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Sheep and goat medicine / [edited by] D.G. Pugh.-1st ed.

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Includes bibliographical references and index.

ISBN-13: 978-0-7216-9052-0 ISBN-10: 0-7216-9052-1

1. Sheep-diseases. 2. Goats-diseases. I. Pugh, D.G. (David G.)

[DNLM: 1. Sheep diseases-therapy. 2. Goat diseases-therapy. 3. Veterinary
medicine. SF 968 S5405 2002]

SF968 .S54 2002

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SHEEP AND GOAT MEDICINE

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C ontributors
David E. Anderson, DVM, MS Virginia R. Fajt, DVM, PhD
Diplomate ACVS Collaborator, Veterinary Antimicrobial Decision Support
Associate Professor, Food Animal Medicine and Surgery System
Department of Veterinary Clinical Sciences Animal Medicine
College of Veterinary Medicine College of Veterinary Medicine
The Ohio State University Iowa State University
Columbus, Ohio Ames, Iowa
A.N. Baird, DVM, MS Alan M. Heath, DVM, MS
Diplomate ACVS Diplomate ACT
Associate Professor, Veterinary Clinical Sciences Assistant Professor, Department of Clinical Sciences
Purdue University College of Veterinary Medicine
West Lafayette, Indiana Auburn University, Alabama
Ellen B. Belknap, DVM, MS Bruce L. Hull, DVM, MS
Diplomate ACVIM Diplomate ACVS
Associate Clinical Professor, Department of Clinical Professor and Head, Food Animal Medicine and Surgery
Sciences College of Veterinary Medicine
College of Veterinary Medicine The Ohio State University
Auburn University, Alabama Columbus, Ohio
Christopher Cebra, VMD, MA, MS Hui-Chu Lin, DVM, MS
Diplomate ACVIM Diplomate ACVA
Department of Large Animal Clinical Sciences Associate Professor, Department of Clinical Sciences
College of Veterinary Medicine College of Veterinary Medicine
Oregon State University Auburn University, Alabama
Corvallis, Oregon
Michael Q. Lowder, DVM, MS
Margaret Cebra, VMD, MS Diplomate ABVP
Diplomate ACVIM Associate Professor, Department of Large Animal
Philomoth, Oregon Medicine
College of Veterinary Medicine
Undine Christmann, DMV University of Georgia
Large Animal Internal Medicine Athens, Georgia
Department of Clinical Sciences
College of Veterinary Medicine Margo R. Machen, DVM, PhD
Auburn University, Alabama Associate Professor, Department of Clinical Sciences
College of Veterinary Medicine, Nursing, and Allied
Carmen M.H. Colitz, DVM, PhD Health
Diplomate ACVO Tuskegee University
Assistant Professor of Ophthalmology Tuskegee, Alabama
School of Veterinary Medicine
Louisiana State University David McKenzie, DVM, MS
Baton Rouge, Louisiana Assistant Professor, Department of Clinical Sciences
School of Veterinary Medicine
Barbara C. Diffay, DVM Tuskegee University
Special Assistant to the Dean Tuskegee, Alabama
College of Veterinary Medicine, Nursing, and Allied
Health
Tuskegee University
Tuskegee, Alabama

• v •
vi • C ontributors
Seyedmehdi Mobini, DVM, MS Debra C. Ruffin, DVM, MS
Diplomate ACT Diplomate ACVIM
Professor of Veterinary Science Department of Clinical Sciences
Research and Extension Veterinarian College of Veterinary Medicine
Georgia Small Ruminant Research and Extension Center Auburn University, Alabama
Agricultural Research Station
College of Agriculture, Home Economics, and Allied Bryan M. Waldridge, DVM, MS
Programs Diplomate ABVP
Fort Valley State University Department of Clinical Sciences, Equine Section
Fort Valley, Georgia College of Veterinary Medicine
Auburn University, Alabama
Christine B. Navarre, DVM, MS
Diplomate ACVIM Lisa Helen Williamson, DVM, MS
Associate Professor, Food Animal Section Diplomate ACVIM
Department of Clinical Science Associate Professor, Department of Large Animal
College of Veterinary Medicine Medicine
Auburn University, Alabama College of Veterinary Medicine
University of Georgia
Darrell L. Rankins, Jr., PhD Athens, Georgia
Associate Professor, Department of Animal and Dairy
Sciences Cindy Wolf, DVM, MS
College of Agriculture Small Ruminant Clinical Specialist
Auburn University, Alabama Department of Clinical and Population Sciences
College of Veterinary Medicine
Laura K. Reilly, VMD University of Minnesota
Diplomate ACVIM St. Paul, Minnesota
Adjunct Assistant Professor of Medicine,
New Bolton Center
University of Pennsylvania
Kennett Square, Pennsylvania

D. Michael Rings, DVM, MS

Diplomate ACVIM
Professor, Food Animal Medicine and Surgery
Department of Veterinary Clinical Sciences
College of Veterinary Medicine
The Ohio State University
Columbus, Ohio
ToJack and Terry, who raised my sister, brother, and me to do the best we could in
order to glorifY the Lord

ToJayne, my soul mate, bestfriend, and love if my life.

To Rebekah, Natalie, and Dylan, who are truly giftsfrom God They give me a
wonderful desire to work hard
Preface
The desire to work with and learn about goats and sheep ers of sheep (Drs. Wolf, Navarre, and Rankins) and goats
can be traced to my life well before veterinary school. The (Drs. Mobini, Diffay, Waldridge, Navarre, and Rankins).
first animals I ever purchased with my own money were In addition, I tried to ensure that the writers repre-
two cross-bred Nubian goats, and the first animal I traded sented different areas of North America so as to bring both
work for was a Hampshire ewe. Over the years my family geographic and production perspectives to the contents of
and I have been involved before and after veterinary grad- this text (Northeast—Dr. Reilly; Northwest—Drs. Cebra
uation as sheep breeders, in sheep 4-H and FFA showing, and Cebra; Midwest—Drs. Anderson, Baird, Hull, Rings,
as meat goat breeders, and as pet goat and sheep owners. and Wolf; and Southeast—Drs. Navarre, Belknap, Diffay,
As a veterinarian both in private and academic practice, Mobini, Heath, Rankins, Ruffin, Lin, and Williamson).
my primary interest has been in small ruminants. Over Although the book is entitled Sheep and Goat Medicine,
the years several good books on either goat or sheep med- it covers surgical and diagnostic procedures, basic nutri-
icine have been published. Chapters in discipline- tion, diet formulations, theriogenology, ophthalmology,
oriented texts deal with disease, surgery, or reproduction and anesthesiology. The book is designed so the private
of sheep and/or goats. However, I have always thought it practitioner, academic clinician, graduate student, veteri-
difficult to find information dealing with the whole of nary student, animal scientist, and some producers can
sheep and goat medicine, surgery, reproduction, and nu- easily access applicable information. To enhance the
trition in a single text. This is where the roots of this book reader’s ability to use this book as a reference, I tried to
began—as an attempt to fill that void. As a faculty incorporate as many pictures, charts, and tables as space
member and small ruminant clinician at Auburn Univer- would allow.
sity, the phone calls I receive from other university clini- The book includes 17 chapters and 3 appendices. The
cians, practicing veterinarians, and producers are based on first chapter (on handling and examination of sheep and
an inability to easily locate applicable information. The goats) and the last chapter (on flock health) are the only
goal of this book is to provide a text on sheep and goat two chapters in which sheep and goats are discussed com-
medicine, nutrition, surgery, and theriogenology in an pletely separately. Because of specific concerns in restraint
easily usable form. and examination as part of a health care program, I felt it
When W.B. Saunders first contacted me, I was appre- was better to discuss the two species separately in these
hensive about committing to such a major undertaking. I two chapters. Dr. Cindy Wolf, an excellent clinician, aca-
knew I would be unable to write this book alone. I con- demician, and sheep producer, wrote much of the sheep
tacted people I knew would be able to bring a wide range sections of those two chapters. My good friend and col-
of experience and ability to their writing. I am proud that league, Dr. Seyedmehdi Mobini, wrote the bulk of the
several former veterinary or graduate students who rode goat sections of the last chapter, and Drs. Barbara C.
in ambulatory trucks with me (Drs. Cindy Wolf, Ellen B. Diffay and David McKenzie wrote most of the physical
Belknap, Alan M. Heath, Bryan M. Waldridge, Virginia examination and handling information on goats for the
R. Fajt, and Michael Q. Lowder) and who have gone on first chapter. Dr. Diffay has spearheaded goat 4-H proj-
after graduation to excel in large animal medicine and ects in Alabama and is the veterinary advisor to the
practice and become experts in a wide range of disciplines Alabama Meat Goat Association. Dr. McKenzie is a very
are included as authors. I also asked colleagues at Auburn fine clinician at Tuskegee University.
University (Drs. Christine B. Navarre, Alan M. Heath, In portions of Chapter 2 (Feeding and Nutrition) and
Debra C. Ruffin, Ellen B. Belknap, Hui-Chu Lin, and Chapter 6 (Theriogenology of Sheep and Goats), sheep
Bryan M. Waldridge) to help me in this endeavor. I in- and goats are discussed separately, but only in situations
cluded clinicians with a sheep focus (Drs. Wolf and where the topic material does not apply to both.
Heath), those who focus on goats (Drs. Diffay, Throughout the remaining chapters and appendices,
Waldridge, and Mobini), and academicians who treat sheep and goats are discussed together.
them both (Drs. Ring, Machen, Anderson, Hull, Three appendices are included in the book to provide
Belknap, Navarre, Christopher and Margaret Cebra, quick reference information for the reader. Appendix I
Reilly, Baird, and Williamson). I also included profes- provides drug dosage information, Appendix II helps the
sionals with specific specialty areas (Drs. Lin [anesthe- reader administer fluid therapy, and Appendix III lists
sia], Colitz [ophthalmology], and Rankins [nutrition]). normal clinical diagnostic values.
Also included were those who had practical experience in Chapter 2 includes information on ways to formulate
production, not only as veterinarians, but also as produc- and implement a total parenteral nutrition program, three
• ix •
x • Preface
methods for balancing a ration using a hand-held calcula- Ruffin, and Belknap (as well as Dr. Bob Carson, therioge-
tor, and ways to balance the mineral component of the nologist extraordinaire), who were my constant sounding
diet. boards throughout the book’s writing and editing. In ad-
Drs. Christopher and Margaret Cebra took on the dition, Dr. Gatz Riddell helped in the review of Chapter
arduous task of writing the catch-all chapter (Chapter 13 (Diseases of the Mammary Gland) and Dr. Chris
14—Diseases of the Hematologic, Immunologic, and Johnson helped review Chapter 9 (Diseases of the Mus-
Lymphatic Systems [Multisystem Diseases]). It covers culoskeletal System). All of these colleagues gave me
some of the same diseases discussed elsewhere, albeit valuable insight and criticism that greatly improved the
from a systemic viewpoint. The two chapters by Drs. final version of the book.
Cebra and Cebra and the chapters by Drs. Waldridge and Special thanks go to those who helped me with orga-
Colitz (Diseases of the Ophthalmologic System) and Dr. nizing, typing, and laying out the book: Debbie Burelle at
Belknap (Diseases of the Respiratory System) were Auburn University’s College of Veterinary Medicine and
written solely by those authors. I served as editor and my dear wife, Jayne Pugh. These ladies deserve the best
layout designer only. All these folks did an outstanding “thank you” I can offer because they worked tirelessly on
job. this endeavor. The staff at the Learning Resource Center
The rest of the book chapters have my “fingerprints” at Auburn University helped with pictures and drawings.
all over them. I was fearful that the book might too Last but by no means least important, I want to thank
closely reflect my personal ideas and experiences as a my teachers in veterinary and graduate school that have
sheep and goat producer and veterinarian. However, I had a profound influence on my life and career. They
truly believe that the co-authors have balanced out the include Drs. Dilmus Blackmon, John McCormack, and
text with their collective expertise. In the final months of the late Tom McDaniel, all of whom taught me in veteri-
preparation the original author of Chapter 11 (Diseases nary school at the University of Georgia, as well as Dr.
of the Neurologic System) had to step down due to other Ronnie Elmore, who directed me as a resident at Texas
commitments. With less than 2 months before the book A & M University. Also, I want to thank Dr. LaRue
was due to the publisher, Dr. Margo R. Machen took on Johnson, from whom I learn something new every time
the task of coordinating and writing much of the chapter. we talk. These gentlemen are my mentors in veterinary
I cannot thank her enough for the outstanding job she medicine and over time and space have greatly influenced
did putting this chapter together with little notice. the writing and editing of this book more than they will
I wish to thank all of the contributing authors who put ever know.
up with my constant hounding to complete their portions
of the book; none complained and all worked very hard! I
want to give special thanks to Drs. Navarre, Heath, D.G. Pugh
 Chapter 1

Hof Sheep
andling and Examination
and Goats
BARBARA C. DIFFAY, DAVID M C KENZIE, CINDY WOLF, AND D.G. PUGH

PHYSICAL EXAMINATION
Purchase and source(s)
OF SHEEP Transportation history
The clinician should note the signalment of the sheep at Stays off the premises (e.g., shows and fairs, breeding)
the start of the examination. Signalment is a significant Feeding and watering history, including consistency
part of the examination process because certain differen- Water source
tial diagnoses are more common in sheep of a particular Management (grazing or confined)
age, breed, pregnancy status or stage, or sex. Although Procedural history (vaccinations, castration, docking,
this statement may seem obvious, it bears repeating— drenching)
consideration of the signalment often provides the practi- Stage of pregnancy or lactation
tioner with information useful in prioritizing the list of
differential diagnoses.
Specific body systems may require further clinical
Handling Before and During Examination
scrutiny after the initial examination. This is especially A good understanding of normal sheep behavior is useful
important if the system in question was difficult to assess when working with this species. Taking advantage of
during the first examination. For example, a 5-month- their desire to escape is a fundamental part of successful
old, crossbred wether that weighs 110 pounds and is on handling. Sheep will readily follow one another; will
ad lib feed (95% concentrate) in a feedlot presents with move away from things that frighten them; will move
the complaint of being off feed. Obstruction of the better around slight corners or curves; will move away
urethra caused by urolithiasis is a high-ranking differen- from buildings; prefer to move uphill; prefer lighted areas
tial diagnosis, but the diagnosis may be missed if no uri- and resist dark barns, alleys, and chutes; and will respond
nation or straining is noted on the initial physical exami- to well-trained herding dogs. Handling areas should be
nation. Reexamination as clinical signs worsen may yield well lighted and free of objects that may project shadows
the correct diagnosis at a later time. into the animals’ visual path and should have solid sides.
The art of taking a useful history improves with For ease in catching an individual animal, the clinician
experience. The clinician should avoid asking leading should first move the group into a small yard or enclo-
questions. Questions need to be thorough enough to sure. The wool or hair should not be grabbed. A crook or
address all important points, but not so lengthy that they lariat is an acceptable catching device. Regardless of the
inhibit the development of a good relationship with the method of capture, excitement and stress should be
client. When taking an animal’s history, the clinician avoided. A sheep can be handled by various handling
needs to consider the client’s knowledge base. Clients points—for example, under the mandible, tail, and flank
with more experience provide better observations. The (Figure 1-1). After it has been caught, a sheep can be “set
clinician should remember to ask for details regarding up” on its rump for examination, shearing, and foot trim-
the previous treatment history and responses to that ming (Figure 1-2). Dairy sheep and hand-reared, bottle-
treatment. fed lambs are more used to human contact than most
The following elements are particularly important other sheep and as a rule are more curious about and less
parts of the animal’s history: wary of people.
• 1 •
2 • Sheep and Goat Medicine

Figure 1-1 The handler is on the left side of the sheep with his left Figure 1-2 There are many variations to sitting a sheep on its
hand under the jaw and his right hand holding the tail. It would be rump. The left arm should be placed around the animal’s neck at the
acceptable for him to be kneeling with one knee (usually the right) on level of the shoulder. The right hand reaches under the sheep,
the ground and the right hand holding the right rump. grasping the right hindfoot and setting it on its rump.

Mismothering of lambs and ewes can readily occur if dental disease, but inability to feed because of lack of
they are disturbed, particularly during the first few weeks bunk space and bullying is not uncommon. Sheep usually
of life. Handling of lambs and ewes should occur with a chew their cud more rapidly than cattle. Compared with
minimum of stress, and it may be prudent to house the goats, sheep are not as particular about the cleanliness of
pair together during treatment to maintain a strong feeders and waterers. Signs of wool or hair abnormalities
bond. should be noted. Loss of wool may indicate recent stress
from fever, external parasitism, insufficient dietary fiber,
or some neurologic diseases. The animals should be ob-
“Over the Fence” Examinations served for any signs of lameness. Feet and joint abnor-
The flocking instinct in sheep is very strong. Therefore malities are common in sheep flocks. Common nervous
any individual animal that separates itself from the flock signs in sheep include circling, head pressing, and appar-
should be suspect. Sheep are relatively undemonstrative ent blindness.
animals; a sick animal may show few signs apart from A diagnosis of pathology in an individual may alert the
isolation and possibly drooping ears and a decreased clinician to a condition affecting other animals in the
flight response (Table 1-1). Any animal that lags behind flock subclinically. In cases in which no clinical diagnosis
(even for a short distance) when the group is moved can readily be made, the clinician should try to persuade
rapidly should be examined. Abnormal respiratory signs the owner to allow a full necropsy. This is of paramount
may be detected by moving animals rapidly for short importance if a large number of animals are at risk.
periods. In sheep with respiratory disease, both respira- A visual judgment of the body condition of sheep
tory rate and effort increase as the animals are moved— cannot be made if they are carrying a heavy fleece. There-
even at a fast walk. Sheep should be observed for evi- fore the clinician should palpate the dorsal spinous and
dence of diarrhea or soiling of the breech area while on transverse spinous processes of the first lumbar vertebra
pasture. Normal fecal pellets are free of blood and mucus. as well as the loin musculature of several animals in the
Because sheep are either fed as a group or graze pasture, flock to estimate body condition. Open ewes and ewes in
their natural feeding behavior should be observed. Reluc- early pregnancy are often purposely kept in light condi-
tance to feed may result from disease, parasitism, or tion. Nevertheless, emaciated sheep may be heavily para-
 Chapter 1 Handling and Examination of Sheep and Goats • 3

TABLE 1-1

SOME BEHAVIOR PATTERNS OF SHEEP AND GOATS

Behavior Pattern

ACTIVITY SHEEP GOATS

Food preference Grass and succulent herbage Browse (weeds, leaves, and twigs)
Food variety Accept monotonous diet Need variety
Habitat selection Lowlands or hilly grasslands Climb on rocks and elevations
Antagonistic behavior Butt head on Sideways hooking motion
Fighting Butt Rear on hind legs
Sexual behavior Less herding Herding of females
Newborn young behavior Remain by mother (“lying in”) Freezing some distance from mothers
(“lying out”)
Alarm signal Snort and stamp one forefoot Frequent high pitch (“sneeze”)
Alarm Form a compact bunch Form a thin line
Hornless condition Fertile Sterile (usually) in males
Tail Hangs down Stands up (erect)
Beard Absent Present in buck and in some females
Wattles Absent May be present
Hears a low-flying plane Frightened and likely to run herd Often stand and watch
Stress (elevated blood cortisol) Results from isolation or subjection More of a problem with young kids and
to an unfamiliar environment doelings

sitized or suffering from various diseases such as paratu- body condition scores are crucial to flock productivity.
berculosis, caseous lymphadenitis, and ovine progressive Ewes should have a body condition score of 2.5 to 3.5 at
pneumonia (OPP). breeding to achieve an optimal ovulation and lambing
A very strong maternal relationship develops in sheep. rate. Ewes that are overly fat at breeding tend to be open
Most ewes vigorously reject any attempt by other lambs at pregnancy checking.
to suckle, although some (even before lambing) will To assess the body condition score of a sheep, the cli-
“steal” lambs. In North America confined ewes are rou- nician must evaluate four areas of the lumbar region:
tinely “jugged” for as long as 48 hours to ensure maternal
1. The prominence of the dorsal spinous process
bonding. A “jug” is a 4- or 5-square-foot pen in which
2. The prominence of and degree of fat covering on
just-lambed ewes are placed to allow the bonding process
the transverse spinous process
to occur. Nearly all lambs suckle within 2 hours of
3. The amount of muscle and fat under the transverse
birth. Lambs suckle very frequently—at least 60 to 70
spinous process—this is assessed based on the ease
times a day.
with which the examiner’s fingers pass beneath the
The clinician should walk or drive through the grazing
transverse processes
land to examine animals under undisturbed conditions.
4. The fullness of the loin eye muscle (longissimus
Sheep do not graze or defecate randomly but select
dorsi) and degree of fat covering between the
campgrounds (generally under trees and near water) to
transverse and dorsal spinous process
rest and ruminate. In very hot weather sheep tend to
graze more often in the early morning and evening. Sheep must be confined to a pen or chute to allow
adequate palpation for body condition scoring (see
Figure 2-1).
External Examination
Examination for body condition score. Body condi-
tion scoring of sheep is an important management tool.
Examination of Body Systems
The scoring scheme depends on assessing fat and muscle While examining the animal, the clinician may observe a
over and around the first lumbar vertebra. The traditional number of problems. The following paragraphs list and
system uses a six-point system, with a 0 representing discuss some common abnormalities and their associated
emaciation and a 5 representing extreme obesity. Target etiologies.
4 • Sheep and Goat Medicine
Wool and hair. Animals with excess wool should be ex- Crustiness—Crustiness, especially under the dew
amined for wool blindness. Wool-blind sheep or those claws, is a common result of chorioptic mange.
with wool hanging over their eyes have difficulty compet- Sunburn—Animals with white, thin skin can become
ing for feed in unconfined settings. Snow can freeze on sunburned, especially on their udders.
the surface of their wool, making the wool-blindness
more pronounced. Shearing the wool from around the Photosensitization causes head shaking, restlessness,
faces of ewes in the late fall helps ensure better body con- itching, swelling, peeling of white or unprotected por-
dition after a harsh winter. tions of the skin, and sloughing of the tips of the ears.
The ears of older sheep may show damage from torn-out
Wool loss. If the clinician observes wool loss, he or she ear tags or predators. Frostbite often affects the extremi-
must then discern whether it is a generalized or local phe- ties, including the ears, limbs, and tail. Skin damage from
nomenon. Chewing of the wool generally implies a short- freezing appears as swelling followed by the loss of the
age of roughage, particularly if many of the flock are tips of ears, tails, and even distal portions of the limbs.
engaged in this activity. A “break” in the wool indicates a
weakness in the wool fiber at the actively growing site.
This occurs secondary to systemic disease or some
Examination of the Head
marked nutritional stress. Head injuries from fighting are not uncommon in rams,
and these injuries are prone to secondary infections and
Skin disease. The clinician should look for evidence of myiasis. Injuries caused by fighting are most frequently
irritation from ectoparasites (e.g., lice, keds, mange mites, seen during the breeding season, before the rams are put
fly strike), parting the wool for close inspection of the with the ewes, and when new rams are first added to a
skin. Specific sites are usually rubbed and scratched by ram group. Rams do not appear to be able to recognize
sheep with clinical scrapie. In endemic areas, the clini- one another immediately after shearing. Separating rams
cians also should examine for evidence of screw-worms. for 24 hours after shearing may help prevent fight-
Myiasis (fly strike) most commonly affects the perineal associated injuries. Horn growth can impinge on or grow
area, poll, breech, and preputial area. into the skull or eye; horns should therefore be trimmed
when necessary.
Wool changes. If matted wool with exudation is noted The clinician should always look for any signs of
by the clinician, a diagnosis of mycotic dermatitis is likely. dyssymmetry during examination. Nervous dysfunction
If the wool is matted without exudation, the sheep prob- such as a lip droop, an eyelid droop, or a tongue deviation
ably have more than 1 year of wool growth or have been often results from trauma or listeriosis. Any facial swelling
chronically sick or underfed. With the onset of warm should be evaluated for abscesses secondary to puncture
weather and sweating, wool can become even more wounds, abscessed lymph nodes (Corynebacterium pseudo-
matted. When numerous sheep are found to have a loss of tuberculosis), trauma, hematomas, or seromas.
crimp and their wool takes on a steely appearance, a nu- The eyes should be examined for watery discharge and
trient (copper) deficiency should be suspected. Fleece rot conjunctival inflammation. These conditions may be ap-
results from prolonged wetness accompanied by bacterial parent from a distance as blepharospasm and wet cheeks.
multiplication. Grass seed infestation may occur in The presence of keratoconjunctivitis suggests a conta-
range- and browse-grazing sheep. Hairiness and/or ab- gious condition, especially if the pathology is bilateral and
normal wool pigmentation such as brown fibers over the numerous animals in the group are affected. The animal
nape of the neck in wool sheep may indicate border should be examined for signs of anemia (nematode infec-
disease infection. tions), jaundice (copper toxicity), and congestion (fever,
septicemia, toxemia). Certain breeds (e.g., Hampshire)
normally have black pigment in some of the mucous
Hair and Skin in Hair Sheep Breeds membranes, requiring the clinician to use other mucous
Normal shedding—Hair sheep (Barbados, Gulf Coast membranes for examination (sclera, inside the mouth,
Native) shed their winter coat in spring. inside the vulva, inside the prepuce). Entropion, or in-
Pruritus—Mange, allergy, and scrapie are three verted lower eyelid, is a common heritable defect seen in
common causes of pruritus. young lambs. It is often present at birth but not detected
Hair loss—Ringworm, mange, and poor nutrition can until the affected lamb is 1 or more days old. Animals
all result in loss of hair over the entire body or in with entropion are usually brought to the clinician’s at-
small, circumscribed areas. tention because of corneal inflammation. The clinician
Skin nodules—Abscesses, pustules, and demodectic should examine the sheep’s lips and gums for vesicles and
mange cause most skin nodules. scabs. The presence of vesicles is suggestive of contagious
Dandruff—Dandruff and skin flecks are generally ecthyma (sore mouth). Similar lesions also may be found
nonspecific signs of illness or poor nutrition. on the muzzle, around the eyes, near the coronary band,
 Chapter 1 Handling and Examination of Sheep and Goats • 5

on the prepuce, around recently docked tails, and at the The clinician should carefully palpate the abdomens
base of the udder and teats. of young lambs for pain and swelling, particularly in the
umbilical area (omphalophlebitis). The perineal area
Teeth. If any incisors are missing, as is common in aged should be examined for evidence of active diarrhea. The
ewes, the descriptive term is broken mouth. This pathology nature of the diarrhea can be helpful in generating a list
can result in poor body condition in grazing animals, al- of differential diagnoses. The presence of blood may
though lost incisors are less of a problem in sheep being suggest coccidiosis in lambs older than 4 weeks of age. A
fed harvested feedstuffs. Mottling and pitting of enamel foul odor suggests salmonellosis in sheep of any age. Di-
may indicate fluorosis. Grinding of the teeth may indicate arrhea caused by cryptosporidiosis is often grayish-
abdominal pain or nervous disease. The bottom incisors yellow, may contain blood, and usually occurs in 2- to 4-
should meet the upper pad of the mandible. If the molar week-old lambs. Rectal prolapse is not uncommon in
teeth are missing, overgrown, or not apposed, the clini- fattening lambs, especially those whose tails were docked
cian may note poor body condition, draining or fistulous excessively short. Normal rectal temperature in sheep is
tracks from the mandible, or bony enlargement over the 101.8 to 103.5 degrees Fahrenheit (° F), but it may tran-
affected tooth (Figure 1-3). siently exceed 104° F during periods of excitement
Teeth wear varies greatly with diet and soil types. (Table 1-2).
Older sheep develop periodontal disease and are prone to
tooth loss. Molar or cheek teeth are most important to Respiratory system. A clear, bilateral, watery nasal
the welfare of the sheep; they can be examined by careful discharge is relatively common in sheep; it generally
palpation of the cheeks or by using a mouth speculum occurs during times when sheep are housed in poorly
and a light source. However, molar examination may be ventilated buildings. This serous nasal discharge is most
difficult because sheep are unable to open their mouths frequently seen in areas where the temperature fluctuates
very wide and usually resist this type of examination. considerably during the day. Discharge from just one
Replacement breeding stock (ewe and ram lambs) should nostril is less common but can occur with Oestrus ovis
be evaluated for overshot or undershot jaws. Mild cases (nasal bot) infections, tumors, or foreign bodies. Sheep
will not affect the ability to grow and maintain body with nasal bot infections sneeze and have an intermit-
condition, but these animals should not be used for tent, clear serous nasal discharge. Bilateral purulent nasal
breeding. Excessive salivation (ptyalism) may indicate discharge may indicate upper or lower respiratory tract
local irritation caused by glossitis from a foreign body or infection. Bilateral bloody nasal discharge is seen with
trauma; the gingival lesions of contagious ecthyma also some infectious conditions (e.g., anthrax) or after the in-
may produce excessive salivation. An inability to swallow gestion of root crops that have undergone freezing and
because of a neurologic disorder (e.g., tetanus, rabies) is thawing before consumption. Sheep that have pneumo-
another cause of ptyalism. Nasal bot migration may nia cough intermittently, have an elevated respiratory rate
result in sneezing and serous nasal discharge. A cyanotic (above 20 breaths per minute), and may show increased
tongue is strongly suggestive of bluetongue especially if it respiratory effort. Pneumonia is more common in young
occurs in regions of the country where the disease is and very old animals. The normal respiratory rate for a
prevalent. healthy unexcited sheep is 12 to 20 breaths per minute
(see Table 1-2).
Body Systems Cardiovascular system. Damp wool can make auscul-
Digestive system. The clinician should palpate the tation difficult. Therefore the clinician should attempt
pharynx for injuries, particularly those that may result the heart examination in a quiet area with the use of a
from improper use of drenching equipment. Bloat often good quality stethoscope. The normal heart rate for a
occurs in sheep, especially those with diets high in healthy unexcited sheep is 70 to 80 beats per minute. The
legumes (alfalfa). Anesthetized sheep should be evaluated pulse can best be evaluated by palpating the femoral
throughout anesthesia for the development of bloat, artery on the medial aspect of the rear leg (see Table 1-2).
which may impinge on their ability to breathe. Usually, if
a handful of skin can be grabbed in the left paralumbar Urinary system. Urine samples can usually be obtained
fossa, the sheep is not bloated sufficiently to affect respi- from ewes by briefly occluding their nostrils. The urethral
ration. If the skin cannot be grabbed, the bloat should process of a male can be examined after the ram lamb
promptly be relieved to prevent respiratory arrest. Normal reaches puberty and the preputial adhesions have de-
rumen contractions for sheep occur at the rate of one or tached. Placing the ram in a sitting position and manually
two per minute. Percussion of the abdomen is rarely as reflecting the prepuce caudally allows exteriorization of
useful in sheep as in cattle because sheep do not usually the penis. A gauze placed around the penile shaft makes
develop the gas-filled viscus (displaced abomasum) that is grasping and examination easier. Uroliths can occasion-
commonly noted in dairy cattle. ally be palpated and/or seen in the urethral process.
6 • Sheep and Goat Medicine

A B

C D

E F

Figure 1-3 The dentition of sheep. A, Dentition at 6 months to 1 year. B, Dentition at 1 to 1.5 years.
C, Dentition of a 2-year-old. D, Dentition of a 3-year-old. E, Dentition of a 4-year-old. F, Dentition of an aged
or a broken-mouthed ewe.
 Chapter 1 Handling and Examination of Sheep and Goats • 7

TABLE 1-2

SOME PHYSIOLOGIC PARAMETERS OF SHEEP AND GOATS

PARAMETER SHEEP GOATS

Rectal temperatures (vary according to 102° F (with a range of 101.5° 102° to 104° F
ambient temperatures and fleece or to 104° F)
hair coat)
Ruminations 2 per minute 1 to 2 per minute
Pulse 70 to 80 beats per minute 70 to 90 beats per minute
Respiration 12 to 20 breaths per minute 15 to 30 breaths per minute
Puberty 5 to 12 months 4 to 12 months
Estrus 36 hours 12 to 24 hours
Estrus cycle 16 to 17 days 18 to 23 days
Gestation 147 days 150 days
Average birth weight Breed dependent Breed dependent
Single 8 to 13 pounds
Twins 7 to 10 pounds
Fleece weight 7 to 15 pounds

Passing a catheter in male sheep is difficult because of the rams—presumably because of a previous subclinical
presence of the urethral diverticulum where the urethra episode of urolithiasis or trauma. The urethral process
crosses the caudal border of the pelvic floor. Dribbling of may slough secondary to urolithiasis. Vaginal prolapse is
urine, abdominal straining, or urethral pulsing noted on seen in ewes in the last 2 weeks of pregnancy. If the pro-
digital palpation of the rectum all indicate urethral ob- lapse is not replaced within approximately 12 hours, it
struction. As urolithiasis progresses, abdominal disten- may enlarge to contain the bladder, the cervix may be
sion develops. Enlarged urinary bladders can be visual- traumatized, and the mucus plug may be disrupted. All
ized by ultrasonographic examination, and urine may be ewes with a vaginal prolapse should be carefully moni-
drained by cystocentesis. If the urethra remains ob- tored for anorexia, depression, and ascending uterine in-
structed, the urethra and bladder will usually rupture. fection. Such infections are usually fatal for the fetus and
Scabs or ulceration on the prepuce may indicate ulcera- can result in toxemia and death of the ewe. Uterine dis-
tive posthitis. This condition is most commonly found in charge or lochia is normally seen after lambing for up to 3
wethers being fed high concentrations of protein. weeks. Normal lochia should be reddish-brown in color
and nonodorous. Any other discharge from the vagina
Genital system. The scrotum should be examined by warrants further evaluation and may indicate an abortion.
palpating its contents and noting its external appearance. Ewes that have recently aborted should be considered in-
The skin and wool or hair covering should be intact and fectious to other animals and should be examined and
uniform. A ram’s scrotum can have chorioptic mange in- quarantined.
festations, localized injuries, frostbite, and hernias. Close Sheep are seasonal breeders. In the Midwest, breeding
examination helps detect these abnormalities. The testes season begins in late summer and continues throughout
and epididymes must be palpated carefully for abnormal- the fall, with lambing in late winter and spring. The
ities of shape (epididymitis), size (orchitis, hypoplasia), breeding season and lambing period in other locales is
freedom of movement in the scrotum (adhesions, sper- based on season and demand for sales and markets.
matocele or varicocele, abscesses), and turgidity (poor tes-
ticular tone is usually associated with suboptimal sperm Mammary glands. If a lamb is starving or a ewe resists
production). The phrase that “big is beautiful, mobility suckling by her own lamb, the clinician should carefully
meaningful, resilience respectable, softness suspicious” is examine the udder for bilateral symmetry and abnor-
helpful to remember when evaluating rams for breeding malities of color, pliability, temperature, turgidity, and
soundness. Rams selected for breeding should always volume of milk produced. Both teats should be evalu-
have symmetric scrotal contents and meet the breed and ated for patency and milk flow. A physiologic prepartal
age criteria for scrotal circumference measurements (see udder edema occurs in some sheep. A diffusely hard or
Chapter 6). The urethral process is normally visible at the firm udder in the first few days after lambing may indi-
end of the penis. This structure may be absent in some cate OPP. Affected glands secrete scant quantities of
8 • Sheep and Goat Medicine
normal-appearing milk. No signs of inflammation are toxemia exhibit ataxia and blindness. Sheep observed in
present in most cases of OPP, and both glands are equally sternal recumbency with the head deviated toward the
affected. The udder should be carefully palpated for evi- flank may be hypocalcemic, severely anemic, or pro-
dence of acute or chronic bacterial mastitis lesions. Mas- foundly dehydrated and acidotic (secondary to rumen
titis generally affects only one gland. Abscesses com- acidosis), or may suffer from meningitis. When sheep
monly form as a result of chronic mastitis. A California circle to one side, the practitioner must consider listerio-
Mastitis Test (CMT) is useful for diagnosing the condi- sis, brain abscesses, and parasitic lesions. Sheep with grass
tion. The first sign of acute bacterial mastitis may be an tetany (hypomagnesemia) generally stagger. Hypomag-
abduction of the rear leg in order to minimize contact nesemic animals are often grazing rich, fast-growing
with the inflamed gland. This is often perceived as lame- forage. Ataxia in lambs may be caused by copper defi-
ness. Contagious ecythma, udder impetigo, and bites or ciency, spinal abscesses resulting from an ascending tail
abrasions from suckling can cause external lesions at the docking infection, nematode larval migration (Para-
base of the udder or on the teats. Lamb-induced injuries lephastrongyles tenuis), or trauma.
often occur on the medial aspect of the teat, and generally Tetanus is common on some farms. Affected sheep
at the base of the udder. initially demonstrate a localized stiffness such as a semi-
erect tail, erect ears, and prolapsed third eyelids. As the
Locomotor system. The stance and gait should be disease progresses, the animal’s entire body becomes stiff
carefully observed. Sheep should be forced to walk away and goes into tetanic spasms secondary to external stimu-
from the examiner. Observation from the side greatly aids lation. Affected animals also develop opisthotonos. Sheep
in diagnosis. Lameness is best determined with the usually have the paralytic form of rabies rather than the
animal at a walk rather than a run. Difficulty in walking furious form. Pseudorabies also occurs in animals in
or lameness in young lambs can result from septic arthri- direct contact with infected swine. Sheep that are clini-
tis or white muscle disease, among other causes. Arthritis cally affected with scrapie may have an abnormal gait.
can be a problem in older rams and has a variety of Scrapie-infected sheep may bunny hop, be hypermetric
causes. Carpal swellings are commonly seen in older on the rear legs, or have proprioceptive deficits of the
animals; however, some thickening of the skin over the forelimbs. They are generally weak. They also may be
carpi (hygromas) can occur naturally when sheep are emaciated yet interested in eating, have wool rubbed off
housed on hard surfaces. Enlargement of the epiphyseal of their hindquarters and flanks, and may even have areas
areas is seen in lambs with rickets and those that have de- of skin excoriation. Ewes in late pregnancy that have clin-
veloped calluses from healing rib fractures. ical scrapie are often misdiagnosed as having pregnancy
Sheep with footrot commonly graze on their knees. toxemia, and vice versa.
Feet should be examined, pared, and smelled during the
routine examination. Virulent footrot produces a charac- Lymphatic system. The superficial lymph nodes of
teristic foul odor. Initially the examiner observes an inter- sheep are hidden beneath their wool and fiber. The clini-
digital dermatitis, followed by necrosis and underrunning cian should palpate them to assess for size and consis-
of horn. The footrot lesions start at the abaxial part of the tency. Lymph nodes that are infected with Corynebac-
heel and move proximally toward the toe. The entire sole terium pseudotuberculosis enlarge and rupture. They drain a
may be underrun and sloughed if the virulent strain of thick yellowish-green, nonodorous purulent fluid. Exter-
Dichelobacter nodosus is present or if affected sheep do not nal lymph nodes that should be palpated during a routine
receive timely treatment. In most cases of footrot, more examination include the mandibular, parotid, retro-
than one foot is affected; the condition more commonly pharyngeal, prescapular, prefemoral, supramammary, and
affects the front feet. Secondary myiasis is a common popliteal lymph nodes. The internal lymph nodes can
finding during fly season in some parts of North only be evaluated by ultrasound and radiographic exami-
America. nation or necropsy examination.
Acute pain and swelling often accompany foot ab-
scesses. Over time, suppuration occurs, often on the
lateral aspect of the coronary band of the affected claw.
Examination of the Environment
Foot abscesses usually affect only one foot. Abscess of the The clinician should evaluate the environment for its
foot is a sporadic condition, whereas footrot occurs in fitness for the particular group of sheep. Questions to
outbreaks. consider include: Does the environment contain an ap-
propriate diet and water source? Does it provide suitable
Nervous system. To begin an evaluation of the nervous shelter? Do the sheep have enough space to meet their
system, the clinician should observe the sheep carefully needs? The practitioner must be familiar with the needs
from a distance. Behavioral abnormalities may be associ- of the particular production group to answer these ques-
ated with either primary nervous system disease or a tions correctly. Objective data such as a forage analysis
metabolic condition. For example, ewes with pregnancy may be required to address the group’s needs.
 Chapter 1 Handling and Examination of Sheep and Goats • 9

Examination of the Ration ties. Poorly designed and maintained facilities contribute
Many producers describe the diet of their sheep in terms of to inefficiency and can lead to livestock and human in-
buckets of grain and bales of hay fed per day. Practitioners juries and loss of time and money. When performing vet-
should work to help clients discuss the sheep diets as follows: erinary procedures, the clinician must recognize the po-
tential for zoonoses. An assessment of the herd’s health
• Production group being fed such diet
status through histories and physical examinations guards
• Number of sheep in that group
clinicians, technicians, and farm personnel and families
• Average body condition score and body weight
against zoonotic infections.
• Pounds of grain fed per day
Stress and trauma to the livestock are to be avoided.
• Feed analysis of that grain
Producers who are able to have frequent, nonthreatening
• Pounds of hay (or other roughage source such as
interactions with their goats will reduce the herd’s appre-
haylage or silage) given and consumed each day
hension of being handled.
• Forage analysis of the hay
• Availability, form, and analysis of trace mineral salt
The water source and its cleanliness and delivery
Physical Restraint
system also are important features of the diet. The When planning procedures that require physical restraint
amount of roughage fed compared with the amount con- of goats, practitioners should consider the layout and sur-
sumed is not the same because of wastage, which varies roundings of the working facility, the physical condition
depending on the quality and feed delivery system. and temperament of the animals, and human and animal
Placing feed on the ground or in some styles of round safety. One person can easily restrain and carry out
bale feeders generally results in more wastage than certain procedures on goats that have been frequently
feeding in sheep-proof bunks and collapsing bale feeders. handled in a quiet, nonaggressive manner. However, for
efficiency and safety, when goats have had only occasional
human contact, animal restraint and procedures should
Necropsy Findings be performed with an assistant. If a goat has been mis-
Wherever possible, the practitioner should perform handled, it will be wary of future attempts to confine and
necropsy on recently dead sheep. The gross necropsy find- constrain it. Patience and an easygoing manner of treat-
ings of a thin adult sheep with no well-described signs is ment hold rewards for the clinician.
frequently sufficient to make a diagnosis regarding the
cause of weight loss. If no gross lesions are evident, major Restraint for Physical Examination
tissues (fresh and fixed) should be submitted to a diagnostic
laboratory for further investigation. The practitioner can To catch and lead a goat, it is acceptable to use the horns,
improve the chance for a diagnosis by providing a thorough beard, collar, or halter (Figure 1-4). The techniques of
case history and requesting specific tests where indicated.

F URTHER READING
Hindson JC, Winter AC: Outline of clinical diagnosis in sheep, Cam-
bridge, MA, 1996, Blackwell Science.
Martin WB, Aitken ID: Diseases in sheep, ed 3, Malden, MA, 1999,
Blackwell Scientific.
Boden E: Sheep and goat practice, London, 1991, Bailliere Tindall Pub-
lishing.
Leahy J, Barrow P: Restraint of animals, Ithaca, NY, 1953, Cornell
Campus Store.

RESTRAINT AND HANDLING

OF GOATS
Safety and Health Considerations
According to the United States Department of Agricul-
ture, agriculture ranks as one of the three most hazardous Figure 1-4 Goats can be restrained by their horns, if the handler
grasps near the skin and keeps the rear of the animal under control.
industries in the United States along with mining and If the handler does not control the animal’s rear and the goat flips
construction. The safety and welfare of animals and per- around, it may injure its neck. Grasping the horn near the tip may
sonnel must be considered when planning working facili- result in breaking the horn and possibly fracturing the skull.
10 • Sheep and Goat Medicine
looping an arm around the goat’s neck or grabbing its After the head is stabilized, the goat’s ears, eyes, nose,
gastrocnemius tendon can be used to catch and hold a and mouth can be inspected. For an oral examination, the
goat (Figure 1-5). A goat being held by a hind limb may use of a speculum is recommended to ensure a clear view
possibly dislocate a hip joint in an attempt to jerk itself of the oral cavity and prevent the goat from biting instru-
free. Goats find restraint by their ears painful and owners ments or the clinician’s fingers.
consider it abusive.
The use of an assistant or restraining devices facilitates
physical examinations, vaccinations, blood collections, ar-
Restraint for Administration of Medications
tificial insemination, hoof trimming, and other proce- The administration of oral and injectable medications
dures. Equipment such as stanchions, tilt tables, squeeze and the collection of blood samples are best accomplished
chutes, cages, and raceways can be used. Some procedures by positioning the goat as described previously for physi-
can be completed while an assistant steadies the goat cal examination and head restraint.
against a wall or fence by firmly holding a leg against the
goat’s flank or thorax behind its elbow. A handler can Oral drugs. When drenching, dispensing boluses, or
gently flip, place, and then hold a goat in lateral recum- passing an orogastric tube, the clinician should hold
bency by placing a knee on the goat’s neck. Another the goat’s head in a straight, natural position with the
useful strategy is to have the handler straddle the goat, mandible parallel to the ground. The dose syringe is
then back it into a corner and firmly press his or her knees inserted well into the cheek pouch via the commissure
against the goat’s shoulders or neck. Kids weighing up to of the lips. The goat must be given time to swallow
30 pounds that are used to being handled can be placed as the fluid is slowly dispensed. Tilting the head upward
with their legs folded under them on the lap of an assis- can lead to aspiration pneumonia. To safely and prop-
tant while the clinician examines the head of the kid. erly place a bolus, the clinician moves the balling gun
over the base of the tongue, but not into the pharynx.
After administering the tablet, the clinician maintains
Restraint of the Head the position of the head and holds the goat’s mouth
While straddling the goat’s withers or neck, the clinician closed until the goat swallows. This prevents the animal
can control the animal’s head by gripping its cheeks, beard, from spitting out the medication. Using a speculum,
or horns. One method for head restraint is to place one the clinician can pass a 1.2- to 1.5-cm diameter stomach
hand on each cheek and wrap the fingers under the tube through the mouth of an adult goat. An 8 French
mandible, being careful to avoid pressure on the trachea. red rubber urethral catheter with an attached 60-cc
Alternatively, the clinician can hold the beard with one catheter-tip syringe can be used as an orogastric tube
hand and wrap the other arm around the goat’s neck. A to feed or provide oral medications to very young and
third method involves gripping the horns. The ability to weak kids.
control a horned goat’s head depends on the temperament
of the goat as well as the skill and strength of the handler. Injectable drugs. The veterinarian should ask the
owner the purpose for which he raises the goats (e.g.,
leather, meat, breeding, exhibition, pet). Reactions to vac-
cines and antibiotics can cause lesions in commercially
valuable skin and muscle and cosmetic flaws in hobby,
pet, and show goats. Meat producers prefer that injec-
tions be placed in the neck, a meat cut of low value.
Breeders prefer the axilla, where a nodular mass of scar
tissue is not visible and cannot be readily mistaken for
caseous lymphadenitis.

INTRAMUSCULAR INJECTIONS: Intramuscular injec-

tions are commonly given in the area of the neck enclosed
by the cervical vertebrae ventrally, nuchal ligament dor-
sally, and shoulder caudally. Other muscles used for injec-
tions include the longissimus in the lumbar region as well
as the gluteals, semitendinosus, semimembranous, and
triceps (Figure 1-6). The clinician must pay special atten-
tion to the location of the sciatic nerve in the thighs
Figure 1-5 In this case the handler uses his left hand to hold the
jaw–throat latch area and his right hand to hold the tail. If the goat because irritating drugs can cause permanent damage.
tries to free itself, the handler can move the left hand onto the jaw Additionally, the small muscle masses in young goats
and pull the animal closer to help control it. limit the volume of the injectable substance.
 Chapter 1 Handling and Examination of Sheep and Goats • 11

SUBCUTANEOUS INJECTIONS: Subcutaneous injections Before giving intramammary infusions, the clinician
can be given in the axilla or on the chest wall (Figure 1-7). should clean and swab the teat with alcohol. Single-use
The triangular area of the neck described previously also teat cannulae are used for each teat and inserted just deep
is used. However, shot reactions near the prescapular enough to gain entry into the teat cistern. In does with
lymph node may be erroneously diagnosed as caseous small teat orifices, sterile tomcat catheters can be used to
lymphadenitis. infuse medications.

ADDITIONAL INJECTION ROUTES: The jugular vein is

often used to administer intravenous drugs and collect
Restraint for Hoof Trimming
blood samples. It is advisable to use a 4-cm, 20-gauge With the goat standing, the clinician flexes the pastern
needle for venipuncture. Intradermal injections call for and raises the foot and limb until the sole faces upward.
1.8-cm, 25-gauge tuberculin needles. Intraperitoneal in- The clinician can then work facing the head or tail of the
jections, primarily used in neonates, are given with 1-inch, goat while positioned at the animal’s side (Figure 1-8).
18- or 20-gauge needles inserted no deeper than 1.8 cm. An assistant can hold the goat, place the goat in a stan-
While the kid is held hanging by its front legs, the clini- chion, or halter tie the goat while the clinician trims the
cian inserts the needle perpendicular to the skin about 1 hooves. In caring for fractious animals, sitting them on
cm to the left of the navel. their rump (as is done with sheep) may be useful.

Facilities
An important goal of well-planned working facilities is to
gather, restrain, and handle animals with minimal stress
and prevent injuries to animals and personnel.

Fencing. Fencing is used to confine stock, separate

animals into management subgroups, exclude predators,
and protect ornamental and commercial crops from con-
sumption by goats. The selection of appropriate fencing
material is dictated by purpose, size, and cost. When
planning permanent enclosures, owners may want to
consult fence contractors and suppliers of commercial
handling equipment, as well as other goat keepers who
may have proven ideas for consideration. Smooth-wire,
Figure 1-6 An injection is being made into the high-tensile, multiple-strand electric fencing deters goats
semimembranosus/semitendinosus area. Injections in this area can
and predators alike and is easily maintained. However, if
result in lameness from local muscle irritation or nerve damage.
However, this is a good intramuscular injection site in animals not
being raised for meat if a large volume of medication is required.
Other preferred sites, particularly for small dose volumes, are
indicated by the arrows.

Figure 1-8 Goats can be restrained in a variety of ways for hoof

trimming. In this case the handler is restraining the goat by pressing
his left and right legs and knees into the goat’s side while pressing the
Figure 1-7 Administering a subcutaneous injection in the chest left arm and elbow into the goat’s shoulders and neck. The left hand is
region of a goat. holding the foot and the right hand is doing the trimming.
12 • Sheep and Goat Medicine
the power source fails, goats may find freedom by step- spring. Housing for does at parturition enables the goat
ping through the wire strands. keeper to manage difficulties experienced by the doe or
Goats can damage field fencing by standing on their her kids in a timely manner. Limiting the doe to a stall
hindlimbs and leaning their front feet against the fence. gives her a quiet, undisturbed environment for bonding, a
A single strand of electric wire placed near the top and crucial event that calls for a minimum of 5 minutes.
bottom of a woven wire fence discourages goats from In large herds, it may be impractical to provide indi-
leaning on the fence and may prevent predators from vidual stalls for preparturient does. In such cases, does
crawling underneath. Horned goats, particularly those may be group-penned 2 to 4 weeks before parturition,
with backward-pointing horns, are likely to get caught giving the owner ample opportunity to monitor for po-
when withdrawing their heads from the 6-inch wide by tential problems. Neonates are highly susceptible to
5-inch high spaces in the fencing. This renders the goat hypothermia in cold or wet weather; therefore owners
indefensible against being butted by herd mates or at- should take precautions against their does delivering in
tacked by predators. A possible fatal outcome is strangu- the field.
lation of the entrapped goat. Similarly, a goat can catch its
foot in the open spaces of a chain-link fence and fracture Feed and water. Good feed and water hygienics should
a leg in its struggle to free itself. be practiced to promote healthy goats and reduce wastage
Although welded-wire panels can withstand the pres- of feed. In contrast to tales of tin can–eating goats, goats
sure of goats, they can entrap horned goats if the panel will decline wet or moldy feed and dirty water. Feedstuffs
openings are the standard size of 8 inches wide by 6 inches should be provided in well-designed troughs that mini-
high. Furthermore, kids weighing less than 15 pounds can mize contamination with feces, urine, and dirt deposited
step through these spaces to escape confinement. Welded- by hooves.
wire panels with openings smaller than 8 inches wide by 4 A 15-inch-long feed trough space can accommodate
inches high can eliminate these concerns. one adult goat. Kids, when penned or pastured with
mature goats, should have free access to a creep feeder, ef-
Housing. Housing facilities provide shelter for live- fectively eliminating competition with adult animals.
stock; storage for feed, equipment, and supplies; and a Bunk space in the creep area should be 10 inches per kid.
work area for routine animal care procedures. Shelter that Despite ample trough space and the use of creep feeders,
provides warmth, shade, and protection from wind, pre- goats low in the herd hierarchy may not be allowed access
cipitation, and predators establishes an environment of to feed. To alleviate the effect of dominance, multiple
comfort and calmness in the herd. Unlike cattle, goats will feeders may be used, or distressed goats can be isolated
interrupt their grazing to seek cover from rain. The shelter and fed individually. Alternatively, goats simultaneously
should promote the productivity and well-being of goats. restrained and fed in individual stanchions or keyhole
Heating and cooling, ventilation, flooring, and water mangers will be unable to dominate or be dominated by
supply should be considered under the guidance of a herd mates.
person knowledgeable and experienced in farm building The volume of water consumed by livestock is influ-
construction. Additionally, space should be planned for enced by the water content of feed sources, environmen-
loafing areas, feed and water troughs, kidding stalls, and tal temperature, and water quality. To encourage con-
shelter for disabled goats and animal groupings specific to sumption, the keeper should offer clean water ad lib.
the facility (e.g., young does and bucks, recently shorn Typical water troughs or self-waterers can be used. In
goats, research study groups). Feed and equipment cold climates the use of water heaters improves intake.
storage areas must be designed to eliminate the potential Adequate drainage should be provided under watering
for consumption of excessive amounts of grain and inges- devices.
tion of stored chemicals.
Floor space alone does not determine adequate living Avoiding drug residues in meat and milk. Veterinari-
space for animals. Enclosure shape, floor type, ceiling ans and goat producers working as a team can ensure that
height, the location and dimensions of feeders and water- only wholesome meat and milk products enter the human
ers, and other physical and social elements affect the use- food chain. Extra-label drug use and chemical contami-
fulness of the space. Mature does require an average of 16 nation of feed and pasture give rise to drug residues in
square feet of stall space, excluding troughs. A buck may products for human consumption. Veterinarians should
need as much as 30 square feet, whereas a kid needs ap- advise their clients on the ethical and legal limitations of
proximately 10 square feet. Shelters in outside pens or not following all labeled guidelines for drugs used in
pastures should allow 5.5 square feet per goat. Fence food-producing animals.
heights vary between 4 to 5 feet for does and 5 to 6 feet Particular effort should be made to educate livestock
for bucks in rut. producers who administer pharmaceuticals without an es-
A clean, dry, draft-free, well-bedded stall or pen is tablished veterinary-client-patient relationship (VCPR).
ideal for kidding and bonding of the dam with her off- Conscientious record keeping is essential in residue avoid-
 Chapter 1 Handling and Examination of Sheep and Goats • 13

ance. Records should include animal identification Forte VA, Jr, Devine JA, Cymerman A: Research stanchion and
numbers; drug names; dates, amounts, and routes of admin- transporter for small ruminants, Lab Anim Sci 38:478, 1988.
istration; withdrawal times; and contact information for the Gubernick DJ: Maternal “imprinting” or maternal “labeling” in goats,
Appl Anim Behav 28:124, 1980.
person who administers treatment. Awareness of potential
Houpt KA: Domestic animal behavior for veterinarians and animal scien-
risk factors for disease and conscientious management prac-
tists, ed 3, 1998, Ames, IA, Iowa State University Press.
tices on the part of the keeper lead to reduced disease inci- Lager K: Apparatus and technique for conditioning goats to repeated
dence and the subsequent need for drug use. In these ways blood collection, Lab Anim Sci 27(3):38, 1998.
an individual owner can ensure that his or her goats are Leahy JR, Barrow P: Restraint of animals, ed 2, Ithaca, NY, 1953,
wholesome and safe to enter the human food chain. Cornell Campus Store.
National Research Council (Grossblatt N, editor): Guide for the care
and use of laboratory animals, Washington, DC, 1996, National
Biosecurity Academy Press.
Sick or injured animals. Goat keepers should provide O’Brien PH: Feral goat home range. Influence of social class and envi-
an area separate from the herd where disabled animals ronmental variables, Appl Anim Behav 12:373, 1984.
can be housed while receiving veterinary and nursing Smith MC, Sherman DM: Goat medicine, Malvern, PA, 1994, Lea &
Febiger.
care. The potential is great for disease transmission to
Sonsthagen TF: Restraint of domestic animals, Goleta, CA, 1991, Amer-
herd mates that may later occupy a previously contami-
ican Veterinary Publications.
nated stall or pen. Consequently, the area reserved for dis- Stricklin WR, Gonyou HW: Housing design based on behavior and
abled animals must be easily cleaned and disinfected after computer simulations. In Stricklin WR, Gonyou HW, editors:
discharge of recovered animals. Animal behavior and the design of livestock and poultry systems, Ithaca,
NY, 1995, Northeast Regional Agricultural Engineering Service.
Introducing new animals to the herd. A pre-purchase
health examination by a veterinarian is an important
aspect of disease prevention and the establishment of a PHYSICAL EXAMINATION
new VCPR. Taking precautions to reduce the risk of in-
troducing disease in a stable herd is a sound business de- OF GOATS
cision that contributes to increased profitability through Clinical diagnosis begins with history taking and the per-
reduced veterinary expenses, time, and effort. formance of a systematic physical examination.
A pre-purchase evaluation includes a health assess- History information obtained from the client falls into
ment of the herd of origin. Based on the history, physical two main categories. The first is the presenting complaint,
examinations, and knowledge of diseases occurring on which includes the duration, onset (acute, chronic, sea-
nearby livestock farms, the veterinarian may perform di- sonal), and associated signs of disease. The second is man-
agnostic tests to assess the health and reproductive agement factors, which include pasture and soil type, diet
soundness of animals offered for sale. and diet changes, sources of water, housing (hygiene, shelter
Veterinarians should advise owners to restrict a re- from weather, ventilation, humidity, temperature), previous
cently purchased goat to clean housing that minimizes diseases, treatments, vaccinations and tests in individual
physical and aerosol contact with the owner’s existing animals or in the herd, recent transportation and introduc-
herd. An isolation period of 4 weeks allows the animal to tions to the herd, and separation of different age groups.
become acclimated to its environment with minimal Physical examination enables the identification and lo-
stress. In addition, the owner is better able to observe the calization of a problem to a particular organ system or
goat for incubating disease conditions, nutritional re- systems. Problem identification is the most crucial compo-
quirements, and behavior patterns. nent of successful diagnosis and treatment. To form an
overall impression of the goat’s general condition, the vet-

F URTHER READING
The American Sheep Industry Association, USDA Extension Service:
erinarian should observe it from a distance. Parameters to
be assessed include posture, gait, body condition and con-
formation, alertness, breathing pattern, and interaction
Producing high quality consumer products from sheep, Englewood, CO, with the herd (sick animals often isolate themselves). The
1995, Colorado State University. animal should then be restrained for the hands-on exami-
Bell HM: Rangeland management for livestock production, ed 2, Norman, nation, which begins at the head and ends at the tail.
OK, 1978, University of Oklahoma Press.
Bowen JS: Bringing quality assurance concepts to goat producers,
Large Animal Practice, p 24, July/August 1997. Head and Neck
Diffay BC: Avoiding introduction of contagious diseases on your goat
farm, fact sheet no. 2, Tuskegee, AL, 1996, Tuskegee University Press. Skin and musculoskeletal systems. The clinician
Federation of Animal Science Societies: Guide for the care and use of should note the general symmetry of the lips, nostrils,
agricultural animals in agricultural research and teaching, Savoy, IL, muzzle, cheeks, eyes, and ears. Next, wearing gloves if
1999, Federation of Animal Science Societies. suspicious of a zoonotic disease, the clinician examines
14 • Sheep and Goat Medicine
the lips and muzzle for raised lesions such as vesicles, caused by gastrointestinal parasitism. Congestion may in-
pustules, crusted lesions (e.g., contagious ecthyma), dicate fever or toxemia. Icterus may be a sign of liver
papules, or nodules (e.g., papillomas). Diseased animals disease, as may repeated yawning (which also is sugges-
often have a dry, rough, and dull hair coat. Matted hairs tive of pregnancy toxemia or hepatic lipidosis).
may be a sign of dermatophilosis. Scratching the base of Prognathism or brachygnathism should be readily ap-
the ears and shaking the head may indicate ear mites, as parent. A soft fluctuant mass in the maxillary region may
may the presence of debris deep within the ear canal. Cir- be a salivary mucocele or retained cud (the differentiation
cumscribed areas of hair loss without pruritus also may is made by oral examination). Submandibular edema sug-
indicate dermatophilosis. Areas of hair loss and excoria- gests hypoproteinemia (such as that caused by gastroin-
tions may be a sign of pruritus. Parting the hairs allows testinal parasitism). A firm mass behind the laryngeal
closer examination of the skin. External parasites and area may be an enlarged thyroid gland secondary to
areas of erythema, hyperpigmentation, and raised lesions iodine deficiency.
should be identified and examined. The clinician should carefully palpate the jugular fur-
The hydration status should be assessed by pinching the rows. The esophagus may be palpable in the left jugular
skin of the upper eyelid and noting the presence or absence furrow if it is distended by a bolus of food or a foreign
of tenting (the upper eyelid should retract rapidly on body.
pinching). Color and vascular engorgement of the sclera
and conjunctiva also are to be evaluated. Reddened con- Respiratory system. Symmetry of airflow from the
junctiva with an ocular discharge suggests keratoconjunc- nostrils can be assessed with the back of the hand or a
tivitis, corneal ulceration, foreign body, or entropion. The feather. Uneven airflow may be caused by a nasal passage
clinician should examine the ears for raised lesions and skin blocked by a foreign body or nasal adenocarcinoma (rare).
color. Erythema of the ear tips in light-skinned breeds sug- The character of any nasal discharge should be noted
gests photodermatitis. Hornless goats should be examined (i.e., consistency, volume, unilateral or bilateral, continu-
to determine whether they are naturally horned (horn buds ous or intermittent). Food and water containers should be
and whorls of hair over the horn buds) or polled (no horn examined for nasal exudate. The appearance of “scalded”
buds and central whorl of hair). The naturally polled phe- skin or hair loss below the nostrils suggests an intermit-
notype may be associated with the intersex genotype. tent discharge. A serous discharge may be a sign of nasal
Wattles may be found in either sex, occurring on the neck inflammation or early viral infection. A mucoid discharge
and sometimes the face and ears. Benign cysts may occa- may result from early pneumonia, lungworm infestation,
sionally be found at the base of the wattles and should not Oestrus ovis larval infection (occasionally seen in goats),
be confused with abscessed lymph nodes. trauma, or abscess formation. A mucopurulent nasal dis-
The male goat commonly urinates on his head and charge may be seen in advanced pneumonia with bacte-
forequarters when sexually aroused. Clinicians should rial superinfection. A hemorrhagic discharge usually in-
wear gloves and protective clothing when handling them. dicates more severe nasal trauma.
The clinician should auscultate the trachea for wheez-
Digestive and gastrointestinal systems. Incisors can ing (collapsed trachea, obstructive lesion) and crackling
be used to determine the age of goats. Deciduous incisors sounds (tracheitis). A cough can be elicited by palpating
erupt as follows: the larynx and squeezing the trachea. A normal animal
coughs once or twice, whereas a diseased animal may
I1 at birth to 1 week
cough repeatedly after tracheal compression. Upper
I2 at 1 to 2 weeks
airway disease (e.g., early pneumonia, foreign body, com-
I3 at 2 to 3 weeks
pressive lesion) is usually characterized by the acute onset
I4 at 3 to 4 weeks
of a loud, harsh, dry, nonproductive cough. Affected goats
Permanent incisors erupt as follows: do not swallow after coughing. Lower airway disease is
usually characterized by a chronic, soft, productive cough.
I1 at 1 to 1.5 years
The goat swallows after coughing and coughs only occa-
I2 at 1.5 to 2 years
sionally. Examples of lower airway disease include
I3 at 2.5 to 3 years
chronic pneumonia, lung abscess, and lungworm infec-
I4 at 3.5 to 4 years
tion. Coughing up blood suggests aspiration pneumonia
Foul breath suggests dental disease (alveolar periostitis or pharyngeal abscess.
or root abscess). Dropping feed from the mouth or con- A foul, rotten breath suggests pharyngitis, laryngitis,
stant drooling of saliva may indicate uneven tooth wear, or fungal pneumonia. A dull sound produced on percus-
stomatitis, or neurologic disease. Regurgitation may sion of the sinus area indicates fluid accumulation caused
result from pharyngeal or esophageal obstruction. Milk by an inflammatory disease (e.g., tooth root abscess
regurgitation in a kid suggests a cleft palate. Pallor of the [maxillary sinuses], infected dehorning site, ascending
conjunctiva and mucous membranes suggests anemia respiratory infection [frontal sinuses]).
 Chapter 1 Handling and Examination of Sheep and Goats • 15

Cardiovascular and hemolymphatic systems. En- The cranial border of the lung field is deep to the
larged submandibular, retropharyngeal, parotid, and triceps, the dorsal border extends from the point of the
prescapular lymph nodes may indicate regional inflam- shoulder to the last rib, and the caudoventral border
mation or abscessation (caseous lymphadenitis). The arches from the point of the elbow to the last rib. The cli-
ears should be warm to the touch. Cold ears may nician can place a stethoscope well forward under the
result from decreased peripheral blood flow (toxemia or triceps to auscultate the cranial lung fields. Because of the
hypocalcemia). goat’s relatively thin chest wall, normal breath and
The clinician should observe and palpate the jugular bronchial sounds are readily detectable and may sound
furrows. In normal animals a jugular pulse may be noted harsh (louder on inspiration than expiration). Bronchial
extending about one third of the distance from the tho- sounds are usually loudest over the craniodorsal lung field
racic inlet toward the mandible. A distended jugular at the level of the tracheal bifurcation. Increased breath
vein with a pulse extending all the way up the neck may sounds suggest the conditions listed previously as causing
indicate congestive heart failure and/or tricuspid valve tachypnea. Decreased breath sounds may be appreciated
insufficiency. with pneumothorax.
Abnormal lung sounds include crackles (air moving
Neurologic systems. Signs of neurologic disease through inflammatory fluid in the airways) and wheezes
include asymmetric pupil size and face, nostril, ear, and (air moving through inflamed, narrowed airways). Respi-
eye positions. Additional signs include depression or hy- ratory conditions causing abnormal lung sounds include
perexcitability, head pressing, facial tremors, and reten- pulmonary edema and pneumonia. Because significant
tion of feed in the buccal pouches (see Chapter 11). lung disease can be present without causing an audible
abnormality, other signs of respiratory disease (e.g., signs
of dyspnea along with fever, cough, and nasal discharge)
Thorax and Forelimbs must be assessed. The clinician should be aware of the in-
terrelationship of the respiratory and cardiovascular
Skin and musculoskeletal systems. Examination of systems; detection of disease in one system warrants
the skin over the thorax and forelimbs is the same as that careful examination of the other.
for the head and neck. Careful observation for abnormal
conformation is crucial for long-term production and Cardiovascular and hemolymphatic systems. Auscul-
survival of animals in range-grazing programs. Goats tation of the heart is performed by slowly moving the
should be observed for gait abnormalities; a goat walking stethoscope over the valves and locating the point of
on its carpi may have footrot or caprine arthritis- maximal intensity. On the left side of the thorax, the cli-
encephalitis (CAE) virus infection. Excessive growth or nician can auscultate the pulmonic valve (low third inter-
wear on the lateral and medial surfaces of each claw costal space, below the elbow), the aortic valve (high
should be noted. The clinician should check the coronary fourth intercostal space, above the elbow), and the left
band for inflammation or separation from the foot and atrioventricular (A-V) or mitral or bicuspid valve (low
assess odors and discharges from the interdigital space. fifth intercostal space, at the level of the elbow). On the
The joints should be palpated for swelling or pain and right side of the thorax the clinician auscultates the right
moved through a full range of motion. Swollen carpi may A-V or tricuspid valve (high fourth intercostal space,
be caused by a carpal hygroma (no pain on manipulation) above the elbow). Rate, rhythm, character, and intensity
or CAE (painful when manipulated). of the heart sounds should be assessed. Tachycardia (the
normal heart rate ranges between 70 to 90 beats per
Respiratory system. The clinician can note the respira- minute in an adult goat and 90 to 150 beats per minute
tory rate without disturbing the goat by observing the in a kid) may occur as a normal condition in young, ru-
movements of the costal arch or nostrils at a distance. The minating, lactating, late-pregnant, or excited goats. Ab-
average respiratory rate for an adult goat is 15 to 30 normal conditions causing tachycardia include anemia,
breaths per minute; kids have a respiratory rate of 20 to 40 congestive heart failure, pain, and inflammation. Brady-
breaths per minute (see Table 1-2). An increased respira- cardia may result from a conduction block (A-V node
tory rate may be a sign of excitement, high environmental block). A sinus arrhythmia is often detectable during late
temperature or humidity, pain, fever, respiratory or cardio- inspiration, and is normal. Abnormal arrhythmias may be
vascular disease, or respiratory compensation for meta- noted (e.g., in atrial fibrillation).
bolic acidosis. A decreased respiratory rate may result
from respiratory compensation for metabolic alkalosis. Neurologic system. Signs of neurologic disease include
The clinician should carefully note signs of dyspnea or incoordination and ataxia, proprioceptive deficits such as
respiratory distress, including tachypnea, extended head knuckling, stumbling, adduction, abduction, circumduc-
and neck, open-mouth breathing, flaring nostrils, ab- tion, abnormal postural placement, and flaccid limbs fol-
ducted elbows, and anal pumping. lowing repeated joint flexion.
16 • Sheep and Goat Medicine
Abdomen males). In urethral obstruction the clinician may note a
solid-feeling distended bladder on deep palpation of the
Skin and musculoskeletal systems. A goat’s body con- caudal abdomen. The left kidney also may be noted on
dition score can be estimated by palpating the lumbar deep palpation of the mid-dorsal abdomen and assessed
vertebrae, rib cage, and sternum (see Chapter 2). Goats for size, shape, and consistency. In young goats the um-
tend to deposit most of their body fat internally, around bilicus should be examined for signs of inflammation
the abdominal viscera, so that an animal in normal health from an umbilical infection or dripping urine from a
may appear thin on lumbar palpation. Examination of the patent urachus.
abdominal skin is essentially the same as that described
for the head and neck.
Pelvis and Hindlimbs
Digestive and gastrointestinal systems. Standing Skin and musculoskeletal systems. The ventrum,
behind the goat, the clinician should observe the contours teats, and genitalia should be examined for papules (papil-
of the abdomen, looking at the left and right sides and lomas), pustules, and ulcerations (contagious ecthyma).
upper and lower quadrants. These areas should be auscul- The skin and musculoskeletal examination of the pelvic
tated with alternating percussion and ballottement. limbs is similar to that performed for the forelimbs.
Distention of the left upper quadrant, with a gaseous
“ping” on percussion, suggests ruminal tympany or bloat. Digestive and gastrointestinal systems. The normal
A severely bloated rumen may distend the left upper, left rectal temperature of a goat ranges between 38° and 40° C
lower, and right lower quadrants. Distention of the lower (see Table 1-2). Hyperthermia may result from elevated
left quadrant with a firm feel on ballottement may indi- environmental temperature and humidity, stress and ex-
cate rumen impaction. Rumen contractions are counted citement, or inflammatory disease. Hypothermia may
by auscultating the left upper quadrant while gently occur in malnourished or older animals. The perineum
placing a hand on the area to hear and feel the contrac- and the back of the hindlegs should be examined for fecal
tions. Normally one or two primary contractions occur soiling. In young kids the presence or absence (atresia ani)
each minute, associated with mixing of the ingesta. In ad- of the anus should be noted.
dition, one secondary contraction occurs per minute, as-
sociated with eructation. Indigestion, metabolic or min- Cardiovascular and hemolymphatic systems. The cli-
eral imbalances, or generalized pain may decrease the rate nician should palpate the prefemoral and supramammary
of contraction. (female) or scrotal (male) lymph nodes and note any en-
Distention of the right upper quadrant, with a fluid largement (caseous lymphadenitis). The rate and charac-
wave on ballottement or a gaseous sound on percussion ter of the pulse can be assessed by gentle palpation of the
and auscultation, suggests distention of the cecum or femoral artery in the inguinal region. An irregular pulse is
spiral colon. Distention of the lower right quadrant with occasionally noted in cases of atrial fibrillation or my-
a firm feel on ballottement may result from a severely im- ocarditis. A strong pulse may occur in young, excited, lac-
pacted abomasum or an advanced pregnancy. tating, ruminating, or late-pregnant animals, or in
Ventral abdominal distention of the lower left and animals with anemia or inflammation. Recumbent
right quadrants suggests chronic indigestion or ascites animals or animals with hypovolemia, hypocalcemia, or
secondary to hypoproteinemia resulting from gastroin- left ventricular failure often have weak pulses.
testinal parasitism or severe liver disease. A grossly en-
larged liver (such as that seen in severe congestive heart Urogenital and reproductive systems. The clinician
failure) may be palpable on the right side of the abdomen observes the scrotum for lesions, assesses the testicles for
behind the costal arch. Generalized abdominal disten- firmness and heat, and examines the prepuce and penis.
tion, with no audible gastrointestinal motility, may be a Ulceration or occlusion of the preputial orifice suggests
sign of gastrointestinal ileus. ulcerative posthitis (which occurs most commonly in
goats on a high-protein diet). The preputial hairs should
Respiratory system. Pronounced abdominal move- be examined for the presence of crystals or blood and for
ments may be observed in an animal with dyspnea. unusual dryness (in urethral calculi or obstructive
urolithiasis). Anal pumping and perineal urethral pulsa-
Cardiovascular and hemolymphatic systems. Bilateral tions (with the goat unable to urinate or dribbling urine)
ventral abdominal distention may indicate ascites result- also may indicate obstructive urolithiasis. Edema in the
ing from congestive heart failure. prepuce and ventral abdomen, with tissue sloughing, may
be a sign of a ruptured urethra.
Urogenital and reproductive systems. Bilateral ventral The penis of the male goat is difficult to examine di-
abdominal distention also may indicate uroperitoneum rectly without sedation. However, the clinician may be
caused by a ruptured bladder (common in castrated able to exteriorize the penis by placing the goat on his
 Chapter 1 Handling and Examination of Sheep and Goats • 17

The vulva and udder of the female should be examined

for color and size (Figure 1-9). Swelling and hyperemia
may indicate estrus or impending parturition. Crystals on
the vulva hairs below the urethral orifice suggest a urinary
tract infection. The clinician should note the color, con-
sistency, and volume of any discharge from the vulva. A
moderate, serous to cloudy discharge is common in late
estrus. A reddish-brown, odorless discharge seen 1 to 3
weeks after parturition is probably lochia, the normal
breakdown product of the cotyledonary attachments. The
finding of large protruding vulva lips or clitoris or a short
anogenital distance is suggestive of an intersex.
The udder should be palpated for symmetry, size,
shape, and texture. A cold, dark udder suggests gan-
grenous mastitis. If the animal is lactating, the clinician
should examine the teats for patency by expressing a
small amount of milk, and note the color and consistency
of the milk. Discolored, thick, or clumpy milk can indi-
cate mastitis.

Neurologic system. Findings suggestive of neurologic

disease include posterior paresis with a distended bladder
on deep palpation, as well as loss of anal and tail tone.

Figure 1-9 The vulva of a pluripara dairy doe. A subtle dermatitis

is visible on the dorsal vulvar lips, but it is of no consequence in this
F URTHER READING
Gay CC: Clinical examination of sheep and goats. In Radostits OM,
case. No discharge, erythema, or enlargement of the clitoris is
Mayhew IGJ, Houston DM, editors: Veterinary clinical examination
evident. After the area has been carefully washed and dried, a sterile
vaginal speculum can be introduced to visualize the cervix. and diagnosis, Philadelphia, 2000, WB Saunders.
Kelly WR: Clinical examination and making a diagnosis. In Radostits
OM et al, editors: Veterinary medicine, ed 9, Philadelphia, 2000, WB
side and pulling back on the prepuce while pushing Saunders.
forward on the sigmoid flexure at the level of the per- Kelly WR: Veterinary clinical diagnosis, ed 3, London, 1984, Bailliere
ineum, then gently grasping the penis to keep it ex- Tindall.
tended. The surface of the penis should be examined first. Smith BP: Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
The clinician can then examine the urethral process for Wilson JH: The art of physical diagnosis, Vet Clin North Am: Food
calculi or other lesions. Animal Pract 8(2):169, 1992.
 Chapter 2

Feeding and Nutrition

DARRELL L. RANKINS, JR., DEBRA C. RUFFIN, AND D.G. PUGH

Sheep and goats are small ruminants with a worldwide content of the diet selected by goats is greater than the
range. They are found under varying production average of the vegetation present on a pasture. These at-
schemes—from backyard pets to expansive range land tributes have led to the use of goats for brush manage-
grazing operations. The common goal of goat or sheep ment in many regions of the world, whereas sheep are
production units is conversion of forage to usable animal maintained in mostly pasture settings. Use of goats for
products (e.g., meat, milk, fiber). With regard to their weed and brush control predispose this specie to the in-
grazing preferences, ruminants are categorized as browse gestion of toxic plants. Some of the browse consumed by
selectors, grass and roughage grazers, or intermediate goats contains high concentrations of essential oils,
types.1 Sheep are predominantly grass and roughage lignin, or tannins, all of which depress digestion or are
grazers, whereas goats are generally classified as interme- poorly digestible. Whenever browse is the predominant
diate types. Sheep tend to graze selectively and prefer forage consumed, mineral uptake may be better than that
higher-quality portions of the plant. As sheep age, they expected from grasses grown on the same land. Many
may be unable to consume adequate forage in range con- species of browse tend to have deeper roots, resulting in
ditions because of dental disease. Goats have small rich mineral content, possibly to the point of toxicity.
mouths and prehensile lips and are active foragers that Therefore goats maintained for brush control should
will readily consume flowers, fruits, and leaves. Goats can be closely monitored for changes in body weight, body
use browse that has woody stems or thorns. Similar to condition score, and hair coat; the clinician should note
sheep, goats tend to select highly digestible portions of any signs of toxicosis. Sheep also are excellent converters
grasses. They will graze, but prefer to eat at head height, of browse and brush to meat, fiber, and milk, but they are
which is a natural protection mechanism against some raised mostly as grazing animals.
nematode parasites. When given a choice, goats tend to
select grass over legumes and browse over grass. They
prefer to graze along fence lines and rough or rocky
WATER
pasture areas. Goats flourish in areas featuring browse or Although it is often taken for granted, water is an ex-
numerous plant species to graze. However, they usually tremely important nutrient. It is the major constituent of
perform poorly compared with sheep or cattle on flat, im- an animal’s body. If an animal were deprived of all nutri-
proved, monoculture pastures. If given a choice, many ents it would succumb to water deprivation first. Al-
meat goats (e.g., Boer, Spanish) prefer a diet of 80% to though sheep and goats may lose most of their body fat
85% browse and 15% to 20% grasses. Both sheep and and 40% to 50% of their total body protein and survive, a
goats use their mobile lips and tongue to consume their water loss of only 10% can prove fatal. Both sheep and
diets selectively. Goats have been mistakenly labeled as goats are particular about the quality of their water
animals that will eat anything and subsist on feedstuffs of sources. In general, a clean, fresh source of water should
inadequate nutrient content. To the contrary, goats are be available at all times. Each ewe or doe should have at
extremely particular about their diet and refuse to least 1 foot of water trough space; a paved surface 8 to 10
consume feeds that have been soiled. The goat’s inquisi- feet around the water source helps prevent unsanitary
tive feeding habits result in their use of most species of conditions conducive to many diseases, including footrot.
forage present in the environment. The nutritional Daily water intake can be affected by several factors.
• 19 •
20 • Sheep and Goat Medicine
Pregnancy and lactation increase water requirements and TABLE 2-1
consumption—water intake is increased by the third
month of gestation and is doubled by the last month. In GENERAL RECOMMENDATIONS FOR TOTAL
addition, water intake is greater for females carrying DISSOLVED SOLIDS IN DRINKING WATER
twins than for those carrying only a single.2 Likewise,
lactating ewes or does consume twice as much water as TOTAL DISSOLVED
nonlactating females: 7 to 15 liters compared with 3.5 to SOLIDS (PPM) COMMENTS
7 liters per day, respectively. Animals grazing lush spring
pastures where the forage water content may exceed 80% Less than 3500 Safe
consume markedly less water than those consuming dry 3500-5000 May take animals time to adapt to
hay, which may be only 10% to 12% water. Obviously, lac- this concentration; if sulfates are
tating dairy animals require even greater quantities of the predominant type of solid,
water. When high-protein diets are being fed or when some diarrhea may occur
mineral consumption increases, water consumption also 5000-10,000 Safe for nonpregnant, nonlactating
increases. Sheep may increase their water intake by adults; may cause depressed water
twelve-fold during summer compared with intake during intake or production in young
the winter months.2 Water quality also can affect daily animals
water consumption. For maintenance, individual goats More than Unsafe
and sheep usually consume 3.5 to 15 liters of water 10,000
per day.3 From Bauder J: When is water good enough for livestock? Montana
Water varies in quality according to the amount and State Extension Bulletin, 2000; Guyer PQ: Livestock water quality,
type of contaminant. The most common dissolved sub- University of Nebraska Extension Service Bulletin G79-46A; Meyer
stances in water are calcium, magnesium, sodium chlo- KB: Water quality in animals, 1999, Purdue University Extension
Bulletin WQ9.
ride, sulfate, and bicarbonate.3 If the salts of these min-
erals are present in high enough concentrations,
depressed performance, illness, and occasionally death
can result. In addition to causing various problems in
animals, dissolved salts are additive in their suppression TABLE 2-2
of production and health. As salt concentrations in- POTENTIALLY DANGEROUS CONCENTRATIONS
crease, water consumption is usually depressed, with OF NITRATE NITROGEN IN DRINKING WATER*
young animals generally being more affected than adults.
Over time, animals tend to adapt to water with high con- NITRATE NITROGEN
centrations of dissolved salts. However, quick or abrupt (PPM) COMMENTS
changes from water with relatively low concentrations to
water with high concentrations of dissolved substances Less than 100 Safe
are poorly tolerated.3 Table 2-1 provides general guide- 100 to 300 Potentially unsafe when
lines for total dissolved solids in drinking water.4-6 High animals are consuming high-
sulfate concentrations in the 3500 to 5000 parts per nitrate feedstuffs (e.g., during
million (ppm) range may result in suppressed copper a drought)
absorption from the intestine. Nitrates, and less com- More than 300 Not safe
monly, nitrites, are occasionally encountered in toxic con- *High sulfate concentrations in the 3500 to 5000 ppm range may
centrations from ground water (Table 2-2). Most safe, result in copper absorption abnormalities.
drinkable water has a pH of 7 to 8. As the alkalinity of From Bauder J: When is water good enough for livestock? Montana
water increases, its suitability for consumption decreases. State Extension Bulletin, 2000; Guyer PQ: Livestock water quality,
Table 2-3 provides standards for various other water University of Nebraska Extension Service Bulletin G79-46A; Meyer
KB: Water quality in animals, 1999, Purdue University Extension
contaminants. Bulletin WQ9.
Although water contaminated with coliform bacteria
has been associated with disease in humans, only rarely is
coliform contamination of drinking water implicated as a
causal agent of disease in sheep and goats. Only very temperature. In addition, they possess the ability to
young animals are generally affected. reduce urine and fecal water losses during times of water
Maloiy and Taylor7 observed that goats are quite effi- deprivation.
cient at water conservation. Goats tend to adapt to high In summary, sheep and goats should have access to a
ambient temperatures better than other domestic rumi- continuous supply of fresh, clean water in order to ensure
nants and require less water evaporation to control body that productivity is not compromised.
 Chapter 2 Feeding and Nutrition • 21

TABLE 2-3 terms of the net energy system (calories) or in terms of

total digestible nutrients (TDN) as a percentage of the
RECOMMENDED STANDARDS FOR UPPER LIMITS feed. The two expressions are interchangeable by use of
OF POTENTIALLY TOXIC CONTAMINANTS various prediction equations; this chapter uses TDN as
THAT MAY OCCUR IN WATER the measure. Currently, most feed and forage testing lab-
oratories estimate TDN using the Van Soest fiber analy-
UPPER LIMIT OF sis. A representative sample is analyzed for neutral and
CONTAMINATION acid detergent fiber contents, and then TDN is predicted
CONTAMINANT (PPM) based on one or both of these values. This system works
Aluminum 5
effectively for most forages but is less reliable for feeds
that are high in starch (e.g., corn). In general, warm-
Arsenic 0.2 season, perennial grass hays are about 50% to 54% TDN,
Cadmium 0.01-0.05 whereas many of the cereal grains are usually 80% to 90%
Chromium 0.05-1 TDN. Most forages in the green, vegetative state are
Cobalt 1 about 62% to 70% TDN on a dry matter basis. Stemmy,
Copper 0.5 dry, poor-quality hay is less than 50% TDN. By compar-
Fluoride 2-3
ing these typical values with the requirements of various
classes of sheep and goats, keepers can ascertain when
Iron 1-3 supplemental energy sources are needed for forage-based
Lead 0.05-1 rations. For example, a 150-pound ewe requires a diet
Mercury 0.01 containing 55% TDN for maintenance, 59% for late ges-
Selenium 0.05 tation, and 65% for the first 6 weeks of lactation. There-
Vanadium 0.1 fore the dry, non-pregnant ewe could use low-quality
Zinc 25
forage, but the pregnant or lactating ewe needs a diet
of lush, vegetative forage. If a good to excellent forage is
Carbonate and bicarbonate 2000 unavailable, some type of energy supplement is required
From Bauder J: When is water good enough for livestock? Montana for the late pregnant or lactating ewe. Similarly, a 110-
State Extension Bulletin, 2000; Guyer PQ: Livestock water quality, pound doe requires a diet containing 56% TDN for
University of Nebraska Extension Service Bulletin G79-46A; Meyer maintenance.2,8
KB: Water quality in animals, 1999, Purdue University Extension A variety of choices are available for energy supple-
Bulletin WQ9.
mentation. The most common choice is cereal grains,
corn being the most common of these. Corn is dense in
energy, and most of that energy is in the form of starch.
ENERGY When appreciable levels of starch are supplemented to
Energy is probably the first limiting nutrient of most ruminants consuming forage-based diets, the general re-
practical conditions where sheep and goats are main- sponse is a decrease in forage intake and digestibility.
tained throughout the world. Energy requirements vary However, the sheep or goat receiving corn supplementa-
greatly depending on level and stage of production, level tion still has a higher energy status because of the energy
of activity, and intended animal use. Except in situations from the corn. Several other feedstuffs are available for
where rapid growth rates are desired or milk production is use as energy supplements for ruminants consuming
to be maximized, the energy requirement can usually be forage-based diets (e.g., oats, barley, rye). Two other non-
met with medium- to high-quality forage. However, traditional energy supplements are soybean hulls and
under maximal production pressures, some sort of supple- wheat middlings. Soybean hulls are the outermost layer
mentation may be required. Energy-deficient diets can of the soybean and are comprised of abundant quantities
result in poor growth rates, lower body condition scores, of digestible fiber. Unlike corn, soybean hulls do not sup-
decreased fiber production, decreased fiber diameter, de- press fiber digestion but may increase hay digestibility.
creased immune function, and increased susceptibility to Even though soybean hulls have a TDN value 62% less
parasitic diseases and other pathologies. Angora goats than corn, they produce similar results when used as an
and many wool breeds of sheep are prone to various fiber energy supplement for ruminants consuming forages.
production changes, whereas cashmere goats may be less Wheat middlings, a by-product of wheat milling, elicit
susceptible. similar responses. Often these by-product type feeds are
The majority of the energy that is used by sheep and much more economical than corn.2,8
goats comes from the breakdown of structural carbohy- Another source of energy supplementation is fat. In
drates from roughage. Therefore roughage should com- general, total fat content should not exceed 8% of the
prise the bulk of their diet. Energy can be expressed in diet, or 4% to 5% as supplemental fat. In the southern
22 • Sheep and Goat Medicine
United States, where cotton production is prevalent, Non-protein nitrogen (NPN) is an inexpensive way to
whole cottonseed (which contains approximately 24% increase the protein concentration of rations for sheep or
fat) is used as an energy supplement for both sheep and goats. NPN is any source of nitrogen in the non-protein
goats. Sheep or goats should be supplemented with no form, but the most commonly used type is urea. When-
more than 20% of their daily intake as whole cottonseed, ever NPN is used, the diet should have sufficient amounts
assuming that the remainder of the diet contains no fat. of highly fermentable energy components. Feeding grain
with NPN can result in a decrease in rumen pH. This de-
presses the ability of the ruminal urease enzyme to
PROTEIN ferment urea, resulting in a slower release or breakdown
As a general rule, a minimum of 7% dietary crude protein to ammonia and carbon dioxide (CO2). Slowing this
is needed for normal rumen bacterial growth and func- metabolic pathway allows more efficient protein synthesis
tion for sheep and goats. If dietary protein drops below by the rumen microbes. On the other hand, diets of poor
7%, forage intake and digestibility are depressed. Protein quality roughage result in a higher rumen pH and en-
deficiency is associated with decreased fiber production, hanced urease activity. This results in a quicker release of
slowed growth, decreased immune function, anemia, de- ammonia, a poorer “marriage” of chains of carbon atoms
pressed feed use, edema, and death. All of the protein and nitrogen for microbial protein synthesis, and a poten-
reaching the small intestine is in the form of bacterial or tial increase in the incidence of urea/ammonia toxicity.
protozoal protein or dietary protein that escaped ruminal Whenever NPN is added to the diet, feeds containing a
digestion. The quality (amino acid content) of the bacte- urease enzyme should be limited or avoided. Such urease-
rial protein is, surprisingly, quite good. Therefore the containing feeds include raw soybeans and wild mustard.
quantity of dietary protein provided to adult ruminants is Signs of urea-ammonia toxicity include dull or depressed
much more important than the quality. The opposite is demeanor, muscle tremors, frequent urination and defeca-
true of the pre-ruminant lamb or kid. If lambs or kids are tion, excessive salivation, increased respiration, ataxia,
fed a milk replacer, it should be composed of milk by- tetanic spasms, and death. Treatment includes the infu-
products in order to have an adequate amino acid compo- sion of a 5% acetic acid solution (vinegar and water) into
sition for maximal growth. the rumen through a stomach tube. In severe cases,
Crude protein content varies widely among the various rumenotomy and fluid therapy may be required.
feedstuffs. Warm-season, perennial grass hay samples can The following rules of thumb are useful when feeding
range from less than 6% to more than 12% crude protein, urea as a protein source:
whereas legumes in the vegetative state may occasionally
1. Never use urea for more than one third of the
be more than 28% crude protein. The protein content of
protein in the diet or 3% of the grain portion of
plants declines with maturity. Similar to energy needs,
the diet.
crude protein requirements vary with the animal’s stage
2. Ensure that a highly fermentable source of
of production. For maintenance, a 150-pound ewe re-
carbohydrates (e.g., corn, milo) is fed along with
quires a diet including 8% to 9% protein, and a 110-
NPN.
pound doe needs a diet with 7% to 8% protein. During
3. Avoid the sudden introduction of urea into the diet
lactation both the ewe and doe require in excess of 13.5%
(allow at least 8 to 10 days for its introduction).
protein, depending on the number of offspring suckling
4. Ensure proper mixing of feedstuffs whenever urea
or, in the case of dairy goats and sheep, level of milk pro-
is used.
duction. Supplementation of protein may be necessary for
5. If 1 pound of urea and 6 pounds of ground corn
the heavy producing animals. Whenever grass hay is fed,
are cheaper than 7 pounds of cottonseed meal
protein deficiency should be a concern, particularly for
(CSM) or soybean meal (SBM), then the former
growing or lactating animals. The most consistent sign of
diet may be efficiently fed. However, if 7 pounds
protein deficiency in lactating animals is poor weight gain
of either CSM or SBM is less expensive, the urea
or slow growth in their lambs or kids, particularly for
should be avoided.
twins or triplets.2,8
6. If the crude protein of the diet is greater than
Typical protein supplements include the oilseed meals
14% of the dietary TDN, NPN is of little value.
(cottonseed meal, soybean meal), commercially blended
For example, if TDN is 45%, which is typical of
supplements containing both natural protein and non-
many dry hays during winter, NPN is of limited
protein nitrogen (range cubes or pellets, molasses-based
or no value if the crude protein of the diet is
products), and various by-products (whole cottonseed,
greater than 6.3% (45  0.14  6.3).
corn gluten feed). Protein should be fed to meet, but not
greatly exceed, requirements. Excess protein usually Because of varying dietary intakes and their relation-
results in increased feed costs and higher incidences of ship to body condition scoring, NPN is best used in sheep
diseases (heat stress, pizzle rot, urolithiasis). or goats with body condition scores greater than 2.5; they
 Chapter 2 Feeding and Nutrition • 23

should be avoided in animals with a body condition score tool of choice. The technique for liver biopsy is covered in
of less than 2. If NPN is offered to animals, it should be Chapter 4.
fed daily; less is used for protein synthesis if the supple- Calcium and phosphorus are interrelated and are
ment is fed less frequently. In an Australian study9 the in- therefore discussed together. Nearly all of the calcium in
clusion of NPN in poorly digestible forage diets for lambs the body and most of the phosphorus is found in the
resulted in increased weight gain and wool production skeletal tissues. Diets deficient in calcium and phospho-
and decreased signs of parasitic nematode infestation. rus may delay growth and development in young lambs
and kids and predispose them to metabolic bone disease
(e.g., rickets, osteochondrosis) (see Chapter 9). Likewise,
MINERALS calcium and phosphorus deficiencies in lactating ewes
Clinicians generally consider seven macrominerals and and does can dramatically reduce milk production. Serum
eight microminerals when assessing mineral nutrition for phosphorus concentrations are not highly regulated but
sheep and goats (Table 2-4). The designations macro and are still maintained between 4 and 7 mg/dl for sheep and
micro do not reflect the minerals’ relative importance, but between 4 and 9.5 mg/dl for goats. Phosphorus defi-
rather the amount of each that is required as a portion of ciency is the most commonly encountered mineral defi-
the diet. Macromineral needs are usually expressed as ciency in range or winter pastured animals. Most forage
percentages of the diet, whereas micromineral needs are tends to be high in calcium and relatively low in phos-
generally expressed as ppm or mg/kg. The seven com- phorus; this is especially true in legumes. Beet pulp and
monly assessed macrominerals are calcium, phosphorus, legumes (such as clover and alfalfa) are good to excellent
sodium, chlorine, magnesium, potassium, and sulfur. The sources of calcium. For lactating dairy goats and sheep,
eight microminerals are copper, molybdenum, cobalt, supplemental calcium and phosphorus are necessary to
iron, iodine, zinc, manganese, and selenium. Trace meet high demands for milk production. Range goats
mineral deficiency is less common than energy, protein, may need less supplemental phosphorus than sheep
or macromineral deficiency. They occur slowly over time because of their preference for browse and plants that
and rarely cause the dramatic effects on productivity and tend to accumulate phosphorus. Phosphorus serum con-
body condition seen in protein deficiency.2,8 In some centrations of less than 4 mg/dl may indicate phosphorus
cases of mineral deficiency a liver biopsy is the diagnostic deficiency.2 Phosphorus deficiency results in slow growth,
listlessness, an “unkempt” appearance, depressed fertility,
and depraved appetite or pica.2
TABLE 2-4 Sheep and goats fed high grain or concentrate diets
typically need supplemental calcium and little to no addi-
MINERAL REQUIREMENTS OF SHEEP AND GOATS tional phosphorus. Grains are relatively low in calcium
but contain moderate to high concentrations of phospho-
MINERAL SHEEP GOATS rus. Although serum calcium is tightly held in a narrow
range, serum concentrations consistently below 9 mg/dl
Sodium, % 0.09-0.18 0.09-0.2 are suggestive of chronic calcium deficiency.2 Chronic
Calcium, % 0.20-0.82 0.20-0.90 parasitism can decrease the body stores of both calcium
Phosphorus, % 0.16-0.38 0.14-0.40 and phosphorus.2 Common calcium supplements include
Magnesium, % 0.12-0.18 0.12-0.18 oyster shells and limestone. Defluorinated rock phos-
Potassium, % 0.50-0.80 0.50-0.80 phate is an excellent source of phosphorus. Dicalcium
phosphate or steamed bone meal (where available) are
Sulfur, % 0.14-0.26 0.16-0.32
good sources for both. The calcium-to-phosphorus ratio
Iodine, ppm 0.10-0.80 0.60 should be maintained between 11 and 21.2,8
Iron, ppm 30-50 more than 30 Sodium and chlorine are integral components of
Copper, ppm 7-11 10 many bodily functions. Salt (sodium chloride [NaCl]) is
Molybdenum, ppm 0.10-0.5 0.10 the carrier for most ad lib mineral supplements. If salt is
Cobalt, ppm 0.10-0.20 0.10 not offered ad lib, it should be incorporated into a com-
plete ration at a level of 0.5% of the diet. Sodium is pre-
Manganese, ppm 20-40 20-60
dominately an extracellular ion and is important for
Zinc, ppm 20-33 45-50 normal water metabolism, intracellular and extracellular
Selenium, ppm 0.10-0.20 0.10-0.3 function, and acid-base balance. Conversely, chloride is
an intracellular ion, functions in normal osmotic balance,
From Nutrient requirements of sheep, Washington, DC, 1985,
National Academy Press; Bratzlaff K, Henlein G, Huston J: Common and is a component of gastric secretions. Sheep or goats
nutritional problems feeding the sick goat. In Naylor JM, Ralston SL, that are deficient in salt intake routinely chew wood, lick
editors: Large animal clinical nutrition, St Louis, 1991, Mosby. the soil, or consume other unlikely plants or debris. The
24 • Sheep and Goat Medicine
NaCl content of feeds may be increased to 5%, particu- nitrogen-to-sulfur ratio in sheep and goat diets.2,8 This
larly for feeding males, to help increase water intake and has been recently substantiated by Qi et al,11 who re-
reduce the incidence of urolithiasis. ported ideal ratios of 10.41 for maximal gains and 9.51
Salt is commonly used as a carrier to ensure trace for maximal intake in growing goats. However, a ratio as
mineral intake because sheep and goats have a natural low as 7.21 has been suggested for optimal mohair pro-
drive for NaCl. If the clinician, nutritionist, or rancher duction.12 If the forage is low in sulfur content or large
elects to use a salt-containing mineral mixture to ensure quantities of urea are used in the diet, weight gain and
mineral intake, he or she should be aware that individual fiber production can be increased by providing supple-
consumption may vary drastically. Furthermore, improp- mental sulfur. In sheep and goats, sulfur deficiency may
erly prepared salt mixtures or blocks, feed supplements, result in anorexia, reduced weight gain, decreased milk
liquid feeds, or certain types of food or water contamina- production, decreased wool growth, excessive tearing, ex-
tion can drastically alter mineral consumption. Salt also is cessive salivation, and, eventually, death. Browsing
useful as an intake limiter for energy-protein supple- animals such as goats may ingest enough tannins to de-
ments. A 10% to 15% NaCl mixture of two parts ground crease sulfur availability. Sulfur deficiency also depresses
corn and one part soybean meal is approximately 20% digestion, decreases microbial protein synthesis, decreases
crude protein. The added salt usually limits intake to 0.45 use of NPN, and lowers the rumen microbial population.
kg of this mixture per adult goat per day. Whenever using Whenever NPN is fed to fiber-producing animals, sulfur
salt-limited feeding, the keeper should take care to intro- supplementation is indicated. With the possible excep-
duce the feedstuffs slowly over 2 to 3 weeks and provide tion of oats and barley, the sulfur content of most cereal
access to adequate quantities of fresh clean water. Only grains is usually low to deficient, although corn-soybean
white salt should be used as in intake limiter. If trace diets usually meet requirements for the ruminal synthesis
mineral salt or ionized salt is used, mineral (e.g., copper, of sulfur-containing amino acids.
iodine) toxicity is likely, particularly in sheep. Sulfur toxicity is occasionally seen where calcium
Magnesium is important for normal functioning of sulfate is used as a feed intake limiter. It also occurs when
the nervous system and is required for many enzymatic ammonium sulfate is fed as a source of NPN or as a urinary
reactions. Skeletal magnesium can be used by the animal acidifier. If sulfur is supplemented in the form of sulfate,
during times of deficiency, but the skeletal magnesium toxicity may occur, particularly if the sulfur content is
reserve is much smaller than the calcium reserve. Most greater than 0.4% of the diet.2 Sulfate can be reduced to
fast-growing, heavily fertilized cereal grains or grass pas- sulfide in the rumen or lower bowel. Sulfide in large
tures are deficient in magnesium. Magnesium absorption enough concentrations can result in polioencephalomala-
is depressed by high concentrations of plant potassium cia that is only partially responsive to thiamine.
and/or rumen ammonia. Legume and legume-grass Copper deficiencies can be primary (as a result of low
mixed pastures are good sources of magnesium. A mag- intake) or secondary (caused by high concentrations of
nesium deficiency can lead to a condition known as grass molybdenum, sulfur and iron, or other substances in
tetany in either sheep or goats. Magnesium toxicity is feedstuffs). In the rumen, copper, molybdenum, and
very rare. sulfur form thiomolybdates, which reduce copper avail-
Potassium is required for normal acid-base balance ability. Copper’s ability to function as part of the enzymes
and is an integral component of many enzymatic path- needed for specific biochemical reactions is depressed.
ways; it functions as an intracellular ion. The requirement This impairment in metabolism results in clinical signs of
is between 0.5% and 0.8% of the diet depending on the deficiency. Other factors that alter copper absorption
stage of production. Most grains contain less than 0.4% include high concentrations of dietary cadmium, iron,
potassium, whereas fresh green forages generally contain selenium, zinc, and vitamin C in the animal, as well as
more than 1%. However, dormant forages may have alkaline soils. Roughage grown on “improved pastures”
much lower potassium concentrations. Potassium defi- (fertilized, limed) is more likely to be deficient. Liming
ciencies or toxicities are rare for sheep and goats. reduces copper uptake by plants, and many fertilizers
However, deficiencies may occur in highly stressed contain molybdenum. Good quality lush grass forages
animals being fed diets composed mostly of grain. There- have less available copper than most hays, and legumes
fore, under stressful situations (such as weaning), supple- have more available copper than most grasses. Liver
mental potassium may be indicated for animals fed copper reserves last up to 6 months in sheep.2,8
predominantly on grain.2,8 Signs of copper deficiency include microcytic anemia,
Sulfur is a component of many bodily proteins. It is depressed milk production, lighter or faded hair color,
found in high concentrations in wool and mohair because poor quality fleeces, heart failure, infertility, increased
of the large amounts of sulfur-containing amino acids susceptibility to disease, slowed growth, enlarged joints,
(cystine, cysteine, and methionine) in keratin. Sulfur defi- lameness, gastric ulcers, and diarrhea. These signs appear
ciency can reduce mohair production in Angora goats.10 to be more severe with primary copper deficiencies than
The general recommendation is to maintain a 101 with a lowered copper-molybdenum ratio. Sheep with
 Chapter 2 Feeding and Nutrition • 25

copper deficiencies have inferior wool, which is usually normal but dietary molybdenum is high or if the copper-
characterized as “stringy” or “steely.” Such wool lacks both to-molybdenum ratio is less than 41. In this case the
tensile strength and crimp. Growing lambs and kids are assayed copper may not be available for use in body me-
more susceptible to copper deficiency, followed by lactat- tabolism. The dietary copper–to-molybdenum ratio
ing females. should be maintained between 51 and 101. Liver is the
Several breed differences have been observed with best tissue to determine body copper status, but it has
regard to copper metabolism. For example, some Finnish- limitations and is a poor indicator of short-term copper
Landrace sheep may have lower serum copper concentra- balance. If liver copper is marginal, but plasma or serum
tions than Merinos, which in turn have lower serum copper is in the normal range, the animal may have a fa-
copper levels than British breeds at similar levels of vorable response to copper supplementation. In such a
intake.13 Milk is usually deficient in copper, and molyb- case, dietary copper is probably deficient, and the liver
denum is concentrated. Lambs suspected of having the stores of copper are being depleted. If the clinician sus-
swayback condition usually have a liver copper concentra- pects a herd problem, he or she should sample not only a
tion of less than 80 ppm dry weight. cross-section of ages and production status, but also as
Anecdotal reports indicate that goats offered only many animals who are showing clinical signs as possible.
sheep mineral (with low to absent added copper and Forage samples should be taken for copper and trace
added molybdenum) may succumb to copper deficiency. mineral analysis. Core samples of hay should be properly
This deficiency may be magnified in pygmy goats and collected. Feed samples should be placed in plastic bags,
young, growing animals. Merino sheep and dwarf goat not brown paper boxes or bags. Dietary copper should
breeds require 1 to 2 ppm more copper than other breeds. range between 4 and 15 ppm. In areas where copper defi-
Copper is absorbed more efficiently by young animals ciency is a problem in goats, a mineral mixture with 0.5%
than adults.2,8 copper sulfate should be offered free choice. However,
Very young lambs or kids can present with enzootic this level of copper may be toxic for sheep.2,8 In extremely
ataxia. Affected animals are born from copper-deficient deficient areas, copper needles can be administered orally
ewes or does. The swayback condition of lambs or kids is or copper can be injected parenterally.
usually seen at birth but may be diagnosed in animals up Copper toxicity is a much larger problem in sheep than
to 3 months of age. Neonates may experience a progres- goats. The magnitude of difference between copper defi-
sive ascending paralysis. Signs of this ataxia include mus- ciency and copper toxicity is quite small. Copper toxicity
cular incoordination (especially in the hindlegs), lack of can occur in sheep as a result of simple mixing errors
nursing, and death. Most neonates die within 3 to 4 days during the formulation of mineral premixes or by feeding
of the first symptoms. Affected older animals may survive mineral mixes formulated for species other than sheep.
or die, depending on severity. Rear limb ataxia, muscle Sources of toxic concentrations of copper include pre-
atrophy, and weakness are seen in lambs or kids from 2 mixes, trace mineral supplements made for species other
weeks to 3 months of age. A definitive diagnosis is made than sheep, copper sulfate–containing foot baths, high
with necropsy. Histopathologic examination of the spinal copper-containing feedstuffs (horse, hog, or chicken
cord reveals myelin degeneration and cavitations of cere- feeds), and some nontraditional feedstuffs (broiler litter).
bral white matter. Liver copper concentrations are invari- Signs of copper toxicity include increased respiration, de-
ably depressed. Prevention and treatment require copper pression, weakness, hemoglobinuria, icterus, and acute
supplementation (oral supplements, copper needles, a death. Gross pathology of affected animals includes signs
trace mineral mixture, or injectable copper) and attaining of a massive hemolytic crisis and dark, hemoglobin-filled
a good dietary copper-to-molybdenum ratio. kidneys. Treatment includes the use of D-penicillamine
If copper deficiency is suspected, the copper, molybde- (50 mg/kg once a day) and ammonium tetrathiomolyb-
num, sulfur, and iron concentrations of the diet should be date (3.4 mg/kg every other day)(see Chapters 4 and 10).
determined. To confirm copper deficiency, the nutrition- Goats are closer to cattle than sheep in susceptibility to
ist or clinician should measure body tissue concentration. copper toxicity.
Serum copper is commonly used to determine body Cobalt is used by rumen bacteria in the formation of
copper status, but much of the copper is bound in the vitamin B12. It is deficient in some highly organic and/or
clot, making plasma a more reliable indicator of body poorly drained soils. Cobalt deficiency in sheep or goats is
copper status. Unfortunately, from a body assessment characterized as a classic B12 deficiency, with symptoms
standpoint, blood copper concentrations may be falsely including lack of appetite, emaciation, anemia, and
increased by stress or disease. If serum copper is overtly “wasting disease.” Cobalt deficiency is associated with
low and animals were not stressed during sampling, white liver disease, although phosphorus and copper defi-
copper deficiency is likely. If serum copper concentrations ciencies and chronic parasitism also play roles in patho-
are used for assessment, and copper concentrations fall genesis. Animals with this condition have excessive oph-
within normal ranges, additional copper supplementation thalmic discharge and become extremely pale. Necropsy
is of little or no value. An exception is if serum copper is reveals a fatty liver (see Chapter 4). To determine whether
26 • Sheep and Goat Medicine
a cobalt deficiency exists, the clinician must evaluate the animals and 0.2 ppm for nonlactating ewes or does are
complete diet. Serum or urinary methylmalonic acid is usually sufficient. Applying iodine (tincture or Lugol’s, 1
increased, and serum vitamin B12 and liver cobalt concen- to 2 ml) to the skin of a pregnant female once each week
trations are depressed in cobalt deficiency. However, di- is a labor-intensive but rewarding method of preventing
agnosis may be difficult because of the normally low iodine deficiency–induced hypothyroidism. Occasionally
tissue concentration of cobalt. A diet with a cobalt con- hyperiodinism is associated with the feeding of kelp or
centration of 0.1 ppm is adequate in most instances, but related plants in mineral mixtures. This is a clinical
dietary levels below 0.06 ppm should be considered defi- problem in the occasional pet or dairy goat. Simply re-
cient. If a frank deficiency exists, a cobalt-supplemented moving the iodine source may be all that is required for
trace mineral mixture should be fed ad lib. Cobalt toxicity treatment of toxicity.2,8
is of minimal concern for sheep and goats under practical Zinc is associated with deficiency-related disease or
conditions in North America.2,8 dysfunction in sheep and goats. Zinc availability is im-
Iron deficiency in sheep and goats is quite rare under proved by the presence of vitamin C, lactose, and citrate
grazing conditions. Lambs or kids raised in total confine- in the diet. Oxalates, phytates, and large dietary concen-
ment and deprived of access to pasture and earth-floored trations of calcium, cadmium, iron, molybdenum, and or-
stalls or paddocks may become deficient. Iron deficiency thophosphate all depress zinc availability. Zinc concen-
is exacerbated when young animals are fed a milk replacer trations are usually higher in legumes than in grasses,
deficient in iron. Newborn kids and lambs are born with but legumes invariably contain large concentrations of
minimal iron stores. Iron is an important component of calcium, which can depress zinc availability. Zinc tends to
hemoglobin, and a deficiency can result in microcytic- be less available from cereal grain. Signs of zinc deficiency
hypochromic anemia. Iron deficiency is a rare problem in include dermatitis and parakeratosis, depressed milk pro-
adults, except in cases of excessive parasitism. In kids and duction, impaired appetite, poor feed utilization, slowed
lambs with diagnosed iron deficiency, iron dextran (150 growth, increased susceptibility to footrot, less hair on
mg intramuscularly) at 2- to 3-week intervals may prove a legs and head, swollen joints, poor growth, deceased re-
valuable therapy.10 Parenteral iron dextran may be toxic, productive performance, reduced testicular development,
and clinicians should exercise caution when using it.10 If impaired vitamin A metabolism, and increased vitamin E
selenium deficiency also exists, the use of iron dextran can requirements. Male goats appear more sensitive to mar-
result in painful muscle reactions. The iron requirement is ginal zinc intake.
generally 30 to 40 ppm of the diet. When zinc deficiency is suspected, the clinician
Iodine deficiency is more common in certain geo- should carefully sample all constituents of the diet. Serum
graphic regions of North America, particularly the north- or plasma should be properly collected into tubes specifi-
ern tier states of the United States. Iodine availability is cally designed for trace mineral analysis (royal blue top or
depressed by methylthiouracil, nitrates, perchlorates, trace mineral tubes). Hemolysis alters the accuracy of
soybean meal, and thiocyanates. Minerals that interfere serum and plasma samples, because red blood cells have
with iodine absorption include rubidium, arsenic, fluo- high zinc concentrations. Liver samples yield the most
rine, calcium, and potassium. Iodine appears to be most reproducible measurements of the zinc status of the
available for use by the body during winter months and animal. Both polystyrene containers and brown paper
during lactation. The form or “state” in which iodine bags may be contaminated with zinc and should not be
exists in the feed alters availability—iodates are absorbed used for sample collection. Diets containing 20 to 50 ppm
more readily than iodides. Signs of iodine deficiency of zinc are usually sufficient except for animals that
include goiter, poor growth, depressed milk yield, preg- consume a high percentage of legumes in their diets. In
nancy toxemia, and reproductive abnormalities (e.g., these cases a chelated form of zinc is indicated. Trace
abortion; stillbirth; retained placentas; irregular estrus; in- mineral-salt mixes with 0.5% to 2% zinc usually prevent
fertility; depressed libido; birth of small, weak, and either deficiency. The difference between required and toxic
hairless or short, fuzzy-haired newborns). Lambs or kids amounts is quite large, and therefore zinc toxicity is rare
born to iodine-deficient dams may have enlarged thyroid under most conditions.2,8
glands. Affected kids can be treated with 3 to 6 drops of The absorption of selenium from the small intestine is
iodine (Lugol’s solution) daily for 7 days. Commonly the enhanced by adequate dietary levels of vitamins E and A
enlarged thyroid in the kid is a congenital problem unas- and histidine. Large dietary quantities of arsenic, calcium,
sociated with dietary iodine (see Chapter 7). After a thor- vitamin C, copper, nitrates, sulfates, and unsaturated fats
ough examination of the diet, if iodine deficiency is still inhibit selenium absorption. Legumes are usually better
suspected, the clinician can use serum or plasma thyrox- sources of selenium than are grasses, which, in turn, are
ine to assess the body status; these markers are lowered in superior to cereal grains (see also Chapter 9).
deficient states. Iodine is readily absorbed, so most The signs of selenium deficiency include nutritional
sources will work well in salt-mineral mixtures or feed muscular dystrophy, particularly of the skeletal and
supplements. Iodine levels of 0.8 ppm for lactating cardiac muscles of fast-growing young lambs or kids, and
 Chapter 2 Feeding and Nutrition • 27

retained placentas. Signs associated with insufficient sele- tions, vitamin D should be supplemented. Vitamin D defi-
nium include poor growth, weak or premature lambs or ciency can occur in heavily wooled lambs raised with
kids, depressed immune function, mastitis, and metritis. limited access to sunlight or sun-cured forages. Winter
Most often, selenium deficiency is observed in lambs months tend to be the most common time for marginal
between birth and 8 weeks of age. Serum selenium con- blood vitamin D concentrations. Vitamin D, along with
centrations are difficult to interpret because they may calcium and phosphorus, is important for normal bone in-
reflect the dietary intake in the past 2 to 4 weeks. Whole tegrity. Deficiencies can result in rickets (see Chapter 9).
blood selenium is reflective of dietary selenium intake Plants, both fresh and in the form of hay (particularly sun-
over the past 100-plus days. Liver concentration is the cured hay), contain abundant quantities of ergocalciferol
measurement of choice for diagnosing selenium defi- (vitamins D2 and D3). The vitamin D requirement for
ciency. However, the authors of this chapter prefer to use sheep is 5 to 6 IU per kg of body weight per day, except for
whole blood selenium to determine selenium adequacy. early weaned lambs, which have a requirement of 6 to 7 IU
Diets containing 0.1 to 0.3 ppm of selenium are usually per kg of body weight per day.2 For conversions, 1 IU of
adequate. The upper limit (0.3 ppm) should be fed during vitamin D equals 0.025 mg of crystalline D3.2,8
the final trimester of pregnancy. Mineral-salt mixes Vitamin E is a biologic antioxidant that plays a major
should contain between 24 and 90 ppm selenium in defi- role in cell membrane integrity. It is closely associated
cient regions. Of course, dietary limits may be restricted with selenium in its mode of action, and a deficiency of
to different levels in different countries and states of the either can lead to white muscle disease, depressed
United States. In cases of frank deficiency, injectable immune function, and depressed fertility in sheep and
vitamin E and selenium preparations may be given. Sele- goats. Lambs from vitamin E–deficient ewes may experi-
nium toxicity may occur, but deficiency is the more preva- ence stiffness, paralysis, and pneumonia. If a higher than
lent problem. Toxicity is characterized by wool break, expected incidence of infection and disease is noted in
anorexia, depression, incoordination, and death2,8 (see lambs or kids, the keeper or clinician should investigate
Chapter 9). the herd’s vitamin E intake. In selenium-deficient areas,
young lambs should generally be given extra vitamin E
and selenium by injection. Vitamin E is poorly stored in
VITAMINS the body, so daily intake is crucial. Although vitamin E is
Because the rumen normally synthesizes B vitamins in found in most good-quality forages, if females are con-
healthy sheep and goats, the only vitamins needed in the suming poor-quality hay (particularly in selenium-
diets of nonstressed animals are the fat-soluble vitamins: deficient areas), supplementation is required. Feeds rich
A, D, E, and K. If an animal has altered rumen function, in vitamin E include alfalfa meal, cottonseed meal, and
is parasitized, is on a low-fiber diet, or is being given brewer’s grain. Some feedstuffs (e.g., corn, high sulfur-
long-term antibiotic therapy, supplemental B vitamins containing feeds, onions) decrease vitamin E availability.
may be of value. The current National Research Council (NRC) recom-
Vitamin A is involved in numerous bodily functions. It mendations for vitamin E requirements of sheep are 20
is essential for growth, proper skeletal development, IU per kg of feed in dry matter for lambs weighing less
normal reproduction, vision, and epithelial tissue in- than 20 kg. Lambs heavier than 20 kg and ewes require
tegrity. Signs of vitamin A deficiency include weight loss, 15 IU per kg of feed in dry matter.2
depressed immune function, night blindness, decreased If a ruminant animal is healthy, the keeper does not
fertility, and hair loss. Vitamin A can be stored in the liver need to supplement vitamin K. Vitamin K is important
for 4 to 6 months or longer. Green, vegetative forage for normal blood clotting and vision. In healthy animals it
meets the daily vitamin A requirement of all classes of is produced in sufficient quantities in the rumen and
sheep and goats, which is 45 to 50 IU per kg of body lower gut.
weight per day for nonlactating animals.2 During late
gestation and lactation the requirement increases to 85
IU per kg of body weight per day. Plants do not contain
MINERAL FEEDING
preformed vitamin A, but instead have vitamin A’s A salt block or loose salt is just that—a block or loose
carotenoid precursors.2,8 Hay that is brown and dry and mixture of NaCl. Trace mineral salt in block or loose form
has been stored for long periods is probably deficient. is composed of NaCl (usually 98% to 99%) with added
Vitamin-mineral supplements that also contain oxidizing trace microminerals. The adequacy or content of certain
agents (e.g., copper, iron) are subject to oxidative destruc- minerals in the block or loose salt mixture is generally not
tion during storage. Although the label may suggest that specified. The nutritionist or clinician should carefully
vitamin A is present, its activity may be minimal. evaluate the type of salt-mineral supplement that is being
Vitamin D requirements are generally met if the offered to sheep or goats.
animals are exposed to sunlight. In confinement feeding Most adult ewes consume around 0.3 to 0.8 kg of a
operations or during sustained overcast or cloudy condi- mineral mix per month, or about 10 to 28 g daily. Sheep
28 • Sheep and Goat Medicine
and goats maintained in dry lots usually consume more human consumption in the United States. If the
than this, whereas those that graze or browse on range ionophores are fed to ewes or does 30 days before they
consume less. Although commonly used, salt blocks are give birth, they can reduce the shedding of infective
inappropriate for both sheep and goats, and their use can oocysts and may reduce pasture contamination and re-
lead to inadequate mineral intake and the occasional sultant coccidiosis infection in young lambs or kids. Both
broken tooth. A commonly used mixture of 40% dical- have value in improving weight gain and feed efficiency
cium phosphate and 60% trace mineral salt offered ad lib in adults and young growing animals. Ionophores also
generally provides an effective yet inexpensive salt- enhance proprionic acid fermentation in the rumen, thus
mineral supplement. If vitamin E supplementation is re- increasing the pool of glucose precursors and aiding in
quired, 1 kg (21⁄4 lb) of a vitamin E supplement contain- the prevention of pregnancy toxemia in late-term ewes
ing 44,100 IU per kg can be combined with 22.7 kg (50 and does. These drugs have the added benefit of decreas-
lb) of trace mineral salt. If animals consume 10 to 17 g of ing the incidence of free-gas bloat in animals on high
the mixture daily, requirements for vitamin E should be grain–low forage diets (show lambs, feedlot lambs).
met. If the keeper is concerned that sheep or goats are not Decoquinate is another anticoccidial feed additive that
consuming enough of the mineral, he or she can monitor is licensed for use in sheep and goats in the United States.
intake by weighing the mineral being offered weekly. If However, it is not approved for use in animals producing
animals are not consuming enough of the supplement, milk for human consumption. Decoquinate acts early in
the addition of corn, molasses, or soybean meal may the life cycle of coccidia, before they can cause gastroin-
enhance uptake. If too much of the mixture is being con- testinal damage, therefore preventing some of the more
sumed, the addition of white salt will curtail intake. serious consequences of infection. Decoquinate is very
safe and can be added to feed, mineral mixtures, and milk
or milk replacers. Lambs or kids at risk of developing coc-
FEED ADDITIVES cidiosis because of stress or environmental contamination
To date, very few feed additives have been approved in and ewes or does in late gestation are likely candidates for
the United States by the Food and Drug Administration the use of this feed additive. To maximize their effective-
for use in sheep and goats (see Appendix I). Two anti- ness, decoquinate-containing feeds should be fed contin-
biotics, chlortetracycline and oxytetracycline, have been ually for a minimum of 28 days.
approved as feed additives for sheep in the United States. The dewormer morantel is approved as a feed additive
Dietary antibiotics may improve average daily gain, in- for goats to control gastrointestinal nematodes. Feed ad-
crease feed conversion, and reduce the losses associated ditive anthelmintics are valuable for use in animals that
with certain diseases (e.g., pneumonia, enterotoxemia) of are difficult to handle individually because of demeanor
lambs and kids when incorporated into creep feeds or fin- or lack of facilities. However if anthelmintics are fed con-
ishing diets. Responses are variable and depend on man- tinuously and consistent therapeutic intake is not met,
agement and the degree of stress the lambs are experienc- anthelmintic resistance will occur.
ing. Chlortetracycline and tetracycline are labeled in the The anionic salts ammonium chloride and ammonium
United States for increased feed efficiency and improved sulfate are both urinary acidifying agents, that help
body weight gain (20 to 60 g per ton of feed), for the pre- prevent certain types of urolithiasis when added to the
vention of Campylobacter fetus abortion in breeding ewes diets of rams, bucks, and wethers. Urolithiasis may occur
(80 mg per animal per day), and for the treatment of bac- in males (who have smaller urethral diameters than
terial pneumonia caused by Pasteurella multocida and en- females) consuming high-grain diets. This is particularly
teritis caused by Escherichia coli (22 mg per kg of body true in pet goats, breeding bucks or rams, and feedlot
weight per day). Both of these antibiotics have been suc- lambs. However, these anionic salts tend to be unpalatable,
cessfully used in similar dosages in goats (off label) to and because of their effective dosage rate (200 mg per kg
treat the conditions listed for sheep. These antibiotics per day), their use may result in depressed feed intake.
may be milled into complete diets or top-dressed onto The term yeast culture refers to yeast and the medium
feeds to treat footrot or conjunctivitis in situations where on which it is grown. It can be dried, preserved, and used
individual animal treatment is difficult. Individual animal as a feed additive. Although the mode of action has not
intake may vary, with resultant alterations in response to yet been determined, it appears that the feeding of some
therapy. Whenever feed-based antibiotics are used, yeast cultures may stimulate dry matter intake and fiber
anorexic animals will have insufficient intake for proper digestion, especially in mildly stressed animals. These
therapy. yeast cultures may stimulate the growth of ruminal bac-
Two ionophores, lasalocid and monensin, are approved teria, which utilize lactic acid. The quality of these prod-
in the United States as feed additives for control of coc- ucts should be examined closely before their use. Yeast
cidiosis in sheep and goats, respectively. Both are ap- culture may be useful in easing animals onto grain-rich
proved only for confinement feeding, and neither are ap- diets and minimizing rumen upset during the diet transi-
proved for use in animals whose milk is to be used for tion phase.
 Chapter 2 Feeding and Nutrition • 29

Buffers are salts that resist pH changes, whereas neu- destroy much of the vitamins A, E, and K in the feed.
tralizing agents neutralize acid and therefore increase pH. Therefore, when pelleting feeds, manufacturers should
Some feed-grade buffers include sodium bicarbonate, fortify these nutrients in the pellet.
sodium sesquicarbonate, sodium bentonite, and calcium
carbonate. Magnesium oxide, sodium carbonate, and
sodium hydroxide are neutralizing agents. Buffers and
FEED ANALYSIS
neutralizing agents can be added to high-grain diets (e.g., Both sheep and goats can derive nutritional value from
diets fed to feedlot lambs, show lambs, and dairy animals) numerous feeds. A listing of a wide array of feeds and
to help ease the rapid changes in ruminal pH associated their nutritional content can be found in Table 2-5. For
with the ingestion of excessive concentrates. Sodium bi- simplicity, energy values are reported as TDN. Many
carbonate is probably the most widely used of these feeds have limitations on their use because of such
chemicals. The response to feeding buffers appears to be factors as fat content, palatability, moisture content, anti-
variable except when they are used in dairy animals re- nutritional factors, and other attributes beyond the scope
ceiving high-grain diets. Buffers are of less value when of this chapter.
forage-based diets are fed. In dairy goats and sheep, To analyze the nutrient content of a given feedstuff,
buffering agents improve milk production, minimize the clinician must obtain a representative sample. For hay
milk fat depression, decrease the incidence of lactic samples, random sampling of approximately 10% of the
acidosis-rumenitis complex, and improve overall health. bales is adequate. For large round bales a core sample into
These buffers may be fed ad lib to dairy goats, included the round side of the bale to a depth of approximately 78
in a total mixed diet at around 1%, or top-dressed onto cm is ideal. Most sampling devices provide an approxi-
the feed.10 mate 2.5-cm diameter core from the bale. All of the core
samples should be combined into one container and thor-
oughly mixed. From this combined mix, the clinician
FIBER should properly package a subsample of approximately
Fiber is an important component of the diet of a ru- 0.22 kg and send it to a laboratory for analysis. Samples
minant animal. Without adequate fiber in the diet, of silage and other high-moisture feeds should be frozen
normal rumination does not occur. In sheep, feeding a before shipment to the testing laboratory. To analyze bulk
concentrate-based diet with limited amounts of fiber feeds that are stored in bins or other storage facilities, the
results in “wool pulling” as the animals seek a roughage clinician should take several random grab samples as the
source. To promote a healthy rumen, the dietary fiber feed is being augered or unloaded. Forage can be evalu-
content should generally be greater than 50%. ated by appearance, albeit with much less accuracy than
Fiber also is required in the diet to maintain accept- with some sort of analysis. Green, leafy forage that is free
able levels of milk fat. The particle size of the fiber is im- of mold or weeds is usually more nutritious.
portant. It is generally suggested that a minimum parti- After a representative sample arrives at the laboratory,
cle size of 1 to 2.5 cm be fed to stimulate normal it is analyzed for a variety of nutritive components. First,
rumination, although the effect of smaller particles is not the sample is assayed for moisture content. Most feeds
well documented in sheep and goats. Pelleted roughage contain approximately 10% to 15% moisture, possibly less
does not meet the requirement for fiber size. Animals in arid environments. The dry matter of a feed is there-
being fed pelleted forage or lush pasture should be fore important, and for comparison the nutrient content
offered hay.14 of the feed is reported as a percent of its dry matter. If the
moisture content exceeds 15%, mold contamination is a
problem. In addition, total ash content also may be deter-
PELLETED FEEDS mined and individual minerals measured. Total ash
The process of pelleting compacts feeds by forcing them content may be of value for various by-product feeds in
through a die. Pelleting of feeds decreases waste, allows which dust or soil contamination may be a problem.
for easier storage and mechanization, and decreases labor. The fiber content also should be determined. Most
However, it usually increases the total feeding cost. Com- laboratories use the Van Soest procedure, which is based
pacting the feed ingredients reduces or eliminates fines on the use of detergents. The first step is to boil the
and dust particles and therefore increases palatability. The sample in a neutral detergent solution and separate the
pelleting process reduces separation and feed sorting, pre- cell contents from the fiber. The undissolved fraction is
venting the intake of only certain parts of the total feed. referred to as the neutral detergent fiber (NDF). This NDF
Because pelleting usually entails grinding, particle size is fraction is then boiled in an acid detergent solution, dis-
usually reduced, somewhat improving digestibility. How- solving the hemicellulose and leaving behind the remain-
ever, feeding pellets can result in decreased milk fat in ing fraction, the acid detergent fiber (ADF). This fraction is
dairy animals, urolithiasis in males, and an increased inci- dissolved in 72% sulfuric acid, which solubilizes the cellu-
dence of ulcers and choke. Pelleting also may reduce or lose. The remaining lignin and silica are separated by
30 • Sheep and Goat Medicine
TABLE 2-5

NUTRIENT COMPOSITION OF VARIOUS FEEDSTUFFS FOR SHEEP AND GOATS*

TOTAL DIETARY
FEEDSTUFF DRY MATTER % NUTRITION % CRUDE PROTEIN % CALCIUM % PHOSPHORUS %

ALFALFA
Fresh 26.0 59.8 20.3 1.88 0.27
Hay, sun-cured, early bloom 90.5 56.5 19.2 1.39 0.21
Hay, sun-cured, mature 91.2 55.0 14.5 1.17 0.21
Meal, dehydrated 91.8 60.4 19.1 1.5 0.24

BAHIA GRASS
Fresh 28.7 54.7 12.5 0.45 0.31
Hay, sun-cured 90.0 50.9 9.4 0.45 0.22

BAKERY
Waste, dehydrated 91.2 89.1 11.1 0.15 0.24

BARLEY
Grain 88.6 82.7 13.0 0.06 0.38

BEET, SUGAR
Pulp, dehydrated 91.0 74.4 9.8 0.68 0.1

BERMUDA GRASS, COMMON

Fresh 28.9 56.1 12.7 0.48 0.28
Hay, sun-cured 91.2 48.1 9.7 0.47 0.18

BERMUDA GRASS, COASTAL

Fresh 30.3 58.8 12.8 0.5 0.26
Hay, sun-cured 91.6 54.4 12.2 0.42 0.21

CANOLA (RAPE)
Seeds, meal mechanically extracted 92.0 78.6 38.4 0.72 1.13

CITRUS
Pomace (citrus pulp) 91.1 81.3 6.7 1.88 0.13

CLOVER, CRIMSON
Fresh 17.5 64.0 17.1 1.37 0.28
Hay, sun-cured 87.8 61.2 16.7 1.35 0.22

CLOVER, LADINO
Fresh 17.7 70.2 24.8 1.39 0.38
Hay, sun-cured 89.1 63.5 22.4 1.35 0.31

CORN (MAIZE)
Cobs, ground 89.8 48.5 3.1 0.12 0.04
Gluten, meal 91.3 86.8 47.5 0.16 0.50
*Values are shown as a dry matter basis.
 Chapter 2 Feeding and Nutrition • 31

TABLE 2-5

NUTRIENT COMPOSITION OF VARIOUS FEEDSTUFFS FOR SHEEP AND GOATS—cont’d

TOTAL DIETARY
FEEDSTUFF DRY MATTER % NUTRITION % CRUDE PROTEIN % CALCIUM % PHOSPHORUS %

CORN (MAIZE)—cont’d

Gluten, with bran (gluten feed) 89.9 82.8 25.4 0.35 0.84
Grits byproduct (hominy feed) 90.2 87.9 10.3 0.05 0.57
Grain, grade 2 87.3 88.1 10.0 0.02 0.33
Silage, well-eared 34.1 70.1 8.2 0.26 0.21

COTTON
Hulls 90.4 45.1 4.2 0.14 0.08
Seeds, meal mechanically extracted 92.6 79.5 44.3 0.2 1.17
Seeds, whole 92.2 90.3 23.5 0.15 0.73

FESCUE, TALL
Fresh 24.0 62.5 10.8 0.51 0.46
Hay, sun-cured, early bloom 92.0 54.2 10.3 0.3 0.27

FISH, MENHADEN
Meal, mechanically extracted 91.7 77.2 66.6 5.70 3.28

GRASS
Hay, sun-cured, full bloom 89.3 54.9 9.5 0.57 0.24

JOHNSON GRASS
Hay, sun-cured 90.5 55.7 7.7 0.89 0.31

MOLASSES
Sugar cane 74.3 82.2 5.8 0.99 0.11

OATS
Grain 89.2 77.4 13.2 0.09 0.38
Hay, sun-cured 90.7 60.3 9.6 0.32 0.26

ORCHARD GRASS
Hay, sun-cured 89.6 57.9 11.8 0.41 0.28

PEANUT
Hay, sun-cured 90.7 51.1 11.5 1.12 0.14
Hulls 91.0 21.9 8.7 0.27 0.07

RICE
Bran 91.0 73.8 14.1 0.08 1.66
Hulls 91.9 12.5 3.0 0.12 0.08

RYE
Grain 87.5 82.6 13.7 0.08 0.39
Continued
32 • Sheep and Goat Medicine
TABLE 2-5

NUTRIENT COMPOSITION OF VARIOUS FEEDSTUFFS FOR SHEEP AND GOATS*—cont’d

TOTAL DIETARY
FEEDSTUFF DRY MATTER % NUTRITION % CRUDE PROTEIN % CALCIUM % PHOSPHORUS %

RYEGRASS
Fresh 22.6 70.1 17.6 0.66 0.4
Hay, sun-cured, early bloom 89.9 58.0 14.4 0.56 0.35

SORGHUM (MILO)
Grain 89.4 85.4 11.3 0.03 0.3
Silage 28.8 57.3 6.6 0.35 0.21

SOYBEAN
Seed coats, hulls 90.3 76.7 11.2 0.53 0.19
Seeds, meal mechanically extracted 90.0 85.4 48.1 0.26 0.62
Seeds, meal extracted in solution 89.9 83.6 49.9 0.26 0.64

TRITICALE
Grain 89.2 77.5 13.2 0.05 0.3

WHEAT
Fresh, early vegetative 22.2 78.3 22.1 0.4 0.4
Grain 89.0 87.3 15.1 0.05 0.38

WHEY
Dehydrated 93.3 79.7 14.1 0.91 0.82
*Values are shown as a dry matter basis.

ashing the sample. The NDF is an estimate of the crude protein content. Unfortunately, digestible protein
amount of hemicellulose, cellulose, and lignin the sample is of limited practical value in developing rations. Addi-
contains, whereas the ADF estimates only the amount of tionally, samples may sometimes be analyzed for fat.
cellulose and lignin. As the NDF content of a feedstuff Table 2-6 illustrates sample hay analyses.
rises, the bulkiness of the feed also increases—that is, Different testing laboratories use different equations
NDF is negatively correlated with dry matter intake. As to predict energy values. One common equation is as
the ADF content of a feed rises, its digestibility is de- follows:
creased. Pelleting or grinding usually results in a greater TDN (%)  88.9  (0.79  ADF [%])
dry matter intake, even for feedstuffs with relatively high
NDF contents. Based on the determined levels of the The equation balances using either the ADF (39%) or
various fiber fractions, prediction equations are used to the TDN (58.09%) values from the analysis provided in
compute TDN content and various other values for Table 2-6. This is a simple equation, but the various net
energy content (e.g., metabolizable energy, net energy). energy prediction equations use cubic and quadratic
The last major nutrient that is measured is crude terms that are much more complex. The NDF fraction
protein. The sample is analyzed for nitrogen content, and can be used to estimate the animals’ voluntary dry matter
then crude protein is calculated as percent nitrogen mul- intake:
tiplied by 6.25. The crude protein value cannot indicate
Dry matter intake (% of body weight)  120  NDF (%)
if any or how much of the protein has been damaged by
heat. Heat damage often results in decreased digestibil- Again, using the information from Table 2-6, the
ity. This method of protein analysis does not differenti- equation is solved as follows:
ate between NPN and natural protein. If the protein is
reported as digestible protein, this is formulated from the Dry matter intake  120  62%  1.94% of body weight
 Chapter 2 Feeding and Nutrition • 33

TABLE 2-6
lustrate the method for calculating a diet for a group of
ewes with an average body weight of 150 pounds. These
A SAMPLE ANALYSIS FOR FESCUE HAY animals also are in the last trimester of pregnancy, with a
high expected twinning rate (Table 2-7, A and B). Some
DETERMINED grass hay is available and has been analyzed; it contains
DRY-MATTER 51% TDN and 8.8% crude protein. Both corn and
CONSTITUENT BASIS soybean meal can be purchased as needed. The ewes’ daily
requirements can be determined from this information.
Moisture 12.75%
Table 2-7 illustrates that a 154-pound ewe with a 180%
Dry matter 87.25% to 225% expected lambing rate consumes 4.2 lb of dry
Crude protein 12.31% matter per day and requires 2.8 lb of TDN and 0.47 lb of
Fiber protein. If x  lb of hay, then 4.2  x  lb of corn. TDN
NDF 62.00% can then be determined as follows:
ADF 39.00%
0.51(x)  0.881(4.2  x)  2.8
Total digestible nutrients* 58.09%
Net energy—lactation* 1.31 mcal/kg where 0.51 and 0.881 are the proportion of TDN in the
Net energy—maintenance* 1.25 mcal/kg
hay and corn, respectively. As noted in the table, 2.8
is the daily TDN requirement in pounds. Solving for
Net energy—grain* 0.58 mcal/kg x indicates that feeding 2.4 lb of hay and 1.8 lb of corn
*Calculated from prediction equations. per day (dry matter basis) provides the ewes’ energy
needs.
The next step is to determine the protein adequacy.
The provided hay contributes 0.21 lb of protein
In other words, animals consuming the hay in Table (2.4  0.088); the corn contributes 0.18 lb of protein
2-6 would consume about 1.9% of their body weight in (1.8  0.1). Total daily intake of protein is therefore 0.39
dry matter. lb (0.21  0.18). However, because the protein require-
Another calculated figure that may be reported on a ment was determined to be 0.47 lb, the diet is still defi-
forage analysis is relative feed value (RFV). This is calcu- cient by 0.08 lb (0.47  0.39). A protein source such as
lated as follows: soybean meal can be used to supplement the grain (corn).
The net gain in protein for this substitution is 0.34 lb for
RFV  digestible dry matter (%)  dry matter intake (%)  1.29
every pound of soybean meal substituted for corn
where digestible dry matter (%)  88.9  (0.779  ADF[%]). (0.44  0.1). Dividing the deficiency (0.08 lb) by the net
Therefore, for this example the equation is completed as gain in protein gained by substituting soybean meal for
follows: corn (0.34 lb) indicates that the ration can be balanced by
adding 0.23 lb of soybean meal and subtracting 0.23 lb of
RFV  (58.52  1.94)  1.29  88
corn. The final daily ration is therefore 1.57 lb of corn,
RFVs can exceed 100 and often do for good-quality 0.23 lb of soybean meal, and 2.4 lb of hay.
alfalfa. However, they do not take into account the crude To convert this to an as-fed basis, and for simplicity’s
protein content of the forage, which must be evaluated sake in this example, the keeper should assume that all
separately. The poorer the quality of a forage, the longer it feeds are 90% dry matter. Therefore the amount of each
requires for digestion. Poor-quality forage remains in the feedstuff should be divided by 0.9, resulting in 1.7 lb of
rumen for a longer period, thereby limiting feed intake. corn, 0.25 lb of soybean meal, and 2.7 lb of hay.
Keepers purchasing feeds would do well to make deci- From a practical standpoint, the authors of this
sions based on RFV. However, during diet formulation, chapter would probably offer the ewes free-choice hay
TDN and protein concentrations are used most often as and supplement them with 2 lb of a corn-soybean meal
guidelines. mixture that contains 87.5% corn and 12.5% soybean
meal. This ration is fed until lambing commences, at
which time the diet is reformulated to meet the demands
BALANCING A RATION of lactation.
Substitution Method
The substitution method for balancing a ration works
Fixed Ingredients
best when only two or three feedstuffs are to be used on a The next example illustrates a method of balancing a
farm or ranch. (The authors of this chapter use pounds, ration using a fixed set of ingredients. In this example,
not kilograms, in demonstrating this method of ration three different grain sources are used: corn, oats, and
calculation.) As an example, the following paragraphs il- wheat. The diet is balanced for 30-lb kids growing at a
Text continued on p. 38
 34 •

TABLE 2-7, A

DAILY NUTRIENT REQUIREMENTS OF SHEEP (NUTRIENTS PER DAY)

Weight Change Total Dietary Digestible Metabolizable

Sheep and Goat Medicine

Body Weight Per Day Dry Matter Nutrition Energy Energy Crude Protein Calcium Phosphorus

% BODY
KG LB G LB KG LB WEIGHT KG LB MCAL MCAL G LB G G

EWES
Maintenance
50 110 10 0.02 1.0 2.2 2.0 0.55 1.2 2.4 2.0 90 0.21 2.0 1.8
60 132 10 0.02 1.1 2.4 1.8 0.61 1.3 2.7 2.2 104 0.23 2.3 2.1
70 154 10 0.02 1.2 2.6 1.7 0.66 1.5 2.9 2.4 113 0.25 2.5 2.4
80 176 10 0.02 1.3 2.9 1.6 0.72 1.6 3.2 2.6 122 0.27 2.7 2.8
90 198 10 0.02 1.4 3.1 1.5 0.78 1.7 3.4 2.8 131 0.29 2.9 3.1
Flushing—2 weeks prebreeding and first 3 weeks of breeding
50 110 100 0.22 1.6 3.5 3.2 0.94 2.1 4.1 3.4 150 0.33 5.3 2.6
60 132 100 0.22 1.7 3.7 2.8 1.00 2.2 4.4 3.6 157 0.34 5.5 2.9
70 154 100 0.22 1.8 4.0 2.6 1.06 2.3 4.7 3.8 164 0.36 5.7 3.2
80 176 100 0.22 1.9 4.2 2.4 1.12 2.5 4.9 4.0 171 0.38 5.9 3.6
90 198 100 0.22 2.0 4.4 2.2 1.18 2.6 5.1 4.2 177 0.39 6.1 3.9
Nonlactating—first 15 weeks of gestation
50 110 30 0.07 1.2 2.6 2.4 0.67 1.5 3.0 2.4 112 0.25 2.9 2.1
60 132 30 0.07 1.3 2.9 2.2 0.72 1.6 3.2 2.6 121 0.27 3.2 2.5
70 154 30 0.07 1.4 3.1 2.0 0.77 1.7 3.4 2.8 130 0.29 3.5 2.9
80 176 30 0.07 1.5 3.3 1.9 0.82 1.8 3.6 3.0 139 0.31 3.8 3.3
90 198 30 0.07 1.6 3.5 1.8 0.87 1.9 3.8 3.2 148 0.33 4.1 3.6
Last 4 weeks of gestation (130% to 150% lambing rate expected) or last 4 to 6 weeks’ lactation suckling singles
50 110 180(45)* 0.40(0.10) 1.6 3.5 3.2 0.94 2.1 4.1 3.4 175 0.38 5.9 4.8
60 132 180(45) 0.40(0.10) 1.7 3.7 2.8 1.00 2.2 4.4 3.6 184 0.40 6.0 5.2
70 154 180(45) 0.40(0.10) 1.8 4.0 2.6 1.06 2.3 4.7 3.8 193 0.42 6.2 5.6
80 176 180(45) 0.40(0.10) 1.9 4.2 2.4 1.12 2.4 4.9 4.0 202 0.44 6.3 6.1
90 198 180(45) 0.40(0.10) 2.0 4.4 2.2 1.18 2.5 5.1 4.2 212 0.47 6.4 6.5
 Last 4 weeks of gestation (180% to 225% lambing rate expected)
50 110 225 0.50 1.7 3.7 3.4 1.10 2.4 4.8 4.0 196 0.43 6.2 3.4
60 132 225 0.50 1.8 4.0 3.0 1.17 2.6 5.1 4.2 205 0.45 6.9 4.0
70 154 225 0.50 1.9 4.2 2.7 1.24 2.8 5.4 4.4 214 0.47 7.6 4.5
80 176 225 0.50 2.0 4.4 2.5 1.30 2.9 5.7 4.7 223 0.49 8.3 5.1
90 198 225 0.50 2.1 4.6 2.3 1.37 3.0 6.0 5.0 232 0.51 8.9 5.7
First 6 to 8 weeks of lactation suckling singles or last 4 to 6 weeks of lactation suckling twins
50 110 25(90) 0.06(0.2) 2.1 4.6 4.2 1.36 3.0 6.0 4.9 304 0.67 8.9 6.1
60 132 25(90) 0.06(0.2) 2.3 5.1 3.8 1.50 3.3 6.6 5.4 319 0.70 9.1 6.6
70 154 25(90) 0.06(0.2) 2.5 5.5 3.6 1.63 3.6 7.2 5.9 334 0.73 9.3 7.0
80 176 25(90) 0.06(0.2) 2.6 5.7 3.2 1.69 3.7 7.4 6.1 344 0.76 9.5 7.4
90 198 25(90) 0.06(0.2) 2.7 5.9 3.0 1.75 3.8 7.6 6.3 353 0.78 9.6 7.8
First 6 to 8 weeks of lactation suckling twins
50 110 60 0.13 2.4 5.3 4.8 1.56 3.4 6.9 5.6 389 0.86 10.5 7.3
60 132 60 0.13 2.6 5.7 4.3 1.69 3.7 7.4 6.1 405 0.89 10.7 7.7
70 154 60 0.13 2.8 6.2 4.0 1.82 4.0 8.0 6.6 420 0.92 11.0 8.1
80 176 60 0.13 3.0 6.6 3.8 1.95 4.3 8.6 7.0 435 0.96 11.2 8.6
90 198 60 0.13 3.2 7.0 3.6 2.08 4.6 9.2 7.5 450 0.99 11.4 9.0

EWE LAMBS
Nonlactating—first 15 weeks of gestation
40 88 160 0.35 1.4 3.1 3.5 0.83 1.8 3.6 3.0 156 0.34 5.5 3.0
50 110 135 0.30 1.5 3.3 3.0 0.88 1.9 3.9 3.2 159 0.35 5.2 3.1
60 132 135 0.30 1.6 3.5 2.7 0.94 2.0 4.1 3.4 161 0.35 5.5 3.4
70 154 125 0.28 1.7 3.7 2.4 1.00 2.2 4.4 3.6 164 0.36 5.5 3.7
*Values in parentheses are for ewes suckling lambs in the last 4 to 6 weeks of lactation.
Chapter 2
Feeding and Nutrition
• 35
 36 •

TABLE 2-7, B

DAILY NUTRIENT REQUIREMENTS OF SHEEP (NUTRIENTS PER DAY)*

Weight Change Total Dietary Digestible Metabolizable

Body Weight Per Day Dry Matter Nutrition Energy Energy Crude Protein Calcium Phosphorus

% BODY
KG LB G LB KG LB WEIGHT KG LB MCAL MCAL G LB G G
Sheep and Goat Medicine

Last 4 weeks of gestation (100% to 120% lambing rate expected)

40 88 180 0.40 1.5 3.3 3.8 0.94 2.1 4.1 3.4 187 0.41 6.4 3.1
50 110 160 0.35 1.6 3.5 3.2 1.00 2.2 4.4 3.6 189 0.42 6.3 3.4
60 132 160 0.35 1.7 3.7 2.8 1.07 2.4 4.7 3.9 192 0.42 6.6 3.8
70 154 150 0.33 1.8 4.0 2.6 1.14 2.5 5.0 4.1 194 0.43 6.8 4.2
Last 4 weeks of gestation (130% to 175% lambing rate expected)
40 88 225 0.50 1.5 3.3 3.8 0.99 2.2 4.4 3.6 202 0.44 7.4 3.5
50 110 225 0.50 1.6 3.5 3.2 1.06 2.3 4.7 3.8 204 0.45 7.8 3.9
60 132 225 0.50 1.7 3.7 2.8 1.12 2.5 4.9 4.0 207 0.46 8.1 4.3
70 154 215 0.47 1.8 4.0 2.6 1.14 2.5 5.0 4.1 210 0.46 8.2 4.7
First 6 to 8 weeks of lactation suckling singles (wean by 8 weeks)
40 88 50 0.11 1.7 3.7 4.2 1.12 2.5 4.9 4.0 257 0.56 6.0 4.3
50 110 50 0.11 2.1 4.6 4.2 1.39 3.1 6.1 5.0 282 0.62 6.5 4.7
60 132 50 0.11 2.3 5.1 3.8 1.52 3.4 6.7 5.5 295 0.65 6.8 5.1
70 154 50 0.11 2.5 5.5 3.6 1.65 3.6 7.3 6.0 301 0.68 7.1 5.6
First 6 to 8 weeks of lactation suckling twins (wean by 8 weeks)
40 88 100 0.22 2.1 4.6 5.2 1.45 3.2 6.4 5.2 306 0.67 8.4 5.6
50 110 100 0.22 2.3 5.1 4.6 1.59 3.5 7.0 5.7 321 0.71 8.7 6.0
60 132 100 0.22 2.5 5.5 4.2 1.72 3.8 7.6 6.2 336 0.74 9.0 6.4
70 154 100 0.22 2.7 6.0 3.9 1.85 4.1 8.1 6.6 351 0.77 9.3 6.9

REPLACEMENT EWE LAMBS

30 66 227 0.50 1.2 2.6 4.0 0.78 1.7 3.4 2.8 185 0.41 6.4 2.6
40 88 182 0.40 1.4 3.1 3.5 0.91 2.0 4.0 3.3 176 0.39 5.9 2.6
50 110 120 0.26 1.5 3.3 3.0 0.88 1.9 3.9 3.2 136 0.30 4.8 2.4
60 132 100 0.22 1.5 3.3 2.5 0.88 1.9 3.9 3.2 134 0.30 4.5 2.5
70 154 100 0.22 1.5 3.3 2.1 0.88 1.9 3.9 3.2 132 0.29 4.6 2.8
 REPLACEMENT RAM LAMBS

40 88 330 0.73 1.8 4.0 4.5 1.1 2.5 5.0 4.1 243 0.54 7.8 3.7
60 132 320 0.70 2.4 5.3 4.0 1.5 3.4 6.7 5.5 263 0.58 8.4 4.2
80 176 290 0.64 2.8 6.2 3.5 1.8 3.9 7.8 6.4 268 0.59 8.5 4.6
100 220 250 0.55 3.0 6.6 3.0 1.9 4.2 8.4 6.9 264 0.58 8.2 4.8

LAMBS FINISHING—4 TO 7 MONTHS

30 66 295 0.65 1.3 2.9 4.3 0.94 2.1 4.1 3.4 191 0.42 6.6 3.2
40 88 275 0.60 1.6 3.5 4.0 1.22 2.7 5.4 4.4 185 0.41 6.6 3.3
50 110 205 0.45 1.6 3.5 3.2 1.23 2.7 5.4 4.4 160 0.35 5.6 3.0

EARLY WEANED LAMBS—MODERATE GROWTH POTENTIAL

10 22 200 0.44 0.5 1.1 5.0 0.40 0.9 1.8 1.4 127 0.38 4.0 1.9
20 44 250 0.55 1.0 2.2 5.0 0.80 1.8 3.5 2.9 167 0.37 5.4 2.5
30 66 300 0.66 1.3 2.9 4.3 1.00 2.2 4.4 3.6 191 0.42 6.7 3.2
40 88 345 0.76 1.5 3.3 3.8 1.16 2.6 5.1 4.2 202 0.44 7.7 3.9
50 110 300 0.66 1.5 3.3 3.0 1.16 2.6 5.1 4.2 181 0.40 7.0 3.8

EARLY WEANED LAMBS—RAPID GROWTH POTENTIAL

10 22 250 0.55 0.6 1.3 6.0 0.48 1.1 2.1 1.7 157 0.35 4.9 2.2
20 44 300 0.66 1.2 2.6 6.0 0.92 2.0 4.0 3.3 205 0.45 6.5 2.9
30 66 325 0.72 1.4 3.1 4.7 1.10 2.4 4.8 4.0 216 0.48 7.2 3.4
40 88 400 0.88 1.5 3.3 3.8 1.14 2.5 5.0 4.1 234 0.51 8.6 4.3
50 110 425 0.94 1.7 3.7 3.4 1.29 2.8 5.7 4.7 240 0.53 9.4 4.8
60 132 350 0.77 1.7 3.7 2.8 1.29 2.8 5.7 4.7 240 0.53 8.2 4.5
*These values represent different weight losses and sizes than in Table 2-7, A.
Chapter 2
Feeding and Nutrition
• 37
38 • Sheep and Goat Medicine
rate of 0.20 lb per day. In addition, cottonseed hulls are An equation similar to the previous example, in which
available as a roughage source and cottonseed meal as a x  pounds of cottonseed hulls and 0.765  x  11
source of protein. The wheat was purchased at a bargain mixture of corn and oats is now used to solve for TDN:
price, but potential problems exist with feeding large
0.451(x)  0.8275(0.765  x)  0.47
amounts of it. Therefore wheat is limited to 15% of the
diet. In this example the owners have requested that equal where 0.451 is the TDN content of the cottonseed hulls
quantities of corn and oats be used in the diet formula- and 0.8275 is the TDN content of a mixture of equal
tion. Table 2-8 describes the daily requirements for these parts of corn (0.881) and oats (0.774) [0.881  0.774] 
goats as follows: dry matter intake of 0.9 lb, protein 2  0.8275.
intake of 0.119 lb, and TDN of 0.59 lb. First, the nutri- Solving for x reveals that balancing the ration requires
ents being provided by the fixed level of wheat should be 0.52 lb of cottonseed hulls and 0.24 lb of the corn/oats mix,
taken into account: which equates to 0.12 lb (0.24 lb divided by 2) of each.
So far, the ration consists of 0.52 lb of cottonseed hulls,
Daily intake  0.90 lb  15%  0.135 lb of wheat per day
0.135 lb of wheat, 0.12 lb of corn, and 0.12 lb of oats.The
TDN from wheat  0.135 lb  0.873  0.12 lb of TDN
hulls provide 0.022 lb of protein (0.52 lb  0.042), the
Protein  0.135 lb  0.151  0.020 lb of protein
corn provides 0.012 lb of protein (0.12 lb  0.10), and the
Subtracting these amounts from the requirement oats provide 0.016 lb of protein (0.12  0.132). Total
yields the following results: protein in the ration thus far is 0.05 lb (0.022  0.012 
0.016). The requirement is 0.099 lb, leaving a deficit of
Dry matter  0.90  0.135  0.765 0.049 lb.
TDN  0.59  0.12  0.47 lb Cottonseed meal can be substituted for some of the
Crude protein  0.119  0.020  0.099 lb grain. An equal mix contains 11.6%, so the net gain of the

TABLE 2-8

DAILY NUTRIENT REQUIREMENTS FOR GOATS

CLASS OF GOAT BODY WEIGHT (LB) DRY MATTER INTAKE* (LB) TOTAL DIETARY NUTRITION (LB) CRUDE PROTEIN (LB)

Dry doe, early 50 1.25 0.64 0.091

pregnant 70 1.75 0.83 0.117
90 2.25 1.00 0.141
110 2.75 1.17 0.164
130 3.25 1.32 0.186
Doe, late 50 1.25 1.12 0.159
pregnancy 70 1.75 1.45 0.205
90 2.25 1.75 0.248
110 2.75 2.04 0.288
130 3.25 2.31 0.327
Doe, lactating Add 0.35 pound of total dietary nutrition and 0.072 pound
of protein per pound of 4% milk produced
Kid, growing at 30 0.9 0.59 0.119
0.2 lb/day 40 1.2 0.70 0.134
50 1.5 0.79 0.148
Kid growing at 30 0.9 0.66 0.147
0.3 lb/day 40 1.2 0.77 0.162
50 1.5 0.86 0.176
Kid growing at 30 0.9 0.74 0.176
0.4 lb/day 40 1.2 0.85 0.191
50 1.5 0.94 0.205
*Daily dry matter intake for does is estimated at 2.5% of body weight but can be as high as 2.75% of body weight. For growing kids, intake is
estimated at 3% of body weight but can be as high as 4.5% depending on diet and types of kids being fed.
 Chapter 2 Feeding and Nutrition • 39

substitution is 32.7% (44.3%  11.6%). Therefore to previous example is used. Values for the calcium and
balance the ration the keeper should add 0.15 lb (0.47 lb phosphorus content of these two feedstuffs are provided
divided by 0.327) of cottonseed meal and take out 0.075 in Table 2-5:
lb of corn and 0.075 lb of oats from the diet.
CALCIUM PHOSPHORUS
The final daily ration is as follows:
Corn grain, grade 2 0.02% 0.33%
LB DRY MATTER LB AS FED* % AS FED Soybean meal, mechanically
Cottonseed hulls 0.52 0.58 58.0 extracted 0.26% 0.62%
Wheat 0.135 0.15 All values are provided on a dry matter basis. Calcium
Corn 0.045 0.05 5.0 supplementation is to be made with limestone, and phos-
Oats 0.045 0.05 5.0 phorus supplementation is to be made with dicalcium
Cottonseed meal 0.15 0.15 17.0 phosphate. The corn/soybean meal mixture comprises
*To determine this column, the keeper should determine the percent- 97% of the diet. This allows for the addition of a calcium
age of dry matter and divide it into the amount of dry matter being and phosphorus source (dicalcium phosphate) and a
fed (e.g., cottonseed hulls 0.52 lb dry matter at 90% dry matter, or calcium source (limestone) for needed trace minerals, as
0.52 divided by 0.9  0.58 lb of feed). In this example, all the feeds well as a urine acidifier (if needed). Corn is therefore
are 90% dry matter.
81.7% of the diet (84.25%  0.97), whereas soybean meal
comprises 15.3% of the diet (15.75%  0.97). Assuming
a requirement of 0.5% for phosphorus and knowing the
Pearson Square
percentage of phosphorus in dicalcium phosphate
The Pearson square is a simple technique that is quite (18.5%) allows the calculation of the amount of phospho-
useful for blending two ingredients on the basis of one rus supplementation (as dicalcium phosphate) by multi-
nutrient. In the following example, corn and soybean plying each feed ingredient by the percentage of phos-
meal are blended to attain a concentrate mixture of 16% phorus in that feed and adding the results:
crude protein. The square is formed by placing the per-
0.5%  (81.75%  0.0033)  (15.3%  0.0062)  (x  0.185%)
centage of the nutrient that is desired in the center and
then placing the percentage of the nutrient present in the where 0.5% is the daily phosphorus requirement, 81.75%
two feeds at the left corners: is the percentage of corn in the diet, 0.0033 is the per-
centage of phosphorus found in corn, 15.3% is the
Corn 10.0% 32.1 parts corn percentage of soybean meal in the diet, 0.0062 is the
percentage of phosphorus found in soybean meal, x is
16% the amount of dicalcium phosphate required for sup-
plementation, and 0.185% is the percentage of phospho-
Soybean meal 48.1% 6.0 parts soybean meal rus in dicalcium phosphate. The equation is solved as
38.1 total parts follows:
0.5%  0.27%  0.095%  (x  0.185%)
The square is solved by subtracting diagonally across
0.5%  0.365%  (x  0.185%)
the square without regard to the sign of the differences (in
(0.5%  0.365%)  0.185%  x
other words, no negative numbers) and recording the dif-
x  0.73%
ference at the right corners. Using the individual and total
parts, the percentage of each ingredient can be calculated: Therefore dicalcium phosphate must comprise 0.73%
of the diet to satisfy the phosphorus requirement.
32.1/38.1  84.25% corn
It is now possible to solve for the required calcium
6/38.1  15.75% soybean meal
supplementation in the form of limestone, assuming a
Therefore a mixture composed of 84.25% corn and daily requirement of 0.6% and knowing both the amount
15.75% soybean meal mixture yields a feed with a crude of dicalcium phosphate in the diet (0.73%) and the per-
protein content of 16%. This quick method can be used centage of calcium in limestone (38%):
for any class of nutrient.
0.6%  (81.75%  0.0002)  (15.3%  0.0026)
 (0.73%  0.22%)  (x  0.38%)
Calculating for Phosphorus
where 0.6% is the daily calcium requirement, 81.75% is
and Calcium Supplementation
the percentage of corn in the diet, 0.0002 is the percent-
The next example illustrates the way to calculate require- age of calcium found in corn, 15.3% is the percentage of
ments for phosphorus and calcium supplementation. The soybean meal in the diet, 0.0026 is the percentage of
84.25% corn and 15.75% soybean meal mixture from the calcium found in soybean meal, 0.73% is the percentage
40 • Sheep and Goat Medicine
of dicalcium phosphate in the diet, 0.22% is the percent- 13. Hayter S, Wiener G: Variation in the concentration of copper in
age of calcium in dicalcium phosphate, x is the amount of the blood plasma of Finnish-Landrace and Merino sheep and
limestone required for supplementation, and 0.38% is the their crosses with reference to reproductive performance and age,
Anim Prod 16:261, 1973.
percentage of calcium in limestone. The equation is
14. Holland C, Kezar W: Pioneer forage manual. A nutritional guide,
solved as follows:
Des Moines, IA, 1995, Pioneer Hi-Bred International.
0.6%  0.016%  0.04%  0.16%  (x  0.38%)
0.6%  0.216%  (x  0.38%)
(0.6%  0.216%)  0.38%  x
F URTHER R EADING
Naylor JM, Ralston SL: Large animal clinical nutrition, St Louis, 1991,
x  1%
Mosby.
Therefore limestone must comprise 1% of the diet to Ensminger ME, Oldfield JE, Heineman WW: Feeds & nutrition, ed 2,
satisfy the calcium requirement. Clovis, CA, 1990, Ensminger Publishing.
The ration calculated in the previous examples would
therefore be composed of the following:
BODY CONDITION SCORING
Corn 81.7%
Theoretically, the exact amount of nutrients required for
Soybean meal 15.3%
each stage of production should be provided; however,
Dicalcium phosphate 0.73%
this is usually not practical under field conditions. There-
Limestone 1%
fore the animal is subject to seasonal periods of undernu-
Total ration 98.73%
trition and overnutrition. A useful system to help assess
This is on an as-fed basis. Given that a standard 0.5% the overall nutritional status of the flock is to assign a
(0.5 lb) of sodium chloride and 0.05% (0.05 lb) of trace body condition score to the animals. The body condition
minerals are usually added, the resultant mixture is score system most commonly used for sheep and goats
99.28% complete on a dry matter basis. has a range of 1 to 5, with 1 being extremely thin and 5
being extremely obese. Body condition scoring is accom-
plished by palpating a relaxed ewe or doe for the degree of
R EFERENCES
1. Hofmann RR: Anatomy of the gastrointestinal tract. In Church
fat covering on the spinous processes and transverse
processes in the lumbar region (Figure 2-1).1 Because
DC, editor: The ruminant animal digestive physiology and nutrition,
more than 85% to 90% of all healthy ewes receive a score
Englewood Cliffs, NJ, 1988, Prentice-Hall. of 2, 3, or 4, half-scores are often assigned for greater ac-
2. Nutrient requirements of sheep, Washington, DC, 1985, National curacy. For example, if the animal scores higher than a 3,
Academy Press. but not quite a 4, it should be classified with a condition
3. Water requirements for livestock, 2000, Alberta Agriculture Food and score of 3.5. Ideally, the majority of the flock should have
Rural Development Extension Bulletin. a condition score of 2.5 to 3 at breeding and parturition.
4. Bauder J: When is water good enough for livestock? Montana State If the flock was scored 45 days before parturition, and
Extension Bulletin, 2000. the average was less than 2.5 to 3, the keeper should in-
5. Guyer PQ: Livestock water quality, University of Nebraska Exten- crease the flock’s energy intake so that the animals reach
sion Service Bulletin G79-46A.
an average of 2.5 to 3 by the time of parturition. Animals
6. Meyer KB: Water quality in animals, 1999, Purdue University Ex-
in thin body condition at parturition give birth to weaker
tension Bulletin WQ9.
7. Maloiy GMO, Taylor CR: Water requirements of African goats
babies and generally produce less milk during early lacta-
and haired sheep, J Agric Sci 77:203, 1971. tion. An ideal body condition score is especially impor-
8. Nutrient requirements of goats: angora, dairy and meat goats in tem- tant in accelerated breeding systems in which the females
perate and tropical countries, Washington, DC, 1981, National are rebred within 60 to 90 days after parturition. Like-
Academy Press. wise, if the average condition score 30 days before breed-
9. Knox MR, Steel JW: The effects of urea supplementation on pro- ing is less than 3, the keeper should consider flushing the
duction and parasitological responses of sheep infected with females. Moreover, condition scoring all the females
Haemonchus contortus and Trichostrongylus colubriformis, Vet Parisit allows the keeper to move the thin females (those with a
3:123, 1999. score less than 2) into one feeding group while leaving the
10. Bratzlaff K, Henlein G, Huston J: Common nutritional problems
others (those with a score higher than 3) in another
feeding the sick goat. In Naylor JM, Ralston SL, editors: Large
feeding group. In this way the thin females can receive
animal clinical nutrition, St Louis, 1991, Mosby.
11. Qi K, Lu CD, Owens FN: Sulfate supplementation of growing
additional supplementation without the others becom-
goats: effects on performance, acid-base balance, and nutrient di- ing overconditioned. A universally accepted condition
gestibilities, J Anim Sci 71:1579, 1993. scoring system is not available for goats. The authors
12. Qi K et al: Sulfate supplementation of Angora goats: metabolic follow the system in Table 2-9 and use many of the same
and mohair responses, J Anim Sci 70:2828, 1992. principles described for sheep.2 Figure 2-2 shows a crude
 Chapter 2 Feeding and Nutrition • 41

Figure 2-1 Body condition scores for sheep. These drawings show a cross-section through the
lumbar region and depict the fat covering (or lack thereof). Score 1, The spinous and transverse
processes are sharp and no fat is detectable on the loin area. These animals are emaciated. Score 2,
Animals are still thin with prominent spinous and slightly rounded transverse processes. The examiner’s
fingers can be passed under the edge of the transverse processes. Score 3, Animals have smooth, slightly
rounded spinous and transverse processes. Slight pressure is required to palpate the transverse process.
Continued
42 • Sheep and Goat Medicine

Figure 2-1, cont’d Score 4, These animals are fat. The spinous processes are barely palpable.
Score 5, These animals are obese, with a midline concavity running over the spinous process. Because
these scores are broad, many owners or managers round up to half-scores (e.g., 2.5) if the animal has
more fat covering then one score but not quite as much as the next whole-number score up.

TABLE 2-9

THE BODY CONDITION SCORING SYSTEM FOR GOATS

SCORE APPEARANCE

0 No subcutaneous tissue seen.

1 Dorsal aspect of vertebral column forms a continuous ridge, hollow flank, ribs easily seen. Sternal fat easily
moved laterally. Chondrosternal joints easily palpable. No muscle or fat between ribs or bones. Transverse
processes of lumbar vertebrae easily visualized, and articular processes easily palpable.
2 Sternal fat moveable, but 1 to 2 cm thick. Tissue visible between skin and chondrosternal joints. Some tissue
around transverse processes of lumbar spine, but it is more difficult to palpate than in Score 1. Need slight
pressure to palpate articular processes.
3 Dorsal aspect of vertebral column is less prominent. Sternal fat is thick and barely moveable. Chondrosternal
joints are difficult to palpate. Lumbar vertebrae have thick tissue covering. Articular processes of transverse
processes not palpable.
4 Sternal fat, costochondral fat, and rib fat continuous. Transverse process difficult to palpate. Spinous processes
not palpable.
5 Sternal fat and rib fat bulges between pressed fingers. Spinous and transverse processes not palpable.
From Santucci PM et al: Body condition scoring of goats in extensive conditions. In Morand-Fehr P, editor: Goat nutrition, Wageningen,
Netherlands, 1991, Pudoc.
 Chapter 2 Feeding and Nutrition • 43

Figure 2-3 These mixed breed sheep are grazing a fescue

pasture. They have free range to the pasture and, in this case, no
pasture rotation is being used.

legumes to a grass pasture improves the nitrogen content

of the soil and increases pasture productivity. Legumes
Figure 2-2 The clinician can estimate the weight of a sheep or improve the nutritional value of a pasture, but may
goat by measuring the circumference or heart girth just behind the predispose to calcite calculi or bloat. Still, the benefits
shoulder and elbow (a) and the body length from shoulder to rump or
tuber ilium (b) in inches. Heart girth  heart girth  body length 
far outweigh the problems if the legumes are used
300  weight in lb. The wool of unshorn animals should always be judiciously.
compressed during this estimation. One of the authors (Dr. Pugh) uses Where possible, a pasture grazing system should
this formula on sheep and goats of varying size with acceptable include warm-season perennial grasses for use by the
results. (Adapted from Ensminger ME, Oldfield JE, Heinmann WW: ewes after weaning. During early gestation, these same
Feeds and nutrition, ed 2, Clovis, CA, 1990, Ensminger Publishing.)
grasses can be used as mature forage. Approximately 60
days before parturition and through the first 90 days of
lactation the females can graze on cool-season, annual
method of estimating the body weight of sheep and grasses. In some environments the warm-season grasses
goats. then begin their seasonal production. With this system,
very little supplemental feeding is required. As long as
quantity of the various forages is not limited, grain sup-
FEEDING PROGRAMS plementation is usually not required. However, under
In North America, most farm flocks of sheep and goats most practical settings, weather limits forage quantity for
are maintained on pasture- or range-based systems. 60 days or longer each year. A good-quality, pasture-
Worldwide, about 80% of all nutrients for sheep and based forage feeding system often requires minimal
goats are derived from forage.3 Both species are adept at energy and protein supplements for non-lactating, non-
converting forage into high-quality products for human growing animals.
consumption and use. Whenever sheep (and possibly For proper forage management, adequate amounts of
goats) graze large pastures or range, their maintenance grazeable land and several pastures are needed for a rota-
energy requirements may be more than 60% higher than tional grazing program (Figure 2-3). Forage must have
those of animals raised in dry lots.5 The more walking re- some periods of rest from grazing to maintain optimal
quired or the larger the range, the more work the animal productivity. Therefore pasture rotation is essential. The
must perform to consume enough forage to support pasture layout does not need to be elaborate or comprised
maintenance, growth, lactation, and fiber production. of many small paddocks. However, pastures do need to be
divided for proper maximization of forage production.
Approximately 6 to 10 separate paddocks or pastures are
PASTURES desirable, and further subdivisions can be added as
Producing and providing good-quality forage ultimately needed (Figure 2-4). The divisions should be based on
reduces feeding costs, increases overall health, and usually the productivity of the soil and natural breaks in the to-
results in a more profitable farming operation. In a typical pography. They will not necessarily be of equal size. The
fall breeding/spring lambing operation, supplemental forage should be grazed in a way that optimal leaf mate-
grain feeding can be kept to a minimum if a good forage rial is produced. Depending on the time of year and
management program is followed. A variety of perennial amount of moisture, the length of time grazing an area
grasses (e.g., fescue, orchard) can be used by sheep and and rest between each rotation vary. For example, the
goats. Strategic incorporation of legumes (e.g., clover) keeper might have his or her flock graze each of 10 pad-
and some annual grasses (e.g., rye grass) can provide ex- docks for an average of 3 days at a time; at the end of the
cellent nutrition for the flock. The addition of 30% rotation the first paddock has had 30 days of rest and
44 • Sheep and Goat Medicine
soil types. In general, phosphorus should be supple-
mented under most range land conditions. Regardless of
its composition the salt-mineral supplement should be
made available free choice as the only source of salt.
Additional supplements containing protein or energy
may be used as needed. Body condition scoring can help
in making the decision to supplement energy. If the level
of desirable performance can be attained by using a sup-
plemental grain less than or equal to 0.5% of body
weight, feeding grain can be economical. However, if
greater quantities of grain are needed, negative effects of
the grain on forage use will occur (depressed digestibility
of forage). Several grain by-products are acceptable sup-
plements for ruminants consuming a forage-based diet.
Figure 2-4 These Boer and Boer-crossed goats are in a pasture
rotation program in which they are moved every 5 days.
For example, soybean hulls and wheat middlings can
provide economical supplies of energy without negative
effects on forage use. Protein supplements in the form of
soybean meal or cottonseed meal are often used and may
should have good forage regrowth. This type of grazing actually enhance the digestibility of moderate- or poor-
management may not necessarily increase animal gains, quality forage.
but it may increase the land’s carrying capacity as well as Whenever hand feeding is difficult, salt-limited
the overall quality of the pastures. Pasture rotation rations may be useful for range-fed sheep or goats used
systems that increase grass production do not necessarily for brush control. Depending on requirements, supple-
aid in parasite control. Between four and six ewes (and mental energy (e.g., corn, oats) or protein (e.g., cotton-
their lambs) and five to eight does (and their kids) can be seed meal, soybean meal) should be ground and mixed
maintained on the same amount of land that will support with salt in a 31 to a 61 salt-to-grain ratio, depending
one cow and her calf. However, in woodland or brushy on intake. If intake is too great, more salt should be
areas the same land that will nutritionally support one added. If intake is too low, salt should be removed. In all
cow and her calf will provide enough forage for about 10 cases only white salt (NaCl) should be used. The use of
goats and their kids. salt-limited feeds decreases trace mineral intake. If trace
A complete mineral supplement should be offered at mineral deficiencies exist locally, and salt-limited feeds
all times. An adequate mineral supplement for animals are to be used, the keeper should add a suitable trace
grazing grass pasture contains 15% to 30% salt, 6% to mineral salt to the feed at a level where trace mineral con-
12% calcium, 6% to 12% phosphorus, and 1% to 4% mag- sumption does not exceed 0.02% of the animal’s weight.
nesium (except in early spring when magnesium should Salt-limited supplemental feeding should be introduced
be 8% to 14% of the minerals). Trace minerals suitable for slowly over 2 to 3 weeks, and the animals should be mon-
the area and soil type also should be offered. itored daily, particularly in times of stress (predator
attacks, weather changes).
RANGE
Many of the world’s sheep and goats graze on range
CONFINEMENT FEEDING
lands. The common goal among all range land enterprises Confinement feeding of sheep or goats in various small
is to use as much standing forage as possible with little vegetation-free enclosures or dry lots is used in certain
use of harvested forage or other supplements. Supple- locales for all or part of the year. In climates with colder
mental feeding should only be practiced when nutrient winters and areas that lack winter grazing, some produc-
demands far exceed the nutrient supply of the forage. ers move sheep (and occasionally goats) to a sheltered dry
Some deficiencies are acceptable because of the female’s lot or barn for protection. Such situations usually require
ability to regain body condition during the period from more start-up money (for construction of a barn to house
weaning until breeding. The amount and type of supple- animals, feeding floor or lot, and water system) than
mentation needed are variable across range conditions. range or pasture operations. Confinement management
The two most important factors in supplementation de- also may increase the incidence of some contagious dis-
cisions are stage of animal production (lactation) and eases, external parasites (particularly during winter),
weather conditions (moisture or snow cover). A good feeding costs, bedding costs, and the need to handle and
range mineral mixture includes equal parts of dicalcium dispose of manure. Still, the advantages can more than
phosphate and trace mineral salt. The trace mineral salt outweigh the disadvantages in operations where a cheap
component should be designed for the local forage and source of feed and labor is available.
 Chapter 2 Feeding and Nutrition • 45

TABLE 2-10

EXAMPLE RATIONS FOR DRY LOT FEEDING FOR NON-DAIRY ANIMALS (LB/DAY)

150-Pound Ewe 70-Pound Doe

Ingredient* MAINTENANCE GESTATION LACTATION MAINTENANCE GESTATION LACTATION

A† B† A B A B A B A B A B

Alfalfa hay 2.9 4.25 5.5 2.0 2.8 2.6

Grass hay 2.9 3.6 4.8 1.67 2.3 2.2
Corn 0.25 0.75 1.0 1.0 0.33 0.5 0.4 0.4
Soybean meal 0.15 0.75 0.4
*See Table 2-5 for average nutrient contents for each ingredient.
†A and B are different sample diets for each stage of production.

When properly performed, confinement or dry lot avoided, as should bundle-fed, uneaten, frozen, moldy, or
feeding can all but eliminate two of the most serious spoiled silage. Where possible, the use of square bales of
problems with sheep and goat production: internal hay results in less wastage than large round bales, but they
parasites and predators. However, during confinement usually cost more and require more labor to use.
feeding, some access to outdoor dry lots is needed to Feed bunk design should minimize animal contamina-
improve hoof and udder health and decrease the need for tion. Adults and kids (lambs) should be prevented from
supplemental vitamin D. Because no grazing is allowed crawling into feed containers and soiling the feed.
and feedstuffs (hay, silage, grains) are fed in bunks or Dry lot feeding is also of value when implementing a
other types of feeders, production losses resulting from parasite control program. If oral anthelmintics of the
parasites can be curtailed. Also, less energy is required for benzimidazole class are to be used in a deworming
maintenance (walking to a feed bunk versus grazing). program, forcing the animals to fast or feeding dry hay for
Animals require 2 to 4 hours to consume the same 12 to 24 hours before deworming and then providing dry
amount of dry matter from hay that they do in 16 to 22 lot feeding for as long as 72 hours improves the results.
hours of grazing pasture. Heavy-wooled breeds of sheep This technique also allows for parasite egg–laden feces to
in full fleece require 1.5 times more space in a confined be “cleaned” or “passed” from the bowel before placing
area than those that have been shorn. Adult sheep and animals on a safe pasture. Therefore animals may be
goats require 0.6 and 0.3 m of linear bunk space per moved to pasture after deworming in a relatively parasite-
animal, respectively. free state, reducing pasture contamination. Examples of
With confinement systems, ewes and does are more confinement or dry lot rations are shown in Table 2-10.
easily separated by age (ewe lambs, adult ewes) and pro-
duction (lactating, dry or early lactation, late lactation).
The ability to feed groups separately can improve the use
FEEDING THE ADULT MALE
and efficiency of available feedstuffs and help decrease Males should enter the breeding season in good body con-
the incidence of some production diseases (e.g., preg- dition without excessive fat. Rams and bucks should be
nancy toxemia, hypocalcemia). A dry lot program can be maintained at a prebreeding body condition score of 3 to 4
used not only during winter; but also when pasture because they may lose more than 10% of their body weight
becomes scarce or when feeding young lambs or kids for in 11⁄2 months of a breeding season. Condition scores
rapid gains. should be assessed as part of a breeding soundness evalua-
In dry lot feeding, sheep or goats may be fed hay, tion about 2 months before breeding. It is usually benefi-
silage, haylage, or green chop, just as would be used for cial to feed a concentrated energy-protein supplement to
cattle. The dietary habits of sheep and goats vary and the males beginning approximately 4 to 6 weeks before the
affect intake. However, dietary preference appears to limit breeding season. Depending on the body condition and
the use of certain feedstuffs more greatly in goats. The size of the males, 0.5 to 1 kg (1 to 2 lb) of concentrate
smell, taste, and variety of feeds also affects intake. Silage usually suffices. A good-quality supplement for grass-
can be fed to sheep and goats, but both may take time to based forage is 80% corn and 20% soybean meal. After the
adapt to its smell and consistency. Silage that has been breeding season some concentrate may need to be fed to
poorly packed, exposed to air, or has not attained a low help the males regain an adequate body condition. For the
enough pH (less than 5.5 ) may mold or be contami- remainder of the year, adult males can be fed at a mainte-
nated with Listeria monocytogenes. Such silage should be nance level. If grass forage is fed, animals should have free
46 • Sheep and Goat Medicine
access to a mixture of 50% dicalcium phosphate and 50% and continue for an additional 2 to 3 weeks into the
trace mineral salt. If legumes are a significant portion of breeding season.
the diet, a mixture of 50% trace mineral salt, 25% dical- The effects of flushing include increased body condi-
cium phosphate, and 25% defluorinated rock phosphate tion, increased ovulation rate, and increased number of
can be offered. In both instances, these mineral-salt mix- lambs born. Adequate body condition is necessary for ac-
tures should be the only source of salt offered to encourage ceptable conception rates. Outside certain biologic limits
adequate intake. The trace mineral component should be a flushing effect cannot be observed. For example, an ex-
designed for the local soil types. For sheep, low-copper tremely thin (condition score 1) female would probably
mineral mixtures are optimal, but goats can safely not have an increased ovulation rate because she is too
consume trace mineral mixtures made for cattle. Because thin to have normal reproductive cycles. However, within
of the possibility of urolithiasis in males, the keeper should normal ranges (condition score 2.5 to 3) the ovulation
take steps to prevent stone formation by adding ammo- rate appears to respond to a short-duration increase in
nium chloride or other urine acidifiers to the mineral energy, and, to a lesser extent, to increased protein intake
mixture (see Chapter 10). (see Figure 2-1). Flushing does not always increase
lambing or kidding rates; however, it does increase the
number of females cycling early in the breeding season,
FEEDING THE FEMALE resulting in a greater proportion of the offspring being
Breeding females have different nutrient requirements as born early in the lambing or kidding season. Females at or
the stage of production changes. Although requirements just under a body condition score of 2.5 to 3 are optimal
are much lower for maintenance than they are for lacta- for most breeding flocks.
tion, meeting these requirements is important for effi-
cient production. Body condition scoring all females
every 2 to 3 weeks is an important and cost-effective
Early to Middle Gestation
management tool. Mineral feeding as described for the After the female has conceived, early gestation is the time
adult male is applicable for the female. of partial fetal and placental development. Nutrition is
important for adequate development, but requirements
are not greatly increased over those of maintenance. If the
Maintenance diet is lacking in energy, protein, and certain minerals,
During maintenance the objective is to maintain the poor placental development may occur, resulting in poor
female’s weight and health and replenish any losses fetal growth. A reduction in lamb survival rates at birth
experienced during lactation. Most pasture or range set- can result from inadequate feeding during early gestation.
tings provide adequate levels of nutrient intake to main- Likewise, adequate nutrition is required for proper at-
tain dry, non-pregnant sheep and goats for this entire tachment of the embryo to the uterus. Mid-term stress
period. If extremes in environmental conditions occur abortions can occur in Angora goats as a result of energy
(e.g., drought, snowfall), some supplemental feeding is deficiency. This is more common in range conditions,
required. particularly after a weather change, predator attack, or
decreased feed intake. The incidence can be minimized
by not breeding the female until she has attained 60% to
Breeding 70% of her projected mature weight, and by maintaining
At the time of breeding, the practice of flushing the a steady nutritional state during pregnancy4 (see Chap-
females has been used with some success. The basic ters 6 and 7). During early gestation ewes and does can be
premise is that increased nutrition, specifically energy, maintained on winter range or pasture or moderate-
just before and during the early breeding season increases quality hay. As seasonal decreases in feed availability or
the ovulation rate and therefore the lambing or kidding weather-associated increases in feed requirements occur,
rate. The female’s age and body condition and the time of some supplemental grain may be required. Females
year all affect the response to flushing. Mature females in should be fed to maintain a body condition score of 2.5 to
marginal body condition usually respond best to flushing. 3 during early gestation. The scores should be assessed
Moreover, the practice appears to be more beneficial every 2 to 3 weeks, and any flock condition score change
when trying to breed the group early or late as opposed to acted on immediately.
during the peak of breeding season. Overconditioned
females either do not respond or appear to respond only
marginally to flushing. Flushing can be accomplished by
Late Gestation
the provision of lush pastures or by supplementation with The nutrition of the female during the last 6 weeks
about 0.14 kg (0.33 lb) to 0.45 kg (1 lb) of a 10% to 12% of gestation is extremely important. Approximately 70%
crude protein grain per head per day. It is best to begin of fetal growth occurs during this period. Undernutrition
approximately 2 weeks before the males are introduced can result in poor colostrum production, low birth–
 Chapter 2 Feeding and Nutrition • 47

weight lambs and kids, lower energy reserves in the time frame promotes significant mammary development
newborn animals, and increased death loss, especially during the last 30 days of pregnancy. Stillbirths, preg-
during cold and inclement weather. Birth weight is an nancy toxemia, and poor milk production are all indica-
important factor affecting newborn survival. It can be in- tors of feeding an energy-deficient diet in late gestation.
fluenced by breed, number born, age of dam, and the Adequate nutrition should be provided to support milk
dam’s preparturient diet. Extremely low birth weights and colostrum production.
(lambs weighing less than 2 kg) can result in an increased Feed or mineral supplements that contain added ion-
incidence of death during the first 24 hours. Conversely, ophore, antibiotics, or decoquinate may help control or
overfeeding of energy can result in obesity and contribute prevent coccidiosis, abortion, and pregnancy toxemia (see
to dystocia. Proper nutrition is crucial. In general, more the section on Feed Additives in this chapter, as well as
problems result from underfeeding than from overfeeding Chapters 4 and 6 and Appendix I).
during late gestation.
The process of converting dietary energy into fetal
growth is quite inefficient. Because 70% to 80% of fetal
Lactation
growth occurs during the final 6 weeks of gestation, the In both sheep and goats, milk production peaks within
dam’s energy requirements increase substantially. In many 2 to 3 weeks after parturition, then declines rather rapidly
instances the only way to provide the extra nutrition is to to a low by 8 to 10 weeks after parturition. In dairy
increase the amount of concentrate being offered. This animals this drop in milk production is less profound. A
sharp increase in energy requirements is compounded if dam nursing a single kid or lamb produces less milk than
the dam has multiple fetuses. A large uterus filled with a female nursing twins or triplets. This is because one
several fetuses physically limits rumen capacity. This can lamb or kid is unable to consume the amount being pro-
result in a situation whereby the mature female cannot duced, allowing a reduction of total mammary output. A
consume enough forage to meet her needs. Under these dam nursing twins produces approximately 30% more
conditions the keeper may wish to feed between 1⁄3 to 1 lb milk than one nursing a single. Likewise, a lactating dairy
of grain per day, depending on the size of the dam. goat being milked two to three times per day for maximal
During late gestation, feeding regimens should be de- milk production also produces greater amounts. A dairy
signed to minimize the energy being supplied by body fat goat usually weighs 10% of a dairy cow’s weight, but may
reserves. This is especially crucial for late-gestating ewes. require 12% to 14% of the nutrients. Lactating does may
Excessive catabolism of body fat can result in pregnancy be capable of consuming 4% to 5% or more (up to 10% to
toxemia. The dam is at greater risk for this condition 11% in some females) of their body weight in dry matter,
if some environmental or disease stressor is occurring making feed intake the most important limiting factor af-
concurrently. Pregnancy toxemia is characterized by a fecting milk production.
buildup of ketones in the blood as a result of accelerated Milk production during the first 4 weeks of lactation is
fat catabolism. Affected ewes appear listless and have a important for good lamb and kid growth. If milk produc-
distinct acetone smell. Maintaining the flock at a body tion is lacking, the lamb or kid can compensate by in-
condition score of 2.5 to 3 and promoting adequate creasing solid feed consumption. However, because feed
energy intake during late gestation help prevent preg- is less digestible than milk, suckling animals cannot
nancy toxemia. During late gestation, ewes with a single consume enough feed to make up for a milk deficiency
fetus may consume as much as 3.5% to 4% of their body and may therefore exhibit suppressed growth rates during
weight in dry matter in grain or excellent-quality forages. early lactation.
Intake may reach 5% in some does. If poor-quality forage Underfeeding energy during late gestation or early lac-
is fed, these pregnant females may only be able to tation results in greater than expected death losses in
consume 2% to 3% of their body weight in dry matter. lambs, particularly twin lambs. Depressed milk produc-
Treatment can be successful, but as is the case with all nu- tion results in lambs that are “scruffy,” poorly kept, thin,
tritional problems, prevention is the best strategy. Ewes and weak. Necropsies of affected lambs show nondescript
should be fed approximately 1 kg (2.2 lb) of a cereal grain signs—the gastrointestinal tract is filled with straw, and
(e.g., corn, oats) during the final month of gestation the lambs have little or no abdominal fat. Lambs older
to prevent pregnancy toxemia. Goats also can develop than 1 month are less likely to starve as they begin to eat
pregnancy toxemia but appear to be more resistant (see on their own.
Chapter 4). Dairy goats that are grazing or being fed During peak lactation it is nearly impossible for a ewe
good-quality grass hay can be fed 0.5 to 1 kg (1 to 2 lb) of or doe to consume enough feed to meet their nutrient
a 16% crude protein grain per 100 lb of body weight daily demands. During this time, good to excellent dairy
the final 11⁄2 months of gestation. The amount of grain animals use body fat to make up for this deficit and there-
may need to be adjusted depending on body condition. fore experience a downward shift (often by more than
In addition to encouraging healthy lambs and prevent- 1 point) in body condition score. This is why an adequate
ing pregnancy toxemia, adequate nutrition during this body condition before parturition is paramount. To make
48 • Sheep and Goat Medicine
efficient use of her body fat a ewe or doe must have ade- flavor. If certain feed sources cannot be avoided, feeding
quate levels of protein in the diet. For example, the NRC5 these off-flavor producers just after milking may reduce
recommends a protein concentration of 13.4% for ewes some of their ill effects. Still, avoiding the offending feed-
nursing a single versus 15% for those nursing twins. Like- stuffs is the best method of prevention. Other non-feed
wise, for does producing milk containing 3.5% fat, the influences on milk flavor are disease (metritis, mastitis),
NRC6 recommends an additional 68 g of protein per day filthy living conditions, and gastrointestinal upset.
for each additional kg of milk being produced. Many pro-
ducers feed dairy goats 0.23 to 0.4 kg (0.5 to 1 lb) of a
16% to 18% crude protein grain per 0.5 kg of milk pro-
NUTRITIONAL DISORDERS
duced up to 1.8 kg (4 lb); they then feed 0.5 to 1 kg (1 to The most common nutrition-related diseases seen in late
2 lb) of grain for each additional 1.8 kg (4 lb) of produced gestation in goats and sheep are pregnancy toxemia (see
milk. Whenever diets containing large quantities of cereal Chapter 4), hypocalcemia, and hypomagnesemia.
grain are fed, some form of rumen buffer should be in-
cluded in the diet or offered free choice.
Because feed intake can limit production in heavy pro-
Hypocalcemia
ducing dairy animals, increasing the diet’s energy density Hypocalcemia can be a problem in dairy goats and to
in early lactation may be required. The addition of fat to some extent in ewes, meat and fiber goats, and pet
the diet is an excellent way to increase the energy density animals. It usually occurs shortly before or after parturi-
of the diet. As a general rule, supplemental fats should not tion and is a result of low concentrations of serum
exceed 4% to 5% of the diet. Oil seed (whole cottonseed), calcium. Some cases also are complicated by hypophos-
where locally available, is an excellent way to add energy to phatemia and hypermagnesemia or hypomagnesemia.
the diet. About 2% to 3% of the added fat can effectively Ewes appear most susceptible in late gestation and early
come from oil seeds. If more fat is needed, 2% to 3% more lactation, particularly when experiencing some sort of
fat can be added in the form of specialty fats, including stress (e.g., hauling, predator attack, no feed). Sheep may
calcium or magnesium salts or fatty acids. These specialty succumb to hypocalcemia 6 weeks before to 10 weeks
fats are expensive, but for the most part bypass the rumen. after parturition. The greatest demand for calcium for the
The fatty acids and calcium or magnesium salts are broken non-dairy animal occurs 3 to 4 weeks before parturition
apart for digestion in the small intestine. in females with more than one fetus, as a result of the cal-
Obviously, the concentrate portion of the grain can be cification of fetal bones. Goats may have hypocalcemia
adjusted based on body condition scores. These recom- before parturition; however, in high-producing dairy
mendations show the importance of adequate protein goats the disease generally occurs after the dam gives
concentrations for maximal milk production. Whole cot- birth. Whenever an abrupt demand for calcium occurs,
tonseed can be included in the diets of lactating animals the body requires 1 or more days to accrue the enzyme
as an excellent energy (greater than 90% TDN) and systems capable of mobilizing bone stores of calcium.
protein (21% to 23% crude protein) source. Whole cot- High intake of calcium, phosphorus, or some cations
tonseed should account for no more than 20% of the diet. (potassium, sodium) decreases the production of parathy-
The requirements of most lactating ewes can be met roid hormones. During decreased parathyroid function,
by feeding 3.2 to 3.6 kg (7 to 8 lb) of a 12% to 14% less 1,25 dihydroxycholecalciferol is produced. This
crude protein, 55% to 60% TDN diet. If hay is fed, a results in lowered absorption and mobilization of calcium
grass-legume or legume only hay helps supply protein from the intestines and bones. Low dietary calcium or in-
demands. If silage is fed, it usually takes 1.36 kg (3 lb) to creased amounts of dietary anions enhances the produc-
supply the equivalent amount of energy in 0.68 kg (1.5 tion and release of parathyroid hormones.
lb) of good-quality hay.
With the exception of dairy goats or ewes, milk pro- Clinical signs. Early in the course of the disease
duction decreases quickly; by 8 to 10 weeks postpartum it animals have a stiff gait, tremors, and tetany. Affected
has become an insignificant nutrition source for the suck- animals may be ataxic or constipated and have decreased
ling lambs or kids. During this time the dam’s require- rumen motility. As the disease progresses, an increased
ments can be met by grazing moderate- to good-quality heart and respiratory rate, regurgitation of rumen
pasture or range. If animals are grouped and fed by pro- content, bloat, and depression to the point of opis-
duction, first-lactation dams with one kid or lamb should thotonos can occur. Corneal and pupillary light reflexes
be fed with mature females with twins. Also, if these first- appear normal at first, but become depressed before
lactation dams have twins, they should be fed with disappearing entirely. The rectal temperature usually
mature dams with triplets. remains in the normal range, but may be slightly low.
Some dairy goats are susceptible to “off-flavor” milk
production. Cabbage, onions, wild garlic, and some Diagnosis. Diagnosis is usually based on a history and
species of weeds or browse can all negatively affect milk signalment conducive to hypocalcemia, as well as re-
 Chapter 2 Feeding and Nutrition • 49

sponse to therapy. Serum calcium concentrations less poor-quality grass hay (with low magnesium content)
than 4 to 5 ml/dl in sheep and goats are fairly diagnostic and in lambs or kids fed only low-magnesium milk re-
of this disease. placers. Kids or lambs with access to grain or legume-
grass hay are more resistant to hypomagnesemia. Ewes
Treatment. In clinical cases, immediate treatment is with poor dentition and those that lose excessive weight
needed, usually in the form of intravenous (IV) adminis- during winter are prone to the condition.
tration of calcium borogluconate (50 to 100 ml of a 23%
solution). Subcutaneous delivery of these calcium solu- Clinical signs. Hypomagnesemia generally occurs in
tions or the oral administration of a calcium gel designed ewes 2 to 4 weeks after lambing. It is more common in
for cattle, but based on sheep or goat body weight, helps females with twins. Affected animals are excitable and
prevent relapse. If the subcutaneous route is chosen to may develop paddling convulsions, clonic-tonic muscle
supply a “reservoir” of calcium for affected animals, solu- spasms, and an increased respiratory rate. They also
tions containing dextrose or numerous electrolytes should may simply be found dead in the pasture. Rectal tem-
be avoided if possible, because some result in abscesses. perature is commonly normal. Convulsions may be
During treatment, the clinician should monitor the triggered by any number of stimuli, from being chased
animals’ hearts and slow or stop therapy if arrhythmias by predators to acute changes in weather patterns.
occur. If the treatment is successful, the animals should Lambs or kids with the milk replacer–associated form
stand and urinate within 20 minutes. If left untreated, af- are usually anorexic and hyperexcitable and may salivate
fected animals usually die. profusely.

Prevention. To prevent or minimize hypocalcemia, Diagnosis. Diagnosis is often based on signalment and
particularly in dairy goats, the diet should be low in history, as well as response to treatment. Serum magne-
calcium and have a low cation-to-anion ratio. The dietary sium levels less than 1.5 mg/dl may be indicative of this
modifications used for the prevention of milk fever in disease; levels less than 1 mg/dl should be considered di-
cattle may be of value in dairy sheep and goats. Therefore agnostic. Postmortem serum samples are of limited value.
reducing or eliminating diets rich in cations (alfalfa) or Magnesium concentrations in cerebrospinal fluid (for 12
calcium and phosphorus in the late dry period may aid in hours after death), urine (for 24 hours after death), or an-
prevention. Many legumes are rich sources of potassium terior eye chamber fluid (for 48 hours after death) are
and calcium and can therefore contribute to hypocal- good postmortem tests.
cemia. Immediately after parturition the calcium levels in
the diet should be increased. This strategy improves Treatment. Treatment consists of the IV administra-
calcium reabsorption for bones and absorption from the tion of 20% to 25% calcium borogluconate and 4% to 5%
intestine. Hauling or other forms of stress should be min- magnesium (50 ml). Oral calcium magnesium gel and
imized in sheep during the final 8 weeks of gestation. subcutaneous injection of calcium magnesium salts are
Even with this strategy some incidence of hypocalcemia both beneficial to prevent relapse.
may be experienced.
Prevention. Because grass tetany results from a reduc-
tion in available magnesium, a number of methods can be
Hypomagnesemia used to increase consumption. Properly balanced fertiliz-
Hypomagnesemia (grass tetany) can be a problem in ers and magnesium compounds can be applied to the soil
sheep and, to a lesser extent, goats grazing on lush, to increase plant concentrations of magnesium. These are
rapidly growing forage. It usually occurs during the early helpful but not very economical because the primary
spring on pastures that are well fertilized with nitrogen problem with the occurrence of hypomagnesemia is
and potassium. A combination of elevated nitrogen and reduced absorption by the animal rather than low plant
potassium levels in the forage leads to a reduced absorp- concentrations. Therefore prevention is best accom-
tion of magnesium from the gastrointestinal tract of the plished by offering high-magnesium mineral supple-
animal. The primary problem in hypomagnesemia is ments before the growth of lush spring forage and
reduced absorption by the animal rather than low plant lambing or kidding. Most mineral supplements with high
concentrations. Cattle, sheep, and goats that graze lush levels of magnesium are unpalatable; feeders should be
cereal grains (e.g., wheat, rye), particularly in early lacta- checked frequently to ensure proper consumption. To
tion or late gestation, are predisposed to this condition. enhance intake the keeper can mix magnesium oxide with
Any type of stress (e.g., weather changes, transportation, molasses, corn, salt, or other feedstuffs. Daily consump-
predator attack) can increase blood concentrations of free tion is important because magnesium in a readily usable
fatty acids, and excess blood from fatty acid concentra- form is poorly stored in the body. An average adult lactat-
tions depresses blood magnesium. Other forms of hypo- ing ewe needs 7 to 9 g of magnesium oxide daily. An eco-
magnesemia occur during winter when animals are fed nomical supplement is a 1:1 mix of trace-mineral salt and
50 • Sheep and Goat Medicine
magnesium oxide, but this combination appears to be un- leave the strongest, most vigorous newborn with the dam
palatable. A more acceptable substitute may be equal and raise the weakest artificially. Although immunoglob-
parts of ground corn, trace-mineral salt, and magnesium ulin may not be absorbed after 12 to 36 hours, it is a rich
oxide. Other palatable grains can be used in place of the source of vitamin A, energy, protein, and local gut-acting
corn. Legumes (e.g., alfalfa, clover, bird’s foot, kudzu) are antibodies. It also acts as a laxative. If possible, colostrum
much better sources of both calcium and magnesium and should be fed for 2 to 3 days.
their inclusion in a pasture helps reduce the incidence of If lambs or kids are to be hand-fed, feeding 10% to
hypomagnesemia.4 Maintaining a high soil pH (greater 20% of their body weight in the form of good-quality
than 5.5) enhances magnesium availability and intake by milk replacer divided into four equal daily feedings is
plants. The inclusion of vitamin D (5 to 10 IU/kg/day) in usually acceptable. Milk replacers for goats should be
a milk replacer helps prevent hypomagnesemia in lambs around 20% protein and 20% fat, with most of the
or kids fed indoors. protein supplied by an animal source (whey proteins). If
the milk replacer appears brown, the protein sources may
have been overheated, resulting in decreased digestibility.
FEEDING THE LAMB OR KID Antibiotics are commonly added to help reduce the inci-
dence of bacterial respiratory and enteric diseases. Milk
Bottle Feeding replacers should be fortified with vitamin A (20,000 to
Rearing orphaned lambs or kids on milk replacer is quite 30,000 IU/kg of dry matter), vitamin E (30 to 40 mg/kg
expensive and labor intensive. If at all possible, keepers of dry matter), and vitamin D (2500 to 3500 IU/kg of dry
should attempt to graft the orphans onto another dam, matter). Table 2-11 shows the composition of sheep and
rearing them on milk replacer only if this cannot be ac- goat milk.6 If lamb milk replacers are used for goats, they
complished. Ideally, orphans need to consume small should be diluted because they contain more fat than nat-
quantities of milk many times per day, which is generally urally occurs in goat milk. Good-quality milk replacers
not possible for most sheep and goat producers. Most designed for calves may be fed to goats and lambs in small
producers feed “bottle babies” only one to three times quantities over numerous feedings (10% to 20% of body
each day. Many dairy kids or lambs are removed from weight divided into four to six equal feedings). Whenever
their dams somewhere between birth and 72 hours of age mixing milk replacers, the keeper should take care to
and fed as orphans. The most economical way to raise ensure that the powder and milk are properly mixed into
orphans is to get them onto a dry concentrate feed as a suspension. Feeding small quantities over numerous
soon as possible. feedings helps reduce the incidence of bloat. By the third
The newborn needs to receive 10% to 20% of its body week of life, some kids or lambs can be switched to a
weight in colostrum, preferably within 3 to 12 hours after twice-daily feeding regimen. Because milk replacers are
birth. If it is not available from the dam, frozen colostrum expensive, animals should be weaned as soon as possible.
can be thawed and used. Colostrum absorption decreases If lambs or kids are underfed or fed a poorly digestible re-
rapidly from birth through 36 hours of age (see Chapters placer, they may become emaciated, weak, or comatose.
6 and 14). Hemolytic crisis has been observed in some Death is possible. Lambs or kids with this condition have
lambs fed cow colostrum. Still, cross-species colostrum lower than normal blood glucose, and necropsy reveals a
is often better than no colostrum. Dairy cow colostrum body devoid of fat stores. The abomasums of starved
is usually available, but is dilute in its immunoglobulin neonates often become impacted with hair or poorly di-
content. Any colostrum fed to an orphan should be free of gestible items.
caprine arthritis-encephalitis (CAE) and Johne’s disease.
If lambs or kids are unable to nurse, they need to be tubed.
After the initial amount of colostrum is fed, additional
feeding should be withheld from newborns that are to be TABLE 2-11
bottle-raised for as long as 5 hours. This encourages
COMPOSITION OF SHEEP AND GOAT MILK
sucking, easing the transition and aiding in training to a
AS A PERCENTAGE OF DRY MATTER
bottle, nipple pail, or bucket. If the owner wishes to feed
by hand, a lamb nipple attached to a soda bottle is a good ELEMENT SHEEP MILK GOAT MILK
system. The nipple should be placed in the mouth and the
newborn’s jaw moved in a chewing motion by the feeder. Protein 32% 25%
This usually stimulates the nursing reflex in all but very Carbohydrate 25% 31%
weak young. Lambs or kids left with their dams for more Fat 38% 34%
than 2 days require longer training to become accustomed
Total solids as fed 19% 13%
to a bottle or pail. If a ewe or doe has too little milk to
support more than one newborn, it is imperative that suf- From Naylor JM, Bell R: Raising the orphaned foal, Vet Clin North
ficient colostrum be given to all. The keeper should then Am (Equine Pract) 1(1):173, 1985.
 Chapter 2 Feeding and Nutrition • 51

The most efficient and least labor-intensive system is spring in the area for a few days (with limited feed, of
to place the orphans on a self-feeder using refrigerated course), and putting all the animals in a small, confined
milk. This helps the orphans consume less milk and space adjacent to the creep area.
therefore nurse more frequently throughout a 24-hour Creep feeds need not be complex but they must be
period. In effect this regimen imitates the normal palatable because they are competing with milk. Pellet-
dam/newborn nursing regimen. Keeping the milk cold ing or coarse grinding feeds usually increases intake.
also may help prevent spoilage and lessen the extent to Fine grinding usually results in decreased intake as
which the milk replacer separates out of suspension. In animals (particularly lambs) age. Pellets should be small
addition, kids or lambs using a self-feeder should have enough for consumption. In goats, pellets larger than 5
access to an extremely palatable dry diet. A mixture of to 7 mm may decrease intake. After the lambs or kids
corn, oats, alfalfa pellets, molasses, and soybean meal that have begun to consume the creep feed, cheaper ingredi-
provides 14% to 16% crude protein works well. Top- ents can be used to enhance the economics of the prac-
dressing the feed with a dry milk replacer also may stim- tice. However, until the animals reach 3 to 4 weeks of
ulate early intake of the dry feed. Other extremely palat- age, palatability is the key to successful creep feeding. If
able ingredients to young ruminants are soybean hulls increased performance is to be attained from creep
and various sources of bran, including wheat bran. feeding lambs, they must consume more than 0.23 kg
(0.5 lb) daily from 3 weeks of age to weaning. Enhanced
performance may be attained if salt (0.5% of the creep
Creep Feeding feed), ammonium chloride (0.2 kg/440 kg feed, or 10
The term creep feeding refers to the use of supplemental lb/ton), and vitamin E are added to most creep feeds.
feed for the nursing lamb or kid. The goals of a creep Some examples of creep feeds are shown in Table 2-12.
feeding program are to promote an adequate intake with In general, creep feeding should provide an additional
a palatable feed, provide all necessary nutrients, and be as 0.5 kg of gain for each 1.8 to 3.2 kg (4 to 7 lb) of feed
economical as possible. Both lambs and kids use feed- consumed. This efficiency varies from one set of condi-
stuffs more efficiently before weaning. tions to another, but generally when feed costs are low
Lambs and kids will only nibble at the creep feed until and sale prices are high, creep feeding is usually prof-
they are 3 to 4 weeks old. Still, the creep feed should be itable. It is less profitable when feed costs are high and
made available as soon as possible to help the orphans get sale prices are low. In the final analysis it is simply a
used to eating from one location and establish rumen matter of feed costs versus animal sale prices that deter-
function. The feeder should be placed in a dry, well-lit mines the feasibility of creep feeding.
area where lambs or kids can easily gain access but
still retain visual contact with their dams. A variety of
methods can be employed to maximize the acceptance of
Weaning
the creep area. Some of these include hanging a light over Lambs and kids can be weaned as early as 3 or 4 weeks,
the creep feeder, retaining one or two dams and their off- but better results may occur if weaning is delayed until

TABLE 2-12

SAMPLE CREEP DIETS FOR LAMBS AND KIDS*

ELEMENT SAMPLE 1 SAMPLE 2 SAMPLE 3 SAMPLE 4

Ground corn 33% 60% 63% 40%

Oats — — — 11%
Soybean hulls — — 10% —
Soybean meal 6% 8.5% 10% 6.5%
Alfalfa hay 55% 25% — 35%
Bran — — 10% —
Molasses 5% 5% 5% 6%
Trace mineral salt 0.5% 0.5% 0.5% 0.5%
Ammonium chloride 0.5% 0.5% 0.5% 0.5%
Limestone — 0.5% 1% 0.5%
*Diets 1, 2, and 3 should be fed with an excellent-quality hay offered free choice. Diet 4 is a complete, pelleted feed.
52 • Sheep and Goat Medicine
8 to 12 weeks. Because of labor constraints, many keepers Feeding beyond the lamb’s ideal finish results in higher
attempt to wean milk replacer–fed young as soon as pos- cost of gain because of decreased feed efficiency. Adding
sible. Kids of most meat and dairy breeds should weigh at lean muscle is much more energy efficient than adding
least 9.1 to 11.4 kg (20 to 25 lb) and consume 0.23 kg body fat. Blackfaced sheep and meat goat breeds gener-
(0.5 lb) of a 16% to 18% crude protein grain per day. ally finish at greater body weights.
Because weaning is such a stressful event, the goal If high-quality forage is available, lambs can be fin-
should be to get the lamb or kid accustomed to eating ished on it. This generally works best for smaller, younger
out of feedbunks and drinking from a water trough. The lambs. Older, heavier lambs require some concentrate
decision to wean lambs or kids depends on age, season feeding. For example, a small-framed lamb born in
of birth, whether they have been consuming creep feed, January in the southeastern United States could be ready
existing parasite or predator problems on the farm, for slaughter in June having been grazed on only cool-
market price, and available labor. Feedbunk location is season annual grasses (rye grass) or grass-legume pas-
important in helping newly weaned animals consume tures. However, a large-framed, spring-born lamb in the
adequate amounts of dry matter. However, if excellent- western United States may come off of range in the fall at
quality forage is available, it can be used as the sole 6 months weighing 31.8 to 41 kg (70 to 90 lb) and need a
source of feed. A good strategy is to place the feedbunks concentrate-based diet to be finished by 1 year.
perpendicular to the fence line so that the weanlings Many lambs in North America are finished in a
are forced to see and possibly investigate the feed as feedlot or dry lot. These lots vary in size and may be open
they walk (usually continually) the fence line. For the areas, confinement barns, or a combination of both. An
first 2 days of the weaning period, good-quality hay excellent feeding regimen is stepwise feeding whereby
should be offered free choice. The weanlings should lambs (and occasionally kids) are given more grain as they
then be introduced to a concentrate feed offered at a get larger. By the end of the finishing period many are
level of about 1% of body weight per day. A lamb weigh- typically consuming about 80% concentrate and 20%
ing 31.8 kg (70 lb) therefore consumes approximately roughage. However, when given free access to both
0.32 kg (0.75 lb) per day. After the lambs or kids have roughage and concentrate, lambs consume about 60% to
been introduced to the grain, the keeper can gradually 70% concentrate and 30% to 40% roughage. A variety of
increase the amount. cereal grains can be used by lambs, including corn, oats,
Some managers prefer to remove all grain supplements barley, milo, and to some extent wheat. Amounts used are
and place the dam on a poor-quality forage 1 week before based on local economics. A protein supplement may be
weaning. This reduces milk production and decreases the included depending on the amount of protein being pro-
incidence of mastitis. By 7 months, most dairy breed kids vided by the roughage source. Alfalfa is commonly used
should weigh between 27.3 and 36.4 kg (60 to 80 lb). A as a roughage source because of its wide availability, and
good-quality mineral mixture should be offered free animals feeding on it may not need additional protein.
choice. The same guidelines described for mineral Mineral and vitamin premixes also are added to some
feeding of the male (50% dicalcium phosphate and 50% diets. Because the finishing period is usually accompanied
trace mineral salt) are applicable for weanlings. by diets that emphasize grains, the nutritionist or clini-
cian must be aware that excessive grain intake can predis-
pose to urolithiasis, enterotoxemia, and bloat.
Finishing With the possible exception of sorghum, processing of
Finishing of lambs for slaughter can be accomplished in a grains does not appreciably increase lamb performance.
variety of ways. There is no one perfect diet for finishing. Cracking, rolling, or flaking milo to break its hard seed
Instead, each feeding facility accomplishes the goal by coat increases its use by lambs. Feeding other grains
using feedstuffs that are available and economical to the whole may actually tend to decrease the incidence of aci-
area. Feedlots designed specifically for goats are not as dosis and other digestive disturbances. Pelleting bulky
common as those designed for lambs. Most goats are rations may be of some benefit because of the increased
slaughtered off of forage-based diets with little use of level of consumption. The most important factor to con-
concentrate feeding. sider with regard to pelleting or other processing is the
At slaughter the lamb should have approximately 0.23 potential for the lamb or kid to “sort” the feed and
to 0.46 cm of backfat. However, the amount of backfat consume only a portion of the diet. For example, if the
often depends on specific market preferences. Slaughter protein, mineral, and vitamin premix is a loose meal,
weights have a wide range because of the variation in cracking the grain may be beneficial in minimizing
frame size among North American sheep, although they sorting, despite its lack of effect on use. Pelleted feeds
generally fall between slightly below 45.4 kg (100 lb) and help ensure a more uniform intake and are less dusty and
68 kg (150 lb). Ideally, the lambs should be marketed at easier to handle. However, they are more expensive and
the proper degree of finish, regardless of their weight. may increase the incidence of some diseases.
 Chapter 2 Feeding and Nutrition • 53

As stated earlier, goats are generally not finished under

FEEDING YEARLINGS
commercial settings. Most of the goats consumed in
North America are slaughtered by the consumer; by
Females
small, local processing facilities; or in niche marketing Every sheep and goat enterprise is different in terms of
systems. With some exceptions, goats tend to be sold in overall goals. Some operations place importance on
small groups over the course of the year. Because of this breeding ewes and does so that they have their first off-
method of marketing, goats are generally kept on a spring by 1 year of age. Other farms or ranches may find
forage-based diet rather than year-round feeding of it much more practical and economical to breed their
grain. Still, some feedlots, or “grain on grass” operations animals to have their first offspring as 2-year-olds. A
do exist. If a group of kids is placed on a concentrate- ewe’s lifetime production can be as much as 20% greater
based diet for finishing, the same basic principles dis- if she is bred as a ewe lamb rather than as a yearling.8
cussed previously for lambs apply. Table 2-13 provides ex- If the goal is to have the females lamb or kid as year-
amples of growing and finishing diets for lambs and kids. lings, nutrition is crucial from weaning to breeding. In
Growing diets, which contain 14.5% protein and 68% general, the female should obtain 65% of her projected
TDN, are used for younger, lighter lambs and kids. Fin- mature weight by the time of breeding. In reality a range
ishing diets, which contain 10% protein and 80% TDN, of weights probably exists within which small-framed
are more effectively fed to the older, heavier animals. sheep and goats may have acceptable conception rates at
Regardless of the specie being fed, the introduction to 55% to 60% of their projected mature weights, while
and consumption of energy-dense diets in a feedlot some large-framed animals may need to be closer to 70%
setting is stressful and associated with many metabolic of their mature weights.
diseases. The nutritionist or clinician should ensure that Depending on their weaning weights, most females
animals being fed in the finishing stages be slowly intro- need to gain between 0.11 and 0.23 kg (0.25 to 0.5 lb) per
duced to these diets and vaccinated for Clostridium day from weaning until breeding. Under most situations
perfringens C and D, and possibly other diseases (e.g., this requires some supplemental energy or concentrate
contagious ecthyma, pasteurellosis) that are locally prob- feeding. However, overfeeding young females can result
lematic. On arrival animals should be offered free access in excessive fat deposition in the mammary glands and
to a good-quality legume-grass hay, fresh clean water, and decreased lifetime milk production. After the females
a mineral mixture. Animals should be introduced to the have been bred, moderate and steady weight gain is desir-
finishing diet slowly over a 2- to 4-week period. If males able until parturition, with a weight goal of 85% to 90%
are fed, ammonium chloride or other urine acidifiers of the projected mature weight by 1 year of age.
should be fed to prevent urolithiasis (see Chapter 10). If females are to be bred as yearlings, a moderate
The use of rumen buffers, antibiotics, ionophores (see the growth rate is most desirable. As long as a good, well-
section on Feed Additives in this chapter), and free- planned forage system is available, females can achieve
choice hay are all effective in minimizing some produc- desired weight gains with little or no grain supplementa-
tion diseases. tion. Sheep or goats that can successfully breed out of

TABLE 2-13

SAMPLE GROWER AND FINISHER DIETS FOR LAMBS AND KIDS

ELEMENT GROWER 1 GROWER 2 GROWER 3 FINISHER 1* FINISHER 2* FINISHER 3*

Corn 33.5% 28.5% 32.1% 73.2% 76.0% 74.6%

Alfalfa 55% — — 20% — —
Grass hay — 50% — — 17% —
Cottonseed hulls — — 40% — — 14%
Soybean meal 5.5% 15% 21% — — 4%
Molasses 5% 5% 5% 5% 5% 5%
Trace mineral salt 0.5% 0.5% 0.5% 0.5% 0.5% 0.5%
Limestone — 0.5% 0.9% 0.8% 1.0% 1.4%
NH4Cl 0.5% 0.5% 0.5% 0.5% 0.5% 0.5%
*Finisher diets should contain enough limestone (or other calcium source) to provide a 21 calcium-phosphorus ratio in the diet.
54 • Sheep and Goat Medicine
season should be bred at 13 months so they can lamb concentrate. Lambs should be slowly exposed to the con-
or kid at 18 months. This requires less nutritional input centrate portions of the feed, taking 10 to 14 days to
than breeding 7-month-old females but still provides make the transition from little grain to the full amount.
an acceptable generation interval for increased female Feeds should never be switched abruptly and fresh clean
productivity. water should always be offered free choice.
Regardless of the breeding system, animals should be
weighed and body condition scored regularly whenever
possible. If the body condition scores of the group begin
Mature Sheep
to drop below 2.5, the keeper should offer supplemental Mature show ewes and rams should consume approxi-
energy; conversely, if the scores rise above 3.5, he or she mately 1.36 to 2.27 kg (3 to 5 lb) of concentrate per day,
should provide less energy. A good-quality mineral depending on their size. They also should be offered
mixture as described for adult males is applicable for good-quality hay free choice. The requirements for
yearlings. mature sheep are found in Table 2-7. Adult show animals
should be maintained in good condition but should not
be obese. A good exercise regimen is necessary to prevent
Males overconditioning. Where possible, forcing animals to
Feeding developing males is quite straightforward. They graze or walk some distance from grain to hay to water
should be developed using as much forage as possible, may prove valuable.
with just enough supplemental feeding to produce desir-
able gains (0.34 kg or 0.75 lb per day). This is easily ac-
complished with good genetics. Growing males should be
Show Goats
offered a good-quality mineral mixture as described pre- The feeding of young meat goats for show is similar to
viously, with the keepers taking steps to prevent urolithi- the feeding of show lambs discussed previously. The goal
asis and other production-related diseases. is to use a simple diet that provides the desired level of
gain and degree of bloom. The same forages and concen-
trates discussed for lambs in Table 2-14 are appropriate
FEEDING SHOW ANIMALS for goats.
Lambs
FEEDING FOR FIBER
All show animals should be offered a good-quality
mineral mixture and given free access to fresh, clean PRODUCTION
water. Feeding show lambs should be as simple as possi-
ble while providing the desired rate of gain and appropri- Sheep
ate “bloom.” Ideally, the lamb should be fed 30% to 40% Wool production is highly heritable; however, nutrition
of its total daily intake as good-quality hay or forage; the can affect wool growth and character. Within certain bio-
remaining 60% to 70% of the diet should be in the form logic limits, energy intake is directly proportional to wool
of a concentrate or grain mixture (Table 2-14). A lamb production,9 although separating protein effects from
can eat as much as 3% to 4% of its body weight daily. At energy effects is difficult. As long as the minimal protein
least 0.45 kg (1 lb) of hay per day should be fed with the requirement is met, additional dietary protein does not
appear to increase wool growth. Wool does contain an
abundance of the sulfur-containing amino acid cystine.
TABLE 2-14 Therefore feedstuffs rich in sulfur-containing amino
acids are important for optimizing wool growth.
CONCENTRATE MIXES FOR SHOW LAMBS* In general, the effects of nutrition on wool production
are associated with quantity rather than quality. Increased
ELEMENT SAMPLE 1 SAMPLE 2 nutrient intake can increase wool production, within
limits. However, quality can be affected during periods of
Corn 50% 45% severe nutrient deprivation. Under these conditions, fiber
Oats 35% — diameter is decreased. Extreme underfeeding can result in
Soybean hulls — 40% weak fiber with limited value.
Soybean meal 10% 10% The nutritional status of the ewe during gestation can
Molasses 4% 4% influence the wool production of the subsequent off-
spring. Kelly et al10 bisected embryos to produce clones
Mineral mix 1% 1%
that were then placed in ewes fed at maintenance or sub-
*Animals should be introduced to high-grain diets slowly over 2 to 3 maintenance energy and protein levels from day 50 to
weeks. 140 of gestation. The lambs that were born to the ewes
 Chapter 2 Feeding and Nutrition • 55

fed a submaintenance diet produced 0.136 kg (0.3 lb) less energy and protein intake for range-fed goats (and possi-
wool from 0.4 to 1.4 years of age. The wool from those bly sheep). Careful intake monitoring is important.
lambs was coarser than that produced by lambs born to Adequate shelter should be provided to fiber-produc-
ewes fed at a maintenance level. These effects have been ing animals, particularly young animals and Angora
attributed to decreased hair follicle development in goats, that have just been sheared. In early spring or late
fetuses whose dams were fed deficient diets, and they fall, animals may be susceptible to cold stress for as long
continue for the rest of the offspring’s life. as 4 weeks after shearing. The provision of shelters or
wind breaks and an additional 0.23 to 4.5 kg (0.5 to 1 lb)
per day of an energy supplement (cracked corn) above the
Goats normal feeding regimen can help minimize freezing and
Angora goats produce large quantities of fiber per unit of stress loss.
body weight (Figure 2-5). The 2 to 3.6 kg (4.5 to 8 lb) of
mohair produced per cutting can greatly increase nutri- FEEDING GERIATRIC SHEEP
tional demands. As with wool, mohair production can be
improved with increased energy intake. However, protein OR GOATS
appears to elicit more of a response on mohair growth Pet sheep and goats can live much longer than animals in
than it does on wool growth. Cashmere appears to be production units (Figure 2-6). Whenever feeding older
only minimally affected by dietary manipulation. Increas- sheep or goats, keepers should strive to maintain a proper
ing dietary protein above requirements increases mohair body condition and weight. Body weight and condition
volume and diameter.4 Angora does fed isocaloric diets loss are common problems among geriatrics. A complete
containing either 12% or 19% protein had an increase in physical examination, complete blood count, and serum
grease fleece weight and fiber diameter with the high- chemistry analysis may be indicated to identify ongoing
protein diet (approximately 0.57 kg or 1.25 lb).8 Mohair disease. Older animals may require special feeding
also contains abundant amounts of sulfur, making sulfur- because of dental disease, parasite damage to the bowel,
containing amino acids important in Angora goat nutri- and other general health problems. Good-quality hay,
tion. Recently, Qi et al11 indicated that the NRC6 may be moistened pellets, lush forage, and palatable concentrates
erring on the low side in its recommendation of a 101 are often required for animals with dental disease (see
nitrogen-to-sulfur ratio for maximal mohair production, Chapter 3).
and that a ratio of 7.21 may be more useful. Therefore, if
NPN is used as a protein source, sulfur supplementation
is necessary.
Ranged Angora goats should receive nutritional sup-
plementation during late gestation and early lactation.
Salt-limited feeds can be used for both energy and
protein under range conditions. Cottonseed or soybean
meal (or other protein sources), corn, and salt (non-
iodized, non-mineralized) can be added at a 131 ratio.
The keeper should introduce the supplement slowly,
adding more white salt if the animals are overconsuming
and decreasing salt if they are underconsuming. This salt-
limited feeding system can be an effective way to increase

Figure 2-5 Angora goats are maintained on pastures and range. Figure 2-6 The care of geriatric sheep and goats is an often
They tend to be used for brush control less commonly than other types overlooked area of veterinary practice. Pet sheep or goats that
of goats. However, if they are used for brush control, they may require receive proper care may live for more than 15 years. At the time of this
supplemental sulfur because of excess tannin intake from some writing, one author (Dr. Pugh) routinely treats goats and sheep in their
browse. late teens and early 20s, including this pygmy buck.
56 • Sheep and Goat Medicine
Allowing older animals access to feed, particularly if
their social status has changed, and longer periods of non-
competitive time to consume it helps maintain a good
F URTHER R EADING
Ensminger ME, Oldfield JE, Heinemann WW: Feeds and nutrition, ed
body condition score. Because many geriatric animals have 2, Clovis, CA, 1990, Ensminger Publishing.
arthritic conditions, minimizing excess body weight, Naylor JM, Ralston SL: Large animal clinical nutrition, St Louis, 1991,
Mosby.
properly trimming feet, and placing water and feed so
animals are not forced to walk great distances are all valu-
able in case management. Diets designed for the geriatric
horse can be used. However, if copper concentrations are
PARENTERAL NUTRITION
greater than 10 ppm, these diets should not be fed to any Parenteral nutrition (PN) is the IV administration of
sheep or to goats with a history of hepatic disease. If the energy, protein, fat, vitamins, and minerals for the nutri-
animal has renal disease, the protein content of the diet tional support of animals. PN may be warranted in any
should be maintained at 7% to 8%, and the calcium-to- state of debilitation where oral nutritional support is
phosphorus ratio should be kept at 11. A good-quality either contraindicated (e.g., enteritis, obstructions) or dif-
granular mineral mixture of equal parts dicalcium phos- ficult to impossible (e.g., esophageal disease). Total par-
phate and trace mineral salt should be offered free choice. enteral nutrition (TPN) can be used to supply 100% of
If older animals are losing weight, the keeper can slowly the animal’s nutritional demands intravenously. Partial
increase caloric intake by 7% to 10% in the form of fat. parenteral nutrition (PPN) may be used to supply a
However, protein, fats, and copper should be restricted in portion of the animal’s nutritional demands if limited oral
animals with hepatic disease. Animals with hepatic or nutrition is feasible. TPN must include both carbohy-
renal disease may benefit from the addition of B vitamins drates and lipids as energy sources, as well as protein
(orally or parenterally). If renal disease exists, the protein amino acid sources for body homeostasis and repair. Al-
requirement should be met but not exceeded. If anorexia is though TPN and PPN may be used in all ages of sheep
a problem, varying the diet, offering lush grazing, and and goats, cost often restricts its use to young animals or
adding energy-dense feeds are useful strategies. Obviously, valuable adults. The duration for which the PN is to be
all husbandry practices that aid in overall health (e.g., used for nutritional support determines the components
proper shelter, deworming) enhance long-term survival. of the nutritional requirements that will be used. When
instituting PN with an expected duration of less than
2 weeks, energy, protein, and some electrolytes are the
R EFERENCES
1. Russell A: Body condition scoring of sheep. In Boden E, editor:
most crucial components. However, in the rare event that
PN is used for more than 2 weeks, the solutions must be
Sheep and goat practice, London, 1991, Bailliere Tindall. balanced not only for energy, protein, and electrolytes, but
2. Santucci PM et al: Body condition scoring of goats in extensive also for micronutrients and vitamins.
conditions. In Morand-Fehr P, editor: Goat nutrition, Wagenin- As a general rule, all fluid deficits and electrolyte ab-
gen, Netherlands, 1991, Pudoc. normalities should be corrected before the institution of
3. Holland C, Kezar W: Pioneer forage manual, a nutrition guide, Des either TPN or PPN.1 Most PN solutions are hypertonic
Moines, IA, 1995, Pioneer Hi-Bred International. and their use may result in hyperglycemia, hyperosmo-
4. Bretzlaff K, Heinlein G, Huston E: Common nutritional prob- lality, hyperlipemia, acidosis, electrolyte imbalances, or
lems feeding the sick goat. In Naylor JM, Ralston SL, editors:
thrombophlebitis.2 A Silastic or polyurethane catheter
Large animal clinical nutrition, St Louis, 1991, Mosby.
5. Nutrient requirements of sheep, Washington, DC, 1985, National
should be used to reduce the risk of thrombophlebitis.2
Academy Press. Animals on PN are at high risk for sepsis and should be
6. Nutrient requirements of goats: angora, dairy and meat goats in tem- monitored closely for signs of sepsis (e.g., elevated body
perate and tropical countries, Washington, DC, 1981, National temperature, neutrophilia or left shift, hyperfibrinogen-
Academy Press. emia, hyperglycemia).3 Strict attention should be paid
7. Naylor JM, Bell R: Raising the orphaned foal, Vet Clin North Am to aseptic technique when mixing PN solutions and
(Equine Pract) 1(1):173, 1985. when working with IV lines containing PN solutions.
8. Sahlu T et al: Dietary protein level and ruminal degradability for Other complications of TPN include hypoglycemia,
mohair production in Angora goats, J Anim Sci 70:1526, 1992. fatty liver, azotemia, dehydration, and anuria. The sheep
9. Allden WG: Under nutrition of the Merino sheep and its sequela: or goat also should be monitored for derangements in
II the influence of finite periods of arrested growth on the subse-
serum electrolytes, alterations in acid/base status, in-
quent wool growth, fleece development, and utilization of feed for
wool production of lambs, Austr J Ag Res 19:639, 1968.
creases in serum lipids, changes in blood glucose, and
10. Kelly RW et al: Nutrition during fetal life alters annual wool pro- changes in blood urea nitrogen. In addition, urinary
duction and quality in young Merino sheep, Austr J Exp Agric output should be monitored to ensure normal hydration
36:259, 1996. and proper renal perfusion. Table 2-15 shows some
11. Qi K et al: Sulfate supplementation of Angora goats: metabolic serum chemistry changes that indicate improper PN
and mohair responses, J Anim Sci 70:2828, 1992. supplementation.
 Chapter 2 Feeding and Nutrition • 57

TABLE 2-15 BOX 2-1

CHANGES IN SERUM CHEMISTRY VALUES

INDICATIVE OF PROBLEMS WHEN USING PN
C ALCULATION OF THE D E AILY NERGY

CONDITION COMMENT
R EQUIREMENT FOR S G
HEEP AND OATS*

140 kcal/kg0.75/day
Hypoglycemia Caloric needs not being met
Hyperglycemia Sepsis or inappropriately
Calculate body weight in kg (lb  2.2)
high caloric content of PN
40 lb  2.2 lb/kg  18.2 kg
fluid
(140 kcal) (18.20.75)/day  1233 kcal/day
Elevated BUN Dehydration or calorie:NPN
imbalance *This example uses a 40-lb animal. A calculator with an xy function
key is useful for this calculation.
Depressed BUN Inadequate protein
supplementation or hepatic
disease caloric density and osmolality of the solution should be
Elevated liver Lipid content of solution increased slowly over 2 to 3 days.4 A polyionic IV fluid
enzymes exacerbating fatty liver or should be used during the acclimation period to maintain
other hepatic disease hydration.
To calculate the protein requirement for young lambs
or kids, the authors of this chapter extrapolate from other
species and use 2 to 3.75 g of amino acids per kg/day.1,4
As a general rule, the fluid requirement for most Throughout this discussion, values are given in kg of
animals is 66 ml/kg per day. Of course, continuing fluid body weight of the animal being fed per day (kg/day). For
losses should be factored into replacement therapy. Oc- adult animals, the authors again extrapolate from other
casionally a separate fluid line for electrolyte-fluid sup- species and use the requirement of 1 to 1.5 g of amino
plementation is needed when using PN, because con- acids per kg/day.1 The ratio of non-protein calories to
centrated electrolyte solutions may precipitate in PN grams of nitrogen should be maintained at 1001 to
solutions. 3001.4,5 Because protein is about 16% nitrogen, the
The authors of this chapter suggest that clinicians grams of nitrogen can be calculated by dividing the
preparing PN solutions first calculate the animal’s energy number of grams of amino acids by 6.255:
requirements. The caloric requirements for most animals
g amino acids  6.25  g nitrogen
can be calculated with the formula provided in Box 2-1.
With respect to meeting the energy requirement, carbo- For much of the rest of this discussion of PN, the
hydrates (50% dextrose solution) and fats (20% lipid so- authors use the example of supplying nutritional support
lution) are the two sources generally used. Dextrose is through TPN for a 15-kg goat. This example can serve as
the most commonly used carbohydrate source and has a template for sheep and for animals of different weights.
an energy value of 3.4 kcal/g. As a general rule, the If the goat weighs 15 kg, the formula for energy require-
maximum infusion rate of carbohydrates should not ment presented in Box 2-1 of 140 kcal/kg0.75/day is
exceed 5 to 7 mg/kg per minute. Highly concentrated so- solved as follows:
lutions should be administered through a central venous
(140 kcal) (15 kg0.75)/day  1067 kcal/day
catheter because hypertonic PN solutions may result in
phlebitis if small peripheral vessels are used. In neonates, In this example, if the 15-kg goat needs 990 ml of fluid
rarely should a greater than 5% to 10% dextrose solution daily and the clinician decides to administer an amount
be given in peripheral veins. A 20% dextrose solution may 1.5 times greater than the maintenance amount to replace
be safely administered to adults via a jugular venous ongoing losses, the clinician should administer 1500
catheter. Unlike dextrose, lipids are isotonic and do not ml/day of fluid to the animal that is receiving nothing by
increase the osmolality of the TPN solution, yet they are mouth. As previously mentioned, unless a central venous
very dense in energy. Lipids supply 9.1 kcal of energy per line is used, the maximum dextrose concentration should
gram and can be infused at a rate of 2.5 to 3 g/kg per day. not exceed 10%. Therefore 150 g of dextrose could be in-
Usually, the clinician or nutritionist should try to supply cluded in the daily 1500 ml to make 10% dextrose. This
30% to 60% of the calories as lipids. If the clinician amount of dextrose supplies 510 kcal of energy per day
notes evidence of hepatic disease, he or she should use the (150 g  3.4 kcal/g  510 kcal). In this example, 300 ml
low end of this lipid range (30%) and monitor serum sor- of a 50% dextrose solution supplies 150 g of dextrose (150
bitol dehydrogenase closely. All the nutritional require- g  50 g/100 ml  300 ml). Therefore 300 ml of 50%
ments cannot be met safely on the first day; instead, the dextrose should be included in the daily 1500 ml of total
58 • Sheep and Goat Medicine
fluid. However, 557 kcal of energy are still needed to whether this amount meets the non-protein calorie-
meet the energy requirements: nitrogen ratio of 1001 to 3001:
1067 kcal  510 kcal from dextrose g of nitrogen  g of protein  6.25
 557 kcal of energy still needed per day Ratio  kcal  g nitrogen

The clinician in this example can supply the remaining In this example, 30 g of protein  6.25  4.8 g of ni-
calories with 61.2 g of fat: trogen. Because the non-protein calories from both car-
bohydrates and fats in this example are 1067, the ratio is
557 kcal needed  9.1 kcal/g  61.2 g of fat
2221 (1067 kcal  4.8 g of nitrogen  222), which is
The maximum lipid utilization rate for this 15-kg in the range of 1001 to 3001 and therefore acceptable.
animal is 45 g daily (3 g/kg/day  15 kg  45), but A central venous catheter must be used when administer-
61.2 g of fat are needed. Therefore it is impossible to meet ing more than 1 to 1.5 g of protein/kg/day.
the energy requirements by using a solution of less than Although the plan is to administer 1500 ml of TPN so-
10% dextrose (which only supplies 510 kcal of energy) lution per day, it may be more convenient or practical to
because enough lipid cannot be safely administered to mix the solution in 1-liter aliquots. Table 2-16 provides
make up the difference. If the dextrose concentration is recipes. As previously mentioned, the clinician should
increased to 15% (and a central venous catheter is used to begin PN with a solution containing only 25%4 of the cal-
avoid phlebitis), 1500 ml of a 15% dextrose solution sup- culated amounts of dextrose, lipid, and amino acids and
plies 765 kcal: make up the difference in volume with a polyionic isotonic
fluid (Table 2-16, column D). The energy and protein
15 g/100 ml  1500 ml  225 g
density should then be gradually increased over a period of
225 g  3.4 kcal/g  765 kcal
2 to 3 days (Table 2-16, column C). During this acclima-
The 765 kcal supplied by the 15% dextrose solution is tion period the animal should be monitored closely for
in contrast to the 510 kcal of energy supplied by a 10% hyperglycemia or hypoglycemia, elevated blood urea ni-
dextrose solution. If a 15% dextrose solution is used, only trogen (BUN), acidosis, and electrolyte derangements.
302 kcal of energy are needed from fat (1067 kcal re- Monitoring these parameters while slowly increasing the
quired/day  765 kcal supplied by the dextrose  302 energy and protein density of the TPN solution allows the
kcal needed from fat). In this example, only 33 g of fat are clinician to adjust the protein, lipid, carbohydrate, and
now needed (302 kcal  9.1 kcal/g  33 g). This is well electrolyte concentration of the solution to the individual
within the daily fat utilization rate for this size animal needs and tolerance of the animal. If the animal’s blood
(2.5 to 3 g/kg/day, or 45 g for the 15-kg animal). work remains normal during the acclimation period, the
The protein/amino acid (AA) requirement for a young full maintenance PN solution can be administered on the
goat is 2 to 3.75 g of AA/kg/day. For example, an 8.5% third or fourth day (Table 2-16, columns A and B). The
AA solution has approximately 1.3 g of nitrogen/100 ml. sheep or goat also should be weighed daily to ensure that it
Using the base requirement of 2 g of AA/kg/day, a 15-kg maintains or gains weight. The transition back to enteral
goat needs 30 g of AA daily (2 g/kg/day  15 kg). Ap- nutrition should be made gradually.4
proximately 353 ml/day of an 8.5% AA solution is re- Balanced polyionic isotonic electrolyte solutions are
quired to provide 30 g of AA (30 g  8.5 g/100 ml  usually adequate to correct minor electrolyte derange-
353 ml). The following formulas are used to calculate ments and mild acidosis or alkalosis. In the absence of

TABLE 2-16

RECIPES FOR PN SOLUTIONS FOR A 15-KG SHEEP OR GOAT (TO BE INFUSED AT THE RATE OF 1500 ML PER DAY)

A B C D

1500 ML 100% 1000 ML 100% 1000 ML 50% 1000 ML 50%

INGREDIENT MAINTENANCE* MAINTENANCE MAINTENANCE MAINTENANCE

50% dextrose 450 ml 300 ml 150 ml 75 ml

8.5% amino acid† 350 ml 240 ml 120 ml 60 ml
20% lipid‡ 165 ml 110 ml 55 ml 30 ml
Isotonic fluid 535 ml 350 ml 675 ml 835 ml
*Caloric and protein maintenance
†These volumes have been rounded to the nearest 10 ml for ease of measurement.
‡Because adding lipid directly to 50% dextrose can result in destruction of the lipid droplets, the lipid should be added last.
 Chapter 2 Feeding and Nutrition • 59

blood gas analysis, it is relatively safe to use total serum rate of 37.5 ml per L of TPN so as to deliver the 56 ml of
carbon dioxide (TCO2) for evaluation of acid-base status bicarbonate in the total daily 1500-ml fluid volume.
if respiratory disease can be ruled out by thorough physi- A similar formula has been used to calculate the deficit
cal examination. TCO2 accounts for 95% of serum of other electrolytes such as potassium (K), chloride (Cl),
HCO3 and therefore can be used if HCO3 or blood and calcium (Ca):
gas analysis is unavailable. If the potential exists for respi-
Body deficit  kg body weight  (normal electrolyte value
ratory disease, complete blood gas analysis should be per-
 patient’s electrolyte value)  ECF  cf
formed before the administration of alkalinizing agents.6
Treatment of severe acidosis (TCO2 less than 18 mmol/L) Acid-base status greatly affects the movement of
or alkalosis (TCO2 greater than 31 mmol/L) may require potassium ions (K) in and out of cells and the binding
specific fluid therapy. The fluid of choice to treat alkalosis of Ca to albumin. Therefore correction of acid-base status
is sodium chloride. Treatment of severe metabolic acido- often corrects minor imbalances of these electrolytes.
sis usually requires bicarbonate replacement therapy. The Acidosis causes K to move extracellularly and increases
base deficit is calculated as follows7: serum K, whereas alkalosis causes K to move intracel-
lularly and decreases serum K.8 A pH change of 0.1
Base deficit  kg body weight
units results in a 0.6 mEq/L reciprocal change in K.8
 (normal Tco2  patient Tco2)  ECV  cf
Although the previous equation has been used to calcu-
where ECV-cf is the extracellular fluid volume correction late K deficits, an accurate prediction of such a deficit is
factor (0.5 to 0.6 for neonates and 0.3 to 0.5 for adults). difficult because serum K depends on acid-base status.5
To avoid the complications of bicarbonate therapy, the Abomasal outflow obstruction results in hypochloremic,
clinician may wish to correct only half of the base deficit hypokalemic metabolic alkalosis.8 In this case infusion of
initially and reevaluate the patient after initial volume normal saline supplemented with K may be indicated.
and electrolyte replacement therapy. When possible, However, the infusion rate of K should not exceed 0.5
acid-base abnormalities should be corrected before the mEq/kg/hour.9 Acidosis causes increased serum ionized
institution of TPN. If TPN is already underway, the clini- calcium, whereas alkalosis causes decreased serum ionized
cian may choose to deliver bicarbonate therapy by a calcium, which may cause an animal with normal total
second IV line. The clinician or nutritionist should avoid serum calcium to exhibit signs of hypocalcemia.10 It is
adding more than 250 ml of 5% bicarbonate per liter of safest to administer K and calcium ions (Ca)
TPN solution to prevent the solution from becoming ex- through an IV line containing only polyionic isotonic
cessively hypertonic. As an example of base deficit re- fluids so as not to cause precipitation of these cations in
placement therapy, the authors will calculate bicarbonate solution. Mineral supplementation is rarely necessary
replacement therapy for the same 15-kg goat if the TCO2 until after day 7 to 10 of PN. Minerals should be moni-
is 15 mmol/L (which is the same as 15 mEq/L): tored with serum electrolyte analysis and supplemented if
needed (Box 2-2). Both trauma and diarrhea may in-
Base deficit  15 kg  (24  15 mmol/L)  0.5
 67.5 mmol of HCO
3

BOX 2-2
Bicarbonate is commonly supplied as a hypertonic 5%
solution (1200 mmol/L). Isotonic bicarbonate (300
mmol/L) is a 1.3% solution that contains 150 mmol of G ENERAL G UIDELINES ON M INERAL
HCO3 per liter (half of the 300 mmol/L ). Therefore
this 15-kg goat requires 450 ml of isotonic bicarbonate:
S UPPLEMENTATION*

67.5 mmol deficit  150 mmol/L Calcium 0.8 mEq (2 for growth or
 0.45 L, or 450 ml, of isotonic bicarbonate lactation)
Magnesium 0.33 mEq
A simpler way to replace the deficit is to add enough
Sodium 2.26 mEq
5% bicarbonate to the TPN to supply the 67.5 mmol
Phosphorus 3.6 mmol/day (2 for
deficit. Because 5% bicarbonate is 1200 mmol/L (half is
growth or lactation)
Na and half is HCO3 ), it contains 600 mmol/L, or 0.6
Zinc 0.6 mg
mmol/ml, of HCO3. Therefore 112.5 ml is required to
Iron 0.6 mg
get the 67.5 mmol needed to replace the base deficit (67.5
Iodine 1.5 mcg
mmol  0.6 mmol/ml). As previously mentioned, the
clinician may wish to replace only half of the deficit and
*When PPN or TPN are used for less than 7 days, mineral
then reevaluate the acid-base status. In this case 56 ml of
supplementation is rarely required. However, when PN is used for
5% bicarbonate solution can be added to the TPN in longer periods, close monitoring of serum electrolyte status may
place of 56 ml of polyionic fluid. The entire 56 ml could indicate a need for supplementation. All requirements are listed per kg
be included in 1 L of the TPN or it could be added at the of body weight per day.
60 • Sheep and Goat Medicine
2. Chandler ML, Guilford WG, Payne-James J: Use of peripheral
BOX 2-3
parenteral nutritional support in dogs and cats, J Am Vet Med Assoc

E STIMATES OF N UTRITIONAL R EQUIREMENTS

216(5):669, 2000.
3. Lippert AC, Fulton RB, Parr AM: A retrospective study of the use

OF S V
OME ITAMINS FOR P N*
of total parenteral nutrition in dogs and cats, J Vet Intern Med 7:52,
1993.
4. Baker JC, Lippert AC: Total parenteral nutrition in the calf,
Vitamin A 25 IU Compend Food Animal 9(2):F71, 1987.
Vitamin D 6.6 IU 5. Spurlock SL, Furr M: Fluid therapy. In Koterba AM, Drummond
Vitamin E 224 mcg WH, Kosch PC, editors: Equine clinical neonatology, Philadelphia,
1990, Lea and Febiger.
6. Constable PD: Clinical assessment of acid-base status, Vet Clin
*Vitamin supplementation is indicated if solutions are being
North Am: Food Animal Pract 15(3):447, 1999.
administered for more than 7 days. All requirements are listed per kg
of body weight per day. 7. Berchtold J: Intravenous fluid therapy in calves, Vet Clin North Am:
Food Animal Pract 15(3):505, 1999.
8. Sweeney RW: Treatment of potassium balance disorders, Vet Clin
North Am: Food Animal Pract 15(3):609, 1999.
crease loss of zinc (and possibly other nutrients). Vitamin
9. Tremblay RRM: Intravenous fluid therapy in calves, Vet Clin North
supplementation (Box 2-3) also is not generally needed
Am: Food Animal Pract 6:77, 1990.
until after day 7 to 10 of PN, with the possible exception 10. Goff JP: Treatment of calcium, phosphorus, and magnesium
of the B vitamins, which may be of value if given every balance disorders, Vet Clin North Am: Food Animal Pract 15(3):619,
2 to 3 days at labeled dosages from the onset of TPN. As 1999.
a general rule, vitamin K (10 mg intramuscularly) can be
given once a week.

R EFERENCES
1. Spurlock SL, Ward MV: Parenteral nutrition in equine patients:
principles and theory, Compend Contin Educ Pract Vet 13(3):461,
1991.
 Chapter 3

Oral-Esophageal Diseases
CHRISTINE B. NAVARRE, MICHAEL Q. LOWDER, AND D.G. PUGH

Although few diseases affect the oral cavity and esopha- barium suspension (200 ml) or barium cream (100 ml) is
gus in sheep and goats, the ones that do usually result in recommended for adult sheep or goats.2
depressed performance, weight loss, and occasionally
death. Although exceptions exist, most problems of the
oral cavity and esophagus are noninfectious diseases.
Endoscopy
The most common oral cavity abnormality that affects Endoscopy can be useful for examining the pharynx and
production is dental disease. Excessive dental wear and esophagus, as well as diagnosing pharyngeal abscesses,
broken or missing teeth are common in geriatric animals esophageal foreign bodies, and megaesophagus. Most
or those living on range. Before beginning an oral- flexible endoscopes used in large animal practice are too
esophageal examination, the clinician should attain large for use in small ruminants, but endoscopes appro-
a complete history, perform a complete physical exam- priate for small animals can be used. Sedation or general
ination (including body condition scoring), and observe anesthesia is recommended to facilitate restraint. Passage
the animal grazing or eating grain, swallowing, and of the endoscope through the nasal passages is preferred,
ruminating. but an endoscope with a small enough outside diameter is
To perform a complete oral examination, the clinician not always available. A speculum must be used if the en-
should physically restrain or sedate the animal and place doscope is passed through the mouth to avoid damage to
an oral speculum or gag in the mouth to enhance the vi- the endoscope from the teeth.
sualization of the oral cavity. The clinician should note
broken, worn, or missing teeth; ulceration, cracking, or
swelling of the mucosa of the gums, dental pad, and
tongue; and any fetid or abnormal odors. Incisor teeth in
R EFERENCES
1. Spence J, Aitchison G: Clinical aspects of dental disease in sheep. In
healthy adults should sit closely together. Grazing on Boden E, editor: Sheep and goat practice, London, 1991, Bailliere
rough, rocky pastures can wear grooves in the incisor Tindall.
teeth close to the gum margins.1 The neck and throat 2. House JK et al: Ancillary tests for the assessment of the ruminant
areas should be palpated for swelling and other abnor- digestive system, Vet Clin North Am: Food Animal Pract 8(2):203,
1992.
malities. This chapter covers some of the diagnostic pro-
cedures, diseases, and treatments for problems of the
mouth, its surrounding structures, and the esophagus.
DISEASES OF THE ORAL CAVITY
DIAGNOSTIC PROCEDURES Normal Dental Anatomy
The normal dental formula of the permanent teeth for
Radiography both sheep and goats is 2 (incisors 0/3, canines 0/1, pre-
Radiography of the head and neck can be performed in molars 3/3, molars 3/3) for a total of 32 teeth; the canine
sheep and goats using the same techniques used on other teeth function as fourth (lateral or corner) incisors
small animals. Fluoroscopy with contrast media may be (Figures 3-1 and 3-2).1 The ages of permanent tooth
needed to diagnose functional esophageal problems. A eruption for sheep and goats are provided in Table 3-1;
• 61 •
62 • Sheep and Goat Medicine

Figure 3-1 A lateral view showing the normal dentition of the

goat. As the animal ages, excessive wear, wave mouth, tooth toss, and
sharp points may all occur.

Figure 3-3 These frontal views of the incisors of sheep and goats
show the small teeth characteristic of the pre-yearling animal (A), the
two large permanent central incisors of the yearling (B), the dentition
of 2- and 3-year-old animals (C and D), and the full dentition of the 4-
year-old (E). Deciduous teeth are smaller than the permanent teeth
that replace them.

Figure 3-2 A lateral view showing the normal dentition of the

sheep. the appearance of the incisors during the first few years of
life is shown in Figure 3-3. Teeth should be white to
translucent. The molars normally have sharpened points
on the lateral or buccal aspect of the upper arcade and the
medial or lingual aspect of the lower arcade. Unless these
TABLE 3-1
points are causing damage to the oral mucosa or tongue,
AGES OF PERMANENT TOOTH ERUPTION IN SHEEP they do not require routine removal by floating. Fluorine
AND GOATS toxicity may result in soft, chalky areas on the teeth
and/or irregular dental wear. Brown staining and tartar
PERMANENT TOOTH AGE OF ERUPTION accumulation are common and rarely cause disease except
when severe. Normal attrition is noted as a change in the
Incisor 1 1 to 1.5 years shape of the incisors from rectangular to round; the teeth
Incisor 2 1.5 to 2 years eventually become stubs and fall out.2,3 The speed of this
Incisor 3 2.5 to 3 years process is influenced mostly by diet, but soil type, maloc-
clusions, and dental trauma also are contributing factors.
Incisor 4 3.5 to 4 years
Dental caries may be seen as holes in the teeth at the gum
Premolars 1.5 to 2 years margin.3 These are seen more commonly in lambs.3
Molar 1 3 months Grain-fed animals exhibit less dental attrition than those
Molar 2 9 to 12 months grazing on pastures on sandy to sandy loam soils. Animals
Molar 3 1.5 to 2 years grazing on sandy soils have more dental wear than those
browsing or grazing lush forage pastures. Malocclusions,
 Chapter 3 Oral-Esophageal Diseases • 63

whether congenital or acquired (through trauma), usu-

ally result in excessive wear opposite to the site of the
malocclusion.

Dental Attrition
Abnormal dental attrition occurs more commonly in
sheep than in goats. The most common cause is the mas-
tication of ingested sand and soil when forage length is
short. Calcium-deficient, fluoride-toxic, or unbalanced
diets also cause or contribute to this problem.4,5 The
highest incidence of dental attrition in sheep occurs in
range ewes older than 4 years. Tooth loss can result in a 2-
year decrease in the productive lives of sheep.4 Most Figure 3-4 The arrow points to a large hook on the upper last
sheep and goats can accommodate the loss of an incisor, molar. Note the way the hook protrudes into the lower mandible. This
hook was associated with significant difficulty when chewing and
but molar loss is more serious because the molars are weight loss in this animal.
needed for chewing roughage.7 Clinical signs of abnor-
mal dental attrition include weight loss and worn, loose,
or missing teeth.4,6 A decrease in water intake can ac-
company dental disease as the teeth become sensitive to has become controversial and has been outlawed in some
cold water. The clinician should examine the molars care- countries.8,10,11 The cutting or rasping of incisors to the
fully and not rely just on the appearance of the incisors to point of exposing the pulp cavity may result in excessive
diagnose this problem because molar attrition may be pain or tooth abscesses and is of only limited benefit in
related more to weight loss than incisor attrition.8 The improving production.3 Dental care is commonly needed
authors of this chapter prefer to examine and visualize the and may be most effective in the aged animal. Excessive
upper molars directly; however, these teeth also may be enamel points that cause oral discomfort and ulceration
palpable in some animals through the cheeks.9 Managing and hooks or wave mouths can effectively be managed by
grazing areas carefully, providing supplemental feed, en- floating the arcades. Wave or “sheer” mouth usually
suring the proper concentration of calcium in the diet, occurs in only a few animals in the flock.3 Before floating,
and paying attention to the calicumphosphorus ratio all the clinician should flush the animal’s mouth with water
help prevent abnormal attrition. The inclusion of a trace and administer mild sedation if necessary. Floating of the
mineral supplement also may be beneficial for dental cheek teeth can be performed more efficiently using a
health. However, keepers should take care when using full-mouth speculum (such as a Bailey mouth speculum
salt or mineral blocks. Sheep and goats can break their or a pony or miniature horse full-mouth speculum) or a
teeth while trying to ingest adequate salt from salt blocks. retractor to open the animal’s mouth and allow inspection
The incidence of broken teeth may be reduced by provid- and visual guiding of the equipment. Miniature horse
ing salt in a “loose” or granular form. floats work well and provide an effective means for exces-
Uneven molar wear can lead to wave mouth (Figure sive tooth removal. Pneumatic horse floats work excep-
3-4), and loss of molars can lead to accumulation of feed tionally well because the head is flat and small and the
in the empty socket and overgrowth of the opposing float has only a 1⁄4 in reciprocating action. This small
tooth.2 This condition may first be manifested as an in- stroke distance is atraumatic to the oral mucosa. Individ-
crease in the incidence of pregnancy toxemia or excessive ual sharp points can be cut with obstetrical wire or
body condition score losses, as animals are unable to cutting pliers.9 In cases of uncorrectable wave mouth or if
consume enough feedstuffs to meet requirements.3 These an animal’s teeth are worn away, a presoaked, well-bal-
problems occur more commonly in goats than in sheep. A anced, pelleted diet may be fed as a mash.7
foul odor from the mouth may be noted, along with signs
of weight loss, quidding, and an abnormal head position
(turning it to one side) when eating. In these cases an oral
Periodontitis
examination and floating the teeth may be necessary. Periodontitis is inflammation of the tissues around and
supporting the teeth. It occurs mainly in sheep and is
usually seen as a slight redness around some or all of the
General Dental Care teeth. Periodontitis commonly causes loss of incisor
Tooth disease caused by metabolic, nutritional, or toxic teeth. The underlying etiology is unknown, but mechani-
insults in sheep and goats probably occurs more com- cal or chemical gingival trauma from poor feedstuffs, nu-
monly than noted in the scientific literature. The once- tritional deficiencies, and bacterial plaque–induced gin-
common practice of “trimming” or grinding sheep teeth givitis are implicated as causes of acute inflammation.
64 • Sheep and Goat Medicine
Bacteroides gingivalis and other bacteria also have been swelling may be observed. Oral examination can reveal
implicated as a cause of periodontal disease, although the swelling of the gingiva around the affected tooth, tooth
etiology is still poorly understood. In severe cases edema fractures, or normal findings. Radiographs may reveal
may occur at the gingival surface.3 If left untreated, gin- boney lysis and periosteal reaction around the tooth
givitis may progress to chronic inflammation and break- roots.14 Differential diagnoses include osteodystrophia
down of the periodontal tissue.1,4,12,13 This can result in fibrosa, lymphosarcoma, actinomycosis, trauma, and
the incisors becoming long and loose initially. As the con- foreign body. Systemic administration of antimicrobials
dition progresses, the incisors, premolars, and molars for 2 to 4 weeks may cure the problem, especially if the
begin to fall out.1,4,12 Tooth root abscesses may also abscess is not open and draining and no obvious tooth ab-
develop.4 The gums or dental pads may be damaged in normalities exist. Broad-spectrum antimicrobials (e.g.,
some animals. Malocclusion and gum recession or pro- oxytetracycline, florfenicol) have been used with success
liferation also may occur in some sheep and goats. by the authors of this chapter. If systemic administration
However, ulcers caused by trauma usually heal without of antimicrobials fails to correct the problem or if the
treatment.3 Loss of body condition may or may not be condition is severe or the tooth is fractured below the
evident, depending on the diet. gum line, the clinician should consider extraction.
The use of periodontal disease (especially incisor loss Intraoral extraction can be performed in the small ru-
alone) as a reason for culling is questionable.1 Sheep with minant with a full-mouth speculum, dental picks, small
periodontitis or missing incisors may do well if hand fed (40-cm) molar forceps, and a fulcrum. A piece of wood or
(Figure 3-5). However, subclinical production losses may plastic (4 to 6 cm  2 to 4 cm) can be used as a fulcrum.
occur with periodontal disease4 and often a loss of incisor The gingiva is elevated away from the buccal and lingual
teeth is concurrent with premolar and molar loss. Herd sides of the affected tooth. Next, the clinician applies
treatment with antibiotics may be impractical and is slow, steady pressure to the tooth in either the buccal or
rarely effective from a therapeutic or economic stand- lingual direction for approximately 10 to 15 seconds and
point.1,3 Treatment of valuable individual animals with then moves the fulcrum in the opposite direction. After
antimicrobials (oxytetracycline 20 mg/kg ever 48 hours loosening the tooth, the clinician positions the fulcrum
for 2 to 3 treatments) and appropriate surgical techniques beside the head of the molar forceps, which is attached to
may be indicated. Until the exact causes and predisposing the tooth. Downward pressure is slowly applied on the
factors are known for periodontal disease, prevention in- forceps until the tooth is extracted. Packing of the empty
cludes optimizing nutrition. alveolus is usually not required, although flushing of the
mouth twice daily for 3 to 5 days facilitates the healing
process. A weak antiseptic or iodine solution can be used
Tooth Root Abscesses to flush the area. Animals with underlying or periapical
Small ruminants with tooth root abscesses usually exhibit infections may benefit from systemic administration of
a localized bony enlargement of the maxilla in the area of broad-spectrum antimicrobials (e.g., oxytetracycline).
the maxillary sinus or more commonly on the ventral Comparison of preextraction and postextraction radio-
surface of the mandible. Purulent drainage from the graphs ensures complete tooth removal and helps the
clinician determine whether postextraction curettage of
the bony alveolus is required. In cases in which intraoral
extraction is not indicated (e.g., if the tooth is fractured at
the level of the gum), surgical repulsion is an option to be
considered. A bacterial culture and sensitivity assay can
be performed before or during surgery to ensure the use
of the appropriate antimicrobials postoperatively. Pain
medication should be administered as appropriate. Ex-
traction of diseased teeth in sheep has been shown to in-
crease production.15

Miscellaneous Tooth Abnormalities

Congenital absence of the lower incisors or premolars,
persistent deciduous incisors, brachygnathism, and prog-
nathism have all been reported in goats.2,16 In sheep,
persistent deciduous incisors, dentigerous cysts, brachyg-
Figure 3-5 This more than 20-year-old ewe has missing incisors nathism, and prognathism are commonly seen dental ab-
and periodontal disease. (Courtesy Dr. Cindy Wolf, St. Paul, normalities.3,8,17,18 Most of these problems are not treat-
Minnesota.) able, and animals should therefore be culled if health or
 Chapter 3 Oral-Esophageal Diseases • 65

production is depressed. Many pet animals with dental teodystrophia fibrosa also may lead to pathologic frac-
abnormalities lead full lives with special care, but because tures.20 Fractures of the maxilla and mandible present
their pathologies may indicate genetic involvement, these acutely, with soft tissue swelling around the fracture and
animals should not be bred. possibly bony crepitus. Animals are usually anorexic and
may drool excessively. If the injury is discovered quickly, a
fracture can be repaired with routine small animal ortho-
Actinobacillosis pedic techniques. However, often these fractures go un-
Actinobacillosis is caused by the gram-negative rod Acti- noticed and present as chronic healed fractures. If this
nobacillus lignieresii. This organism normally resides in occurs, mandibular fractures in particular may not heal in
the mouth of ruminants and can gain entry to and infect correct alignment, which can result in malocclusion.
the deeper soft tissues of the head after trauma. Acti- Chronic malocclusion can lead to uneven growth and
nobacillosis is reported in sheep, where it can cause gran- wear of the teeth, interfering with prehension and masti-
ulomatous abscesses of the lips, parotid and submaxillary cation of food. Nondisplaced maxillary fractures may heal
regions, or other areas of the head. Tongue lesions are not without fixation.
as common as in cattle.

Clinical signs. The clinical signs depend on the site of

Pharyngeal Abscess
infection but usually include weight loss if eating Pharyngeal trauma can lead to pharyngeal abscesses in
becomes difficult.4,14,19 The drainage from the lesions sheep and goats.21 The clinical signs include anorexia,
may contain granules. Because the organism is a gram- excessive drooling, halitosis, swelling and pain in the
negative rod, a Gram’s stain of drainage can help differen- pharyngeal area, and, in severe cases, dyspnea and
tiate this infection from caseous lymphadenitis. bloat.22 Affected animals may become dehydrated from
decreased water intake and develop metabolic acidosis
Diagnosis. Culture and biopsy of the lesions are from loss of saliva. Sheep and goats are too small for the
needed for definitive diagnosis.14 clinician to perform oral digital examination of the area.
Radiography and endoscopy are needed to determine the
Treatment. Sodium iodide given intravenously (70 extent and severity of the problem and assess for foreign
mg/kg as 10% to 20% solution) and repeated 1 week later bodies. The primary differential diagnosis in small rumi-
is the treatment of choice. Treatment is usually successful nants is abscessation of the pharyngeal lymph nodes
and the prognosis is good, although regression of the from caseous lymphadenitis. Pharyngeal abscesses asso-
lesion may be slow.14 Refractory cases can be treated ciated with trauma are usually acute and accompanied by
orally with organic iodides (ethylene diamine dihydroio- cellulitis and diffuse swelling of the entire pharyngeal
dide [EDDI]) at 60 mg/kg/day for as long as 3 area. In contrast, pharyngeal lymph node abscesses are
weeks.14,19 Mild signs of iodism (e.g., epiphora, saliva- chronic and produce localized swelling of the lymph
tion, dandruff ) are of no clinical significance, but the cli- nodes.
nician should immediately discontinue treatment if more Administration of broad-spectrum antimicrobials and
severe signs (e.g., coughing, inappetence, diarrhea) occur. antiinflammatory drugs is indicated, as is intravenous
fluid support. In refractory or severe cases or cases in
which a foreign body is present, surgery may be indi-
Actinomycosis cated. If the original trauma occurred to the pharyngeal
Actinomycosis (lumpy jaw) is caused by the organism mucosa, the abscess should be drained into the pharynx,
Actinomyces bovis. This condition is uncommon in sheep if possible. This procedure requires general anesthesia;
as compared with cattle and has not been reported in endoscopy may provide better visualization of the area.
goats. Actinomycosis must be considered as a differential A temporary tracheostomy may be necessary because
diagnosis for tooth root abscesses in sheep because it also these animals may experience short-term dyspnea after
causes localized bony swellings on the mandible. surgery.

Treatment. Treatment is the same as for actinobacillo-

sis, although sulfadimethoxine (1 g/kg once a day) or iso-
Salivary Cysts
niazid (15 mg/kg orally [PO]) also may be used. Any Salivary cysts occur in sheep and goats as discrete, fluctu-
treatment should be continued for weeks to months. ant nodules on or behind the mandible. They can be dif-
ferentiated from caseous lymphadenitis by needle aspira-
tion. Fluid from a salivary cyst is clear and mucoid as
Fractures of the Maxilla and Mandible opposed to the purulent fluid drained from an abscess.14,21
Fractures of the maxilla and mandible are usually trau- Treatment is the same as for similar conditions in other
matic in origin. However, tooth root abscesses and os- species.
66 • Sheep and Goat Medicine
Bluetongue can be isolated from blood, semen, or tissues (spleen and
Etiology and pathogenesis. Bluetongue is an acute brain from aborted fetuses). Viral isolation from blood
viral disease caused by a ribonucleic acid (RNA) orbivirus obtained during the viremic, febrile state is the most de-
that affects both domestic and wild ruminants. It is trans- finitive means of diagnosis. Serologic evaluation involves
mitted mainly by gnats of the genus Culicoides, although two types of viral antigen-group antigens called P7 and
sexual and transplacental transmission can occur. Because P2. The former is found in all BTVs, whereas the latter
of the vector transmission, the disease is more common in determines the serotypes. Sera are commonly tested with
late summer and early fall.4,23 Bluetongue virus (BTV) is complement fixation, agar gel immunodiffusion (AGID),
endemic in many areas, particularly southern regions that or one of several enzyme-linked immunospecific assay
are vector friendly. Cattle and other wild ruminants act as (ELISA) tests. A competitive ELISA is considered the
reservoirs; the virus can circulate in the blood of these best serologic test for detection of group antibodies to
animals for months to years, even though clinical disease BTV. A direct fluorescent antibody test also is available.
is rare.23,24 Many strains of the virus exist, and disease Polymerase chain reaction (PCR)–based tests for blue-
usually occurs when a new strain or an animal naive to the tongue have recently become available and are extremely
endemic strains is introduced.4,23 sensitive and specific. Other laboratory tests and observa-
The incubation period of bluetongue in sheep is tions that aid in diagnosis include leukopenia during the
usually 7 to 10 days. The virus appears to cause a vasculi- early febrile stage of the disease and an increase in serum
tis resulting from infection of vascular endothelial cells. creatinine kinase corresponding to the latter phase of
This vasculitis results in edema and necrosis of epithelial muscle stiffness and lameness. Necropsy lesions are non-
and mucosal surfaces. Teratogenic effects are caused by specific. A definitive diagnosis of BTV requires virus iso-
disruption of organogenesis by the virus in the develop- lation from blood or tissue from acutely infected animals
ing fetus. The disease is most severe when previous expo- (particularly the spleen) and aborted fetuses (especially the
sure has occurred (sensitization). In cattle the disease brain) or detection of RNA specific to BTV by PCR.23
operates through an immunoglobulin E (IgE) hypersen-
sitivity reaction. Different breeds of sheep show differ- Treatment. Treatment is supportive only. Broad-
ences in susceptibility to BTV—meat breeds are more spectrum antimicrobials are indicated if secondary bacte-
susceptible than wool breeds and native African sheep rial infections develop. Nonsteroidal antiinflammatory
are resistant to the disease. Feeder lambs are the most drugs are indicated for inflammation, fever, and pain. Nu-
susceptible. tritional and fluid support may be needed if affected
animals cannot eat or drink.
Clinical signs. Clinical signs are seen most commonly
in sheep and all ages are susceptible. Goats are commonly Prevention. Prevention mainly involves controlling the
infected with the virus but rarely show clinical signs.2 Culicoides vector, but this can be difficult. Eliminating
Clinical signs result from generalized vasculitis and vector breeding grounds (mud with a high organic matter
include a transient fever and edema of the muzzle, face, content) and housing animals at dusk and through the
and ears. Profuse serous nasal discharge is seen initially; it night (periods of peak gnat activity) may help.4,23
later becomes mucopurulent, causing crusting around the Because of the complicated immunologic response to
nose. Oral mucous membranes are initially hyperemic. As BTV, vaccine development is difficult.25,26 Modified live
the disease progresses, petechiae and ulcers develop, espe- virus (MLV) vaccines are available in some parts of the
cially on the dental pad and commissures of the mouth. world. However, vaccines must contain the serotypes
Cyanosis of the tongue is not common but does occur in present in a particular location to be useful, and they are
some cases, hence the name bluetongue. Pulmonary edema not without risks. The MLV vaccine can be teratogenic in
develops and can result in secondary bacterial pneumo- early pregnancy, and there is a slight risk for abortion in
nia. Lameness caused by coronitis and myositis, diarrhea late pregnancy, as well as infertility in breeding rams.23
(occasionally bloody), and wool breaks can all be seen in Sheep that have recovered from an attack of bluetongue
affected animals. Some animals may slough their hooves. are solidly resistant for months to infection by the same
The most dramatic clinicopathologic finding is severe viral strain and to some different viral types. Active im-
leukopenia. Differential diagnoses include other vesicular munity in sheep requires both humoral and cellular im-
diseases and photosensitization. The virus also is terato- munity (see Chapters 6 and 18).
genic and can cause abortions, stillbirths, and weak
lambs.4,23
Contagious Ecthyma
Diagnosis. Antibody tests of serum are not definitive Contagious ecthyma is a zoonotic disease of sheep and
because some antibodies persist for years after exposure goats caused by a poxvirus. It also is commonly known as
and cross-reactivity with other orbiviruses can occur. In contagious pustular dermatitis or sore mouth. Young animals
parts of the world where the disease is common, the diag- are most susceptible, but older naive animals also can be
nosis is usually based on clinical signs alone. The virus infected.
 Chapter 3 Oral-Esophageal Diseases • 67

Clinical signs. Clinical signs include proliferative, 7. Clarkson MJ, Winter AC: Teeth. In Clarkson MJ, Winter AC,
crusting lesions, the majority of which occur on the mu- editors: A handbook for the sheep clinician, Liverpool, 1997, Univer-
cocutaneous junctions of the mouth and nose. Lesions sity Press.
8. Barber DML, Waterhouse A: An evaluation of cutting of incisor
also may occur on other areas of the body, especially the
teeth of ewes in an attempt to control premature tooth loss, Vet Rec
udders of females nursing affected young.
123:598, 1988.
9. Smith MC: Exotic diseases of small ruminants. Geriatric medicine
Diagnosis. Diagnosis is usually made from physical ex- for small ruminants, Proc West Vet Conf, p 144, 1998.
amination findings, but virus identification in tissues can 10. Denholm LJ, Vizard AL: Trimming the incisor teeth of sheep:
confirm the diagnosis. Very transient, early lesions are another view, Vet Rec 119(8):182, 1986.
vesicular and need to be differentiated from other vesicu- 11. Spence JA, Hooper GE, Austin AR: Trimming incisor teeth of
lar diseases. sheep, Vet Rec 118(5):617, 1986.
12. Spence JA, Atchison GU: Early tooth loss in sheep: a review, Vet
Treatment. Nutritional and fluid support are impor- Ann 25:125, 1985.
tant because affected animals are reluctant to eat and 13. Cutress TW, Ludwig TG: Periodontal disease in sheep. 1. Review
of the literature, J Periodontol 40:31, 1969.
drink. Treatment of the lesions is usually not necessary
14. Fubini SL, Campbell SG: External lumps on sheep and goats, Vet
unless secondary bacterial infection or maggot infesta-
Clin North Am: Large Animal Pract 5:457, 1983.
tion occurs. Treatment does not speed the course of 15. Andrews AH: Clinical signs and treatment of aged sheep with
lesion regression, which is typically about 1 month. loose mandibular or maxillary cheek teeth, Vet Rec 108:331, 1981.
Crusts should not be removed; this action may delay 16. Emele-Nwaubani JC, Ihemelandu EC: Anodontia of the incisor
healing, promote scarring, and increase the handler’s and canine teeth in a cryptorchid West African dwarf goat, Trop
chance of acquiring the disease. Animals usually make a Vet 2:172, 1984.
full recovery. 17. Pearson EG: Diseases of the hepatobiliary system. In Smith BP,
editor: Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
Prevention. Prevention is best accomplished by main- 18. Bruere AN et al: A syndrome of dental abnormalities of sheep,
taining a virus-free herd. However, this can be difficult New Zealand Vet J 27:152, 1979.
19. Smith BP: Actinobacillosis. In Smith BP, editor: Large animal in-
because carrier animals may not show lesions. Keepers
ternal medicine, ed 2, St Louis, 1996, Mosby.
should carefully examine herd or flock additions for
20. Andrews AH: Osteodystrophia fibrosa in young goats, Vet Rec
lesions. After a herd is infected, eliminating the disease is 112:404, 1983.
difficult because the virus is stable in crusts that have 21. Linklater KA, Smith MC: Conditions affecting the pharyngeal
fallen from infected animals. A vaccine is available for region and esophagus. In Linklater KA, Smith MC, editors: Color
herds or flocks in areas where sore mouth is endemic, but atlas of diseases and disorders of the sheep and goat, London, 1993,
it is a live, virulent vaccine whose use is controlled in Wolfe Publishing.
some areas by state regulatory officials.27 22. Smith BP: Pharyngeal trauma/abscess. In Smith BP, editor: Large
animal internal medicine, ed 2, St Louis, 1996, Mosby.
23. Michelsen PGE: Bluetongue. In Smith BP, editor: Large animal
Other Viral Diseases internal medicine, ed 2, St Louis, 1996, Mosby.
24. Katz J et al: Diagnostic analysis of the prolonged bluetongue virus
Other viral diseases that result in oral lesions, including
RNA presence found in the blood of naturally infected cattle and
foot and mouth disease (see Chapter 14) and vesicular
experimentally infected sheep, J Vet Diagn Invest 6:139, 1994.
stomatitis (see Chapter 14), are covered elsewhere in this 25. Campbell CH, Grubman MJ: Current knowledge on the bio-
book. chemistry and immunology of bluetongue, Prog Vet Microbiol
Immun 1:58, 1985.

R EFERENCES
1. St-Jean G: Dental and periodontal diseases. In Smith BP, editor:
26. Mahrt CR, Osburn BI: Experimental bluetongue virus infection
of sheep; effect of previous vaccination: clinical and immunologic
studies, Am J Vet Res 47:1191, 1986.
Large animal internal medicine, ed 2, St Louis, 1996, Mosby. 27. Michelsen PGE: Contagious ecthyma. In Smith BP, editor: Large
2. Smith MC, Sherman DM: Digestive system. In Smith MC, animal internal medicine, ed 2, St Louis, 1996, Mosby.
Sherman DM, editors: Goat medicine, Philadelphia, 1994, Lea &
Febiger.
3. Spence J, Atchison G: Clinical aspects of dental disease in sheep, DISEASES OF THE ESOPHAGUS
In Pract, p 128, July 1986.
4. Kimberling CV: Diseases of the digestive system. In Kimberling Esophageal Obstruction
CV, editor: Jensen and Swift’s diseases of sheep, ed 3, Philadelphia,
Esophageal obstruction, or “choke,” occurs sporadically
1988, Lea & Febiger.
5. Sherman DM: Unexplained weight loss in sheep and goats. A
when feedstuffs are swallowed that are too hard for
guide to differential diagnosis, therapy, and management, Vet Clin proper mastication or too large to pass down the esopha-
North Am: Large Animal Pract 5:571, 1983. gus. Common feedstuffs that cause choke are sugar beets,
6. Gnad DP et al: Diagnosing weight loss in sheep: a practical ap- corncobs, potatoes, turnips, apples, and pears.1 Obstruct-
proach, Comp Cont Ed Pract Vet 22:S16, 2000. ing items usually lodge in the cervical portion of the
68 • Sheep and Goat Medicine
esophagus but also may become stuck in the cardia.2 Oc- thesia or heavy sedation is essential in cases where
casionally animals become choked after rapid ingestion of mineral oil is used for lubrication because the animal’s
pelleted rations. This type of choke is usually transient head must be kept in a lowered position to prevent aspi-
and the animal is able to relieve it on its own. However, if ration. After relieving the obstruction, the clinician
esophageal spasm or swelling occurs, the condition may should observe the animal for signs of aspiration pneu-
require treatment. Rarely, secondary esophageal obstruc- monia and esophageal stricture. In cases of long-term
tion may occur after the esophagus has previously rup- choke or suspected esophageal damage, antibiotics (oxy-
tured.3 The clinician should note that animals with either tetracycline 20 mg/kg every 48 to 72 hours or penicillin
rabies or botulism may appear to have esophageal ob- 20,000 IU/kg twice a day) and antiinflammatory drugs
struction. Dental disease also may contribute to choke, (flunixin meglumine 1 to 2 mg/kg) may be indicated to
and a thorough oral examination is indicated after the minimize long-term esophageal damage.
choke has been relieved.
Prevention. The occurrence of choke is sporadic and
Clinical signs. Animals that are choked are agitated sometimes unavoidable. Still, fencing off areas where
and stand with the head and neck extended. Repeated choke-producing feedstuffs (e.g., apples) are located may
coughing and retching motions occur, and saliva con- minimize clinical cases. Placing large stones or bricks into
taining some feed particles may come from the mouth feed bunks, providing adequate feed bunk space, and
and nose. Prevention of normal eructation results in feeding multiple small grain meals may all slow feed
rumen tympany, which may cause death in untreated intake, particularly if pelleted feeds are offered.
animals. Partial obstruction is usually not immediately If choke is a recurrent problem in a particular ani-
life-threatening because bloat is less likely, but chronic mals, pellets or other dehydrated feedstuffs should
loss of saliva can lead to dehydration and metabolic aci- be avoided. Affected animals may benefit from an oral
dosis, pressure necrosis, and esophageal rupture. examination and, where appropriate, dental care (e.g.,
floating).
Diagnosis. Diagnosis is by observation of clinical
signs. The clinician may be able to palpate the offending
object in the esophagus. However, the inability to palpate
Megaesophagus
an esophageal obstruction does not preclude choke as a Megaesophagus is an uncommon abnormality in sheep
possible diagnosis. The clinician also may locate an ob- and goats, but it has been reported in Alpine and Nubian
struction while passing an esophageal tube. goats and Southdown sheep.4,5 Esophageal infection with
Sarcocystis species has been found on histopathology in
Treatment. In cases of life-threatening bloat, rumen some cases and therefore implicated as a cause. However,
gas should be relieved first. This can be done by trocariza- this organism is found routinely in the esophagi of normal
tion of the rumen through the left flank with a 14-gauge animals. Regurgitation, vomiting, and swelling of the neck
needle. After relieving the bloat, the clinician should region are typical signs. No practical or effective treatment
attempt to remove the obstruction. If the obstruction is exists other than supportive care in most cases. If Sarcocys-
just behind the pharynx, forceps can be used to grasp and tis is suspected, the clinician may give injectable folic acid
remove the object. If the obstruction is palpable in the inhibitors (e.g., trimethoprim-sulfadiazine 15 mg/kg once
cervical region, it can be manually massaged toward the a day subcutaneously).
pharynx and then removed. If the object is lodged in
the chest, a well-lubricated stomach tube (10 to 15 mm
outside diameter) can be used to try to push the object
into the rumen. This should be done very gently to
R EFERENCES
1. Matthews J: Abdominal distention. In Matthews J, editor: Diseases
prevent esophageal rupture, especially in cases of chronic of the goat, ed 2, Oxford, England, 1999, Blackwell Science.
partial obstruction in which the esophagus may be very 2. Kimberling CV: Diseases of the digestive system. In Kimberling
CV, editor: Jensen and Swift’s diseases of sheep, ed 3, Philadelphia,
friable. In most cases, either mineral oil or obstetric lubri-
1988, Lea & Febiger.
cant is needed for lubrication of the tube and the ob-
3. Fleming SA, Dallman MJ, Sedlacek DL: Esophageal obstruction as
structing object. Obstruction from pellets can be dis- a sequela to ruptured esophagus in a goat, J Am Vet Med Assoc
lodged by gentle massage with a stomach tube, water, 195(11):1598, 1989.
irrigation, or surfactant (e.g., dioctyl sodium sulfosucci- 4. Ramadan RO: Megaesophagus in a goat, Agri-Pract 14:26, 1993.
nate [DSS]) (see Chapter 16). Heavy sedation or general 5. Braun U et al: Regurgitation due to megaesophagus in a ram, Can
anesthesia may be necessary for these procedures. Anes- Vet J 31:391, 1990.
 Chapter 4

DGastrointestinal
iseases of the
System
CHRISTINE B. NAVARRE AND D.G. PUGH

The gastrointestinal system is, arguably, more prone to acute or chronic inflammation; increases in globulins or
disease than any other part of the sheep or goat. Gas- fibrinogen suggest a chronic inflammatory disease. Low
trointestinal parasitism alone is the most significant cause protein levels, especially albumin, can point to chronic
of production and animal losses in much of North blood loss from intestinal parasitism or infiltrative bowel
America.1,2 There is no substitute for a thorough physical disease. Liver disease should be suspected if liver enzymes
examination when trying to determine the affected body or bilirubin are elevated. However, liver enzymes can be
systems of a sick animal; this is especially true in diseases normal in chronic liver disease. Also, albumin levels rarely
of the gastrointestinal system. A complete physical exam- drop in ruminants with liver disease, as they do in other
ination should include palpation for body condition, as- species.3 Changes in electrolytes can occur with gastroin-
sessment of abdominal shape and rumen motility, obser- testinal disease, especially if the animals are anorexic.
vation of the consistency of the stool, and evaluation for Electrolyte measurements also are helpful in formulat-
the presence of bloat. However, because rectal palpation ing a treatment plan. Hypochloremia and metabolic
cannot be performed in sheep and goats, diagnosis of alkalosis occasionally occur in abomasal disease. A mild
disease in a particular segment of the gastrointestinal hypocalcemia may be encountered in some small rumi-
system can be difficult. Therefore, the clinician may have nants with gastrointestinal atony. Because many animals
to perform ancillary diagnostic procedures to characterize with gastrointestinal disease are dehydrated and therefore
gastrointestinal diseases properly. azotemic and possibly hypoproteinemic, urinalysis is
helpful to eliminate urinary disease as a cause of these
pathologies.
DIAGNOSTIC PROCEDURES Normal ranges for clinicopathologic values are in-
cluded in this textbook (see Appendix III) and also have
Clinicopathologic Data been published in several other textbooks.4-7 However,
Clinicopathologic data consisting of a complete blood clinicians would do well to learn the normal values, espe-
count (CBC), serum biochemical evaluation (SBE), and cially serum biochemistry values, established by the labo-
urinalysis can be helpful in differentiating gastrointestinal ratory most commonly used for analysis.7
diseases, developing a prognosis and plan for treatment,
and monitoring treatment. A CBC rarely identifies a spe-
cific disease, but it can be helpful in evaluating the sever-
Rumen Fluid Analysis
ity of dehydration, anemia, and hypoproteinemia. The Analysis of rumen fluid can help differentiate diseases of
clinician must take care to interpret the packed cell the forestomachs. An appropriately sized orogastric tube
volume (PCV) and total protein in light of the hydration can be passed through the oral cavity for fluid collection
status of the animal as noted on physical examination. An (Figure 4-1). The clinician must properly restrain the
anemic or dehydrated hypoproteinemic animal may have animal, using a mouth speculum (Figure 4-2) to prevent
normal PCV and total protein values. Both the CBC and tube chewing. If the tube is chewed, its roughened surface
SBE can be helpful in characterizing the presence and may damage the esophagus; parts of a broken tube can be
severity of an inflammatory disease process. Changes in swallowed. Rumen fluid also can be collected using per-
the total and differential white blood cell count indicate cutaneous rumenocentesis4,8-12 (Figure 4-3). A 16-gauge
• 69 •
70 • Sheep and Goat Medicine

Figure 4-3 The site for performing a rumenocentesis. The area

should be clipped, cleaned, and surgically prepared.

occur during collection with an orogastric tube, and it

appears to be less stressful. Rumenocentesis presents a
slight risk of peritonitis, but this risk can be minimized
with proper restraint. Percutaneous rumenocentesis
should not be performed on pregnant females.
After the fluid is collected, it can be analyzed for color,
Figure 4-1 Passage of an orogastric tube through a mouth odor, pH, protozoal species and motility, methylene blue
speculum. The tube should be lubricated and passed slowly down the reduction time (MBR), Gram’s staining characteristics,
esophagus. and chloride levels. Normal values are listed in Table 4-1.
Anorexia may cause the fluid to appear darker, the pH to
increase, and the number and motility of protozoa to de-
crease. A gray color, low pH, and dead or no protozoa are
seen in rumen acidosis from grain overload. The MBR is
prolonged with any type of indigestion. Large numbers of
gram-positive rods (Lactobacillus species) also may be
seen in rumen acidosis. Elevated rumen chloride indi-
cates an abomasal or proximal small intestinal obstruction
(either functional or mechanical).

Fecal Examination
The most important reason for examining feces in sheep
and goats is to determine the presence and relative
number of nematode parasites infesting an animal or
flock. The quantitative technique for determining eggs
per gram of feces (EPG) is shown in Box 4-1. Fecal EPG
values of more than 500 to 1000 indicate serious infesta-
Figure 4-2 Mouth speculums for use in passing an orogastric tion and the need for intervention.
tube. Various equipment designs can be used to protect the tube from Fecal occult blood testing and acid-fast staining of
being chewed. fecal smears also can be performed. Fecal occult blood
tests can detect microscopic amounts of blood in the
feces. However, they cannot indicate which part of the
needle can be inserted in the rumen through the abdom- gastrointestinal tract is bleeding. Acid-fast stains of fecal
inal wall caudal to the xyphoid and to the left of midline. smears that reveal clumps of acid-fast rods usually indi-
The clinician then aspirates fluid with a syringe. Local cate infection with Mycobacterium paratuberculosis
anesthesia and sedation of the animal may be necessary. ( Johne’s disease). Generally, individual acid-fast rods
This technique avoids the saliva contamination that can found on fecal examination are nonpathogenic.
 Chapter 4 Diseases of the Gastrointestinal System • 71

TABLE 4-1

NORMAL RUMEN FLUID CHARACTERISTICS

OF SHEEP AND GOATS
CHARACTERISTIC NORMAL VALUES

Color Green
Odor Aromatic
pH* 6.5 to 7.5
Protozoa† Mixed sizes and species
rapidly moving
Methylene blue 3 to 6 minutes
reduction time‡
Figure 4-4 Ventral and caudal sites for performing
Gram’s stain Gram-negative rods abdominocentesis. The needle indicates the ventral site. The caudal
predominate site is the clipped area below the flank (arrow).
Rumen chloride Less than 25 to 30 mEq/L
From Nordlund KV, Garrett EF: Rumenocentesis: a technique for BOX 4-1
collecting rumen fluid for diagnosis of subacute rumen acidosis in
dairy herds, Bovine Pract 28:109, 1994; Keefe GP, Ogilvie TH:
Comparison of oro-ruminal probe and rumenocentesis for prediction MM Q C ASTER’S UANTITATIVE T ECHNIQUE FOR
of rumen pH in dairy cattle, Proc 30th Ann Am Assoc Bovine Pract
Conv, p 168, 1997; Smith MC, Sherman DM: Goat medicine, O N
BTAINING THE UMBER OF N EMATODE E GGS
Philadelphia, 1994, Lea & Febiger.
*Use pH paper with at least 0.5-unit gradations.
†Place a drop of fluid on a warm slide and cover with a coverslip.
P G F
ER RAM OF ECES

Examine under 100 magnification. 1. Weigh 2 g of feces and thoroughly mix with 28
‡Mix one part 0.03% methylene blue to 20 parts rumen fluid.
ml of water. This is the preferred method.
Measure time for blue color to clear to match a control tube of fluid.
However, if a gram scale is not available, feces
can be added to the 28 ml of water until the
Abdominocentesis water level indicates 30 ml. This approximates 2
g of feces.
Abdominocentesis is useful in discerning the causes of 2. Remove 1 ml of well-mixed fecal-water
fluid distention in the abdomen. Two methods can be suspension, add to 1 ml of Sheather’s solution,*
used. The first technique involves tapping the lowest and mix well.
point of the abdomen slightly to the right of midline; it is 3. Fill both sides of a McMaster’s chamber with
useful in ruling out a ruptured bladder as the cause of the Sheather’s solution–fecal-water mixture.
general ascites (Figure 4-4).4,13 The clinician should take 4. Allow to stand for 5 minutes.
care to avoid the prepuce in males. The second technique 5. Count ova inside of chamber lines on both
is useful if peritonitis is suspected. Because localized peri- sides. Multiply the number of ova by 100. This
tonitis is more common than generalized peritonitis, four number approximates the number of eggs per
sites are tapped.14 The two cranial sites are slightly caudal gram of feces.
to the xyphoid and medial to the milk veins on the left
and right sides. The two caudal sites are slightly cranial to *Sheather’s solution consists of 1470 ml distilled water, 5 lb sugar, and
the mammary gland and to the left and right of midline. 30 ml liquid phenol. It is made by heating distilled water and sugar in
For either technique, manual restraint with sedation is the upper half of a double boiler until the sugar is dissolved, cooling,
recommended; the use of real-time ultrasonography may and then adding the phenol.
help locate fluid pockets. A 20-gauge needle or teat
cannula can be used for fluid collection.13 The clinician both sheep and goats. The clinician should minimize the
should prepare the site using sterile technique and ratio of EDTA to fluid because EDTA can falsely elevate
provide local anesthesia when employing a teat cannula. protein levels. Using EDTA tubes made for small animals
Fluid should be collected in a small ethylenediamine or shaking excess EDTA out of large tubes resolves this
tetra-acetic acid (EDTA) tube for analysis and a sterile problem. Normal culture values are similar to those for
tube for culture. Abdominal fluid can be difficult to cattle (clear, colorless to slightly yellow, 1 to 5 g/dl
obtain because of the small amounts normally present in protein, less than 10,000 cells).14 Cytologic examination
72 • Sheep and Goat Medicine
is needed to characterize the cell population and assess laparoscopic exploration of the abdomen used for cattle
for the presence of phagocytized bacteria. can be modified for use in sheep and goats.20 The clini-
cian inserts a cannula in the caudal abdomen and care-
fully inflates the abdomen with carbon dioxide (CO2).
Radiography With the animal restrained in dorsal recumbency and
Radiography of the abdomen can be performed in small either sedated or anesthetized, the clinician places the
ruminants using small animal techniques. In adults, the cannula in the inguinal area as described for laparoscopic
rumen normally fills the entire abdomen. Radiography insemination in Chapter 6. Entrance on the right side
can detect gas distention of the small intestine, abdomi- allows visualization of most of the abdominal organs. The
nal fluid, and foreign bodies.14,15 Contrast techniques are clinician should avoid the rumen when introducing the
useful for diagnosing atresia of the rectum or colon. laparoscope into the abdomen. This procedure may be
Unlike in other small animals, contrast techniques are not enhanced by lowering the head or rear of the animal, al-
practical for characterizing small intestinal problems in lowing better visualization of the entire abdomen.
sheep and goats because the rumen dilutes and slows Animals should be properly ventilated during this proce-
passage of the contrast media.16 dure because inflation of the abdomen and lowering of
the head can put pressure on the diaphragm.
Ultrasonography
Ultrasonography can be used to provide better character-
Exploratory Laparotomy
ization of abdominal distention, internal and external ab- Exploratory laparotomy can be a valuable diagnostic tool
dominal masses, and gross lesions of the liver. Ascites in evaluating gastrointestinal diseases when other tests in-
may be differentiated from fluid in the intestinal tract, dicate abdominal disease. In some cases, therapeutic surgi-
and gas distention of the intestines can be differentiated cal techniques can be performed at the same time. The
from fluid distention. Normal ultrasonographic examina- technique of exploratory laparotomy used in cattle can be
tion of the liver in sheep has been described.17 The liver adopted for sheep and goats as long as the clinician keeps
can be viewed on the right side from the seventh or in mind that these animals are more likely to lie down
eighth rib caudally to the thirteenth rib (Figures 4-5 and during surgery and standing surgery should only rarely be
4-6). Ultrasonography can be used to perform biopsies of attempted.21 Small ruminants should be heavily sedated
organs or masses and to locate pockets of fluid. or placed under general anesthesia during this procedure.
They may show signs of postoperative pain, anorexia, and
depression and should be treated accordingly with a non-
Laparoscopy steroidal antiinflammatory drug (NSAID) (flunixin meg-
Laparoscopy is more commonly used as a reproductive lumine 1.1 to 2.2 mg/kg intravenously [IV]).14 The deci-
tool, but it also can be used diagnostically as an alterna- sion to use perioperative and postoperative antimicrobial
tive to exploratory laparotomy in small ruminants.18,19 agents should be based on the conditions under which the
General anesthesia is recommended. The technique for surgery is performed and the diagnosis made at surgery.

Figure 4-5 Demonstration of the site of liver ultrasonography. In Figure 4-6 Normal ultrasonography of the liver in a goat. Note the
sheep the area should be clipped, but in goats alcohol can be applied degree of contrast. Liver abscesses, fibrosis, and fatty deposition can
to the overlying hair and skin. If the area is clipped, the clinician all be visualized.
should apply a bland coupling material (e.g., methyl cellulose,
vegetable oil) between the skin and the transducer.
 Chapter 4 Diseases of the Gastrointestinal System • 73

Antimicrobial agents are not necessary for exploratory stapled, or, if it is small enough, left alone to heal by
surgery performed aseptically, in a hospital setting, and second intention. The clinician or keeper should apply fly
without complications. However, they are indicated in repellent to the area. The animal should have a history of
field conditions, if infection is already present, and if the Clostridium prophylaxis; if it does not, it should be vacci-
intestinal tract is opened. A combination of ceftiofur nated during or before the biopsy.
(1.1 to 2.2 mg/kg IV twice a day [BID]) and procaine
penicillin G (22,000 IU/kg intramuscularly [IM] BID)
can be administered until culture results indicate an
absence of microbes.
R EFERENCES
1. U.S. sheep health and management practices, Fort Collins, CO, 1996,
National Animal Health Monitoring System.
2. Pugh DG, Hilton CD, Mobini SM: Control programs for gas-
Liver Biopsy trointestinal nematodes in sheep and goats, Comp Cont Ed Pract
Liver biopsy in sheep and goats is performed using the Vet 20:5112, 1998.
same technique and instruments as in cattle.12 However, 3. Roussel AJ, Whitney MS, Cole DJ: Interpreting a bovine serum
sedation and ultrasound guidance are recommended.22 chemistry profile: Part 1, Vet Med 92(6):553, 1997.
The biopsy can be performed in the ninth to tenth inter- 4. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea
& Febiger.
costal space slightly above an imaginary line from the
5. Howard JL, Smith RA: Current veterinary therapy 4: food animal
tuber coxae to the point of the elbow (Figure 4-7). The practice, Philadelphia, 1999, WB Saunders.
site should be surgically prepared, and a local anesthetic 6. Howard JL: Current veterinary therapy 3: food animal practice,
(2% lidocaine hydrochloride) infused subcutaneously. A Philadelphia, 1993, WB Saunders.
small scalpel blade is used to make a stab incision through 7. Keneko JJ: Clinical biochemistry of domestic animals, San Diego, CA,
the skin. A 14-gauge, 11.5-cm liver biopsy instrument is 1989, Academic Press.
inserted through the incision and the intercostal muscles 8. Navarre CB et al: Analysis of gastric first compartment fluid col-
and into the liver. The biopsy instrument should be di- lected via percutaneous centesis from healthy llamas, J Am Vet Med
rected toward the opposite elbow in most cases, but the Assoc 214(6):812, 1999.
use of real-time ultrasonography can help determine the 9. Nordlund KV, Garrett EF: Rumenocentesis: a technique for col-
direction and depth needed (2 to 4 cm). The clinician lecting rumen fluid for diagnosis of subacute rumen acidosis in
dairy herds, Bovine Pract 28:109, 1994.
should avoid the vessels along the caudal border of the
10. Keefe GP, Ogilvie TH: Comparison of oro-ruminal probe and ru-
ribs. On reaching the liver, the clinician will note a slight menocentesis for prediction of rumen pH in dairy cattle, Proc 30th
increase in resistance. Samples can be submitted for Ann Am Assoc Bovine Pract Conv, p 168, 1997.
culture (in a sterile plastic or glass vial or tube), 11. VanMetre DC, Tyler JW, Stehman SM: Diagnosis of enteric
histopathology (in formalin at a 101 ratio of formalin to disease in small ruminants, Vet Clin North Am: Food Anim Pract
tissue); and/or mineral analysis (in a plastic tube). When 16:87, 2000.
performing a liver biopsy for mineral analysis, the clini- 12. Smith MC: Commonly encountered diseases of goats, Proceedings
cian should rinse the biopsy site with distilled and deion- of the 1996 Symposium on the Health and Disease of Small Rumi-
ized water after sterile preparation to minimize sample nants, 1996, Kansas City, MO.
contamination. Samples for mineral analysis should not 13. Matthews J: Colic, ed 2, Oxford, UK, 1999, Blackwell Science.
be placed in formalin. The skin incision can be sutured, 14. House JK et al: Ancillary tests for the assessment of the ruminant
digestive system, Vet Clin North Am: Food Anim Pract 8(2):203,
1992.
15. Tanwar RK, Saxena AK: Radiographic detection of foreign bodies
(goat), Vet Med 79:1195, 1984.
16. Cegarra IJ, Lewis RE: Contrast study of the gastrointestinal tract
in the goat (Capra hircus), Am J Vet Res 38:1121, 1977.
17. Braun U, Hausammann K: Ultrasonographic examination of the
liver in sheep, Am J Vet Res 53(2):198, 1992.
18. Gourley DD, Riese RL: Laparoscopic artificial insemination in
sheep, Vet Clin North Am: Food Anim Pract 6:615, 1990.
19. Seeger KH, Klatt PR: Laparoscopy in the sheep and goat. In Har-
rison RM, Wildt DE, editors: Animal laparoscopy, Baltimore, 1990,
Williams & Wilkins.
20. Anderson DE, Gaughan EM, St-Jean G: Normal laparoscopic
anatomy of the bovine abdomen, Am J Vet Res 54:1170, 1993.
21. Hooper RN: Abdominal surgery in small ruminants, Proceedings of
the 1998 Symposium on the Health and Disease of Small Ruminants,
Figure 4-7 Liver biopsy. After the skin is clipped, anesthetized, 1998, Las Vegas, NV.
and aseptically prepared, the surgeon makes a stab incision in the 22. Pearson EG: Diseases of the hepatobiliary system. In Smith BP,
skin and introduces a 14-gauge biopsy needle. editor: Large animal internal medicine, St Louis, 1996, Mosby.
74 • Sheep and Goat Medicine
DISEASES OF THE passage of the tube. A clinician should then take a thor-
ough history and perform a complete physical examina-
FORESTOMACHS tion to find the cause of the bloat. If the bloat is not re-
lieved with an orogastric tube, the tube should be
Bloat removed and examined for evidence of froth. Frothy bloat
Bloat is less common in small ruminants than in cattle, can be treated with poloxalene (44 mg/kg) or dioctyl
with goats having the condition less commonly than sodium sulfosuccinate (DSS) (28 cc [1 oz]) delivered by
sheep. Bloat is the accumulation of either free gas or froth orogastric tube. The froth encountered in frothy bloat
in the rumen, which causes rumen distention. The causes caused by the ingestion of finely ground grain has a pH of
of bloat can be divided into three categories1,2: less than 5.5. If frothy bloat occurs while animals are
being fed concentrates, mineral oil (100 ml) may work
1. Frothy bloat—caused by diets that promote the better. Peanut oil (20 to 50 mg/kg), vegetable oil (100 to
formation of stable froth 200 ml), and hand soap (10 ml) also have been recom-
2. Free gas bloat—caused by diets that promote mended in emergency situations.3 If the animal is in
excessive free gas production severe respiratory distress, the clinician should insert a
3. Free gas bloat—caused by failure to eructate trocar or large needle into the rumen at the paralumbar
fossa. If gas does not escape, or froth is seen coming out
Pathogenesis. Frothy bloat is usually associated with of the trocar, an emergency rumenotomy should be per-
the ingestion of legume forages or hay (particularly formed (see the Rumenotomy section of this chapter).3
alfalfa) and with grazing on lush cereal grain pastures, but If several cases of bloat are encountered in a group of
it also may occur with high-grain diets.3 In the case of pastured animals, the entire group should be removed
frothy bloat from a finely ground diet (usually corn), mu- from the pasture and reintroduced slowly after gradual
coprotein released from rumen protozoa stabilizes the acclimation. If only one or two cases of bloat are encoun-
foam at a low pH. In legume-associated frothy bloat, tered, the healthy animals can remain on the offending
plant chloroplasts released into the rumen trap gas pasture, but grazing should be limited to ensure gradual
bubbles. Regardless of the form of frothy bloat, the small acclimation.
bubbles fill much of the rumen, preventing clearance of
the rumen’s cardia and resulting in a cessation of eructa- Prevention. Prevention of frothy bloat involves limit-
tion. Free gas bloat also occurs with grain diets, especially ing access to offending pastures or feedstuffs; providing
if the animals are not adapted to the diet. Failure to eruc- supplemental feed and providing poloxalene in mineral
tate has a variety of causes. Physical obstructions of the supplements; and adding ionophores to the ration or sup-
esophagus such as choke or swollen mediastinal lymph plement. When grazing or consuming legumes as “green-
nodes can cause free gas bloat. Any disease of the rumen chop,” animals should be introduced to the feed or
wall can interfere with rumen contractions and eructa- pasture slowly, preferably over 2 to 3 weeks. Animals
tion. Hypocalcemia, endotoxemia, pain, peritonitis, and should be closely monitored after a frost and during the
some pharmaceutical agents (especially xylazine) can all rapid growth phase of plants because legumes, particu-
interfere with rumen function and eructation.1,2,4,5 larly alfalfa, may be more likely to cause bloat at this time.
Certain varieties of legumes that are designed for inten-
Clinical signs. Clinical signs of frothy bloat and free sive grazing systems (e.g., Alfagraze) should be planted
gas bloat from either food intake or physical obstruction and managed in a manner that decreases the incidence of
of the esophagus are usually more severe and immediately bloat (limited or creep grazing). Feeding dry, stemmy hay
life-threatening than bloat seen from rumen wall diseases for 1 to 2 hours before allowing access to the legume
and systemic influences. Abdominal enlargement occurs, pasture also may help minimize bloat. Grass-legume pas-
particularly in the dorsal left paralumbar fossa. This may tures in which legumes are limited to less than 50% of the
be subtle in sheep or Angora goats with full fleece. Signs forage are safer but can still pose a problem for animals
of colic and anxiety are common. The rumen may be that are selective grazers. Grazing legumes with high leaf
either hypomotile or hypermotile. Respiratory distress is tannin concentrations (e.g., arrowleaf clover, kudzu) is
evident, with some animals breathing through their usually safer because tannins help break down rumen
mouths; death can ensue if the bloat is not treated.3 foam. The inclusion of poloxalene (10 to 20 mg/kg daily)
in the feed or mineral supplement is useful in preventing
Diagnosis and treatment. This condition is a medical frothy bloat. If poloxalene supplements are used, keepers
emergency, and therefore diagnosis and treatment should should feed them for 1 to 2 weeks before moving animals
occur almost simultaneously. If the animal is not in im- onto a problem pasture.
mediate danger of dying, an orogastric tube can be Free gas bloat from concentrate feeds can be controlled
passed. Most cases of free gas bloat are relieved with by slow introduction to these feeds to allow for rumen
 Chapter 4 Diseases of the Gastrointestinal System • 75

adaptation and by the inclusion of ionophores in the tion. Rumen acidosis usually occurs in animals that have
diet.1 Monensin (15 mg/head/day in ewes, 1 mg/kg/day been fed predominantly forage-based rations and are sud-
in goats) and lasalocid (0.5 to 1 mg/kg/day in sheep and denly given access to large amounts of highly fermentable
goats) both decrease the formation of free ruminal gas. By concentrates or concentrated forms of energy. It also can
enhancing propionic acid formation, these drugs not only occur in animals that have been receiving concentrates
reduce the amount of methane produced in the rumen, previously, if the amount is suddenly and drastically in-
they also improve the efficiency of nutrient assimilation creased; if access is denied for a time, then suddenly re-
from feedstuffs. turned (e.g., during weather changes and alterations in
Bloat in lambs and kids can have the same causes as in water availability); or if ration mixing errors occur (e.g.,
adults but also can be caused by improper milk feeding. leaving out monensin and rumen buffers)
Overfeeding, feeding of large infrequent meals, and As highly digestible carbohydrates are fermented,
feeding spoiled or cold milk have all been associated with rumen pH drops. Lactobacillus species, which are lactic
bloat in lambs and kids.6 Rapid overdistention of the acid producers, proliferate in the acidic rumen environ-
abomasum and improper chemical or physical composi- ment and further lower rumen pH. As the rumen pH
tion of milk replacers inhibit rumen motility, leading to drops, rumen protozoa and many of the lactate users
bloat. Even though the feeding of cold milk has been as- begin to die. Lactic acid production causes the osmotic
sociated with bloat, the practice can be used effectively in pressure in the rumen to increase. Fluid is drawn from
orphan feeding programs. Lambs and kids tend to limit the systemic circulation into the rumen, resulting in
their intake of cold milk after they have become accus- dehydration and possibly hypovolemic shock. Lactate
tomed to cold milk in a free-choice feeding system. Milk concentrations increase in the blood and may cause sys-
is usually placed in the rumen when animals are tube-fed; temic lactic acidosis. The lactic acid in the rumen also
this may result in milk spoilage.1,6 is toxic to the rumen epithelium. Damage to the ep-
ithelium can result in leakage of bacteria and toxins into
the portal and systemic circulation. Chronic sequelae to
Simple Indigestion rumen acidosis include fungal rumenitis and occasion-
Simple indigestion is a mild form of upset of the reticulo- ally liver abscesses.1,7 Liver abscesses are less com-
rumen caused by a change in feeding routine. It can be monly encountered in sheep and goats than in cattle.
caused by an alteration in the type of feed or in the Laminitis also can occur, but may be more of a problem
amount of feed offered. The most common causes of in sheep than in goats.8 The severity of the disease
simple indigestion are the addition of grain to the diet, an depends on the composition of the feed, particle size,
increase in the amount of grain fed, and an increase in the amount of feed consumed, and the period of adaptation
energy density of the diet. Examples of such dietary to the diet.
changes are replacing oats with corn or changing from
whole to ground corn. If the changes are drastic, rumen Clinical signs. Clinical signs vary with the amount and
acidosis can occur (see the following section). Other type of feed ingested and the time since ingestion. Signs
common causes are changes in hay or pasture, consump- first appear 12 to 36 hours after ingestion of the offend-
tion of moldy hay, and ingestion of weeds and toxic plants ing feed; they vary from anorexia, depression, and weak-
after overgrazing or droughts. Clinical signs include mild ness to a down animal suffering from severe circulatory
anorexia that lasts for 1 to 2 days. Mild diarrhea and bloat shock. Dehydration is usually severe and evidence of
also may occur. Rumen fluid pH can be unchanged, in- toxemia is present (e.g., injected mucous membranes, in-
creased, or decreased depending on the inciting cause. creased scleral injection). Colic, bilateral ventral abdomi-
Most animals improve with no treatment.1 nal distention, rumen stasis, and a “splashy” feel to the
rumen also may be present. Diarrhea can develop, adding
to dehydration.1,8,9 The diarrhea can range from a paste-
Rumen Acidosis like feces to very watery droppings with foam and occa-
Pathogenesis. Rumen acidosis is caused by the rapid sionally pieces of grain easily recognized. Dehydration,
rumen fermentation of highly digestible carbohydrates lactic acidosis, and toxemia result in neurologic signs, in-
that are ingested in excessive amounts. Although corn is cluding ataxia, head pressing, opisthotonos, and seizures.
commonly implicated, other cereal grains (oats, wheat, The body temperature is initially elevated but may drop
barley) may be involved, particularly if they are finely as the condition worsens or the animal becomes toxic.
ground. The smaller the particle size, the more quickly Some animals develop polioencephalomalacia and appear
rumen bacteria are able to ferment the carbohydrates blind.
contained in the feed. The common name of this condi-
tion is “grain overload,” but breads, candy, apples and Diagnosis. The rumen fluid pH may fall below 5.5.
other fruits, beets, and potatoes also can cause this condi- The fluid itself is milky gray and particles of the inciting
76 • Sheep and Goat Medicine
feed may be noticed. Protozoa are usually reduced in rected, transfaunation of the rumen microflora with about
number or absent, and large gram-positive rods (Lacto- 1 qt of rumen fluid from a small ruminant is beneficial
bacillus species) may be seen on Gram’s stain.9 Clinico- (Box 4-2). Thiamine supplementation (vitamin B1, 5
pathology is consistent with dehydration (increased mg/lb subcutaneously [SC] three times a day [TID] to
PCV and total protein, prerenal azotemia) and metabolic four times a day [QID]) is indicated until rumen function
acidosis.9 Liver enzymes (gamma-glutamyl transpepti- returns.11 In certain instances, calcium may be indicated
dase [GGT], aspartate aminotransferase [AST], lactate and can be included in the IV fluids (calcium gluconate).
dehydrogenase [LDH]) may be elevated on serum bio- The clinician should avoid mixing calcium salts and
chemical analysis.1,10 The leukogram can vary from sodium bicarbonate. Bacterial leakage into the rumen
normal to a degenerative left shift, depending on the wall, liver, and systemic circulation makes antimicrobial
severity of the case. Urinalysis reveals an increased spe- therapy necessary. The systemic antimicrobial agent of
cific gravity. choice is penicillin (procaine penicillin G, 22,000 IU/kg
IM BID) because anaerobes are the most likely offending
Treatment. Treatment is aimed at correcting cardio- organisms. If treated aggressively, the prognosis for im-
vascular shock, dehydration, acidosis, and toxemia and re- mediate survival is good. Feed (grass hay only) and water
moving or neutralizing the offending feedstuffs. IV fluids should be limited until rumen contractions return to
containing 5% sodium bicarbonate should be adminis- prevent overdistention of the rumen. The chronic seque-
tered.1,11 Oral fluids are contraindicated because they lae discussed previously influence long-term survival.
cannot be absorbed and may increase the rumen disten-
tion and discomfort of the animal. NSAIDs are indicated Prevention. Prevention involves introducing concen-
for toxemia (flunixin meglumine, 1.1 to 2.2 mg/kg trate feeds slowly to allow rumen microflora adaptation.
IV).1,11 Oral administration of magnesium hydroxide Dietary change from a lower to a higher fermentable
and magnesium oxide (1 g/kg) may neutralize the acidic energy concentration should occur slowly and preferably
pH and is sufficient in mild cases. However, if much of over a 2- to 3-week period. In the case of animals being
the feed is still in the rumen, these two alkalinizing fed high-grain rations (e.g., club lambs, feedlot lambs,
agents will only work temporarily. Oral antibiotics have dairy goats), buffering agents can be added to the diet.
been recommended to kill rumen microflora and stop fer- Rumen buffers may improve milk production, increase
mentation. However, the authors of this chapter feel they feed intake, and increase rate of gain. The crude fiber
are contraindicated because the gram-negative anaerobes content should comprise a minimum of 20% of the diet’s
that need to flourish to reestablish normal rumen mi- total digestible nutrients (TDN). For example, the TDN
croflora are susceptible to most antimicrobials effective is 75%, the minimum acceptable crude fiber is 15%.
against Lactobacillus species. Removing the substrate for Crude fiber levels lower than this can be fed for short
the Lactobacillus species is more effective. Because orogas- periods if the rumen is properly adapted, but problems
tric tubes with large enough bores to reflux feedstuffs are may nevertheless occur. Sodium bicarbonate is probably
too large for sheep and goats, rumenotomy is indicated in the most commonly used buffer; it can be offered free
severe cases to remove the feed (see the section on Ru- choice or included in the diet as 1% of dry matter intake.
menotomy in this chapter). After the rumen pH is cor- Calcium carbonate or limestone (which both have low

BOX 4-2

C OLLECTION, H ANDLING, AND S TORAGE OF R UMEN F LUID FOR TRANSFAUNATION

Collection Collection is easiest from the rumen of a fistulated adult cow. If a fistulated cow is unavailable, fluid
can be collected through a weighted orogastric tube. Alternatively, fluid can be collected from any
normal ruminant at slaughter.
Handling Rumen contents collected from a fistulated cow or at slaughter can be strained through gauze or
cheesecloth to separate the fluid from the fibrous contents. Fluid collected through a weighted tube
should be ready for storage.
Storage Rumen fluid should ideally be administered immediately. However, it can be stored for 24 to 48
hours. The surface of the fluid should be covered with a layer of mineral oil to maintain an anaerobic
environment and stored at refrigerator temperature. CAUTION: Do not store rumen fluid in a closed
container because it may explode.
 Chapter 4 Diseases of the Gastrointestinal System • 77

rumen solubility) and magnesium oxide (which has poor DISEASES OF THE
palatability) also can be included in the feed. Magnesium
oxide should be limited to 0.5% to 0.8% of the dry matter RETICULORUMEN
intake.
Traumatic Reticuloperitonitis
Traumatic reticuloperitonitis is not as common in small
Reticulitis/Rumenitis/Parakeratosis ruminants as in cattle, but it has been reported. Goats are
Pathogenesis. Reticulitis and rumenitis can result from affected more commonly than sheep. This is probably
chemical or mechanical damage to the mucosal lining of because of the dietary habits of small ruminants; they
the reticulorumen. The most common cause of chemical tend to be selective grazers and do not “vacuum” the
damage is rumen acidosis. However, ingestion of caustic ground as cattle do. Offending foreign bodies that cause
toxins also can damage the mucosa. Mechanical damage traumatic reticuloperitonitis include pieces of wire and
can occur from ingested foreign bodies or the formation needles.16,17 The clinical signs are identical to those in
of rumen bezoars. In cattle, some viruses such as the ones cattle and may include anorexia, depression, colic, signs of
that cause bovine virus diarrhea and infectious bovine heart failure, and evidence of draining tracts from the
rhinotracheitis can infect the rumen wall. Similar viruses chest cavity. Treatment is usually difficult.
have yet to be identified in sheep and goats. After the
mucosa has been damaged, secondary infection by bacte-
ria or fungi can occur.12 Previous treatment with oral an-
Rumen Impaction
tibiotics may predispose to fungal infections of the rumen Rumen impaction can occur after dehydration, blockage
wall, especially if the mucosa is already damaged. Acti- of the omasal orifice by a foreign body, sand ingestion, or
nobacillosis, actinomycosis, and tuberculosis rarely affect consumption of diets high in fiber and low in digestibil-
the rumen wall. Tumors of the rumen wall also have been ity.18 Clinical signs are nonspecific, but the firm rumen
reported.1,13 Not all of these causes of reticulitis and ru- can usually be palpated in the left flank. The feces may be
menitis have been reported in sheep and goats, but all are scant and dry. Oral fluids containing magnesium sulfate
potential problems. (60 g) may loosen impactions, but a rumenotomy is re-
quired in severe cases.18
Clinical signs. The clinical signs of these diseases are
vague. Anorexia and forestomach hypomotility may be
the only clinical signs.
Rumenotomy
To reduce rumen fill, sheep or goats should ideally have
Diagnosis. Confirming a diagnosis also may prove dif- feed withheld for 24 hours before rumenotomy. However,
ficult. Samples of rumen fluid may only show changes as- this is usually impossible because in most cases rumen-
sociated with anorexia (alkaline pH, decreased numbers otomy is an emergency procedure. The perioperative ad-
and motility of protozoa, prolonged MBR time; see Table ministration of antimicrobial agents is essential because
4-1 for normal values). Occasionally fungal organisms even with meticulous technique some contamination of
may be seen on Diff Quik stained slides of rumen fluid. the incision site and possibly the peritoneal cavity is in-
In these cases a diagnosis of fungal rumenitis should be evitable. Because the rumen microflora is predominantly
made. An exploratory laparotomy and rumenotomy may composed of anaerobic bacteria, penicillin (22,000
be required to diagnose foreign bodies or masses. Rumen IU/kg) is the antimicrobial agent of choice and should be
parakeratosis is characterized by dark, thickened, and administered 2 to 4 hours before surgery. If the rumen-
clumped rumen papillae. It is seen mainly in feedlot otomy is being performed in an emergency situation,
lambs that consume finely ground or pelleted rations.14 penicillin salts (potassium or sodium) that can be given
The parakeratotic rumen papillae are fragile and pre- IV provide therapeutic concentrations more rapidly than
disposed to damage, which can increase the chances of procaine penicillin. NSAIDs (flunixin meglumine, 1.1 to
rumenitis.1 2.2 mg/kg IV) also are recommended before surgery. If
necessary, treatment of cardiovascular shock and dehy-
Treatment and prevention. Treatment depends on the dration with IV fluids also should begin before surgery
inciting cause. Dietary changes should be made to de- and continue until the animal is rehydrated and in stable
crease energy density and increase fiber intake. Mild ru- condition (see Appendix II).
menitis may improve with time and supportive care General anesthesia is recommended, but heavy seda-
(transfaunation, fluid support, high-quality feed). Fungal tion and local anesthetic infiltration of the incision site
rumenitis can be treated with thiabendazole (25 mg/kg can be efficiently used (see Chapter 16). The clinician
orally).15 Severe changes may lead to scarring and perma- should clip and surgically prepare a square area from 5 cm
nent impairment of rumen function. in front of the last rib to the tuber coxae, and from the
78 • Sheep and Goat Medicine
dorsal midline to the lower abdomen, encompassing the 8. VanMetre DC, Tyler JW, Stehman SM: Diagnosis of enteric
entire left paralumbar fossa. disease in small ruminants, Vet Clin North Am: Food Anim Pract
The surgeon makes a skin incision approximately 5 cm 16:87, 2000.
9. Braun U, Rihs T, Schefer U: Ruminal lactic acidosis in sheep and
longer than the width of the hand 5 cm caudal and parallel
goats, Vet Rec 130(16):343, 1992.
to the last rib. The incision is continued through the
10. Lal SB et al: Biochemical alterations in serum and cerebrospinal
muscle layers into the abdomen. Because the abdominal fluid in experimental acidosis in goats, Res Vet Sci 50(2):208, 1991.
wall is relatively thin, the surgeon should take care not to 11. Smith MC: Commonly encountered diseases of goats, Proceedings
enter the rumen or bowel. The surgeon grasps the rumen of the 1996 Symposium on the Health and Disease of Small Rumi-
wall and pulls it through the incision; suturing it to the nants, 1996, Kansas City, MO.
skin with a simple continuous circular pattern around the 12. Perez V et al: Generalized aspergillosis in dairy sheep, J Vet Med
entire incision. This forms a seal that minimizes rumen 46(9):613, 1999.
content contamination of the deep layers of the incision 13. Norval M et al: Rumen papillomas in sheep, Vet Microbiol
and peritoneal cavity. The rumen wall is then incised 10(3):219, 1985.
inside the circle of sutures. The incision in the rumen wall 14. Kutas F, Galfi P, Neogrady S: Effect of monensin on development
of ruminal parakeratosis in fattening lambs, Zentralblatt fur Veteri-
should be large enough for the surgeon to put his or her
narmedizin 30(7):506, 1983.
hand inside the rumen without traumatizing the rumen
15. Kersting KW, Thompson JR: Lactic acidosis. In Howard JL,
wall. Smith RA, editors: Current veterinary therapy 4: food animal prac-
After the rumen has been explored and emptied and tice, Philadelphia, 1999, WB Saunders.
the primary reason for doing the procedure has been 16. Sharma KB, Ranka AK: Foreign body syndrome in goats—a
completed, the surgeon closes the rumen wall in a contin- report of five cases, Indian Vet J 55(5):413, 1978.
uous inverting pattern (Cushing, Lembert, or Guard’s 17. Maddy KT: Traumatic gastritis in sheep and goats, J Am Vet Med
rumen stitch) with absorbable suture (0 catgut). The area Assoc, p 124, Feb 1954.
should be rinsed with copious amounts of sterile isotonic 18. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea
fluids, and a new set of sterile instruments, sterile gloves, & Febiger.
and surgical attire should be used for the remainder of the
surgery. The surgeon then removes the suture securing
the rumen to the skin and rinses the area again before
DISEASES OF THE ABOMASUM
performing routine closure of the abdominal muscles and
Abomasitis
subcutaneous layers with absorbable suture (0 catgut) in
simple continuous patterns, taking care to close dead Abomasitis and abomasal ulcers in adult sheep and goats
space between layers. The skin is closed with a continu- are associated with rumen acidosis or chronic rumenitis
ous pattern (Ford interlocking) using a nonabsorbable but also can be caused by infections.1-4 Finely ground
suture material. feeds, pelleted rations, systemic stress, and feeding lush
The sheep or goat should be observed closely by the forages have all been implicated. Anecdotal associations
clinician for signs of complications, including peritonitis, with mineral deficiency (copper) have gone unproved.
incisional dehiscence, incisional hematoma, abscess, and
hernia formation. Penicillin therapy (procaine penicillin Clinical signs and diagnosis. This disease often goes
G, 22,000 IU/kg BID) should continue for at least 5 unnoticed in mild cases, and the most common signs are
days. The skin sutures can be removed 10 to 14 days after anorexia and colic. No definitive antemortem diagnostic
surgery. tests are available. Fecal occult blood is often absent. Oc-
casionally dark stool, altered appetite (wood chewing),

R EFERENCES
1. Garry FB: Indigestion in ruminants. In Smith BP, editor: Large
and bruxism are seen. Therefore other causes of colic
should be eliminated. Diagnosis is based on clinical signs.

animal internal medicine, ed 2, St Louis, 1996, Mosby. Treatment. Effective therapy can be difficult. Oral med-
2. Guard C: Bloat or ruminal tympany. In Smith BP, editor: Large ications such as coating agents must first pass through the
animal internal medicine, ed 2, St Louis 1996, Mosby. rumen, and therefore arrive at the abomasum diluted. IV
3. Matthews J: Diseases of the goat, ed 2, Oxford, UK, 1999, Blackwell (not oral) ranitidine (15 mg/kg once a day [SID]) may be
Science. beneficial.5 Herd problems of rumen acidosis may be ad-
4. Brikas P, Tsiamitas C, Wyburn RS: On the effect of xylazine on dressed with buffers in the feed.
forestomach motility in sheep, J Vet Med 33:174, 1986.
5. van Miert ASJPAM, van Duin CTM, Anika SM: Anorexia
during febrile conditions in dwarf goats: the effect of diazepam, Abomasal Hemorrhage
flurbiprofen and naloxone, Vet Quart 8:266, 1986.
6. Chennells D: Bloat in kids, Goat Vet Soc J 2:16, 1981. A syndrome of abomasal hemorrhage, bloat, and ulcera-
7. Nour MSM, Abusamra MT, Hago BED: Experimentally induced tion is seen in lambs and kids 2 to 10 weeks of age.
lactic acidosis in Nubian goats: clinical, biochemical, and patho- Sarcina-like bacteria, Clostridium falax, Clostridium sor-
logical investigations, Sm Rumin Res 31(1):7, 1999. delli, and Clostridium septicum have been isolated from
 Chapter 4 Diseases of the Gastrointestinal System • 79

many of these cases.6-9 C. septicum infections of the ab- Unlike abomasal impaction, this disease is associated
omasum are commonly called braxy.1 The feeding of milk with concentrate feeding and often occurs around
replacer free choice, iron deficiency, and bezoars have lambing time. The clinical signs are chronic weight
been implicated as predisposing factors.10,11 loss, abdominal distention, and anorexia. Clinical pathol-
ogy and rumen chloride levels are the same as de-
Clinical signs. The signs of this syndrome are severe, scribed for abomasal impaction. On necropsy the ab-
acute abdominal distention; colic; and death.6-9 omasum is greatly distended, and the contents may be
liquid or dry. Treatment with laxatives, cathartics,
Diagnosis and treatment. The diagnosis of this condi- motility modifiers, and abomasotomy has been mostly
tion is by postmortem examination. Treatment in sus- unsuccessful.17-19
pected antemortem cases is unsuccessful.

Prevention. Adding formalin to milk replacers and

Azalea, Laurel, and Rhododendron Toxicity
vaccinating for clostridial diseases may decrease the oc- Members of the azalea, laurel, and rhododendron plant
currence of this disease.10,12 Lambs or kids on problem group produce andromedotoxins that alter sodium me-
farms can be vaccinated for Clostridium species during the tabolism, resulting in prolonged nerve depolarization.
first week of life with multivalent bacterins. These plants are cardiotoxic, but affected animals gener-
ally exhibit acute gastrointestinal upset. These evergreen
shrubs produce thick, dark green leaves. They also have
Abomasal Impaction
five-lobed, white to pink, saucer-shaped flowers that
Similar to rumen impaction, abomasal impaction usually bloom around July. Some of these plants are grown as or-
occurs when poor-quality roughage is fed, but it also can namental shrubbery around homes, whereas others grow
be seen with foreign body obstruction of the pylorus.4,13,14 wild along streams, cliffs, and rocky slopes. They can be
Goats appear to be more commonly affected than sheep, short or tall (as large as 10 m) and can form thickets. All
and Boer goats are more commonly affected than Angora parts of these plants are toxic.
goats.15 Pregnant animals may be more prone to this
condition. Clinical signs. Animals browsing a new area, those fed
clippings from trimmed azalea hedges, and underfed,
Clinical signs and diagnosis. Affected animals are hungry animals given access to these plants are likely can-
usually anorexic. They have mild distention of the ventral didates for intoxication. Animals that ingest as few as two
abdomen, and in some cases the firm abomasum can be or three leaves may show signs of salivation, grinding
palpated through the abdominal wall on the right side.16 teeth, nasal discharge, colic, epiphora, and acute digestive
Weight loss may be apparent. Clinicopathologic evalua- upset within 6 hours of ingestion. As the intoxication
tion may be normal, or mild hypochloremic metabolic al- progresses, animals become depressed and exhibit projec-
kalosis may be present, with elevated rumen chloride tile vomiting, frequent defecation, and a slowed pulse.
concentrations (more than 50 mEq/L).16 Terminally intoxicated animals become paralyzed and
comatose. Some sheep and goats develop aspiration
Treatment. Diet changes and mineral oil by mouth pneumonia secondary to intoxication.
(PO) are the most commonly employed treatments.
Abomasotomy can be attempted, but it has rarely been Diagnosis. The diagnosis of this condition is usually
reported in small ruminants and does not usually based on clinical signs coupled with a history of ingestion
improve the animals’ long-term prognosis. When at- of one of these plants and/or the discovery of these plants
tempting abomasotomy, the clinician should perform in the gastrointestinal tract.
the procedure with the animal in dorsal recumbency
and under general anesthesia. The abomasum can best Treatment. Intoxicated animals may recover in 1 to 2
be visualized through an incision parallel and to the days without any therapy if the offending plants are
right of midline, caudal to the xyphoid process. The removed from the diet. However, the administration of
prognosis is poor.13 charcoal (2 to 9 g/kg PO), atropine (0.06 to 0.1 mg/kg
IV), other antiarrhythmic drugs, and IV fluids all may be
Prevention. Dietary manipulation to improve feed or indicated. To manage the aspiration pneumonia, the ad-
forage quality is the best mode of prevention. ministration of antibiotics (penicillin 22,000 units/kg
BID IM) and oral magnesium hydroxide also may be
beneficial. Obviously, any existing dehydration should be
Abomasal Emptying Defect
corrected (see Appendix II).
Abomasal emptying defect is a disease that presents
similarly to abomasal impaction but is recognized only Prevention. Mountainous or hilly areas should be
in Suffolk sheep. The underlying cause is unknown. fenced. Feeding shrubbery clippings is discouraged.
80 • Sheep and Goat Medicine
practices and prevention and treatment strategies, diar-
R EFERENCES
1. Kimberling CV: Jensen and Swift’s diseases of sheep, ed 3, Philadel-
rhea is still the most common and costly disease affecting
neonatal ruminants.1-4
phia, 1988, Lea & Febiger. Some general preventive measures (e.g., improved san-
2. Matthews J: Diseases of the goat, ed 2, Oxford, UK, 1999, Blackwell itation) decrease disease no matter the cause. However,
Science. specific control measures such as vaccination require the
3. Gundula A, Shirley H: Two cases of phycomycotic ulceration in definition of a specific cause of diarrhea. Table 4-2 lists
sheep, Vet Rec 77:675, 1965. the agents most likely to cause diarrhea in lambs and kids,
4. Linklater KA, Smith MC: Color atlas of diseases and disorders of the tissues or other samples required for diagnosis, and com-
sheep and goat, London, 1993, Wolfe Publishing. monly employed test methods. The color and consistency
5. Duran SH et al: pH changes in abomasal fluid of sheep treated
of the feces and any gross lesions can appear similar no
with intravenous and oral ranitidine, Proceedings of the Eleventh
ACVIM Forum, Washington, DC, 1993, American College of Vet-
matter the cause. Therefore laboratory identification of
erinary Internal Medicine. infectious agents and tissue histopathology are key to es-
6. DeBey BM, Blanchard PC, Durfee PT: Abomasal bloat associated tablishing a diagnosis. Because autolysis and secondary
with Sarcina-like bacteria in goat kids, J Am Vet Med Assoc bacterial invasion of the gut begins within minutes of
209(8):1468, 1996. death, necropsy samples taken immediately from eutha-
7. Vatn S, Tranulis MA, Hofshagen M: Sarcina-like bacteria, nized lambs and kids yield the most reliable diagnostic
Clostridium falax and Clostridium sordelli in lambs with abomasal material. Mixed infections with two or more pathogens
bloat, haemorrhage and ulcers, J Comp Path 122(2/3):193, 2000. are common, and pathogens that are a problem on a farm
8. Ellis TM, Rowe JB, Lloyd JM: Acute abomasitis due to Clostrid- change from year to year.3,5,6 In some cases an underlying
ium septicum infection in experimental sheep, Aust Vet J 60(10):308, nutritional deficiency or excess may occur concurrently
1983.
with an infectious agent. Therefore the clinician should
9. Eustis SL, Bergeland ME: Suppurative abomasitis associated with
Clostridium septicum infection, J Am Vet Med Assoc 178(7):732, 1981.
be careful to take a variety of samples to ensure that all
10. Vatn S, Ulvund MJ: Abomasal bloat, haemorrhage and ulcers in pathogens and predisposing factors involved are recog-
young Norwegian lambs, Vet Rec 146(2):35, 2000. nized; continued reevaluation of the causes of diarrhea is
11. Vatn S, Torsteinbo WO: Effects of iron dextran injections on the crucial. Examination of several cases, with a focus on
incidence of abomasal bloat, clinical pathology and growth rates in those in the acute phases, is important. Although exami-
lambs, Vet Rec 146:462, 2000. nation of antemortem fecal samples can be diagnostic,
12. Gorrill AO, Nicholson JWG, MacIntyre TM: Effects of formalin laboratory testing of tissue samples may yield better
added to milk replacers on growth, feed intake, digestion and inci- results. Treatment and preventive measures specific to a
dence of abomasal bloat in lambs, Can J Anim Sci 55(4):557, 1975. particular disease are discussed with that disease in the
13. Bath GF, Bergh T: A specific form of abomasal phytobezoar in following paragraphs. General supportive treatment and
goats and sheep, J South African Vet Med Assoc 50(2):69, 1979.
control measures are covered at the end of this section.
14. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea
& Febiger.
15. Bath GF: Abomasal phytobezoariasis of goats and sheep, J South Causes of Diarrhea in Neonatal Lambs
African Vet Med Assoc 49:133, 1979. and Kids
16. Kline EE et al: Abomasal impaction in sheep, Vet Rec 113(8):177,
1983. Four major pathogens cause diarrhea in lambs and kids
17. Guard C: Abomasal dilation and emptying defect of Suffolk during the first month of life: enterotoxigenic Escherichia
sheep. In Smith BP, editor: Large animal internal medicine, ed 2, St coli (ETEC), rotavirus, Cryptosporidium species, and Sal-
Louis, 1996, Mosby. monella species. The relative prevalence of these infectious
18. Rings DM et al: Abomasal emptying defect in Suffolk sheep, J Am agents varies greatly among studies. This variance most
Vet Med Assoc 185(12):1520, 1984. likely results from differences in location, season, diagnos-
19. Ruegg PL, George LW, East NE: Abomasal dilation and empty-
tic techniques, and the occurrence of mixed infections.
ing defect in a flock of Suffolk ewes, J Am Vet Med Assoc
193(12):1534, 1988.
Other, less common causes of diarrhea in neonates are
Giardia infections and nutritional diarrhea. Figure 4-8
shows the ages at which diarrhea is expected with certain
infections.
DISEASES OF THE INTESTINES
Diarrhea in Lambs and Kids Enterotoxigenic Escherichia coli
Diarrhea in lambs and kids is a complex, multifactorial Pathogenesis. ETEC employs two virulence factors to
disease involving the animal, the environment, nutrition, cause disease. The first is the ability to attach and colo-
and infectious agents. Decades of research have been nize the intestinal villi, which is accomplished via fimbria
devoted to the study of the pathophysiology of infectious or pili. The most important fimbria in lambs are K99 and
diarrhea of calves; the pathology in lambs and kids is F41.7,8 The fimbrial antigens can be recognized from
quite similar. Despite improvements in management samples sent to most diagnostic laboratories and are im-
 Chapter 4 Diseases of the Gastrointestinal System • 81

Giardia
Salmonella
Cryptosporidium
Rotavirus
Escherichia coli

5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30
Days of Age

Figure 4-8 Ages at which infectious agents cause diarrhea in lambs and kids.

TABLE 4-2

DIAGNOSTIC SAMPLES AND TESTING METHODS REQUIRED FOR DIFFERENTIATION OF THE MOST COMMON
CAUSES OF INFECTIOUS DIARRHEA OF LAMBS AND KIDS
CAUSATIVE AGENT SAMPLE REQUIRED TEST METHOD*

Escherichia coli 2 to 3 g feces Culture and serotyping for K99 and F41
Formalin-fixed small intestine Histopathology
Rotavirus 2 to 3 g feces or colonic contents EM, ELISA, VI, CF, PCR
Formalin-fixed small and large intestine Histopathology
Frozen small and large intestine VI, FA, IP
Cryptosporidia 2 to 3 g feces FA, fecal flotation
Air-dried fecal smear Acid-fast stain
Formalin-fixed small and large intestine Histopathology
Salmonella 2 to 3 g feces Culture, PCR
Formalin-fixed small and large intestine Histopathology
Frozen small and large intestine and mesenteric Culture
lymph nodes
Giardia Wet mount of feces Iodine staining
Feces ELISA, FA
Clostridium perfringens Frozen small intestinal contents and abomasum, Culture, toxin identification
small and large intestine
Formalin-fixed abomasum and small and large Histopathology
intestine
Coccidia 2 to 3 g feces Fecal flotation
Formalin-fixed small and large intestine Histopathology
From Rings DM, Rings MB: Managing Cryptosporidium and Giardia infections in domestic ruminants, Vet Med 91(12):1125, 1996; Cohen ND et
al: Comparison of polymerase chain reaction and microbiological culture for detection of salmonella in equine feces and environmental samples, Am
J Vet Res 57:780, 1996; Drolet R, Fairbrother JM, Vaillancourt D: Attaching and effacing Escherichia coli in a goat with diarrhea, Can Vet J 35(2):122,
1994.
*EM, Electron microscopy; ELISA, enzyme-linked immunospecific assay; VI, virus isolation; CF, complement luxation; PCR, polymerase chain
reaction; FA, fluorescent antibody; IP, immunoperoxidase.

portant in diagnosing this agent as a cause of diarrhea. age-related resistance also may occur in these animals.3,7 It
After the organism attaches to the villi, it produces the usually presents as an outbreak in lambs and kids between
second virulence factor, enterotoxin. Enterotoxin inter- 12 and 48 hours of age. Because ETEC causes a “secretory”
feres with the normal physiology of the gut, with resul- diarrhea, bicarbonate loss in the diarrhea leads to severe
tant diarrhea.8 Calves have an age-associated resistance, acidosis, with lambs and kids quickly becoming dehydrated
most likely related to the blocking of fimbrial attachment and recumbent. However, many infected animals die
to the gut, so ETEC occurs mainly in calves less than a before developing diarrhea. Affected neonates are de-
week old.9,10 The mode of infection is fecal-oral. pressed, stop nursing, and may show excessive salivation.
Fluid sequestration in the abomasum causes a “splashing”
Clinical signs. ETEC is seen in lambs and kids less than sound on movement.This condition results in high mortal-
10 days of age but is most common at 1 to 4 days of age, so ity if animals are not treated promptly.7
82 • Sheep and Goat Medicine
Diagnosis. Fecal culture and serotyping for the K99 techniques on feces or tissue sections is the basis of diag-
and F41 fimbrial antigens are the basis for diagnosis. nosis.13,16 Because these organisms are sloughed with the
Because many nonpathogenic E. coli are normal gut in- villus tip cells they infect, and viral antigens are com-
habitants, simply culturing this organism is usually in- plexed with the lambs’ and kids’ antibodies, tissue samples
significant.8 Occasionally the bacteria do not express the from acutely infected animals are best.17 Rotavirus has
fimbrial antigens in culture, so ETEC cannot be ruled been detected in animals without diarrhea, so other
out if the culture is negative for K99 and F41.11 Histo- causes of diarrhea should be investigated as well.4,5
logic evidence of colonization of the small intestine can
support a diagnosis. Treatment and prevention. Rotavirus is treated with
supportive care. Prevention by vaccination of ewes and
Treatment. Supportive care consisting of fluid therapy does with bovine rotavirus vaccines before they give birth
with either oral, IV, or SC administration of a polyionic is recommended to increase passive immunity.3,4,8
solution is the mainstay of therapy. The use of oral an-
timicrobial agents is controversial. Although antibiotics
may kill the ETEC, they also may interfere with normal
Cryptosporidiosis
gut flora. If fluid support is provided, the diarrhea usu- Pathogenesis. Cryptosporidium parvum is a protozoa
ally subsides without antibiotic treatment. Still, oral that can cause a malabsorptive diarrhea similar to that
neomycin (10 to 12 mg/kg BID) or trimethoprim sulfa seen with rotavirus infection. Unlike other protozoal
(30 mg/kg PO) and systemic ampicillin (10 to 20 mg/kg agents such as the one that causes coccidiosis, cryp-
IM BID) or amoxicillin (10 to 20 mg/kg IM TID) may tosporidia do not require fecal excretion for sporulation to
be beneficial. NSAIDs are indicated to decrease inflam- infective stages.18 They sporulate in the gut and about
mation of the gut and provide some analgesia. The use of 20% become immediately infectious to other villus tip
flunixin meglumine (1 to 2 mg/kg IM) has been shown to cells without ever leaving the intestines. This method of
decrease fecal output in ETEC infections in calves12 and autoinfection can result in severe disease that can be sus-
appears to be beneficial in lambs. tained for long periods. Because some of the oocysts also
are immediately infectious when they are shed in feces,
Prevention. It is recommended that clinicians vacci- spread of infection can occur quickly.
nate ewes and does with bovine ETEC vaccine before
they give birth to increase passive immunity.3,4,8 Mono- Clinical signs. Cryptosporidia can cause diarrhea in
clonal and polyclonal antibody products for calves may be lambs and kids 5 to 10 days of age.4,19,20 Affected animals
beneficial during an outbreak if it can be given to lambs are often active, alert, and nursing. The diarrhea is usu-
or kids within the first 12 hours of life. The use of ally very liquid and yellow. Diarrhea can vary from mild
neomycin (10 to 12 mg/kg PO BID) in lambs that appear and self-limiting to severe, especially with mixed infec-
normal may help stop the progression of an outbreak. tions.4,5,19,21 Relapses are quite common, and this organ-
Shearing ewes prepartum to minimize fecal ingestion by ism usually occurs as a component of mixed infections.
neonates and ensuring that newborns ingest adequate
colostrum both help decrease the incidence of this Diagnosis. Acid-fast staining of air-dried fecal smears is
disease. Making sure that ewes and does give birth at a a quick and easy method of diagnosis. Examination under
2.5 to 3.5 body condition score increases the chance of 40 to 100 magnification reveals round protozoa that
adequate colostrum manufacture by the dam. have taken up the red color of the carbol fuchsin portions of
the stain on a green background (Figure 4-9). Although
they can be diagnosed by fecal flotation, their very small
Rotavirus size (4-6 mm) makes this method difficult and subject to
Pathogenesis. Lambs and kids are infected with group false negative results.22,23 Both immunologic and poly-
B rotaviruses, whereas most other animals and human merase chain reaction (PCR) techniques have been devel-
beings are infected with group A rotaviruses.13 Rota- oped to improve detection limits.22,24 Cryptosporidia also
viruses infect villus tip cells of the small intestine, which can be identified with histology. Cryptosporidiosis is a
results in villus atrophy and malabsorptive diarrhea.14 zoonotic disease, and people can easily become infected
from handling infected animals or feces.18
Clinical signs. Rotavirus generally causes diarrhea in
lambs and kids 2 to 14 days old, but older animals also Prevention. No consistently effective treatment for
can be affected. Young animals can become very de- cryptosporidiosis in ruminants has been identified. Anec-
pressed and dehydrated.3,13,15,16 dotal reports suggest that decoquinate and monensin
sodium may be useful in control of cryptosporosis. Deco-
Diagnosis. Detection of the organism by electron mi- quinate (2.5 mg/kg PO) may be very useful in prevention
croscopy of fecal or colonic samples or by immunologic of cryptospirosis in goats and possibly kids. During an
 Chapter 4 Diseases of the Gastrointestinal System • 83

sionally contain fibrin, but many animals die before this is

observed. Clinicians may note leukopenia or leukocytosis
in the CBC results.

Treatment. Therapy for Salmonella-induced diarrhea

involves supportive care and possibly parenteral antimi-
crobial therapy. The use of antimicrobial agents is contro-
versial and probably does not influence the gastroin-
testinal infection. However, because this is an invasive
organism, parenteral use of antimicrobial agents may be
beneficial in preventing septicemia. Antimicrobial sus-
ceptibility patterns are difficult to predict for Salmonella
species, so antimicrobial therapy should be based on
Figure 4-9 Red-staining Cryptosporidium on a blue-green culture and sensitivity results. Ceftiofur sodium (1.1 to
background in a fecal smear prepared with an acid-fast stain. This 2.2 mg/kg IM BID) or trimethoprim sulfadiazine (15
protozoal parasite induces villous atrophy and decreased digestion. mg/kg SC SID) can be administered until antimicrobial
sensitivity results are known.
outbreak affected animals should be isolated from the rest
of the flock. No new animals should be added to a pen in Prevention. Latent carriers of Salmonella can poten-
which the disease has been diagnosed. Keepers should tially shed organisms to other animals, particularly when
depopulate pens in which the disease has been diagnosed they are stressed.4 Newly introduced animals should be
and attempt to clean the environment. Cryptosporidiosis isolated for 1 month, and fecal culture should be consid-
can be particularly difficult to control because of the or- ered.4 Bleach is an effective disinfectant to use during an
ganisms’ persistence in the environment and resistance to outbreak. Identification of carrier animals by fecal culture
most chemical disinfectants. However, ammonia (5% to is recommended for herd problems. Vaccine efficacy is
10%) and formalin (10%) seem to be most effective.19,25 questionable, and to date its effects have not been thor-
Feeders should be constructed to minimize fecal contam- oughly evaluated in sheep and goats.
ination. Studies are currently underway to develop a
vaccine for cryptosporidiosis in cattle. Early results are fa- GIARDIA: Giardia-induced diarrhea is more com-
vorable, and this may prove the best way to control the monly seen in but not limited to 2- to 4-week-old lambs
disease in the future.26 This is potentially a zoonotic and kids.4,30 The diarrhea is usually transient, but infected
disease, and therefore clinicians and keepers should exer- animals can continue to shed cysts for many weeks, even
cise great caution when handling affected animals. when they are clinically normal.22,31,32 Therefore simply
finding the agent in feces does not mean it is the cause
of diarrhea, especially in older animals. However, these
Salmonellosis animals may be a source of infection for other animals
Pathogenesis. The bacterial genus Salmonella has and possibly humans.22,30 Iodine-stained wet mounts of
thousands of serotypes, and all can potentially cause diar- feces or tissue is the classic method of diagnosing giardia-
rhea in animals. Salmonella can cause diarrhea in lambs sis, but more sensitive immunologic techniques are now
and kids of any age.3,4 The microbes produce enterotox- available.22,30 Infected animals can be treated effectively
ins, are invasive, and cause severe inflammatory disease with fenbendazole (5 to 10 mg/kg BID for 3 days or SID
and necrosis of the lining of the small and large intestines. for 5 days).22 Giardia has historically been treated with
metronidazole (50 mg/kg PO SID for 5 days). However,
Clinical signs. Animals less than 1 week old are more use of this drug class in food animals is currently illegal in
likely to die acutely without clinical signs, whereas the United States.This is potentially a zoonotic condition.
animals older than 1 week are more likely to have diar-
rhea.4,7,27 An acute onset of fever, depression, tenesmus,
and shock is occasionally observed. Salmonella-induced
Nutritional Diarrhea
diarrhea is more likely to contain blood.4 This also is a Infectious agents are not the only cause of diarrhea in
zoonotic disease that warrants protective measures. neonates. Nutritional problems can result in diarrhea, but
these causes are overshadowed in the literature because
Diagnosis. A diagnosis of this condition is based on the resulting diarrhea is usually mild and subsides
culture of the organism in feces or tissues and histologic without treatment. Nutritional diarrhea is most common
examination of the small and large intestine.28 More sen- in orphaned animals as a result of keepers offering poor-
sitive PCR techniques for identifying Salmonella species quality milk replacers, making mixing errors, or feeding
in feces are being developed.29 The diarrhea may occa- large amounts infrequently (see Chapter 2). Diarrhea re-
84 • Sheep and Goat Medicine
sulting from consumption of lush pasture or high-energy but less severe signs are seen in the acute form of the
rations is a common occurrence. In most cases such diar- disease. The chronic form occurs more commonly in
rhea is self-limiting. The incidence of this form of gastric goats.4,39
upset can be minimized by a slow introduction (over 2 to
3 weeks) to energy-dense diets. Diagnosis. Antemortem diagnosis is based on clinical
Calves with infectious diarrhea that develop maldiges- signs. At necropsy, C. perfringens can be cultured from in-
tion or malabsorption can have secondary nutritional di- testinal tissue samples. However, the significance of a
arrhea from an inability to digest carbohydrates (lactose, positive culture can be difficult to interpret because these
xylose).33,34 This has been reported in goats, and also is organisms can be present in the gut normally and then
probably a cause of diarrhea in lambs.35 Diarrhea result- proliferate after death. Histologic examination of sections
ing from primary lactose deficiency also has been re- of the gut can be helpful. Identification of the toxins
ported in calves.36 Calves on poor-quality milk replacers (namely the epsilon-toxin) in intestinal contents is re-
can develop an overgrowth of normal enteric E. coli, re- quired for a definitive diagnosis.4,7 Because the toxin de-
sulting in diarrhea.37 If lactose intolerance is suspected, grades within several hours of death, not finding the toxin
decreasing the amount of lactose fed and using commer- does not preclude enterotoxemia as a diagnosis.38
cially available lactose enzymes may alleviate signs.
Treatment. Treatment is rarely effective but consists
CAUSES OF DIARRHEA IN mainly of aggressive supportive care. C. perfringens type
D antitoxins (15 to 20 ml SC) can be administered to
OLDER LAMBS AND KIDS animals during an outbreak of enterotoxemia if clinical
The most common cause of diarrhea in older lambs and signs are noted before death. The antitoxin may be more
kids is nematode infestation. This condition is discussed effectively used as a preventive in the face of an outbreak.
later in this chapter in the section on causes of adult diar- During an outbreak any animals that have not been vac-
rhea. Other major causes of diarrhea in older lambs and cinated should be given the antitoxin and vaccinated with
kids are C. perfringens and coccidiosis. the toxoid simultaneously; those previously vaccinated
should receive a booster vaccination.
Clostridium perfringens Prevention. Routine vaccination should start at 4 to 6
C. perfringens types A, B, C, and D can all cause diarrhea in weeks of age and be followed by a booster 3 to 4 weeks
lambs and kids, but type D is the most common later. However, on farms where the disease has become
agent.4,7,38 endemic, lambs or kids can be vaccinated and given anti-
toxin during the first week of life. Yearly vaccination,
Pathogenesis. The disease occurs in peracute, acute, preferably a few weeks before the ewes and dams give
and chronic forms and is commonly called enterotoxemia birth increases colostral immunity in neonates and im-
or overeating disease. In the case of type C infection, a proves prevention programs. Goats may not respond as
beta-toxin can cause acute hemorrhagic enteritis. Type C well to vaccination as sheep, so biannual or triannual vac-
infection is seen mostly in lambs or kids younger than 3 cination is recommended, especially in problem herds.4,38
weeks of age. An epsilon-toxin is responsible for pathol- Vaccination with only C. perfringens types C and D and
ogy in type D infections. Enterotoxemia is usually seen tetanus is superior to the use of more polyvalent
in rapidly growing feedlot lambs on high concentrate clostridial vaccines.4 Reducing the energy density of the
rations. It also is associated with other feeding changes, diet and avoiding sudden dietary changes or alterations of
including changes in type of pasture. However, it occa- the feeding routine are crucial to prevention. Reducing
sionally occurs with no reported dietary changes, particu- internal parasites, particularly tapeworms, may further
larly in goats.4,7,39 This disease usually occurs in the reduce the incidence of these disorders.
fastest-growing and most well-conditioned animals. It
can occur in vaccinated herds (again, more commonly in
goats) so it should not be ruled out if a history of previous
Coccidiosis
vaccination is present.4 Pathogenesis. Coccidiosis is a protozoan parasitic
disease that is a common cause of diarrhea in lambs and
Clinical signs. The peracute form of clostridial infec- kids. It also may cause subclinical production losses.19
tion is characterized by the rapid onset of severe depres- Clinical disease is often seen when some form of stress
sion; abdominal pain; profuse, bloody diarrhea; and neu- (e.g., dietary change, weather changes, parturition,
rologic signs. Death occurs within hours of the onset of weaning) is occurring on the farm or in the flock. Eimeria
signs. Sudden death may occur without signs of diar- species cause the disease in sheep and goats; each is in-
rhea. The onset of neurologic signs followed by sudden fested with its own host-specific species. Unlike Cryp-
death is more common in sheep, whereas goats are more tosporidium, which can be shed in feces in the infective
likely to show signs of diarrhea before death.4 Similar stage, coccidia must sporulate outside the host to become
 Chapter 4 Diseases of the Gastrointestinal System • 85

infective. Sporulation occurs under moderate tempera- Treatment. Treatment of affected animals with clini-
tures and high moisture conditions. The nonsporulated cal signs includes supportive care and administration of
and sporulated oocysts can survive a wide range of temper- coccidiostats. All animals in the group should be treated
atures and may survive for years under certain conditions. during an outbreak. The use of coccidiostats has little
effect on the existing infection, but it does prevent the
Clinical signs. Lambs and kids are most susceptible to spread of the disease from continued exposure to infec-
the problem at approximately 1 to 4 months of age, al- tive organisms.40 Many coccidiostats inhibit coccidia de-
though younger animals may become infected. Clinical velopment and prevent disease if given prophylacti-
disease is common after the stress of weaning, feed cally.40 They are of little value if they are given after the
changes, or shipping. Crowded conditions result in exces- onset of clinical disease. Sulfa drugs appear to be clini-
sive manure and urine contamination, which is ideal for the cally beneficial, but they may simply decrease secondary
buildup and sporulation of the oocysts. Under these condi- or concurrent bacteria-induced diarrhea.40 Because coc-
tions, animals may be exposed to high numbers of infective cidia develop some resistance to coccidiostats, these
organisms and develop diarrhea.The diarrhea in lambs and drugs should be administered only before stressful events
kids is usually not bloody, but it can contain blood or mucus (e.g., shipping, weaning, parturition).40 The drugs listed
and be very watery. Anorexia, dehydration, weakness, in Table 4-3 and trimethoprim sulfa (15 mg/kg orally
rough hair coat, and death all may occur.19 Weight loss is SID for 5 days) are approved for use in the United
common, and constant straining can result in rectal pro- States.7,41
lapse. In severe cases the disease becomes protracted
because of necrosis of the mucosal lining. Even if these Prevention. Control involves improved sanitation and
animals are treated appropriately, the diarrhea continues possibly the use of coccidiostats. Preventing overcrowd-
until the intestinal mucosa heals, which can take several ing decreases the buildup of manure and infective
days to weeks. Permanent scarring can result in chronic oocysts. Exposure to sunlight and desiccation are two of
poor development, even if the diarrhea subsides.19,40-42 the most effective means of killing the organisms. Mini-
mizing stress and optimizing nutritional intake also are
Diagnosis. Acute coccidiosis can be easily diagnosed important. Coccidiostats available in the United States
from a direct smear or flotation of feces (Figure 4-10). In are shown in Table 4-3 and Appendix I. To avoid toxicity
the chronic stages, most of the organisms have been shed in growing animals, the clinician or keeper must carefully
and very low numbers are seen on fecal examination. adjust dosages to the changing levels of feed intake as
Because normal animals can shed small numbers of path- animals grow. All agents except amprolium should be fed
ogenic species or large numbers of nonpathogenic for at least 4 weeks.19,40 This allows exposure and subse-
species, interpretation of fecal examinations in the quent development of immunity to occur while prevent-
chronic stages of coccidiosis or in animals with diarrhea ing the detrimental effects of clinical disease. However,
from other causes can be difficult.40-42 In these cases the coccidia can become resistant to coccidiostats; fecal
clinician should rule out other diseases before making a samples should be periodically evaluated after prolonged
diagnosis of coccidiosis. Blood analysis may show both use of a particular product. Anecdotal reports suggest
anemia and hypoproteinemia. amprolium resistance may occur on some farms. More-
over, if amprolium is offered with a creep feed rich in thi-
amine, its ability to act as a thiamine antagonist may be
compromised. Year-round use of coccidiostats increases
the potential for resistance. Therefore they should be fed
only during times of expected risk.40 The inclusion of
lasalocid (1 kg of 6% premix) or decoquinate (1 kg of 13%
premix) in 22 kg of trace mineralized salt fed as the only
source of salt for 30 days prepartum can reduce the
number of oocysts shed in ewe or dam feces. This practice
can reduce the coccidia contamination of pasture and
thereby remove a source of infection for kids and lambs.
The benefits of administering lasalocid and monensin
beyond coccidia control include increased feed efficiency,
enhanced growth rate, and decreased incidence of free gas
bloat. However, if coccidiostats are included in either
mineral or feed supplements, inconsistent or depressed
intake may result in subtherapeutic drug dosing.
Figure 4-10 Parasites found on fecal examination.
Trichostrongylid-type eggs (HOTC complex) (b), Coccidia (c), and Lambs are resistant to infection in the first few weeks
tapeworm “eggs” (d) may be identified with flotation techniques. of life. Exposure to the protozoa during this time confers
Fasciola hepatica (a) eggs are found with sedimentation techniques. immunity and resistance to later infections.40,42
86 • Sheep and Goat Medicine
TABLE 4-3

COCCIDIOSTATS USED FOR TREATMENT AND PREVENTION OF COCCIDIOSIS IN SMALL RUMINANTS*

COCCIDIOSTAT DOSE COMMENTS

Lasalocid 20 to 30 g per ton of feed; 0.5 to 1 mg/kg body Approved for use in sheep in the United States
weight per head per day in feed or salt
Decoquinate 0.5 mg/kg body weight per head per day in feed Approved for use in goats in the United States
or salt
Monensin 10 to 30 g per ton of feed Approved for use in goats in the United States;
may be most effective choice for goats
Amprolium 50 mg/kg body weight per head per day for 21 Not approved for use in small ruminants in the
days (NOTE: This dose is five times the United States; comes in liquid and crumble
recommended calf dose) form; can potentially cause polioencephalo-
malacia at high doses and with
prolonged administration
Sulfaquinoxaline 13 mg/kg body weight per head per day as Approved for use in sheep in the United States
0.015% solution in water for 3 to 5 days
Sulfamethazine 119 to 238 mg/kg body weight per head per day Not approved for use in small ruminants in the
in sheep; 50 g per ton of feed in goats United States
Salinomycin 382 g per ton of feed in goats Not approved for use in small ruminants in the
United States
From Foreyt WJ: Coccidiosis and cryptosporidiosis in sheep and goats, Vet Clin North Am: Food Anim Pract 6(3):655, 1990; Craig TM: Coccidiosis
in small ruminants, Proceedings of the Small Ruminants for the Mixed Animal Practitioner, Western Veterinary Conference, 1998, Las Vegas, NV. Smith
MC: Parasitic diseases of goats, Proceedings of the 1996 Symposium on the Health and Disease of Small Ruminants, 1996, Nashville, TN.
*Not approved for dairy animals in the United States.

MISCELLANEOUS CAUSES OF for calves. Fluids can be administered by bottle or by tube

if the animal will not nurse. The keeper or clinician should
DIARRHEA IN KIDS AND LAMBS carefully adjust the amount of fluids for lambs and kids
Adenovirus, caprine herpesvirus, coronavirus, Campy- (250 to 500 ml, or 8 to 16 oz, as opposed to 4 L in a calf ).
lobacter jejuni, Yersinia species, and Strongyloides papillosus Because most electrolyte solutions designed for calves
can cause diarrhea in lambs and kids of various ages.2,4,6 contain glucose, after they have been mixed they should be
Enterohemorrhagic E. coli (EHEC) and enteropatho- refrigerated and any leftovers discarded within 24 hours.
genic E. coli (EPEC) also have been isolated in the feces IV fluids may be needed to treat more severe dehydration.
of kids with diarrhea.43,44 These E. coli types are K99- If the lamb or kid is too weak to stand, IV fluids are indi-
and F41-negative. Culture and serotyping of these or- cated. Isotonic fluids containing electrolytes should be
ganisms from feces and tissue samples with typical given to replenish losses. Glucose can be added to fluids to
histopathologic lesions is diagnostic. Although ETEC is make a 1% to 2.5% solution. Sodium bicarbonate also may
not zoonotic, EHEC and EPEC can potentially affect be administered, especially if the dehydration is severe. A
humans. rule of thumb is to give one fourth of the calculated fluid
need (see Appendix II) as isotonic bicarbonate (1.3%).
TREATMENT OF LAMBS Extra potassium (10 to 20 mEq/L) can be added to fluids
because most animals are severely dehydrated from diar-
AND KIDS WITH DIARRHEA rhea and depleted in potassium, even though their blood
Although some causes of diarrhea have specific treat- potassium levels may be elevated. If extra potassium is
ments, many animals need to be treated for dehydration added, acidosis must be corrected concurrently. After cor-
and metabolic acidosis regardless of the inciting cause. recting the dehydration, the keeper or clinician can offer
Animals with only mild diarrhea, especially mild nutri- oral electrolyte-enriched fluids to replace ongoing losses
tional diarrhea, may not require therapy unless they caused by continued diarrhea.
become dehydrated. If kids or lambs become less than 8% Removing milk or milk replacer from the diet is not
dehydrated and are only mildly depressed but still willing recommended. Young animals need nutrients, and even
to nurse, they can be treated with oral electrolytes designed high-energy, glucose-containing electrolyte solutions are
 Chapter 4 Diseases of the Gastrointestinal System • 87

no substitute for milk. Animals should continue to passed to the thoracic inlet, colostrum can be adminis-
receive milk replacer in normal amounts or be allowed to tered by gravity flow (see Chapter 6).
nurse; they can be supplemented with oral electrolytes if Prepartum shearing of the dam may decrease the in-
necessary. Animals being hand fed should be offered gestion of feces by lambs. Good sanitation of lambing
small amounts frequently to help minimize problems. and kidding areas is paramount in management programs
Electrolytes should never be mixed with milk, but should that stress prevention. The presence of organic matter in-
instead be given in separate feedings. If lactose deficiency terferes with the effectiveness of many disinfectants, so
is suspected, lactase drops or capsules (available in health removal and proper disposal of feces, carcasses, and pla-
food stores) can be added to milk or milk replacer.35 centas are essential. When disposing of waste material
NSAIDs (flunixin meglumine, 1.1 to 2.2 mg/kg IV; containing either Cryptosporidium or Giardia, the keeper
ketoprofen, 2.2 to 4.4 mg/kg IV) are beneficial, especially should be careful to avoid contaminating water sources.
if toxemia is involved, as in ETEC, enterotoxemia, and Infected animals should be isolated to prevent spread of
salmonellosis. It is the authors’ opinion that antimicrobial the infection throughout the flock. In general, infected
agents should be reserved for proven outbreaks of salmo- animals should remain in the environment where the in-
nellosis and for animals with other causes of diarrhea that fection was first diagnosed, because it is already contami-
do not respond to fluid therapy and NSAIDs; these nated. Removing pregnant ewes or dams to a clean area
drugs should only be administered parenterally. The use before lambing or kidding helps minimize the continued
of oral coating agents and antacids is popular, but it has spread of disease. If possible, lambs and kids already born
not been shown to be beneficial and is not therapeutically but not showing clinical signs should be removed to a
logical in light of the pathogenesis of these diseases. Pro- third area. If “safe” pastures are maintained for internal
biotics may be beneficial in reestablishing the normal nematode control, they are ideal for use in an emergency
flora of the small intestine. The authors’ rule of thumb is situation to control these diseases. Although some
that nothing should be given orally except milk, oral elec- animals may appear normal, they may be incubating and
trolytes, and probiotics. possibly shedding the infective agents of a disease. If such
animals are moved with pregnant females, they can be a
source of contamination in a clean area. If healthy lambs
GENERAL CONTROL and kids cannot be moved to a third, relatively safe area,
MEASURES FOR INFECTIOUS they should be left with the clinically infected animals
because they have already been exposed.
DIARRHEA
Ensuring adequate intake of high-quality colostrum and
minimizing stress are important for prevention of all
neonatal diseases. A normal lamb or kid will stand and
R EFERENCES
1. Sherman DM: Causes of kid morbidity and mortality: an
nurse within 45 minutes to 1 hour of birth. The ingestion overview, Proceedings of the Fourth International Conference on
of colostrum within 2 to 3 hours is essential in prevent- Goats, Brasilia, Brazil, 1987, EMBRAPA-DDT.
ing hypothermia and hypoglycemia and decreasing the 2. Vickers MC: Enteric infections in young goats and their control,
incidence of various diseases. Lambs or kids born as Proceedings of the Sixteenth Seminar, Sheep and Beef Cattle Society,
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3. Blackwell TE: Enteritis and diarrhea, Vet Clin North Am: Large
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Johne’s disease, ovine progressive pneumonia (OPP), and Brazil, 1987, EMBRAPA-DDT.
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colostrum–associated” hemolytic disease sometimes seen lambs, Proceedings of the Third International Symposium on Veteri-
in lambs. If the lamb or kid is unable to nurse, it should nary Laboratory Diagnostics, Ames, Iowa, 1983.
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phia, 1988, Lea & Febiger.
animal handler can sit comfortably holding the lamb or
8. Hodgson JC: Escherichia coli in domestic animals and humans,
kid in sternal recumbency in the lap. A 12 to 14 French Wallingford, UK, 1994, Cab International.
soft feeding tube is then lubricated, inserted into the side 9. Runnels PL, Moon HW, Schneider RA: Development of resist-
of the mouth, and passed slowly. If the tube is placed in ance with host age to adhesion of K99 Escherichia coli to isolated
the trachea, the lamb or kid will become uncomfortable intestinal epithelial cells, Infect Immun 28(1):298, 1980.
and may shake and cough. The tube may be palpated on 10. Zeman DH, Thomson JU, Francis DH: Diagnosis, treatment, and
the left side of the throat. After the tube has been slowly management of enteric colibacillosis, Vet Med 84(8):794, 1989.
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11. Schultheiss P: Diarrheal disease in calves, Large Anim Vet 47(2):24, 37. Roy JHB: The calf, ed 4, London, 1980, Butterworth.
1992. 38. Uzal FA, Kelly WR: Enterotoxemia in goats, Vet Res Commun
12. Roussel AJ et al: Effect of flunixin meglumine on Escherichia coli 20:481, 1996.
heat stable enterotoxin-induced diarrhea in calves, Am J Vet Res 39. Songer JG: Clostridial diseases of small ruminants, Vet Res 29:219,
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13. Theil KW et al: Group B rotavirus associated with an outbreak of 40. Craig TM: Coccidiosis in small ruminants, Proceedings of the Small
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14. Babiuk LA, Sabara M, Hudson GR: Rotavirus and coronavirus in- Conference, 1998, Las Vegas, NV.
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15. Theil KW, Lance SE, McCloskey CM: Rotaviruses associated Nashville, TN.
with neonatal lamb diarrhea in two Wyoming shed-lambing oper- 42. Clarkson MJ, Winter AC: A handbook for the sheep clinician, ed 5,
ations, J Vet Diagn Invest 8(2):245, 1996. Liverpool, UK, 1997, University Press.
16. Munoz M et al: Rotavirus excretion by kids in a naturally infected 43. Duhamel GE, Moxley RA, Maddox CW: Enteric infection of a
goat herd, Sm Rum Res 14(1):83, 1994. goat with enterohemorrhagic Escherichia coli (0103:H2), J Vet
17. Heath SE: Neonatal diarrhea in calves: diagnosis and intervention Diagn Invest 4(2):197, 1992.
in problem herds, Comp Cont Ed Pract Vet 14(7):995, 1992. 44. Drolet R, Fairbrother JM, Vaillancourt D: Attaching and effacing
18. Moore JA, Blagburn BL, Lindsay DS: Cryptosporidiosis in Escherichia coli in a goat with diarrhea, Can Vet J 35(2):122, 1994.
animals including humans, Comp Cont Ed Pract Vet 10(3):275,
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19. Foreyt WJ: Coccidiosis and cryptosporidiosis in sheep and goats, DIARRHEA IN ADULT SHEEP
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20. Berg IE, Peterson AC, Freeman TP: Ovine cryptosporidiosis, J Am
AND GOATS
Vet Med Assoc 173(12):1586, 1978. The differential diagnosis list for acute and chronic diar-
21. Sanford SE et al: Cryptosporidiosis, rotaviral, and combined cryp- rhea in small ruminants is very long.1 The most common
tosporidial and rotaviral infections in goat kids, Can Vet J cause of diarrhea in adult sheep and goats is parasitism;
32(10):626, 1991. another major cause is Johne’s disease. Both of these dis-
22. Rings DM, Rings MB: Managing Cryptosporidium and Giardia in- eases are discussed in the following sections. Other causes
fections in domestic ruminants, Vet Med 91(12):1125, 1996.
of acute diarrhea include rumen acidosis, peritonitis, en-
23. Corwin RM: Cryptosporidiosis: a coccidiosis of calves, Comp Cont
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dotoxemia, and ingestion of toxins. The list of toxins that
24. Webster KA et al: Detection of Cryptosporidium parvum oocysts in cause diarrhea also is very long, and often the diarrhea is
feces: comparison of conventional coproscopical methods and the not the primary clinical sign. Some of the more common
polymerase chain reaction, Vet Parasit 61(1/2):5, 1996. toxins that produce diarrhea are arsenic, toxic amounts of
25. Campbell I et al: Effect of disinfectants on survival of Cryp- salt, levamisole, copper, oak, selenium, and pyrrolizidine
tosporidium oocysts, Vet Rec 111(18):414, 1982. alkaloids.1 Salmonella species and chronic enterotoxemia
26. Perryman LE et al: Protection of calves against cryptosporidiosis can cause diarrhea in adult animals. Coccidiosis can occur
with immune bovine colostrum induced by a Cryptosporidium in adults under severe stress or in animals that possess
parvum recombinant protein, Vaccine 17(17):2142, 1999. limited immunity because of lack of exposure. Hepatic
27. Bulgin MS, Anderson BC: Salmonellosis in goats, J Am Vet Med and renal disease and copper deficiency are sometimes ac-
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companied by chronic diarrhea, but weight loss is a more
28. House JD, Smith BP: Current strategies for managing salmonella
infections in cattle, Vet Med 93:756, 1998.
common sign in adults.
29. Cohen ND et al: Comparison of polymerase chain reaction and
microbiological culture for detection of salmonella in equine feces INTESTINAL PARASITISM
and environmental samples, Am J Vet Res 57:780, 1996.
30. Kirkpatrick CE: Giardiasis in large animals, Comp Cont Ed Pract
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Nematode Infestation
31. Koudela B, Vitovec J: Experimental giardiasis in goat kids, Vet Etiology and pathogenesis. Sheep and goats are in-
Parasit 74(1):9, 1998. fested with many of the same gastrointestinal nematode
32. Olsen ME et al: Effects of giardiasis on production in a domestic parasites as cattle, but these parasites tend to either be
ruminant (lamb) model, Am J Vet Res 56(1):1470, 1995. species-specific or have some amount of host specificity.
33. Nappert G et al: Determination of lactose and xylose malabsorp-
Sheep and goats are susceptible to the same nematodes
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and tend to share resistance to those that infect cattle and
34. Naylor JM: Neonatal ruminant diarrhea. In Smith BP, editor: horses. The major gastrointestinal nematodes that para-
Large animal internal medicine, ed 2, St Louis, 1996, Mosby. sitize pastured sheep and goats are Haemonchus, Osterta-
35. Weese JS, Kenney DG, O’Connor A: Secondary lactose intoler- gia, Trichostrongylus, Cooperia, Nematodirus, Oesophagosto-
ance in a neonatal goat, J Am Vet Med Assoc 217(3):372, 2000. mum, and Bunostomum species. The acronym HOTC
36. Olchowy TWJ et al: Lactose intolerance in a calf, J Vet Int Med comes from the first letter of each of the first four genera
7(1):12, 1993. of parasites listed. The specific parasites that produce
 Chapter 4 Diseases of the Gastrointestinal System • 89

disease vary from flock to flock. Climate usually deter- Diagnosis. Antemortem diagnosis of nematode infes-
mines which parasites are of clinical significance on a tation is made by examining the feces for nematode eggs.
farm, and the weather determines when the parasites will Although a direct fecal smear can be examined, the mere
be transmitted and infective. In much of the United presence of parasite eggs is not helpful in determining the
States, Haemonchus is the most significant parasite with parasite load of an animal or animals. Quantifying of the
respect to both clinical disease and anthelmintic resist- EPG of feces is the best way of estimating parasite loads.
ance. Most of these parasites affect the abomasum or The quantitative McMaster’s technique for determining
small intestine of young, recently weaned animals and oc- the EPG of feces is shown in Box 4-1. Common nema-
casionally adult animals. Sheep (and, to a lesser extent, tode eggs are shown in Figure 4-10.
goats) that are older than 18 months may be less suscep-
tible. Overcrowding and overgrazing with concurrent Treatment and control program. After taking a thor-
pasture mismanagement and malnutrition usually in- ough history of the previous parasite control program
crease susceptibility to these parasites. Inadequate nutri- used on a farm and determining its effectiveness, the cli-
ent or protein intake may result in greater susceptibility.2 nician can design and implement a new control pro-
The life cycle appears to be similar in most of these gram.2,3 However, before deciding to implement a de-
parasite species. Adults lay eggs that are passed in the worming program, the clinician should decide which
feces; except for Nematodirus species, the eggs hatch parasites are in need of control and whether control of
under favorable environmental conditions. The larvae go these parasites is cost effective in a particular flock.
through several free-living developmental stages becom- Whenever possible, a dewormer that can reduce EPG
ing infective. When the infective larvae are ingested by counts on the farm by 90% should be identified and used
the host, the parasite completes its life cycle as an adult. for at least a year. Of all the parasite prevention programs,
Trichuris eggs are the infective stage and can survive for strategic deworming or a combination of strategic and
extended periods in dry lots or barns.4 However, Trichuris tactical programs appear to produce the best results.2,4,5
is associated with minimal pathology. During dry envi- Strategic deworming is used when most of the para-
ronmental conditions, fecal pellets tend to trap the nema- sites are inside the animals and not on the pasture.2 In
tode larvae, whereas in wet conditions, larvae are released northern climates, strategic deworming can best be
onto the pasture. Therefore drought conditions followed carried out during the winter, when the nematode para-
by rain can result in devastatingly high rates of pasture sites are in a hypobiotic state. When environmental con-
contamination as larvae that have remained in fecal ditions are inhospitable for the survival of the infective
pellets are released.2 larvae, some of the most pathogenic nematodes (e.g.,
Very high environmental temperatures result in shorter Haemonchus) may become hypobiotic; that is, they assume
survivability of some stages of infective larvae. Most of the a state of arrested development. They may then mature to
larvae have adapted the ability to over-winter, but can the adult stage when environmental conditions become
survive only for short periods outside the host during conducive for the survival of their eggs or larvae. Prevent-
spring. Nematodirus is an exception in that the develop- ing or decreasing the numbers of maturing adults by
mental stages leading to infective larvae occur while the killing the larvae before the periparturient rise in parasite
microbe is still encapsulated in the egg. However, com- egg production and pasture contamination is an excellent
pared with other species of parasite, Nematodirus is of management tool.4,6,7 Unfortunately, in warmer, more
minor importance. Nematodirus battus may pose a threat to temperate to subtropical environments, this method is
young, newly weaned and therefore immunologically less effective because larvae can survive the environment
naive grazing lambs. The hookworm Bunostomum also is for longer periods. The addition of a protein supple-
different, as it may infect the host by either oral ingestion ment overlapping the expected periparturient rise has
or percutaneous penetration. With the exception of the been shown to decrease the number of parasite eggs shed
small intestinal parasite Strongyloides, lambs or kids fed around the time of parturition. However, the cost of the
indoors or in dry pens tend to be free of parasites. protein supplement may outweigh its benefits.8
A strategic program entails the use of an anthelmintic
Clinical signs. All intestinal nematode infections agent that is capable of killing encysted larvae. Animals
produce similar signs, although infection with the more are then moved to parasite-free or safe pastures—areas in
rarely encountered Bunostomum may perhaps result in which the level of parasite contamination is too low to
more profound anemia. If they infest the animal in suffi- result in infection of grazing animals. Examples of safe
cient numbers, all nematodes may cause poor growth, de- pastures include pastures where sheep or goats have not
creased feed conversion, decreased milk production, grazed for 3 to 6 months in the spring or fall, respectively
weight loss, diarrhea, anemia, ventral edema (bottle jaw), (and depending on the climate); pastures used for hay
midline edema, and death. Again, all these parasites can production; new pastures (i.e., those used for corn,
potentially result in disease, but Haemonchus is the most cotton, or other crops); and pastures grazed by horses or
devastating, particularly in more temperate regions.2 cattle. The use of safe pastures is paramount in any de-
90 • Sheep and Goat Medicine
worming program. Rotating pastures after less than 3 occurs, the more quickly resistance is attained to ant-
months during the warm part of the year or less than 6 helmintics. After deworming, only resistant parasites
months during cooler months is ineffective.3 However, remain to infect the animal and they are able to reproduce
if pastures are tilled and replanted, by the time new freely, resulting in proliferation of resistant strains.2,4
grazeable forage is available, infective parasite larvae will Using drugs that remain in tissues at inappropriately
be dead or significantly decreased.3 low concentrations and treating and retaining immuno-
An alternative to pasture rotation is to perform an compromised animals encourage the development of
initial strategic deworming before lambing or kidding anthelmintic resistance. Practices that ensure adequate
and follow it with two to four more dewormings at 3- dosages, proper treatment techniques, and appropriate
week intervals throughout the lambing and kidding types of anthelmintics should be emphasized.2,13
period.9-11 Treating lambs or kids at weaning and moving The clinician should do everything in his or her power
them to a safe pasture is a form of strategic deworming.4 to minimize the incidence of anthelmintic resistance,
In lambs or kids to be sold at an early age, the adminis- both through their own actions and by counseling owners
tration of a single anthelmintic treatment followed by a in proper use of deworming drugs. The product develop-
move to a safe pasture may be all that is required. A ment market for anthelmintics is the cattle industry. The
“double treat and move” system is required for lambs kept small sheep and goat markets simply use drugs made
for 12 to 18 weeks after weaning, particularly during the available for cattle. Because most available anthelmintics
summer.12,13 This form of strategic deworming requires are highly effective in controlling parasites, anthelmintic
two treatments 6 to 8 weeks apart as well as two safe pas- resistance in sheep and goats must be avoided. The an-
tures. In northern climates where animals are moved to a thelmintics that have been used previously on a flock, the
dry lot or barn for the winter, a strategic anthelmintic ad- route of administration (e.g., PO, SC, IM, pour-on), and
ministration as animals are moved off pasture can help the length of use should be determined. Few dewormers
reduce the parasite burden through the winter.14 If this are approved for use in sheep and goats, but many ap-
deworming is followed by minimal or no exposure to proved for use in cattle and horses may be effective.2,7 If
grazing areas and another dewormer is administered sheep graze with goats that harbor anthelmintic-resistant
before the spring rise in fecal egg counts, the total para- parasites, the sheep also may become infected.4 However,
site burden on spring pasture can be drastically reduced, if sheep are allowed to graze while the goats browse and
effectively controlling parasites until summer or fall. the two groups rarely mingle, less parasite movement will
Tactical deworming programs are used to remove par- occur between these species.
asites from their hosts before they enter their reproductive Resistance to macrolides (e.g., ivermectin, doramectin,
phase and can contaminate the pasture.4 An example of moxidectin) does occur. Resistant worms are generally
tactical deworming is treating animals 10 to 14 days after a not very tolerant of cold temperatures and therefore re-
rain, particularly if the rain has followed a drought. Para- sistance to this drug class in northern environments is not
site transmission is worse in most flocks during this time as large a problem as it is in more temperate or subtropi-
as pastures become heavily contaminated. McMaster’s cal zones.15 Although moxidectin is not approved for use
counts of more than 1000 EPG in the spring or more than in sheep and goats in the United States, it has been
2000 EPG in the fall warrant tactical deworming.2,4,7 shown to be effective in cases where ivermectin resistance
Opportunistic deworming and salvage deworming is encountered.2 Still, this drug should be avoided until all
are usually less effective in long-term flock management. other anthelmintics have failed. Craig3,4 has suggested
Many times salvage deworming programs are used to that clinicians refrain from injecting or using pour-on
save the lives of heavily parasitized animals.4 If animals macrolide preparations designed for cattle in small rumi-
are dewormed only after showing signs of parasitism nants. This practice may enhance the development of re-
(e.g., bottle jaw, anemia), animal and flock productivity sistant strains of some internal parasites because of inap-
have already been depressed. Deworming during han- propriately low drug absorption (with pour-on use) or
dling for other procedures (e.g., castration, vaccination, long-term subtherapeutic levels (with injection).4
shearing) is an example of an opportunistic program. It is If resistance to tetrahydropyrimidines (e.g., morantel,
convenient but is not conducive to long-term flock pyrantel) occurs in a flock, levamisole also may be ineffec-
health. Flock work should be scheduled around parasite tive. Morantel and levamisole resistance in parasites
management programs, not vice versa.2,14 appears to be sex-linked. Therefore if animals are not
Suppressive deworming programs entail the use of exposed to these drugs for several years, reversion to sus-
anthelmintics at regular intervals, usually every 2 to 4 ceptibility can occur.3,4
weeks. Suppressive programs are labor-intensive, tend to If resistance to one of the benzimidazole dewormers
be very expensive, fail to identify animals with superior has been documented in a flock, some resistance to all
immunity to parasites, and ultimately result in an- members of that class is likely.4 Benzimidazole-resistant
thelmintic resistance despite initial effectiveness.2,4 Haemonchus species appear to be more virulent, produce
As a general rule, the more frequently deworming more eggs, cause greater environmental contamination,
 Chapter 4 Diseases of the Gastrointestinal System • 91

and survive in the environment as free-living larvae for effectiveness for many years and on many farms and
longer periods. Benzimidazole-resistant parasites appar- ranches.2,14 The authors randomly collect feces from 5%
ently do not revert to susceptible forms, even over long to 10% (or a minimum of 10 animals) of the sheep or
periods. Therefore the clinician or keeper should exercise goats on the farm. A composite sample is prepared by
caution to minimize resistance.4 Benzimidazole efficacy combining equal amounts of stool from all animals.
can be improved by increasing dosages, dividing dosages Craig3 has suggested that combining stool samples from
into two treatments administered at 12-hour intervals, many animals alters the accuracy of the tests because
and instituting pretreatment fasting.2 great individual variation in fecal egg counts occurs
If resistance to numerous classes of anthelmintics among animals. Composite egg counts more accurately
occurs on a farm, combining two of the resistant classes of reflect parasite burdens in groups of young animals, and
dewormers (fenbendazole and levamisole) has proven ef- individual fecal examinations are more accurate in
fective.16 When using combined dewormers, the clinician adults.2,4 Still, the authors prefer to use composite
should administer the full therapeutic dosage of each. samples unless obvious differences in stool character or
Anthelmintics are metabolized at different rates by sheep body condition score exist among the sampled animals.
and goats. Goats may require larger dosages of some de- Anthelmintic resistance can be minimized by using drugs
wormers than sheep.7 Craig4 has suggested that if no that reduce fecal egg counts by 90%. Pre- and post-
dose rate is known for a particular anthelmintic for sheep deworming changes in EPG should be evaluated yearly or
or goats, the animals should be treated at twice the sug- whenever resistance is suspected.4 In vitro methods of as-
gested cow dosage. Pour-on anthelmintics designed for sessing flock parasite resistance also are available at some
cattle tend to be of limited value when used topically on diagnostic laboratories. In most in vitro tests, larvae are
either goats or sheep.2 A list of dewormers useful in sheep hatched from collected feces and the sensitivity of differ-
and goats is listed in Table 17-3. To maximize a parasite ent anthelmintics is determined by larval exposure. These
control program, anthelmintics that appear effective tests are very accurate but tend to be quite expensive.
should be used for only 1 year before a new class of de- The most effective method to prevent anthelmintic re-
worming drug is used. More frequent rotation (after less sistance is to not use deworming drugs at all.4 One of the
than 1 year) of anthelmintic agents hastens resistance and most overlooked management procedures is the identifi-
should be avoided whenever possible. cation and selection of parasite-resistant sheep and goats.2
Whenever a flock is dewormed, animals should be Some breeds or familial lines within breeds have excellent
treated based on the heaviest animal in the group and not parasite resistance (e.g., Gulf Coast Native and Barbados
on the group’s average weight. Underdosing can hasten sheep, some strains of Spanish, Pygmy, and Tennessee
the formation of parasitic resistance and therefore should myotonic-fainting goats).2 One study17 comparing Boer-
be avoided.4 Holding the sheep or goats in a dry lot crossed goats with non-Boer crosses found that the Boer
overnight or feeding only dry hay for 12 to 24 hours crosses had significantly more parasite infestations. Only a
before and 12 hours after deworming appears to improve small number of flock members contribute the greatest
the efficacy of some orally administered anthelmintic amount of environmental parasite contamination because
agents (benzimidazole). Limiting feed intake before de- susceptible animals shed the most eggs in their feces.
worming slows the rate of passage of ingesta through the Animals with the lowest EPG in a flock may be those that
bowel, enhancing drug effectiveness.2,13,14 Feed should possess the most parasite resistance.4 Salvage deworming
never be withheld from sick or debilitated animals or programs should generally be avoided, but they may be
late-term females.2,13,14 Most dewormers may effectively used as aggressive selection criteria. That is, animals that
control adult or larval parasites but are ineffective against do well with little or no deworming, particularly those
eggs. Therefore animals should be kept on a dry lot for as grazing heavily contaminated pastures, should be identi-
long as 3 days after deworming, then moved to a safe fied and retained in the breeding flock. Those that become
pasture. Use of this procedure minimizes parasite egg infected should be dewormed to salvage them or save their
contamination of the new pasture because most of the lives and then sold when possible. Proper record keeping
egg-contaminated feces is voided within 72 hours of de- and identification of all animals is paramount in selecting
worming. If more than one dosage appears on the drug for parasite resistance.2,14 This aggressive approach can
label, the larvacidal dose should be used (fenbendazole at yield excellent results if it is carefully implemented, but
10 mg/kg rather than 5 mg/kg).2 devastating losses can occur if it is poorly managed.
Anthelmintic effectiveness can be determined by com- When introducing new animals to a flock, keepers
paring a McMaster’s fecal EPG on the day of deworming should have biosecurity programs in place to limit the in-
with one taken 7 to 14 days later. If less than a 90% drop troduction of new or potentially anthelmintic-resistant
in EPG is found, anthelmintic resistance exists and the parasites. New flock additions should be kept in a dry lot
animals should be switched to another class of de- for 3 weeks and dewormed at least twice with two differ-
wormer.2 Although it is a controversial method, the ent classes of dewormers during this period. The effec-
authors have used this technique to identify anthelmintic tiveness of the anthelmintic agent used should be deter-
92 • Sheep and Goat Medicine
mined by fecal examination before the animal is allowed cobacterium avium subspecies paratuberculosis. Transmis-
contact with the rest of the flock.2 sion of the organism is primarily by the fecal-oral route.
Other nontraditional chemical methods of parasite Young animals are more susceptible to infection than
control are used by some owners. Some appear to be adults. It can be transmitted through milk and placenta.
worthless (e.g., diatomaceous earth), but others (e.g., ne-
matophagous fungi, herbal dewormers) may prove effec- Pathogenesis. Bacterial shedding in feces and milk and
tive in some situations. transplacental transmission is more common in animals
showing clinical signs.18-20 Therefore the offspring of in-
fected animals and especially the offspring of animals
Cestode Infestation showing clinical signs are most likely to acquire the infec-
Pathogenesis. The most common gastrointestinal tion. After an animal is exposed, it will either clear the or-
tapeworm of sheep and goats seen in North America ganism or develop a chronic, persistent infection. The in-
belongs to the genus Moniezia. Cestodes (tapeworms) are fection is most commonly isolated to the ileal regions of
usually of more concern to owners than clinicians, who the small intestine, where it causes granulomatous thick-
generally consider them only incidental low-grade ening of the intestine and subsequent malabsorptive diar-
pathogens, particularly in adult animals. Still, several 10- rhea. Infected animals may be asymptomatic for years.
to 20-foot-long tapeworms can compete with the host for
nutrients, hinder normal gut motility, and excrete some Clinical signs. Morbidity rates are low (approximately
toxic wastes into the host’s gastrointestinal tract. Mature 5%), but for every animal with clinical signs, several exist
tapeworm eggs are passed in the feces individually or pro- in the subclinical state, and may be a source of both
tected in proglottides, which are usually visible to the horizontal and vertical transmission.18 Both sheep and
owner. The eggs embryonate and infect a mite, a small goats appear to remain asymptomatic until 2 to 7 years
pasture-living arthropod that serves as the intermediate of age. The most consistent clinical sign in sheep and
host. A sheep or goat ingests the mite while grazing, al- goats is chronic weight loss. Chronic diarrhea occurs in
lowing the tapeworm to complete its life cycle. approximately 20% of cases.18 Signs may appear with or
be exacerbated by stress, especially after parturition.18,19
Clinical signs. Tapeworms may rarely cause disease in Hypoproteinemia and chronic mild anemia are the on-
lambs and kids less than 6 months of age. Anecdotal ly consistent clinicopathologic findings. Because of their
reports suggest a cause-effect relationship between heavy low protein levels, infected animals can develop sub-
tapeworm infestation and an increased incidence of C. mandibular edema.
perfringens enteritis, digestive disturbances (e.g., diarrhea,
constipation), poor condition, and anemia. Ulceration at Diagnosis. Diagnosis is by culture of the organism from
the site of attachment may be seen on necropsy. Rarely feces. Unfortunately, this testing takes between 8 and 14
species of Trypanosoma, the fringed tapeworm, may cause weeks, but it can detect 40% to 60% of clinically infected
liver condemnation. goats. Sheep strains of Johne’s disease and some goat
variant strains seem to be more difficult to culture in media
Diagnosis and treatment. A presumptive diagnosis can used to identify cattle strains of the disease.Therefore fecal
be made by finding proglottides in the stool, eggs on direct culture in sheep and goats appears to be of limited
smears, or eggs on fecal flotations (see Figure 4-10).Treat- benefit.19,20 A relatively inexpensive and easily performed
ment with albendazole (15 mg/kg), fenbendazole (20 to method of identifying approximately 50% of all clinically
25 mg/kg), or praziquantel (10 to 15 mg/kg) may be effec- infected animals is acid-fast staining of fecal smears.18,19
tive either with a single treatment or with daily therapy A PCR test of feces also is available, but its sensitivity is
(e.g., fenbendazole daily for 3 to 5 days). Because of the lower than that of fecal culture. Good diagnostic results
free-living nature of the arthropod intermediate host, can be obtained with serologic testing for antibodies (e.g.,
animals are readily reinfected after treatment, which may agar gel immunodiffusion [AGID], enzyme-linked im-
give rise to the false assumption that the therapy was inef- munospecific assay [ELISA], complement fixation) in
fective. Again, tapeworm infestation may result in disease, animals showing clinical signs. The specificity of all the
but often it is easier to blame the tapeworm segment seen serologic tests is greater than 95% in sheep and goats with
in the stool as a cause of disease than to implicate the signs of clinical disease, although the sensitivity is not as
unseen thousands of HOTC complex parasites in the abo- high.19-21 Therefore a positive serologic test in an animal
masum and small intestine of the animal.3,14 showing clinical signs indicates that the animal has Johne’s
disease. However, the disease cannot be ruled out with a
negative test. Sheep and goats appear to respond differ-
Johne’s Disease ently in regard to the formation of antibodies. Sheep tend
Johne’s disease (also called paratuberculosis) is a chronic to develop antibodies in the later stages of the disease,
wasting and diarrheal disease caused by the bacteria My- whereas antibodies may be detected much earlier in the
 Chapter 4 Diseases of the Gastrointestinal System • 93

goat. The AGID test appears to be the best serologic test 4. Craig TM: Anthelmintic resistance: the selection and successful
currently available.22,23 The ELISA and complement fixa- breeding of superior parasites, Proceedings of the Small Ruminants
tion tests can cross-react with Corynebacterium pseudotu- for the Mixed Animal Practitioner, Western Veterinary Conference,
1998, Las Vegas, NV.
berculosis, making them of limited value in flocks with
5. Menzies P: Control and prevention of specific diseases of sheep
caseous lymphadenitis infections.19,24 Necropsy diagnosis
and goats, Proceedings of the Symposium on Health and Disease of
is based on the finding of thickened, corrugated intestines, Small Ruminants, Nashville, TN, 1996, American Association of
especially in the area of the ileum. Acid-fast staining of Small Ruminant Practitioners.
impression smears (taken from the ileum and ileocecal 6. Herd RP: Control of periparturient rise in worm egg counts of
lymph nodes) can help yield a quick diagnosis. The stain- lambing ewes, J Am Vet Med Assoc 182:375, 1983.
ing of numerous clumps of acid-fast rods is highly sugges- 7. Bretzlaff K: Production medicine and health programs for goats.
tive of Johne’s disease. In Howard JL, editor: Current veterinary therapy in food animal
practice 2, Philadelphia, 1986, WB Saunders.
Prevention. Johne’s disease has no effective treatment, 8. Donaldson J: The effects of dietary protein on establishment and
so prevention and control are imperative. However, pre- maturation of nematode populations in adult sheep. In Barrel GK,
editor: Sustainable control of internal parasites in ruminants,
venting the introduction of Johne’s disease into a herd can
Christchurch, UK, 1997, Lincoln University.
be difficult. Because animals with subclinical infection
9. Herd RP: Nematode infections—cattle, sheep, goats, swine. In
may not shed the organism or may shed only small quan- Howard JL, editor: Current veterinary therapy in food animal prac-
tities of it, fecal culture is helpful only if a positive culture tice 2, Philadelphia, 1986, WB Saunders.
is obtained. The sensitivity of serologic tests of animals 10. Miller JE: Parasites affecting goats in the Southeast, Proceedings
with subclinical disease is low and variable among of Goat Production and Marketing Opportunities in the South,
flocks.19,20 Negative test results in subclinically infected 1995, Fort Valley, GA.
animals are common. However, the specificity of sero- 11. Uriarte J, Valderrabano J: Grazing management strategies for the
logic tests remains high, and therefore a positive test is a control of parasitic diseases in intensive sheep production systems,
valid reason to not purchase an animal.19 Because Johne’s Vet Parasit 37:342, 1990.
disease also occurs in cattle, supplemental colostrum sup- 12. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea
& Febiger.
plies should come only from dairy herds with no history
13. Herd RP, Zajac AM: Helminth parasites of the gastrointestinal
of Johne’s disease.
tract. Nematode infections in cattle, sheep, goats, and swine. In
After Johne’s disease is diagnosed in a herd, several Howard JL, Smith RA, editors: Current veterinary therapy 4,
control measures can be taken. Sanitation is important Philadelphia, 1998, WB Saunders.
because the organism is highly resistant in the environ- 14. Pugh DG, Navarre CB: Parasite control programs in sheep and
ment (able to survive more than 1 year under most condi- goats, Vet Clin North Am: Food Anim Pract, 17(2):, 2001.
tions).20 Reduced stocking rates, frequent cleaning of 15. Wescott RB, Foreyt WJ: Epidemiology and control of trematodes
pens, and use of automatic waterers decrease fecal trans- in small ruminants, Vet Clin North Am: Food Anim Pract 2:373, 1986.
mission. Keepers should cull the offspring of infected 16. Miller DK, Craig TM: Use of anthelmintic combinations against
animals. Culling animals based on the results of AGID multiple resistant Haemonchus contortus in Angora goats, Small
tests or fecal culture of the flock is recommended. Rum Res 19:281, 1996.
17. Hollis A et al: Preliminary investigation of anthelmintic efficacy
Animals should be tested at least once a year. More fre-
against GI nematodes of goats and susceptibility of goat kids to
quent testing as resources allow speeds the identification
gastrointestinal nematode infection, Proceedings of the ARD Sympo-
of infected animals. A vaccine for cattle is only available sium, 2000, Fort Valley, GA.
in some locales and clinicians or keepers may require offi- 18. Greig A: Johne’s disease in sheep and goats, In Pract 22(3):146,
cial permission to use it. Vaccine use does not eliminate 2000.
infection, but it can decrease herd prevalence, delay the 19. Smith MC: Paratuberculosis in small ruminants, Proceedings of
onset of clinical signs, and decrease cross-transmission by the Small Ruminants for the Mixed Animal Practitioner, Western Vet-
infective bacterial shedding in the feces. erinary Conference, 1998, Las Vegas, NV.
20. Stehman SM: Paratuberculosis in small ruminants, deer, and

R EFERENCES
1. Smith BP: Alterations in alimentary and hepatic function. In
South American camelids, Vet Clin North Am: Food Anim Pract
12(2):441, 1996.
21. Clarke CJ et al: Comparison of the absorbed ELISA and agar gel
Smith BP, editor: Large animal internal medicine, ed 2, St Louis, immunodiffusion test with clinicopathologic findings in ovine
1996, Mosby. clinical paratuberculosis, Vet Rec 139(29):618, 1996.
2. Pugh DG, Mobini SM, Hilton CD: Control programs for gas- 22. Thomas GW: Paratuberculosis in a large goat herd, Vet Rec
trointestinal nematodes in sheep and goats, Comp Cont Ed Pract 113(20):464, 1983.
Vet 20(4 suppl.):S112, 1998. 23. Shulaw WP et al: Serodiagnosis of paratuberculosis in sheep by use
3. Craig TM: Epidemiology of internal parasites: effects of climate of agar gel immunodiffusion, Am J Vet Res 54(1):13, 1993.
and host reproductive cycles on parasite survival, Proceedings of the 24. Pepin M, Marly J, Pardon P: Corynebacterium pseudotuberculosis in-
Small Ruminants for the Mixed Animal Practitioner, Western Veteri- fection in sheep and the complement fixation test for paratubercu-
nary Conference, 1998, Las Vegas, NV. losis, Vet Rec 120(10):236, 1987.
94 • Sheep and Goat Medicine
INTESTINAL OBSTRUCTION calcium borogluconate per liter) and potassium (10 to 20
Any cause of intestinal obstruction that occurs in other mEq/L) is a good choice for fluid therapy.
ruminants may occur in sheep and goats. Most of these
diseases produce abdominal discomfort and occasionally
abdominal distention. Diagnosis can be difficult because
Foreign Body Obstruction
rectal palpation cannot be performed on small ruminants. Ingested foreign bodies or bezoars can obstruct portions
Abdominal radiographs and ultrasonography may help of the intestines.3,4 The signs are similar to those of ob-
differentiate these diseases, but exploratory surgery may struction caused by intussusception and depend on the
be required to obtain a definitive diagnosis and select ap- part of the intestine that is blocked. In some cases the ob-
propriate treatment. structing body can be seen with radiography or ultra-
sonography. Surgical removal is required for treatment.
Intussusception
Cecal Volvulus and Torsion of the Root
Intussusception is more common in young animals, but it
can occur in adults. It occurs when one segment of the in-
of the Mesentery
testine telescopes into an adjacent segment. Any portion Cecal volvulus and torsion of the root of the mesentery
of the intestine can intussuscept, but the ileum and ileoce- occur sporadically in sheep and goats.1,3 Extreme abdom-
cal junction are the most common areas involved. When inal pain, rapid abdominal distention, and circulatory col-
intussusception occurs, the lumen of the intestine narrows lapse are typical signs. Immediate surgical correction and
to the point of obstruction. The initiating cause is not circulatory support are needed.
always known.1,2 It is associated with an intestinal mass in
adults and enteritis in young animals.1 Oesophagostomum
infestations have been implicated as a cause in sheep.1
Intestinal Atresia
Atresia of the colon, rectum, and anus can all occur as con-
Clinical signs. The initial complaint is colic (mani- genital problems. The clinical sign of progressive abdomi-
fested as kicking at the abdomen, repeated rising and nal distention usually is noted in the first week of life.
lying down, and vocalization) followed by low-grade Atresia of the anus can be diagnosed on physical examina-
pain. True colic signs are variable in lambs and kids. In tion, but atresia of the colon and rectum may require con-
some cases, after the initial colic episode subsides, trast radiography for a definitive diagnosis. Surgical estab-
animals show no evidence of pain until the abdomen lishment of anal patency can be performed for atresia ani.
becomes distended. The time between the initial intus- A permanent colostomy may be required for atresia of the
susception and abdominal distention depends on where colon and rectum. Atresia of the anus and rectum are con-
the blockage occurs. Intussusception of the ileal area may sidered heritable in cattle.1 In the authors’ experience,
take several days to cause bilaterally symmetric abdomi- atresia ani is more common in sheep than in goats.
nal distention. Fecal output is scant, and what little there If surgical correction of atresia ani is attempted, the
is may be dark or tarry, or may contain mucus. Dehydra- animal should be neutered or kept out of the breeding
tion becomes evident, hypochloremic metabolic alkalosis program because of the potential genetic basis for this
may develop and rumen chloride levels may increase with condition. Occasionally a slight bulge in the skin may
obstructions of the duodenum. occur where the anus should be located, especially in male
lambs. Ultrasonography can be used to locate a feces-
Diagnosis. Abdominocentesis may yield fluid compat- filled rectum. For surgical correction, the clinician should
ible with a transudate (increased protein concentration locate the area where the anus should be, prepare it with
and leukocyte numbers).1 Radiography and ultrasonogra- sterile technique, and infiltrate it with a local anesthetic.
phy reveal fluid-distended intestinal loops. Occasionally The surgeon then makes a circumferential incision to
the intussusception itself can be visualized with ultra- remove the overlying skin covering the rectum. An alter-
sonography or palpable through the abdominal wall. If native is to make an X-shaped incision into the rectum.
the disease is not treated, intestinal rupture and peritoni- Treated animals should be given mineral oil, DSS, or
tis can occur. stool softeners as needed.

Treatment. Surgical correction is required. If the intus-

susception is corrected early, the prognosis is good in the
Intestinal Ileus
absence of peritonitis. Fluid support is needed to correct Ileus of the small intestine is a pseudo-obstruction that
dehydration and metabolic abnormalities. Fluids should occurs when there is an absence of intestinal motility. The
be administered IV until rumen function returns. Ringer’s animal’s failure to pass ingesta leads to signs similar to in-
solution with added calcium (approximately 25 ml tussusception. The cause of ileus is usually unclear, but it
 Chapter 4 Diseases of the Gastrointestinal System • 95

often occurs secondary to systemic diseases. The same el- possibly the descending colon) is usually associated with
ements that cause rumen stasis may potentially result in excessive straining. Straining is seen in lambs with diar-
intestinal stasis and ileus. Symptomatic treatment with rhea caused by coccidiosis, Salmonella, or dietary imbal-
NSAIDs for pain and inflammation and fluids for dehy- ances, in ewes or ewe lambs with vaginal prolapse, in males
dration is usually curative.1 However, if signs persist, sur- with urolithiasis, and in animals grazing lush forage (par-
gical exploration is indicated to rule out true obstructive ticularly legumes such as alfalfa and clover). It also can
diseases. occur secondary to chronic coughing, short tail docking,
and the use of growth implants.5-7 Rabies also can cause
chronic straining and rectal prolapse.5-9 Regardless of the
Peritonitis cause, after the rectal mucosa becomes everted and
Pathogenesis. Infection of the peritoneal lining of the exposed, irritation of the mucosa causes further straining,
abdominal cavity may lead to septic peritonitis. Common which exacerbates the problem. Venous drainage of the
causes include uterine tears; rupture of the rumen or abo- prolapse may be compromised, but the arterial supply
masum secondary to rumenitis, abomasitis, or abomasal usually remains intact and contributes to the swelling.
ulcers; trocarization of the rumen for bloat; and rupture Rectal prolapses are graded as Type I to IV, based on the
of the intestine secondary to obstruction. portion of rectum and distal colon that is everted.5 A de-
scription of these grades in shown in Table 4-4.
Clinical signs. Signs depend on the severity of the
condition. Abdominal discomfort and distention, dehy- Treatment. Correction may be cost prohibitive for
dration, injected mucous membranes, depression, and feedlot lambs, and immediate slaughter is recommended.
death can all occur in cases of peritonitis. The presence of In more valuable animals, very mild, early cases can be
a fever is variable, both heart rate and respiration rate are treated with frequent application of hemorrhoidal oint-
usually elevated, and respiratory effort may be guarded. ment designed for humans and manual replacement of
Animals may be febrile early, but have a normal to low the prolapsed mucosa into the anus. The authors try to
body temperature as the condition progresses. avoid applying purse-string sutures in the anus because
they tend to serve as a nidus and result in further strain-
Diagnosis. Abdominal ultrasound can be useful in ing. However, if less aggressive therapies do not relieve the
locating pockets of fluid for abdominocentesis, which problem in 24 hours, a purse-string suture may become
usually yields fluid with increased protein concentration necessary, particularly in Type I and II prolapse. In all
and leukocyte numbers. On occasion, intracellular bacte- cases and modes of treatment, restricting feed for 24 to 48
ria are observed on cytologic examination. The presence hours and administering mineral oil is recommended.
of extracellular bacteria is not diagnostic because acciden- Dusty feedstuffs (concentrates, pellets, hay) should be
tal enterocentesis can occur. Culture of abdominal fluid avoided because they may contribute to coughing, which
and subsequent antimicrobial sensitivity tests are indi- exacerbates this condition. Adding molasses to feeds and
cated for the implementation of proper treatment. The lightly wetting hay may help reduce problems with dust.
causative organisms vary depending on the source of the Purse-string suture is easily performed. The pro-
bacteria. Rumen bacteria are typically gram-negative lapsed tissue and perineal area are washed with mild soap
anaerobes, and E. coli and other enteric bacteria are and lubricated with petroleum jelly or hemorrhoidal oint-
common if the intestine is the source of infection. Ex- ment before the prolapse is replaced.5,9 After replacing
ploratory surgery may be required to diagnose a gastroin- the prolapsed mucosa, the clinician inserts a tubular
testinal rupture. The CBC can be normal but often shows object (syringe case, wooden dowel, gloved finger) into
an inflammatory leukogram and, in severe cases, a degen- the rectum. He or she then places a purse-string suture of
erative left shift. nonabsorbable suture material (3-5 nylon) in the skin
around the anus, tightens it around the tubular object,
Treatment. Treatment includes the prescription of ap- and ties it off. The suture should be placed around the
propriate antimicrobial agents, the administration of anus using a cutting needle, and entering and exiting at
NSAIDs for pain and endotoxemia, and fluid support for the 12 o’clock position. Tying the knot above the anus
dehydration. The prognosis is guarded, especially if an in- ensures that less fecal soiling of the suture will occur. The
testinal rupture has occurred. clinician should tie the suture in a bow knot to allow easy
identification over the next few days and then remove the
tubular object. The suture should be tight enough to
Rectal Prolapse prevent prolapse but loose enough to allow feces to pass.
Pathogenesis, clinical signs, and diagnosis. Rectal The clinician should regularly reevaluate the animal and
prolapse is more common in sheep than in goats. This if possible loosen the purse-string suture at 24-hour in-
evagination of the rectal mucosa and rectal structures (and tervals until no tension exists. After a full day of no
96 • Sheep and Goat Medicine
TABLE 4-4

GRADES OF RECTAL PROLAPSE

TYPE DESCRIPTION COMMENTS

Type I Small, circular amount of submucosal swelling Good prognosis if there is no damage to mucosa;
protrudes through anus; probing reveals a pocket purse-string suture, iodine injection, submucosal
or fornix just inside anus resection
Type II Slightly more circular submucosal and mucosal Good prognosis if treated quickly and no mucosal
swelling, possibly containing retroperitoneal rectal damage; purse-string suture, iodine injection,
tissue from anus; probing reveals a pocket just submucosal resection, rectal amputation
inside anus
Type III Complete prolapse containing part of the If there is vascular injury to the descending colon,
retroperitoneal structures of the rectum and the prognosis is guarded to poor; submucosal
descending colon; probing reveals a fornix just resection or rectal amputation are the methods of
inside anus; the affected portion of the descending choice
colon does not prolapse through the anus
Type IV The descending colon appears as a tube, and has If there is vascular injury to the descending colon,
intussuscepted through the rectum and anus; prognosis is poor; abdominal exploration may
unlike the previous types, in this case a probe be required to determine the extent of damage to
or finger can be inserted into the prolapse through the descending colon
the anal sphincter for a distance of 5 to 10 cm
From Hooper RN: General surgical techniques for small ruminants: Part II, Small Ruminants for the Mixed Animal Practitioner, Western Veterinary
Conference, 1998, Las Vegas, NV.

tension, the suture can be removed. If animals continue to other 2 to 4 mm distal to the anal sphincter and through
strain, an epidural anesthetic can be administered. Petro- the entire prolapse.5
leum jelly and hemorrhoid gels should be placed on the A circular incision is made 2 to 4 mm distal to the
anus daily.5,9 spinal needles through the mucosa and around the
The injection of counterirritants around the rectum outside of the anus. Another circular incision is made just
(1 ml or less of Lugol’s iodine) either alone or in conjunc- distal to the caudal extent of the prolapse into the point
tion with anal purse-string suturing is a quick and inex- where the mucosa reflects on itself on the innerside of the
pensive treatment.5,6,9 The clinician inserts an 18-gauge prolapse. The clinician connects these two incisions with
needle (5 cm) deeply into the skin around the anus at 12, a longitudinal incision parallel to the prolapse and dis-
3, and 9 o’clock. An injection at the 6 o’clock position sects the mucosa between the circumferential incisions.5
should be avoided because swelling around the urethra The mucosal edges are then sutured with a simple inter-
can result in obstruction. rupted pattern using a suitable absorbable suture mate-
For more severe cases, submucosal resection or rectal rial. After completely suturing the mucosal surfaces, the
amputation of tissue may be necessary.5,9 Rectal amputa- clinician removes the two spinal needles and places a
tion can be performed with a prolapse ring or suture tech- purse-string suture in the anal sphincter. Placement of
nique.7 Prolapse ring usage is a salvage technique. The the suture and follow-up care are the same as described
clinician inserts the prolapse ring into the rectum and for the purse-string suture technique. Submucosal resec-
places an elastrator band or suture around the area to be tion decreases the incidence of both peritonitis and stric-
amputated to induce vascular compromise and necrosis of ture formation compared with other surgical techniques,
tissue. If a ligature is used, it should be tightened to allow but it is expensive.5
purchase on the tube or ring. A fibrosis is induced just In all of these techniques, a caudal epidural anesthetic
proximal to the band or suture, and mucosa subsequently (2% lidocaine, 0.5 ml per 45 kg) is recommended to de-
grow across the areas.5 Strictures, peritonitis, and ab- crease straining and ease pain from the procedures.6,7 A
scesses are possible complications, but this technique may xylazine epidural (0.01 to 0.03 mg/kg as sufficient [QS]
be useful as a field procedure. to 2 ml with 2% lidocaine) may give longer relief (approx-
Submucosal resection can be performed under imately 4 to 6 hours) from straining than lidocaine. An
epidural analgesia after the prolapse and the perineal area alcohol epidural also may prevent straining for extended
have been surgically prepared. The clinician places two periods. Either isopropyl alcohol or ethanol can be used
spinal needles (9 to 10 cm) at 90-degree angles to each to demyelinate the motor and sensory nerves.5 This type
 Chapter 4 Diseases of the Gastrointestinal System • 97

of anesthesia can be permanent and therefore should be Liver enzymes may or may not be elevated. Diagnostic
used only for animals intended for slaughter. Because of ultrasonography of the liver may help detect abscesses, es-
the potential for some loss of sciatic nerve function, the pecially if they are numerous and widespread. However,
clinician should perform a test injection of a local anes- no specific treatment or control measure is available.
thetic (2% lidocaine) before using alcohol. If the epidural Many of the preventive protocols used for feeder cattle
appears effective and no ataxia or muscle weakness of the apply to the control of abscesses in sheep and goats.
rear limbs occurs, the clinician can inject a mixture of These include slowly introducing concentrates into the
equal parts of lidocaine and alcohol into the sites where diet, offering long-stemmed hay free choice, and includ-
the test epidural was performed. Possible problems with ing rumen buffers (alkalinizing agents) and antimicrobial
alcohol epidural anesthesia include injection site necrosis, agents in the feed.
sciatic nerve dysfunction, and the inability to void feces.5
Regardless of the type of epidural used, the clinician
clips, washes, and dries the area before placing a small
Pregnancy Toxemia/Fatty Liver Syndrome
needle (20- to 21-gauge [2.6 cm]) in the most cranial yet Pathogenesis. Fatty liver occurs in conjunction with
moveable intracaudal vertebral space—usually C1 to C2 pregnancy toxemia in ewes and does during the last
or C2 to C3. The needle is placed on the dorsal midline, month of gestation. It is most common in thin or obese
with the needle 90 degrees to the skin and the hub moved ewes or does with a single large fetus, twins, or triplets.1
slightly caudal, and then slowly advanced. During late gestation, particularly in obese females, the
abdominal space is filled with accumulated fat and an

R EFERENCES
1. Guard C: Obstructive intestinal diseases. In Smith BP, editor: Large
ever-expanding uterus. Because of the lack of rumen
space, these females have difficulty consuming enough
feedstuffs to satisfy energy requirements. In most man-
animal internal medicine, ed 2, St Louis, 1996, Mosby. agement systems, late gestation occurs during the winter
2. Mitchell WC: Intussusception in goats, Agri-Practice, p 1918, Dec months, when less pasture is available and poorer-quality
1983. feedstuffs are offered. Energy requirements for ewes and
3. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea does carrying twins or triplets is greatly increased during
& Febiger. the final 2 months of gestation because 70% to 80% of
4. Sherman DM: Duodenal obstruction by a phytobezoar in a goat, J
fetal growth occurs during this time. Ewes with twins
Am Vet Med Assoc 178:139, 1981.
require 180% more energy, and those with triplets need
5. Hooper RN: General surgical techniques for small ruminants: Part
II, Proceedings of the Small Ruminants for the Mixed Animal Practi-
200% to 250% more dietary energy. Pregnancy toxemia
tioner, Western Veterinary Conference, 1998, Las Vegas, NV. also occurs in association with anorexia caused by other
6. Pipkin AB: Rectal prolapse in ruminants and horses. In Smith BP, diseases (foot rot, OPP, CAE) or sudden stresses (feed or
editor: Large animal internal medicine, ed 2, St Louis, 1996, Mosby. weather changes, predator attacks, hauling). Whatever
7. Kimberling CV: Jensen and Swift’s diseases of sheep, ed 3, Philadel- the initiating cause, a period of anorexia and lack of suffi-
phia, 1988, Lea & Febiger. cient energy intake result in a negative energy balance.
8. Welker B, Modransky P: Rectal prolapse in food animals. Part 1: These animals begin to mobilize body stores of fat and
cause and conservative management, Comp Cont Ed Pract Vet transport them to the liver. In the liver, fat is catabolized
13:1869, 1991. to glycerol and free fatty acids (FFAs). FFAs can be used
9. Welker B, Modransky P: Rectal prolapse in food animals. Part II:
in the citric acid cycle (Krebs cycle) as an energy source,
surgical options, Comp Cont Ed Pract Vet 14:554, 1992.
but not in the direct formation of glucose. Anorexic
animals have less ruminal substrate available for produc-
tion of the glucose precursor propionic acid. However,
DISEASES OF THE LIVER oxaloacetate, which is an integral part of the citric acid
cycle, is removed from the cycle and converted into
Liver Abscesses glucose. Depletion of oxaloacetate inhibits the normal
Liver abscesses usually occur as a result of chronic ru- citric acid cycle’s function, inhibiting the use of FFAs. As
menitis in cattle, but they are rare in sheep and goats. the pool of FFAs increases, they are converted to ketone
They can occur in feedlot lambs and kids and other bodies or repackaged into lipoproteins. Because rumi-
animals fed rations high in grain. In lambs and kids, sep- nants are not efficient at transporting lipoproteins out of
ticemia or extension of an umbilical vein infection can the liver and back to the adipose stores, the lipoproteins
cause liver abscesses.1 In most cases, however, liver ab- overwhelm the liver’s ability to handle this massive
scesses are an incidental finding. Weight loss, anorexia, buildup, resulting in a fatty liver. Because less substrate is
depression, and decreased production (growth, milk) may available for glucose formation, more oxaloacetate is “can-
occur. In adults, Corynebacterium pseudotuberculosis is the nibalized” from the citric acid cycle, further inhibiting the
most common cause. Actinomyces pyogenes and Fusobac- body’s ability to use FFAs. This in turn causes the contin-
terium necrophorum also are cultured from abscesses.1-3 ued accumulation of ketone bodies. Hypoglycemia, hy-
98 • Sheep and Goat Medicine
perketonemia, and potentially uremia and death can authors recommend immediate Cesarean section on de-
occur. pressed moribund animals (see Chapters 6 and 16). The
owner should be forewarned of the poor prognosis for
Clinical signs. Animals suffering from fatty liver or animals already in a moribund state. Fluid support during
pregnancy toxemia become anorexic and depressed, and after surgery is crucial.
display altered behavior, and become recumbent. Some Regardless of the therapeutic plan, the animal should
are constipated, grind their teeth, have a ketone smell to be offered a palatable, energy-rich, highly digestible feed-
their breath, and suffer from dystocia. Neurologic signs stuff. The keeper and clinician should take care to mini-
include blindness, circling, incoordination, star-gazing, mize the risk of a confounding disease during convales-
tremors, and convulsions.4,5 Death can occur if the condi- cence (e.g., lactic acidosis, polioencephalomalacia).
tion is left untreated. In the case of in-utero fetal death,
maternal septicemia-endotoxemia and death are common Prevention. Fatty liver and pregnancy toxemia can be
sequelae. prevented through proper nutrition. Maintaining animals
in proper body condition throughout the year and
Diagnosis. Diagnosis is based on clinical signs, the pres- making sure energy and protein levels are adequate in late
ence of multiple fetuses, and typical clinicopathologic find- gestation (see Chapter 2) are two key preventive meas-
ings. CBC results may be normal or show an eosinophilia, ures.2,4 The owner/manager should be taught to assess
neutropenia, and lymphocytosis. These animals may or body condition in individual animals and should main-
may not be hypoglycemic, but ketoacidosis, hypocalcemia, tain emergency stores of feed in case of severe weather or
and hypokalemia are common.2,4 Liver enzymes are natural disasters. The requirement for energy may be one
usually within normal limits but occasionally may be in- and a half to two times maintenance for single fetuses
creased. Azotemia, both from dehydration and secondary and two to three times maintenance for multiple fetuses.
renal disease, is a common finding, and a fatal uremia may Prevention of concurrent disease that may further in-
occur. Blood concentrations of ß-hydroxybutyric acid crease energy demands or cause anorexia (e.g., intestinal
greater than 7 mmol/L are consistent with pregnancy parasitism, foot rot) is crucial. The keeper should take
toxemia. Urinalysis will be positive for both ketones and care to increase the grain portion of the diet slowly
protein. Urine is collected from sheep by holding the because anorexia from rumen upset can lead to this
nares and from does by frightening them and then allow- disease.2 Ewes should be offered 0.5 to 1 kg of a cereal
ing them a perceived escape when they stop, squat, and grain (corn, oats, barley, or a combination) every day
void. Although not commonly performed, liver biopsy during the final months of gestation; does can be offered
1
can help determine the extent of fatty infiltration. This ⁄2 to 1 kg of grain. Keepers should maintain ewes and
syndrome must be differentiated from hypocalcemia, hy- does at a body condition score of 2.5 to 3 (see Chapter 2)
pomagnesemia, polioencephalomalacia, encephalitis, lead throughout gestation and evaluate the animals’ energy
toxicity, and cerebral abscesses. every 2 to 4 weeks.
Ultrasonography can help identify females with multi-
Treatment. Very early cases (before the animal exhibits ple fetuses. These animals should be separated into
recumbency) may be treated with oral or IV glucose. A groups and fed accordingly. Ultrasonographic determina-
balanced electrolyte solution with extra calcium (25 ml of tion of fetal numbers is best accomplished between days
a 23% calcium borogluconate per liter), potassium (10 to 45 and 90 after breeding with a 3.5 mHz transducer; a 5
20 mEq/L), and 5% dextrose is needed. In some cases, mHz transducer produces better results between days 45
sodium bicarbonate is valuable in treating acidosis (see to 50. Either type of transducer may be of value and these
Appendix II). Energy intake must be increased, and windows of time may be expanded by the ability of the
propylene glycol can be administered (15 to 30 ml every operator (see Chapter 6). Determination of fetal numbers
12 hours) as a glucose precursor. Rumen transfaunation may be enhanced by shearing the hair or fiber in front of
and supplementation with vitamin B complex (including the udder, applying a coupling substance to the skin, and
vitamin B12, biotin, niacin, and thiamine) also are recom- viewing as much of the abdomen as possible, building a
mended. After females become recumbent, treatment mental image of its structures and the number of fetuses
must be very aggressive. Removal of the fetuses is crucial while systematically moving from one side of the poste-
in these cases. Chemically inducing parturition (by ad- rior abdomen to the other.
ministering 2.5 to 10 mg of prostaglandin F2a or 0.75 Keepers and clinicians should ensure that ewes are
mg/45 kg of cloprostenol in does and 15 to 20 mg of dex- healthy and free of chronic diseases (e.g., OPP, CAE, foot
amethasone in ewes) and giving the ewe or doe medical rot, chronic parasitism) and that a good-quality trace
support (fluids, B vitamins, glucose) while waiting is a mineral salt mixture is available free choice. The addition
useful protocol in some cases. Unfortunately, during the of lasalocid (0.5 to 1 mg/kg/day) or monensin (1
time before parturition, endotoxemia from dead fetuses mg/kg/day) to the feed or mineral mixture enhances the
further compromises the female. For this reason, the formation of the glucose precursor propionic acid and
 Chapter 4 Diseases of the Gastrointestinal System • 99

improves the efficiency of feed use. However, monensin rhea; sheep may exhibit photosensitization. Clinico-
should be used with caution because toxicity may occur; pathologic findings include a macrocytic, normochromic
the agent should comprise no more than 30 ppm of the anemia and hypoproteinemia.1,2
complete diet. The inclusion of niacin (1 g/head/day) in a
feed supplement or mineral mixture helps prevent preg- Diagnosis. Abnormal serum or liver concentrations of
nancy toxemia. Supplementation with lasalocid, mon- vitamin B12 or liver cobalt are the basis of diagnosis. Liver
ensin, or niacin should begin 2 to 4 weeks before the cobalt concentrations on a dry matter basis of 0.08 
females give birth. 0.02 ppm were reported in goats with white liver disease,
Shearing in the last trimester also is recommended in compared with 0.53  0.11 ppm in controls.6
ewes.5 Many sheep producers routinely clip the wool
around the vulva. If complete body shearing is performed, Treatment and prevention. Sheep can be treated
the incidence of fatty liver or pregnancy toxemia may be with oral cobalt (1 mg/head/day) or vitamin B12 in-
decreased. Sheared sheep require less energy to walk and jections. The condition can be prevented by including
graze. Sheared ewes also tend to shiver on cold days, exer- cobalt in the ration by feeding a good-quality trace min-
cising the enzyme systems that promote the more effi- eral salt.2
cient use of FFAs as energy substrate. These ewes tend to
seek shelter during cold weather, which may decrease
lamb losses resulting from hypothermia. Obviously, if
Liver Flukes
ewes are to be shorn, keepers should make adequate Both Fasciola hepatica and Fascioloides magna can in-
shelter available. fest sheep and goats. The disease occurs along the Gulf
Keepers should avoid hauling or moving females dur- Coast and in the Pacific Northwest and Great Lakes
ing late gestation. Proper predator control measures areas.
should be maintained. Good hoof care programs should
be in place on farms or ranches where grazing is the pre- Pathogenesis. The life cycles of F. hepatica and F.
dominant form of nutrient intake. Sheep and goats magna are similar in that each requires an aquatic snail as
should have their teeth checked to ensure good dentition an intermediate host. Fluke eggs that are passed in animal
before the breeding season. Animals with poor teeth stool hatch in water to form miracidia, which penetrate
should be culled. the intermediate host. The miracidia develop through
Measuring serum b-hydroxybutyric acid concentra- several intermediate hosts to form cercariae, which
tions is useful in assessing energy status in ewes. Values of emerge from the intermediate hosts to encyst as infective
0.8 to 1.6 mmol/L suggest a negative energy balance. metacercariae on forage. Sheep or goats accidentally
Keepers should take steps to correct the problem by ingest the metacercariae, which then encyst in the small
feeding better-quality, more digestible feedstuffs. intestine. They can migrate into the liver in approxi-
mately 6 weeks and may begin to lay eggs within 3
months after infection. F. hepatica is capable of laying
White Liver Disease eggs in sheep for several years. The flukes also can
White liver disease is a form of fatty liver disease reported migrate into the bile ducts or through hepatic tissue,
only in Angora and Angora-cross goats and sheep. It is leaving large anaerobic tracts and producing acute or
associated with cobalt deficiency. chronic disease.7 Sheep and goats are definitive hosts for
F. hepatica, whereas only some species of deer and elk are
Pathogenesis. Cobalt is needed by rumen microflora to definitive hosts for F. magna. F. magna, unlike F. hepatica,
produce cyanocobalamin, or vitamin B12, which is a co- never matures and continues to migrate, causing severe
enzyme for methylmalonyl-CoA mutase. In turn, this damage and death.7,8 F. magna does not complete its life
enzyme is needed to convert propionate to glucose cycle in sheep or goats. The most serious complication of
through the Krebs cycle. Cobalt deficiency leads to the ac- acute liver fluke infestation is black disease (Clostridium
cumulation of methylmalonyl-CoA, or methylmalonic novyi), which presents as sudden death.
acid, which is converted to branched chain fatty acids that
accumulate in the liver.2,6 High-grain diets that are fer- Clinical signs. F. hepatica infestation usually causes
mented to propionate coupled with deficient or marginal acute disease in sheep and goats but can present as a
cobalt intake may predispose to this condition.2,6 White chronic condition. Chronic disease is the result of the
liver disease has not been reported in the United States, mature flukes in the bile ducts and is manifested in de-
but ill thrift from cobalt deficiency has been observed. It is pressed growth and milk production. Acute disease oc-
therefore possible that the disease goes unrecognized.1 curs when large numbers of immature flukes migrate at
once, particularly in animals with limited immunity to
Clinical signs. Signs are most commonly seen in flukes. Signs include anorexia, depression, weakness,
young animals, and include ill thrift, anorexia, and diar- dyspnea, anemia, ascites, colic-like signs, dry feces, and
100 • Sheep and Goat Medicine
sudden death. The clinical signs are identical to those of tions in successive years. Decreasing exposure is the key
nematode infestations (i.e., chronic weight loss, ill thrift, to control. Eliminating the snail is impractical, but
diarrhea, anemia, hypoproteinemia). Similar but more fencing off low-lying areas may prevent ingestion. De-
severe signs occur with F. magna infection, which is pending on local fluke life cycles, keepers should avoid
usually fatal.2,5,8 grazing animals on areas with high fluke populations
during peak infection times. Areas where water stands or
Diagnosis. Antemortem diagnosis of fluke infestation flows over grazing pastures, streams, and irrigation
can be difficult. Finding eggs in feces is diagnostic for F. ditches (particularly those with clay soil) are high-risk
hepatica. Eggs are only produced by adults and not in zones.
great numbers, so a negative fecal test cannot preclude
acute or chronic fascioliasis. Fluke eggs do not float in
routine fecal flotation methods used for nematode diag-
Cysticercosis
nosis; a sedimentation technique should be used for sus- Cysticercus tenuicollis is the larval stage of the dog tape-
pected fluke infestations. To perform a sedimentation worm Taenia hydatigena, of which sheep and goats are in-
test, the clinician mixes 2 to 3 g of feces with 200 ml of termediate hosts. The larval stage migrates through the
tap water and strains the mixture through a tea strainer liver, then attaches to the liver or other abdominal organs
into a beaker. The sediment can be examined 15 minutes and causes black, winding tracts and cysts in the liver.
later under a dissecting microscope. Eggs are light yellow Acute disease occurs only with large numbers of cysticerci
to golden and have an operculum at one end (see Figure and is characterized by depression and weakness resulting
4-10). F. magna does not mature, so eggs are not pro- from liver damage. The chronic cystic stage is usually
duced and fecal examination is of no value. Most fluke in- asymptomatic. No treatment is available and control is
festations are discovered by finding the flukes at necropsy problematic because it requires treating infestation in
or slaughter. An ELISA test may be available in the dogs and preventing contact with dogs.1,2,5
future.2,5,8 CBCs of affected animals may indicate
eosinophilia and anemia. Increased liver enzymes and hy-
poalbuminemia also are occasional findings.
Copper Toxicosis
Pathogenesis. Copper (Cu) toxicosis is more common
Treatment. Because antemortem diagnosis is difficult, in sheep than in goats. Goats appear closer to cattle than
the clinician should institute fluke treatment after ruling sheep in their ability to store and handle Cu and resist
out other differential diagnoses if the possibility of fasci- toxicosis. Toxicity results from chronic accumulation in
oliasis exists. If fascioliasis is diagnosed at necropsy, the the liver from the ingestion of excess Cu in relation to
remaining animals in the herd should be treated. Because molybdenum (Mo) or sulfate in the diet. In sheep, a Cu-
flukicides available in the United States are highly effec- to-Mo ratio greater than 101 leads to the accumulation
tive only against mature flukes, the timing of treatment is of excess Cu. The most common sources of excess Cu in
important. In the southern portions of North America sheep and goats are trace mineral mixtures and feeds for-
the snails are ingested in the spring and the flukes mi- mulated for cattle or horses. Clinical signs are often absent
grate in the summer and mature in the fall. In cooler, during the chronic accumulation phase. Acute disease is
northern climates, snails may remain active during sum- seen when Cu is suddenly released from the liver in large
mer, so flukes can mature in the fall and into the winter. amounts. Stress usually precipitates this acute phase.
Clinicians should begin treatment in the southern United Acute release and subsequent high blood Cu concentra-
States in the late summer or early fall. A single treatment tions cause an acute hemolytic crisis, resulting in anemia,
in late winter or early spring is commonly used in the hemoglobinuria, and acute renal failure. Existing hepatic
northern climates of North America. Albendazole (15-20 disease (such as that caused by liver flukes) may predis-
mg/kg orally) and clorsulon (7 mg/kg orally, 2 mg/kg SC) pose animals to this condition. Some breeds seem to be
are very effective against adult F. hepatica.2,9,10 Clorsulon prone to Cu absorption and storage problems (Merino
has no efficacy against nematode parasites but is highly sheep), whereas others tend to be more resistant and
efficacious against both adult and late-stage immature prone to deficiency (pygmy goats) (see Chapters 2 and 3).
flukes. Albendazole (15 mg/kg orally) is somewhat useful
in controlling F. magna at 8 weeks after infestation, and Clinical signs. Anorexia, depression, diarrhea, and
clorsulon is effective only at very high dosages.11-13 Un- weakness are all signs of Cu toxicity. Many affected
fortunately, neither agent can kill 100% of F. magna, and animals are found dead with hemolysis and icterus. Signs
only a few remaining flukes can be fatal. of abdominal pain and diarrhea are sometimes present.
Port wine–colored urine is evidence of hemoglobinuria.
Prevention. Control of fluke infestations is difficult, al- Hemoglobinemia produces icterus of the mucosal
though timely treatment of animals can decrease infec- membranes and fever.
 Chapter 4 Diseases of the Gastrointestinal System • 101

Diagnosis. On clinicopathologic examination, anemia,

Toxic Hepatitis
hemoglobinemia, hyperbilirubinemia, increased liver Pathogenesis. The liver is vulnerable to toxic insult
enzymes, and azotemia are present. Urinalysis reveals because one of its major functions is detoxification. The
hemoglobinuria and isosthenuria. The combination of most common plants that are gastrointestinal and liver
azotemia and isosthenuria indicates acute renal failure. toxins are shown in Table 4-5. Clinical signs depend on
Definitive diagnosis of acute disease requires measure- the cause. Acute, severe toxicity is more common with
ment of Cu concentrations in serum. Normal blood Cu chemical toxicosis, whereas plant toxins usually cause
concentrations are approximately 50 to 200 mg/dl in chronic disease. A thorough history is important and in
sheep and goats.2,5,14 These concentrations increase 10- many cases inspection of the animals’ environment is
to 20-fold with an acute hemolytic crisis.5 On necrop- required.
sy, kidney Cu concentrations are the most diagnostic
because liver concentrations may be normal from release Clinical signs. The clinical signs of toxic hepatitis can
into the bloodstream. Generally kidney concentrations be vague. Animals may only show anorexia and depres-
greater than 100 ppm and liver concentrations greater sion. Icterus is more common with hemolytic diseases
than 350 ppm on a dry matter basis are diagnostic.2,5 If and is not always seen with liver disease. Photosensitivity
tissue copper is reported in wet weight, the conversion to is a common clinical feature in ruminants and hepatoen-
dry tissue weight can be estimated by multiplying the cephalopathy also can occur.
tissue concentration by a factor of 3.5
Diagnosis. Clinicopathologic data are more helpful in
Treatment. Treatment of acutely affected animals is diagnosing acute toxicity. Serum AST and LDH levels
often futile. It consists of supportive therapy for the acute can increase with hepatocellular necrosis but are not liver-
renal failure and anemia and attempts to lower liver Cu specific, so muscle injury and disease must be ruled out.
stores. Fluid therapy for the acute renal failure (see Ap- These enzymes also increase if serum is not separated
pendix II) is of therapeutic value, and a blood transfusion from a blood clot in a timely fashion.1 Increased levels of
may be needed if the PCV drops precipitously. Ammo- alkaline phosphatase (AP) and GGT indicate biliary
nium tetrathiomolybdate (1.7 mg/kg IV or 3.4 mg/kg SC stasis. AP also is not liver-specific, but increased serum
on alternate days for three treatments) is the most eco- levels of GGT are very specific for liver disease. GGT
nomical agent for treatment for acute cases. In valuable also increases in some hepatocellular diseases, so testing
animals, D-penicillamine (26 to 50 mg/kg BID or 52 for its normal concentrations is important.15 Unfortu-
mg/kg SID PO for 6 days) increases urinary Cu excre- nately, all of these enzymes can be normal with liver
tion. Trientine is used in human beings, but has shown disease, especially if it is chronic. Hyperbilirubinemia, hy-
variable results in sheep.15 Treatment of the remainder of poglycemia, low blood urea nitrogen (BUN), and hypoal-
the flock should include the administration of ammo- buminemia are not always evident as classically taught. If
nium molybdate (50 to 500 mg/head/day PO) and hepatoencephalopathy is suspected, blood ammonia con-
sodium thiosulfate (300 to 1000 mg/head/day PO) for 3 centrations may be elevated. Blood ammonia analysis
weeks.15 Stress should be minimized, so keepers and cli- may be impractical in the field because the blood should
nicians should delay routine maintenance procedures be kept on ice, and the test should be performed within
such as deworming and hoof trimming until after treat- 30 minutes of collection. To enhance the accuracy of
ment. The offending source of Cu should be eliminated. blood ammonia analysis, the clinician should collect
blood from a normal control animal for comparison.
Prevention. Avoiding high dietary Cu (more than 10 Ammonia concentrations three times those of the control
ppm), a high Cu-to-Mo ratio (greater than 101) in the animal are diagnostic.16 Liver biopsy remains the most
feed, Cu-containing foot baths, and other sources of Cu valuable tool in diagnosing liver disease. Although clot-
is crucial. Including supplemental Mo in the diet to lower ting dysfunction may occur in liver disease, it is an un-
the Cu-to-Mo ratio to 61 to 81 is beneficial. This re- common complication in ruminants and should not dis-
quires 2 to 6 ppm of Mo in many instances. Often too courage the clinician from performing a liver biopsy.
much emphasis is placed on the trace mineral component
of the diet. The clinician should be aware that even if no Treatment. If the intoxication is caught in the acute
Cu is added to the trace mineral mixture and the element stage, activated charcoal (500 g per adult animal) can be
does not appear on the product label, the mineral mixture given. Supportive care, especially fluid support with dex-
may still contain Cu. Many components of mineral mixes trose solutions, is the mainstay of therapy. Low-protein
are contaminated with Cu (zinc sulfate may contain 400 diets may suppress ammonia production temporarily, but
ppm of Cu, dicalcium phosphate may contain more than they can be detrimental over time depending on the pro-
30 ppm of Cu). Therefore the clinician needs to perform duction status of the animal. If photosensitization occurs,
a dietary analysis to find and correct the problem. animals should be housed indoors if possible, and broad-
102 • Sheep and Goat Medicine
TABLE 4-5

PLANTS CAUSING GASTROINTESTINAL OR HEPATIC DISEASE

PLANT COMMENTS SIGNS

Cocklebur Erect annual herbage in sandy soils, flood Within hours to days of ingestion—
plains, and overgrazed pastures; seeds are anorexia, vomiting, colic, dyspnea,
toxic gastroenteritis, chronic hepatitis, hepatic
damage, death
Senico-groundsel, Pyrrolizidine alkaloid; excreted in milk and Dullness, weakness, weight loss, icterus,
Crotalaria, heliotropism, urine and can cross placenta; young more fibrosis, hepatocytomegaly, bile duct
amsinckia (fiddleneck), susceptible proliferation, photosensitivity;
echium subcutaneous edema, diarrhea
Lantana Found in sandy, tropical areas; berries, Chronic toxicity—slow hepatic failure;
leaves, and hay are toxic icterus, photosensitization, weakness,
bloody diarrhea, cholestasis, hepatic
toxicity
Sneezeweed, bitterweed, Grows in overgrazed pastures; all parts of Acute toxicity—gastrointestinal upset,
rubberweed plant are toxic depression, serous nasal discharge,
salivation, bloat; chronic toxicity—
vomiting, bittermilk lesions, hepatic and
renal congestion, gastric edema, aspiration
pneumonia; pulmonary edema
Cabbage, kale, rape, Remove from diet; add iodine to diet (for Gastroenteritis, hepatic necrosis, photo-
mustard, wild goiter) sensitization, goiter, hemolysis
mushroom
Horsebrush Stop grazing, keep animals indoors Bighead, itching, uneasiness, inflamed eyes,
blindness, serum discharge from scabs;
degenerative changes in liver and elevated
liver enzymes
Clover (crimson, red, Photosensitization
subterranean burclover)
St. John’s wort Perennial herb; grows along roadsides and Increased respiration, diarrhea, pruritus,
in overgrazed fields; remove from diet and dermatitis, diarrhea, death
keep animals in shade

spectrum (systemic or topical) antibiotics may be neces- drome).1 This is a genetically recessive condition. It is
sary to control secondary bacterial dermatitis. Corticos- characterized by an abnormality in the excretion of con-
teroids (dexamethasone 0.1 to 1 mg/kg IV or IM) may jugated bilirubin and phylloerythrin and is often seen in
be indicated in early cases of photosensitization to de- animals consuming green forage. Clinical signs include
crease inflammation. Neurologic signs can be controlled anorexia, photodermatitis, and icterus. Liver biopsy of af-
with phenobarbital (initial dose: 10 to 20 mg/kg IV fected animals reveals dark to black granules in otherwise
diluted in saline and administered over 30 minutes; sub- normal hepatocytes. The syndrome first manifests itself
sequent doses: 1 to 9 mg/kg IV diluted in saline, as in lambs around 5 months of age.18
needed up to TID). Diazepam (Valium) is contraindi- A similar condition occurs in Southdown lambs
cated in hepatoencephalopathy because it may worsen around 6 months of age (Gilbert’s syndrome). This too is
signs.17 a recessive condition that causes decreased hepatic uptake
of phylloerythrin and bilirubin, with concurrent renal
failure.18 Signs include icterus, photodermatitis, and ul-
Miscellaneous Liver Diseases ceration around the ears and mouth. A liver biopsy
Congenital hyperbilirubinemia, or black liver disease, reveals normal hepatic tissue. In both of these conditions,
occurs in mutant Corriedale sheep (Dublin-Johnson syn- animals should be kept out of sunlight and fed minimal
 Chapter 4 Diseases of the Gastrointestinal System • 103

TABLE 4-5

PLANTS CAUSING GASTROINTESTINAL OR HEPATIC DISEASE—cont’d

PLANT COMMENTS SIGNS

Blue-green algae Toxic after a bloom Vomiting, diarrhea, liver failure, photo-
sensitization; necropsy findings include
swollen bloody liver, edema around
gallbladder, centrolumbar apoptosis, and
necrosis
Pokeweed Vomiting, cramps, diarrhea, weakness,
dyspnea, prostration, tremors, convulsions
Gossypol (cottonseed) Toxicity seen in younger pre-ruminants Poor performance, convulsions, cardiac
toxicity
Rhubarb Contains oxalic acid Gastrointestinal toxicity
Oak Acorns and oak buds are most toxic Abdominal pain, pseudomembranes in
gastrointestinal tract, bloody diarrhea,
depression, renal toxicity
Castor bean Beans most toxic Gastrointestinal irritation, bloody diarrhea,
central nervous system disturbances
Mistletoe Berries not toxic Nausea, diarrhea
Others:
English ivy
Sesbania
Narcissus
Elderberry
Spurge
Buckwheat
St. Anne’s lace
Milkweed
Parsley, giant hogweed

amounts of green forage. Obviously, affected animals 5. Kimberling CV: Jensen and Swift’s diseases of sheep, ed 3, Philadel-
should be neutered or culled. phia, 1988, Lea & Febiger.
Various tumors of the liver, including fibrosarcoma, 6. Johnson EH et al: Hepatic lipidosis associated with cobalt defi-
ciency in Omani goats, Vet Res Commun 23(4):215, 1999.
lymphosarcoma, and cholangiocellular carcinoma, have
7. Craig TM: Epidemiology of internal parasites: effects of climate
been reported.17,18 The use of ultrasonography and ultra-
and host reproductive cycle on parasite survival, Proceedings of the
sound-guided liver biopsy may aid in diagnosis. Small Ruminants for the Mixed Animal Practitioner, Western Veteri-

R EFERENCES
1. Fetcher A: Liver diseases of sheep and goats, Vet Clin North Am:
nary Conference, 1998, Las Vegas, NV.
8. Wescott RB, Foreyt WJ: Epidemiology and control of trematodes
in small ruminants, Vet Clin North Am: Food Anim Pract 2:373,
1986.
Large Anim Pract 5:525, 1983.
9. Foreyt WJ: Efficacy and safety of albendazole against experimen-
2. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea
tally induced Fasciola hepatica infections in goats, Vet Parasit 26(1-
& Febiger.
2):261, 1988.
3. Santa Rosa J et al: A retrospective study of hepatic abscesses in
10. Rehbein S, Visser S: Efficacy of an injectable ivermectin/clorsulon
goats: pathological and microbiological findings, Br Vet J
combination against Fasciola hepatica in sheep, Vet Rec
145(1):73, 1989.
145(16):468, 1999.
4. Parson EG, Maas J: Hepatic lipidosis. In Smith BP, editor: Large
animal internal medicine, ed 2, St Louis, 1996, Mosby.
104 • Sheep and Goat Medicine
11. Foreyt WJ, Foreyt KM: Albendazole treatment of experimentally are useful in females and some males. However, urine
induced Fascioloides magna infection in goats, Agri-Practice, p scalding of the skin may occur in some males. Clinicians
1441, Sept 1980. should closely monitor animals that have undergone
12. Conboy GA, Stromberg BE, Schlotthauer JC: Efficacy of clorsu-
clamping.
lon against Fascioloides magna infection in sheep, J Am Vet Med
Assoc 192(7):910, 1988.
13. Foreyt WJ: Evaluation of clorsulon against Fascioloides magna in
Surgical resection. In cases in which the hernial ring is
cattle and sheep, Am J Vet Res 49(7):1004, 1988. larger than 5 cm, surgical intervention should be carried
14. Kaneko JJ: Clinical biochemistry of domestic animals, ed 4, San out. Animals can be sedated and then infiltrated with a
Diego, CA, 1989, Academic Press. local anesthetic or placed under general anesthesia. The
15. Plumlee KH: Metals and other inorganic compounds. In Smith area around the hernia is clipped and surgically prepared.
BP, editor: Large animal internal medicine, St Louis, 1996, Mosby. The clinician opens the hernial sac and introduces a
16. Roussel AJ, Whitney MS, Cole DJ: Interpreting a bovine serum finger into the abdomen to ensure that no viscera have
chemistry profile: Part I, Vet Med, 92:553, 1997. adhered to the inner lining of the ring and that no en-
17. Divers TJ: Therapy of liver failure. In Smith BP, editor: Large larged or infected umbilical remnants are present. He or
animal internal medicine, St Louis, 1996, Mosby.
she then carefully excises the ring and closes the defect in
18. Ogilvie TH: Large animal internal medicine, Baltimore, 1998,
the abdominal wall. This closure can be made by simply
Williams & Wilkins.
opposing the abdominal wall with a horizontal mattress
pattern stitch (absorbable suture). An alternate closure of
PATHOLOGY the abdominal wall is to suture the peritoneal lining in a
separate pattern and close the abdominal wall defect so
OF THE UMBILICUS one side of the defect is pulled to overlap the other side.
The upper free edge is sutured to the opposite wall with a
Umbilical Hernia near-far-far-near pattern. The authors choose not to
The umbilicus is an opening in the ventral abdominal employ surgical techniques that slow this procedure. The
wall that allows passage of the umbilical vessels and allan- subcutaneous tissue can be closed with simple interrupted
toic stalks. This opening should close within a few day of pattern using absorbable suture and the skin should be
birth. The failure of this opening to close properly is closed with whatever pattern the clinician prefers.
termed umbilical hernia. The hernial sac has an inner Animals should be given tetanus prophylaxis and antibi-
peritoneal layer and an outer layer of skin. These hernias otics. They should be closely monitored for signs of sepsis
are probably of genetic origin but may occur as sequelae and surgical failure. Exercise should be limited for 7 to 14
to umbilical remnant infection. The opening in the ab- days after surgery.
dominal wall is perceived as a ring on palpation. If the cli-
nician can insert more than one finger into the hernial
ring or if the hernia persists for more than 3 to 4 weeks,
Umbilical Infections
surgical intervention is indicated. Infections of the umbilical arteries (omphaloarteritis) and
veins (omphalophlebitis) and urachal disease can occur
Penning. Clamps or rubber bands may be of value for because of failure or partial failure of passive transfer of
closing small hernias (those less than 4 cm in diameter). colostral antibodies and subsequent sepsis. Contamina-
The clinician should either lightly sedate the animal or tion of the umbilicus, retracting of these structures after
infiltrate the skin around the hernia with a local anes- stretching and breaking, and chemical damage (from
thetic (2% lidocaine). The animal should be placed on its strong tincture of iodine) to the amniotic remnants are
back and held by a technician-helper. Any viscera pro- other possible causes.1,2,3 Dipping the umbilicus with
lapsing into the hernial sac should be replaced into the iodine or iodine-chloriodine substances is a common
abdomen. The clinician then inserts two metal pins practice. Aggressive use of these chemicals may precipi-
(baby diaper pins can be used) through the skin and on tate serious inflammation of the cord. Excessive torsion
opposite sides of the hernial ring, just on the edge of the of the umbilical cord, distention of the proximal urachus,
linea alba. The pins should be placed deep enough to sit and some genetic factors may all be associated with
next to the abdominal wall. Slight tension is placed on patent urachus, which also may occur as a sequela to om-
the skin in the center of the umbilical sac, pulling it away phaloarteritis or omphalophlebitis.
from the abdomen. When the clinician is confident that
all viscera have been cleared from the hernial sac, he or Clinical signs and diagnosis. The clinical signs
she places an elastrator band between the pins and the include umbilical swelling, pain, and occasionally
abdominal wall. This results in ischemic necrosis of the drainage or discharge of the umbilical stump. Palpation
skin. The skin will slough and the abdominal defect will and transabdominal ultrasonographic evaluation reveal an
heal in 7 to 14 days. Lambs should be given tetanus pro- enlarged cord-like structure ascending from the umbili-
phylaxis. This procedure and other clamping techniques cus cranially (umbilical vein) or caudally (urachus or um-
 Chapter 4 Diseases of the Gastrointestinal System • 105

bilical artery). Ultrasonographic evaluation may indicate nants. As with urachal surgery, the abdomen should be
an abscess or thickened tissue. Patent urachus is associ- opened lateral to the umbilicus. Depending on the sever-
ated with dermatitis, urine scalding of the ventral abdo- ity of infection and the amount of tissue involved, the cli-
men, and urine dribbling. If the urachus becomes infected nician may need to perform extensive dissection of
it may leak urine intraperitoneally or subcutaneously. necrotic tissue and possibly intestinal resection.3
Both of these developments may be identified with ab- If the infection of the umbilical vein extends to and in-
dominal palpation, ballottement, ultrasonographic evalu- volves the liver, marsupialization of the umbilical vein is
ation, and, when indicated, paracentesis.1 The CBC may an effective method of therapy.2,3 The clinician can pull
indicate neutrophilia. Blood culture is indicated if sepsis the vein to the most cranial portion of the abdominal in-
occurs simultaneously. Occasionally infection of the in- cision and suture it to the muscle layers and skin before
ternal structures may occur with no outward umbilical closing the abdomen as described for umbilical hernia
swelling. Deep abdominal palpation and/or the use of repair. However, a preferable method is to close the ab-
real-time ultrasound are necessary to attain a diagnosis. dominal wall, pull the transected umbilical vein through,
Animals with umbilical infections also may have signs of and suture it to a separate stab incision. This may help
septicemia, anorexia, depression, joint distention, and minimize the incidence of abdominal wall herniation.
fever. Only monofilament, absorbable, non-gut suture material
should be used.3 The venous stump should be flushed
Treatment. If a patent urachus occurs without inflam- daily with antiseptic solution (1% chlorhexidine, 0.1%
mation of the associated tissues, it can be cauterized daily povidone iodine), and the animal should be maintained
with iodine or silver nitrate. However, if it remains patent on antibiotics for more than 14 days. The venous stump
for more than 5 days, it should be surgically closed. The usually closes within a month.3
animal should be placed under general anesthesia (see
Chapter 16). The area around the umbilicus should be Prevention. Umbilical infections can be prevented or
clipped and surgically prepared, and the animal should be drastically reduced by ensuring adequate intake of good-
placed on a broad-spectrum antimicrobial agent 2 to 4 quality colostrum. Lambs and kids also should be only
hours before surgery. The clinician opens the abdomen minimally stressed (particularly during the first 2 to 3
lateral to the umbilicus and digitally explores the adjacent days of life) to enhance colostral absorption. In some
area for adhesion formation. The urachus should be iden- management scenarios, proper dipping of the navel with
tified and followed to the urinary bladder. After this, the non-caustic materials also helps reduce the incidence of
clinician should amputate the urachal attachment to the this disease.
bladder and close the bladder with a double-layered in-
verting pattern (Cushing). The abdominal wall, subcuta-
neous tissue, and skin are closed as described for umbili-
cal hernia repair.
R EFERENCES
1. Lofstedt J: Neonatal conditions, with emphasis on equine neonate.
On occasion some cases of omphalophlebitis-om-
In Ogilvie TM, editor: Large animal internal medicine, Baltimore,
phaloarteritis can be treated medically. Prolonged antibi- 1998, Williams & Wilkins.
otic therapy with a broad-spectrum antimicrobial agent 2. Rings DM: Umbilical hernia, umbilical abscess, and auricle fistula,
(ceftiofur 2.2 mg/kg SID or oxytetracycline 20 mg/kg SC Vet Clin North Am: Food Anim Pract 11:137, 1995.
every 72 hours) may be attempted. However, if medical 3. Hooper RN: General surgical techniques for small ruminants: Part
therapy is ineffective, the infected umbilical remnants II, Proceedings of the Small Ruminants for the Mixed Animal Practi-
should be marsupialized or excised. The authors prefer tioner, Western Veterinary Conference, 1998, Las Vegas, NV.
more aggressive, surgical removal of the umbilical rem-
 Chapter 5

DSystem
iseases of the Respiratory

ELLEN B. BELKNAP

EVALUATION OF THE border is found at the sixth rib, the middle of the thorax is
at the seventh rib, and the caudal border is at the eleventh
RESPIRATORY SYSTEM rib. Auscultation is much easier in goats than in sheep,
but by taking the time to part the wool for greater
History contact, a skilled clinician can achieve good auscultation
While watching and assessing the patient, the clinician in both species. Eliminating as much excess noise in the
should obtain a thorough history, including the duration barn as possible produces better results with this diagnos-
of any problems, exposure to other animals, recent move- tic tool. Normal breath sounds are loudest over the
ment, previous vaccinations and treatments, responses to trachea and base of the lung, but upper respiratory condi-
treatment,1 and number of animals affected. Given ap- tions often result in more abnormal sounds in the trachea.
propriate attention, the history alone may pinpoint the In addition, abnormal sounds may be referred from
diagnosis.2,3 disease within the thorax. However, by localizing the site
of maximal loudness, the clinician can assign the origin of
the abnormal noise to the upper or lower respiratory
Physical Examination tract. Normal breath sounds are loudest on inspiration
Watching the animal from a distance is crucial to evaluat- because it is an active process compared with passive ex-
ing the respiratory system as part of the physical exami- piration. Abnormal sounds include crackles, which are
nation. The animal’s attitude and appearance give clues to caused by the opening of closed airways, and wheezes,
its health. The clinician can make a more accurate assess- which are whistling, squeaking sounds caused by the vi-
ment of the animal’s resting respiratory rates and better bration of airway walls or narrowed airways with air
evaluate the breathing pattern by observing from a dis- going through them.4,5 The clinician should perform
tance. A clinician may note stridor (inspiratory dyspnea) deep palpation over the trachea to assess whether a cough
before even seeing the animal, whereas an exaggerated can be elicited and characterized. The thorax also may
expiratory effort may imply lower respiratory disease. be percussed, although this is more difficult in sheep
Any nasal discharge should be noted. The clinician than in goats. Pleural friction sounds, which are caused
should observe other animals in the herd to assess by the rubbing of altered pleural surfaces, may occur
whether any others are displaying clinical signs of disease, during both inspiration and expiration, but they are rarely
respiratory or otherwise. Close attention should be given auscultated.
to the inspection of the nose, oral cavity, nasal cavity and
sinuses, larynx, trachea, and thorax. Observation, palpa-
tion, percussion, and auscultation all may be employed in
Diagnostics
this inspection. Complete blood count. A complete blood count
(CBC) with a fibrinogen concentration may be useful in
evaluating the type of disease process and the severity of
Auscultation inflammation. Sheep and goats typically do not experi-
Sheep and goats have 13 ribs, which are used by clinicians ence dramatic increases in white blood cell counts during
to define the lung borders. That is, the cranial ventral bacterial infections, but counts greater than 20,000
• 107 •
108 • Sheep and Goat Medicine
cells/ml are usually significant. During acute inflamma- lected, the PE tubing may be advanced and the procedure
tory or infectious processes, a left shift of neutrophils may repeated.
be observed; such a shift is classified as regenerative when
mature neutrophilia coexists and as degenerative with Radiographs. Radiography is a helpful diagnostic indi-
concurrent neutropenia. An understanding of this re- cator that, along with the evaluation of clinical signs, can
sponse can be helpful in monitoring the progression of be used to determine the efficacy of therapy. For example,
the condition, especially in cases of septicemia with a de- the discovery of pulmonary abscesses during radiography
generative left shift. Neutropenia is rare in goats. Fi- warrants a graver prognosis and may indicate the neces-
brinogen responses in ruminants are dramatic and may be sity of a change of therapy. Skull radiographs may be in-
the only observable abnormalities in some inflammatory dicated for intranasal masses, pharyngeal swellings, nasal
conditions. foreign bodies, and cases of severe sinusitis. Many of the
techniques used for other small animals can be applied to
Thoracocentesis. Thoracocentesis is indicated in sheep and goats.
animals with pleural effusion. The use of real-time ultra-
sonography may help guide needle placement, but simply Sinus centesis. Sinus centesis may be diagnostic as
inserting the needle into the seventh intercostal space at well as therapeutic. The clinician clips and aseptically
the costochondral junction level or higher usually works prepares the area, infiltrates the skin and subcutaneous
well. After clipping and surgically preparing the site and tissue with a local anesthetic (2% lidocaine, 0.5 ml), and
infusing a local anesthetic, the clinician should insert then makes a stab incision with a sterile scalpel blade. Al-
the biopsy needle (18-gauge, 3 to 10 cm) just off the ternatively, a Steinmann pin can be used to drill a small
cranial border of the rib to avoid intercostal vessels and hole. Samples should be appropriately taken for cytology
nerves. or culture and lavage should be performed using either
PE tubing or a “tom cat” catheter (if future treatments
Nasal swab. Collecting a nasal swab specimen for virus are required).
isolation is useful if no animals are available for necropsy.
Either a Dacron- or cotton-tipped swab may be used. Ultrasound. Examination of the chest with real-time
The clinician should wipe the external nares with a paper ultrasonography is helpful to evaluate the presence and
towel before inserting the swab and rotating it fairly extent of pleural effusion, pleural fibrin deposits and ad-
vigorously to obtain mucosal cells. The swab should be hesions, atelectasis, consolidation, and some abscesses.
broken above the tissue culture media so as to not Ultrasound also may be used as a guide in thoracocentesis
contaminate the media. Most diagnostic laboratories and lung biopsy. Goats are better subjects than sheep for
provide veterinarians with viral transport media that can ultrasonography because they typically have less body
be kept frozen until needed. Most transport media are fat (Figure 5-1). During real-time ultrasonography the
supplemented with antibiotics, but this should not pre- pleura and superficial lung surfaces may be visualized.
clude clean technique by the clinician attempting virus Moreover, consolidated lung parenchyma provides a
isolation. better acoustic medium and is often well visualized. Pul-
monary abscesses that extend to the surface of the lung
Tracheal sampling. The clinician may use either a may be detected by ultrasonography (Figure 5-2). Diag-
transtracheal wash or an endoscope-collected sample to nostic ultrasonography is more sensitive than radiography
culture pathogens from the lower respiratory tract. A in detecting small amounts of pleural fluid. As the
small endoscope (8 to 9 mm) may be passed through the echogenicity of the fluid increases, the cellular and pro-
nasal passages of adult small ruminants. If this is not pos- tein content of the fluid also increases.
sible, the endoscope can be passed orally with the aid of
a wooden mouth speculum and mild sedation. Transtra- Blood gas analysis. Depending on the age of the
cheal fluid collection may be performed by clipping and animal, an arterial blood gas sample may be taken from the
aseptically scrubbing the middle third of the neck, infil- femoral, auricular, or brachial artery using a heparinized
trating the skin and subcutaneous tissue with local anes- syringe.2 The sample should be sealed with a tube stopper
thetic (2% lidocaine, 0.5 ml), and making a stab incision after the air has been evacuated from the syringe. Analysis
with a scalpel throughout the skin and subcutaneous of the sample may determine whether ventilatory assis-
tissue. The clinician then inserts a 14-gauge needle or tance is required. Hypoxemia (PaO2 less than 85 mm Hg)
trocar through the trachea and sterilely passes tubing may result from hypoventilation, diffusion impairment,
(220 polyethylene [PE]) to a point just past the tracheal ventilation-perfusion mismatch, or right-to-left shunting
bifurcation. Endoscopic visualization of the PE tubing of blood. Not all animals will benefit from the administra-
and pockets of fluid can enhance sample collection. tion of oxygen or assisted ventilation, so it is important
The clinician should inject sterile isotonic solution that the clinician interpret the blood gas results accurately
(20 ml) through the tubing and immediately retrieve and use them in conjunction with other diagnostic tests to
the fluid with continuous suction. If little fluid is col- determine appropriate treatment.
 Chapter 5 Diseases of the Respiratory System • 109

A B

C D

Figure 5-1 Ultrasound image of a normal caprine thorax (A), a normal ovine thorax (B), and a caprine
thorax with pneumonia (C and D) using a 3 MHz probe. Dorsal is to the right and ventral is to the left in the
ultrasounds. The arrows point to the pleural surface. (Courtesy Dr. Margaret Blaik, Auburn, Alabama.)

An ultrasound-guided biopsy at the ninth intercostal

space, approximately 11 cm ventral to the dorsal midline,
may be attempted.6 The clinician then makes a small stab
incision through the anesthetized area using a sterile
scalpel blade, advances a sterile biopsy instrument (14-
gauge), and collects the sample. The procedure can be
performed safely with experience and may help differen-
tiate inflammatory, allergic, emphysematous, edematous,
and neoplastic changes.7

R EFERENCES
1. De Las HM et al: Evidence for a type D-like retrovirus in enzootic
nasal tumour of sheep, Vet Rec 132:441, 1993.
2. Pringle JK: Ancillary testing for the ruminant respiratory system,
Vet Clin North Am 8(2):243, 1992.
3. Pringle JK: Assessment of the ruminant respiratory system, Vet Clin
Figure 5-2 Radiograph of a kid with bronchopneumonia. Note the North Am 8(2):233, 1992.
air bronchograms. 4. Curtis RA et al: Lung sounds in cattle, horses, sheep and goats, Can
Vet J 27:170, 1986.
5. Kotlikoff MI, Gillespie JR: Lung sounds in veterinary medicine.
Lung biopsy. Obtaining a percutaneous lung biopsy is Part I. Terminology and mechanisms of sound production, Comp
not without risks, but it may be beneficial in establishing Cont Ed Pract Vet 5(8):634, 1983.
a diagnosis. As with thoracocentesis, the clinician clips 6. Braun U et al: Ultrasound-guided percutaneous lung biopsy in
and aseptically prepares the skin over the seventh inter- sheep, Vet Rec 146:528, 2000.
costal space and anesthetizes the skin and subcutaneous 7. Braun U et al: Percutaneous lung biopsy in cattle, J Am Vet Med Assoc
tissue (2% lidocaine, 0.5 to 1.0 ml subcutaneously [SC]). 215:679, 1999.
110 • Sheep and Goat Medicine
UPPER RESPIRATORY DISEASES dorsal midline of the dorsum of the face and reflects the
skin flaps. The surgeon then makes another I-shaped in-
Enzootic Nasal Tumor cision into the nasal bones, reflects the nasal bones with
Pathogenesis. Enzootic nasal tumors of sheep and the periosteum, and removes the nasal septum.7 The mass
goats may be unilateral or bilateral conditions; they cause can then be easily accessed and removed. Gauze soaked in
progressive inspiratory dyspnea.1 The tumors originate 1:100,000 epinephrine is used to assist hemostasis. This
from the olfactory mucosa of the ethmoid or nasal procedure can be accompanied by significant blood loss,
turbinates, and their etiology is thought to be associated so a donor animal should be available. Without treat-
with a type D/B retrovirus.2,3 Enzootic tumors have been ment, most affected animals die within 90 days of the
experimentally transmitted from sheep to sheep and goat onset of clinical signs.5,6
to goat.4 Their incidence is sporadic but because they
occur in related flocks they do indicate an enzootic
problem.5 Sheep and goats as young as 15 and 7 months,
Oestrus ovis Infestation
respectively, have been diagnosed with these tumors.1,6 Pathogenesis. The adult Oestrus ovis fly deposits larvae
around the animal’s nostrils. The larvae then migrate up
Clinical signs. Affected animals present with copious the nasal passage into the dorsal turbinates and sinuses,
seromucous to mucopurulent nasal discharge and stridor. where they develop for weeks to months before coming
Exercise intolerance, facial asymmetry, anorexia, head out to pupate on the ground. Few or no signs are associ-
shaking, sneezing, decreased air flow, exophthalmos, and ated with initial infestation, but infestation with subse-
open-mouth breathing have all been reported.6 The quent generations of flies produces excessive clinical
tumor is locally invasive, obliterating the airway, but is signs, probably as a result of a hypersensitivity reaction.
rarely metastatic (Figure 5-3). Erosion of maxillary and
other skull bones and invasion of the orbit may occur oc- Clinical signs. The animal may develop a secondary
casionally.1 Initially, the lesions are small nodules, but bacterial infection and possibly sinusitis. Irritation from
they grow into mucoid, nodular cystic masses that can the adult fly can result in shaking of the head, rubbing of
occlude the caudal nasal cavity and sometimes the the nose, and stomping of the feet—all of which decrease
pharynx or larynx.5 Inflammatory polyps may be present grazing time. Infestation of the nasal cavity with the
in the adjacent nasal cavity.3 larval (bot) stage irritates the tissues, causing rhinitis,
sneezing, mucopurulent nasal discharge, stridor, and de-
Diagnosis. A preliminary diagnosis of a nasal mass is creased airflow (Figure 5-4).8 Both sheep and goats may
made by observation of clinical signs along with percus- be affected, although goats usually acquire the infection
sion of the sinuses. Endoscopy or radiography may be from sheep and have milder clinical signs. Occasionally,
helpful in defining the mass, but only biopsy can confirm secondary interstitial pneumonia will develop.
the diagnosis of an enzootic tumor. Histologically, these
tumors are classified as adenomas, adenopapillomas, and Diagnosis. Endoscopy is helpful in making a diagno-
adenocarcinomas. In goats the tumor tends to originate sis, and radiographs may demonstrate mineralized bots.
from the serous gland cells, whereas in sheep the tumor is The copious nasal discharge of affected animals contains
thought to arise from Bowman’s gland.1 numerous eosinophils and mast cells.

Treatment. Treatment, if warranted, is surgical re- Treatment. Ivermectin (200 mg/kg SC) is used in the
moval. The surgeon makes an I-shaped incision over the late summer to prevent the buildup of heavy infestations

Figure 5-3 Nasal adenocarcinoma. Note the dark mass at the Figure 5-4 A ewe with an Oestrus ovis infestation. Notice the
nares. nasal discharge.
 Chapter 5 Diseases of the Respiratory System • 111

and again in the winter to kill overwintering larvae. An- bandages should be removed in 5 to 7 days, depending
tibiotics may be of some value in treating secondary on the size of the dehorning site and the cleanliness of
pneumonia, but clearing the nasal passages of the bots is the bandage.
usually all that is required.
Pharyngitis
Sinusitis Pathogenesis. Inflammation of the pharyngeal area
Pathogenesis. Inflammation of the paranasal sinuses is usually results from trauma caused by dosing equipment,
an infrequent finding in sheep and goats, but it should be rough feed, or foreign objects. Continued use of older
considered in cases of obvious drainage from previous de- plastic balling guns, specula, and stomach tubes allows
horning sites or facial deformity and swelling. Most the sheep or goat to chew and make the surface even
often, the frontal and maxillary sinuses are involved. more traumatic. Foreign objects that cause swelling
Frontal sinus infections usually occur in animals with a include antibiotic or anthelmintic boluses, wire, and plant
history (weeks to months) of dehorning, whereas maxil- awns. Common organisms associated with disease
lary sinusitis is most commonly observed secondary to include Actinomyces pyogenes, Fusobacterium necrophorum,
tooth problems. Inflammation of both sinuses may occur and Corynebacterium pseudotuberculosis. Mild lesions may
as a sequela to nasal bot infestation, nasal adenocar- resolve on their own. More severe lesions may progress to
cinoma or other neoplasia, facial fractures, and horn abscesses, granulomas, and severe cellulitis (phlegmon).
injuries.
Clinical signs. Clinical signs include coughing, obvi-
Clinical signs. Clinical signs include drainage from a ously painful swallowing, nasal discharge, and anorexia or
dehorning site, facial asymmetry or bulging, softening of only wanting to drink. The animal’s breath may have a
facial bones, nasal discharge, unequal airflow from nos- foul odor and the animal may stand with its head and
trils, foul odor, head shaking or rubbing, head and neck neck extended. Drooling, fever, dehydration, and aspira-
extension, and head resting or head pressing.9 Non- tion pneumonia also may be noted. Stridor may be pro-
specific signs include pyrexia, lethargy, and anorexia. nounced with more obstructive lesions. Depending on
Neurologic signs may be present in chronic cases and the the amount of swelling, the pharynx may be occluded.
animal may hold its head at an abnormal angle or squint Visual inspection of the oral cavity is difficult, but the cli-
its eyes. nician may be able to note hyperemia, swelling, exudate,
food material, and possibly foreign bodies.
Diagnosis. Diagnosis is usually made by clinical signs,
but radiographs or sinus centesis may be helpful. Percus- Diagnosis. External palpation of the pharyngeal area
sion over the affected sinus to detect resonance also may generally induces coughing and a painful response.
aid diagnosis. An oral examination is useful to define Culture of purulent drainage or abscesses can be done, al-
lesions of the teeth or pharyngeal abnormalities. Culture though contamination is difficult to avoid. Radiography
and sensitivity of the purulent material may assist in or endoscopy may be required to diagnose the lesion
treatment. definitively.

Treatment. Lavaging the affected sinus daily with a Treatment. Treatment may include use of nonsteroidal
0.1% chlorhexidine in saline solution using a teat can- antiinflammatory drugs (NSAIDs) and broad-spectrum
nula or French catheter may be helpful. If the animal has antibiotics. Tube feeding and oral administration of an-
systemic signs, the clinician may administer procaine tibiotics should be avoided. A temporary rumen fistula is
penicillin G (22,000 IU/kg twice a day [BID]), flunixin sometimes placed to ensure adequate nutrition. Pharyn-
meglumine (1.1 mg/kg intravenously [IV] or intramus- geal abscesses may be drained into the pharyngeal area
cularly [IM] BID), or ketoprofen (3.0 mg/kg IV or IM and, if possible, flushed with a dilute Betadine (0.1% to
once a day [SID]). Even though the two sinuses usually 0.2%) in saline solution.
communicate, the frontal sinus of the mature sheep or
goat is very compartmentalized, making treatment diffi-
cult. For this reason the clinician may need to drill nu-
Retropharyngeal Abscesses
merous holes into the sinus. The clinician should pack Abscesses of the retropharyngeal lymph nodes may occur
gauze or other material into the sockets of extracted secondary to pharyngeal pathology or result from infec-
teeth to avoid food material contamination. Treatment tion with Corynebacterium pseudotuberculosis. Stridor,
may take as long as 2 weeks to heal the animal. In severe coughing, and difficulty swallowing may be observed.
cases the sinus infection may extend into the calvaria and These abscesses are usually not lanced or lavaged because
result in meningitis. Bandaging the heads of sheep and of the potential to spread the organism. Surgical removal
goats after dehorning may help prevent sinusitis. The is possible but difficult because of the importance of
112 • Sheep and Goat Medicine
avoiding the jugular vein, carotid artery, and vagus nerve. 8. Baker JC: Ruminant respiratory system. In Smith BP, editor: Large
Moreover, reports have described a false carotid aneurysm animal internal medicine, Philadelphia, 1996, WB Saunders.
in sheep resulting in severe inspiratory dyspnea.10 9. Ward JL, Rebhun WC: Chronic frontal sinusitis in dairy cattle: 12
cases (1978-1989), J Am Vet Med Assoc 201:326, 1992.
10. Rings DM, Constable P, Biller DS: False carotid aneurysm in a
Necrotic Laryngitis sheep, J Am Vet Med Assoc 189:799, 1986.
11. Johnson R et al: Nasal squamous-cell carcinoma in a sheep, Mod
Necrotic lesions of the larynx may be caused by Fusobac- Vet Pract 63:897, 1982.
terium necrophorum. The organism is ubiquitous, but re- 12. Lane JG et al: Laryngeal chondritis in Texel sheep, Vet Rec 121:81,
quires a perforated mucous membrane to gain entrance to 1987.
the laryngeal tissue and produce inflammation and necro- 13. Jackson PG et al: Tracheal collapse in a goat, Vet Rec 119:160,
sis of the larynx. Clinical signs include a moist, painful 1986.
cough; inspiratory dyspnea; difficulty swallowing; and 14. Scarratt WK, Bradley RL, Booth LC: Collapsed trachea in two
salivation. Although necrotic laryngitis is a common calves, Comp Cont Ed Pract Vet 7:S49, 1985.
problem in calves, it is not frequently seen in sheep and
goats. It is more common in animals that are housed
indoors or kept in crowded feedlots.
TYPICAL PNEUMONIAS
Pasteurellosis
Laryngeal Chondritis The pneumonic form of pasteurellosis is the most
Laryngeal chondritis has been described in Texel common and is regarded as one of the most important in-
sheep.11,12 Affected animals exhibit increased upper res- fectious bacterial diseases of sheep and goats.1-3 Pas-
piratory noise, dyspnea, and some cyanosis. Endoscopy is teurella haemolytica is a normal inhabitant of the upper
helpful to observe edema and suppuration of the ary- respiratory tracts of sheep and goats. Most cases of pas-
tenoid cartilage. It is thought that the short head charac- teurellosis are caused by P. haemolytica type A, but P. mul-
teristic of this breed may predispose to the disease. The tocida also has been implicated.4 P. haemolytica has two
treatment is the same as for affected horses—removal of biotypes, A and T, that differ morphologically, biochemi-
the affected laryngeal cartilage. cally, biologically, and serologically. Colonies of biotype A
are usually small and gray, whereas biotype T colonies are
larger (2 mm in diameter) and have brown centers5; both
Tracheal Collapse are gram-negative coccobacilli. Biotype A is responsible
Usually considered a congenital defect, tracheal collapse for pneumonic pasteurellosis and also may cause sep-
is characterized by stridor, exercise intolerance, and ticemia in young lambs. Serotype A2 is the most
coughing. In a case reported in a 4-month-old goat, the common isolate in ovine pneumonic pasteurellosis.6,7
kid was smaller than its litter mates but displayed no signs Biotype T has been isolated from cases of pneumonia and
at rest.13 A tentative diagnosis may be made by observing septicemia in older lambs.8 On the basis of surface anti-
the clinical signs and palpating a collapsed trachea, but gens the biotypes are divided into 17 different serotypes.9
radiographs or endoscopy may be necessary for confirma-
tion in some cases. Surgical correction is possible with the Pathogenesis. P. haemolytica produces a number of vir-
use of prosthetic tracheal rings.14 ulence factors, including lipopolysaccharide (LPS), or
endotoxin, which is considered of primary importance

R EFERENCES
1. De Las HM, Garcia de Jalon JA, Sharp JM: Pathology of enzootic
in inducing early pulmonary pathophysiologic changes
and stimulating immune responses in vaccines.10 Stress
in the form of transport, bad weather, poor ventilation,
intranasal tumor in thirty-eight goats, Vet Path 28:474, 1991. nutritional imbalances, parasitism, confinement, han-
2. De Las HM et al: Evidence for a type D-like retrovirus in enzootic dling, and weaning may be involved in the etiology of
nasal tumour of sheep, Vet Rec 132:441, 1993. pneumonic pasteurellosis. Predisposing agents include
3. DeMartini JC, York DF: Retrovirus-associated neoplasms of the parainfluenza-3, adenovirus type 6, respiratory syncytial
respiratory system of sheep and goats, Vet Clin North Am 13:55, virus, Chlamydia, Bordetella parapertussis, and Mycoplasma
1997. ovipneumoniae.11 Stress and either viral-viral or viral-
4. De Las HM et al: Experimental transmission of enzootic in-
bacterial synergism work in concert to overwhelm the
tranasal tumors of goats, Vet Path 32:19, 1995.
host’s defense mechanisms, allowing secondary or oppor-
5. McKinnon AO et al: Enzootic nasal adenocarcinoma of sheep in
Canada, Can Vet J 23:88, 1982.
tunistic invaders (e.g. Pasteurella) to enter the respiratory
6. Rings DM, Rojko J: Naturally occurring nasal obstructions in 11 tract.
sheep, Cornell Vet 75:269, 1985. Experimental inoculation of lambs with P. haemolytica
7. Trent AM, Smart ME, Fretz PB: Surgical management of nasal alone or in combination with adenovirus type 6 of P13
adenocarcinoma in sheep, J Am Vet Med Assoc 193:227, 1988. may cause severe respiratory disease.8-10,12 Combined in-
 Chapter 5 Diseases of the Respiratory System • 113

fections may result in early death or slow resolution of

lesions. More consistent results are obtained when P.
haemolytica is administered 6 to 8 days after the virus.12 P.
haemolytica alone may cause an acute serofibrinous pneu-
monia and pleuritis resulting in death or rapid recovery
depending on the severity of the serofibrinous pneumo-
nia.9 Intratracheal injection of LPS from P. haemolytica
A1 results in an acute fibrinopurulent pneumonia, indi-
cating that LPS contributes to the pathogenesis of
P. haemolytica infection in the lungs.10 The use of dexa- Figure 5-5 A set of lungs and liver from an animal with septicemic
pasteurellosis.
methasone alone to mimic stress was insufficient to pro-
duce infection or pneumonic lesions without another
form of stress (e.g., transport) on an animal that was
previously experimentally challenged intranasally with P.
haemolytica A2.13
Inoculation of goats with P. haemolytica either IV or by
an intratracheal route resulted in consolidated pulmonary
lesions and some fibrinous lesions.14 Certain unknown
factors may be involved in the predilection of P. haemolyt-
ica to colonize the lungs because IV inoculation of other
gram-negative organisms in cattle does not result in pul-
monary deposition.15 Although P. haemolytica has been
isolated from tonsillar tissue in cattle and sheep, intraton-
sillary inoculation of P. haemolytica does not result in pul-
monary lesions.14 Figure 5-6 A set of lungs with Pasteurella pneumonia.
Clinical signs. Septicemia (Figure 5-5), arthritis, and
otitis media may occur secondarily to the pneumonia.
Outbreaks can occur, usually involving one particular peritoneal cavities. Lesions within the lungs consist of
serotype, in any age, breed, or sex. Springtime outbreaks areas of consolidation with one or more foci of necrosis
are most often associated with severe weather and gener- surrounded by hemorrhage.9 Hydropericardium can some-
ally involve nursing lambs 2 weeks to 2 months of age and times be seen. Histopathologic examination may reveal
some ewes. In the fall, outbreaks generally occur in 5- to pneumonitis with multifocal areas of acute fibrinopu-
7-month-old lambs after shipment to feedlots. Morbid- rulent bronchopneumonia, coagulative necrosis, and fibri-
ity rates may reach 50%, but mortality rates are generally nous pleuritis.8 Often areas of necrosis are surrounded
low. Transmission is by inhalation of droplets from car- by masses of basophilic spindle-shaped leukocytes called
riers or direct contact. Nursing lambs may be infected oat cells; their presence is considered by some to be pathog-
by ewes with P. haemolytica mastitis. Goats are suscep- nomonic for pasteurellosis. A tentative diagnosis can be
tible to pneumonic pasteurellosis under natural condi- made with a history of stress, clinical signs of acute bron-
tions.16 One study7 found that of all the pneumonic le- chopneumonia, and the presence of gross lesions at
sions of goats discovered at necropsy, 20% were caused by necropsy. Isolation of P. haemolytica is confirmatory.13
P. multocida.
The first sign of pneumonia may be sudden death. Treatment. Most cases respond to treatment with
Other early clinical signs include fever (105° to 108° F), long-acting oxytetracycline (20 mg/kg SC every 48 to 72
depression, anorexia, weight loss, isolation from the flock, hours).8 Medication of entire flocks is achieved by ad-
mucopurulent nasal discharge or lacrimation, tachy- ministering sulfonamides in the drinking water or orally
pnea, coughing, and increased lung sounds (crackles and (200 mg/kg/day followed by 66 mg/kg daily for 4 days).
wheezes). The disease course is usually 12 hours to 3 Ampicillin and penicillin have been reported to be effec-
days, with recovery occurring in 14 to 20 days. Outbreaks tive. Tylosin (10 to 20 mg/kg), ceftiofur (2.2 to 4.4 mg/kg
may last 1 month. Chronically affected lambs and kids IM or IV every 24 hours), and florfenicol (20 mg/kg IM
have reduced lung capacity, reduced weight gain, and de- every 48 hours) may be used as well. Tilmicosin (10
creased feed efficiency; death is possible.8 mg/kg SC) can be effective in some sheep but should be
avoided in goats.17
Diagnosis. Necropsy of affected animals reveals a sec-
ondary fibrinopurulent pleuropneumonia (Figure 5-6), Prevention. Pneumonia can be prevented by minimizing
with excess serous fluid often present in the pleural and stress and instituting vaccination programs. Susceptibility
114 • Sheep and Goat Medicine
to bacterial infections is at its highest 7 days after viral respi- charge. Body temperature is usually not elevated. The
ratory infection because viral lung titers are declining, pul- disease is more common in lambs younger than 1 year.
monary antiviral antibody titers are peaking, alveolar
macrophages contain peak levels of viral antigen, and the Diagnosis. Diagnosis of PI3 infection is made by iso-
antibacterial activity of the macrophages is severely im- lating the virus from nasal swabs from animals that have
paired.18 Vaccinating with a modified live virus (MLV) been infected for less than 1 week or by measuring sero-
product for bovine herpesvirus 1 (BHV1), parainfluenza-3 logic responses.
(PI3), and bovine respiratory syncytial virus (BRSV) before
shipping to the feedlot may decrease mortality compared Prevention. Protection against experimental and
with nonvaccinated lambs.19 Additional vaccination with a natural cases of pneumonic pasteurellosis by use of a live
Hemophilus somnus bacterin does not appear to increase the intranasal PI3 vaccine has been demonstrated.26-30
level of protection afforded by the MLV vaccine alone. A
vaccination study evaluating the efficacy of a killed P.
haemolytica serotype A1 and A2 vaccine resulted in an out-
Adenovirus
break of primarily pneumonic P. multocida, suggesting that The adenoviruses are deoxyribonucleic acid (DNA)
vaccines for pasteurellosis need to contain antigens afford- viruses. Many different antigenic types exist in rumi-
ing cross-protection against both species and numerous nants.24 Depending on which of the six serotypes is
serotypes.20,21 causing infection, seroprevalence of a flock may range
A later study evaluated a vaccine containing whole cell from approximately 7% to 83%.24,31,32 Although aden-
antigens of P. haemolytica A1 and another containing P. ovirus has been isolated from sheep with respiratory
haemolytica A1 cell surface and leukotoxin antigens. disease, the importance of the virus is not completely
Neither agent provided any clear evidence of a lower rate under-stood. However, it is thought to cause mild respi-
of pneumonia compared with nonvaccinated control ratory disease that increases in severity with concurrent P.
lambs.20,22 Another study found that the most wide- haemolytica infections.26,33 The virus is most often iso-
spread serotype (A2) is not very immunogenic in lated from young lambs with respiratory and enteric
lambs.2,23 The only Pasteurella species vaccines available disease.33
for use in sheep and goats are the whole cell bacterins,
which are generally considered ineffective. Clinical signs. Clinical signs are mild and include
Stress can be induced by many risk factors. Minimiz- pyrexia, anorexia, sneezing, serous nasal discharge, and
ing climatic changes, reducing overcrowding, decreasing pneumonia. Experimental challenge with adenovirus may
transportation, minimizing improper ventilation, and result in a proliferative bronchiolitis and an anteroventral
eliminating major fluctuations in diet can all help de- bronchopneumonia.
crease risk factors known to place more stress on the res-
piratory system. Diagnosis. Diagnosis of adenovirus infection is by
virus isolation from nasal swabs or paired serologic
testing, if available.
ACUTE RESPIRATORY VIRUSES
In all acute respiratory viral pneumonias, therapy should Prevention. No vaccines are used for this virus in the
be directed at preventing or treating secondary bacterial United States.
pathogens and providing supportive measures to help de-
crease the debilitating effects of these diseases.
Respiratory Syncytial Virus
BRSV, a pneumovirus of the family Paramyxoviridae, is
Parainfluenza Type 3 an important respiratory virus of cattle that also has been
PI3, which is a member of the paramyxovirus family, is a implicated in cases of respiratory disease in sheep and
ribonucleic acid (RNA) virus. The one serotype of PI3 goats. The importance of RSV as a primary cause of res-
that infects sheep is related to but distinct from the PI3 piratory disease in sheep and goats is equivocal and many
that infects cattle and human beings.19 Most infections are researchers believe it is of greater importance as a predis-
inapparent because more than 70% of sheep are seroposi- posing pathogen to secondary bacterial pneumonia.
tive for PI3,24 but outbreaks have been reported with high Questions remain about possible interspecies transmis-
rates of morbidity. Although respiratory syncytial virus sion. Prevalence studies have reported 42% of 447 free-
(RSV) and adenoviruses may predispose to pneumonic ranging bighorn sheep and 52.5% of 378 ewes to be
pasteurellosis, PI3 appears to be more important.25 seropositive to BRSV.24,34
Recent studies have suggested the existence of two ru-
Clinical signs. Clinical signs include frequent cough- minant subgroups of RSV, with one subgroup represent-
ing, serous nasal discharge, and occasional ocular dis- ing RSV isolated from calves and goats and the other rep-
 Chapter 5 Diseases of the Respiratory System • 115

resenting RSV obtained from sheep.35 Radiolabeled Prevention. To date no RSV vaccines have been mar-
probes based on differences in the G glycoprotein genes keted for sheep and goats. Identification of viral sub-
were used to characterize the genetic heterogenicity of groups is important for vaccine development so that all
the various ruminant RSV isolates by the ribonuclease subgroups may be included for protection against all pos-
protection assay. Previous reports had suggested that sible strains an animal may encounter.
some ovine RSV isolates should be considered distinct
RSVs based on reverse transcriptase polymerase chain re-
action (RT-PCR) and DNA hybridization using primers
Ovine and Caprine Herpesvirus
and a probe to the fusion (F) protein messenger RNA Caprine herpesvirus (CHV) has been isolated in lung and
(mRNA) of BRSV.36 An RSV-specific whole virus nasal swabs of goats during outbreaks of pneumonia in
enzyme-linked immunospecific assay (ELISA) and a which P. haemolytica also was isolated.50 The specific role
peptide-based ELISA were used to demonstrate anti- of CHV in caprine or ovine pneumonia has been ques-
RSV activity in the majority of sera from sheep, goats, tioned, although some reports describe it as a cause of
cattle, and human beings, whereas antibodies specific to rhinitis, vulvovaginitis, and abortion in adult goats.51,52
BRSV were found in all cattle and the majority of goats Both BHV1 and CHV can infect cattle and goats, but
tested.37 The role of maternal antibodies in ruminant their pathogenicity is restricted to the natural host.51 Pre-
RSV infections is controversial, with some demonstrating vious reports evaluating herpesvirus isolates taken from
a protective effect and others apparently predisposing to sheep and goats with various problems determined by re-
clinical disease and viral shedding.38 striction endonuclease analysis and radioimmunoprecipi-
Experiments have shown that the ovine isolate of tation that the isolates were more closely related to BHV1
RSV, when inoculated in a challenge model, causes mild than CHV.53 Experimental challenge with CHV induced
primary pneumonia in lambs, with lung lesions similar to a clinical rhinitis with histopathologic lesions of tracheitis.
those described in naturally occurring epizootic pneumo- However, none of the challenged goats became severely
nia in sheep.38,39 Pulmonary lesions in lambs experimen- ill.54 Although it may not lead to serious disease, CHV can
tally infected with BRSV are not as pronounced, with less proliferate in the upper respiratory tracts of goats.54 Ovine
peribronchial and perivascular lymphoid accumulation herpesvirus-1 has been isolated from cases of ovine pneu-
and collapse of airways.40-42 The loss of cilia and cell monia.55 Lambs inoculated experimentally with CHV de-
necrosis identified in experimental disease in lambs are veloped subclinical pneumonia with interstitial changes in
thought to lead to decreased efficiency of mucociliary the lungs; after a later administration of corticosteroids,
clearance and predispose to secondary bacterial pneumo- the virus was re-isolated, indicating that the virus may go
nia.43 Other studies have reported a synergistic effect of into a latent state.56 These authors propose that CHV may
RSV and P. haemolytica in experimental challenges in be associated with ovine pulmonary carcinoma.
lambs.44-46 Experimental infection of lambs with BRSV
and RSV-specific antibodies did not influence the sever-
ity and duration of clinical disease, titer of virus shed, or
Mycoplasma Pneumonia of Sheep
humoral and cellular immune responses compared with Mycoplasma pneumonia also is known as enzootic pneumo-
single inoculation with BRSV, although the duration of nia, chronic nonprogressive pneumonia, and atypical pneu-
viral shedding was prolonged.47 The virus has been re- monia. Typically, Mycoplasma ovipneumoniae is thought to
ported as causing acute respiratory disease with a high be the primary organism, with P. haemolytica A, other
rate of mortality in goats,48 although most keepers report Mycoplasma organisms, and Chlamydia psittaci ovis being
mild respiratory disease unless the condition is compli- secondary invaders.2,57
cated by P. haemolytica A.49
Pathogenesis. As with the bovine respiratory disease
Clinical signs. Clinical signs observed in goats with complex, stress and minor viral pathogens may predispose
RSV include anorexia, pyrexia, conjunctivitis, cough, to Mycoplasma pneumonia. The disease occurs in inten-
tachypnea, and tachycardia. Auscultation may reveal in- sively reared lambs that live in areas with poor ventilation
creased bronchial sounds and possible crackles. Friction and in assembled groups of lambs in feedlots; it most
rubs may be auscultated in cases of mixed infection. commonly develops as maternal antibody levels wane.
Reservoirs such as older animals and convalescent adults
Diagnosis. Necropsy of affected animals may reveal infect lambs mainly after weaning. Encapsulation allows
diffuse interstitial pneumonia and firm, edematous lungs. the organism to evade the host’s immune response and
The presence of syncytial cells on histopathologic exami- promotes long-term colonization of the upper respiratory
nation is characteristic of RSV infection. Immunoperoxi- tract.58 Goats also may be affected.59 Transmission is by
dase staining of tissues may indicate RSV antigen in the the respiratory route (contact or aerosol) and results in
epithelial cells of the alveolar and bronchial walls and in ciliostasis and production of an exudate that allows bacte-
syncytial and alveolar lumens.49 rial colonization of the lungs (e.g., with P. haemolytica).57
116 • Sheep and Goat Medicine
The Mycoplasma component of the disease is thought to
Mycoplasma Pneumonia in Goats
restrict the lethality of the Pasteurella. The most important Mycoplasma groups that infect rumi-
nants in known as the Mycoplasma mycoides cluster. It con-
Clinical signs. The disease is mild and is characterized sists of M. mycoides subspecies mycoides small colony, M. my-
by chronic coughing and dyspnea on exertion. Mucopu- coides subspecies mycoides large colony, M. capricolum
rulent nasal discharge, fever, and depression may be ob- subspecies capripneumoniae, M. mycoides subspecies my-
served when Pasteurella is involved. Productivity is usually coides, M. mycoides subspecies capri, M. capricolum sub-
decreased. High morbidity and low mortality rates are species capricolum, and bovine serogroup 7.67 Differentia-
generally associated with this nonprogressive, often sub- tion between members of this cluster by conventional
clinical, condition.60 methods can be difficult, and specific diagnosis may rely on
PCR.68 Immunohistochemical methods using monoclonal
Diagnosis. Diagnosis is based on the presence of mild, antibodies are useful for diagnosing specific strains of the
chronic pneumonia in lambs younger than 1 year. Lesions M. mycoides cluster.69,70 Greater success in isolating the or-
at necropsy include consolidation of the cranial lobes ganism is attained in more acute cases, whereas chronic in-
(and occasionally the anterior border of caudal lobes) fections result in less successful isolation.71 ELISA is re-
with pleuritis. Consolidated areas may be gray to red- ported to be useful for diagnosis.72 Neither M. mycoides
brown with red atelectatic areas and firm, gray-white subspecies capri or M. capricolum subspecies capricolum
nodules on the cut surface. An interstitial, cuffing-type occur in the United States.
pneumonia with nodular lymphoid hyperplasia, bronchi- M. mycoides subspecies mycoides large colony (Mmm)
olar epithelial hyperplasia, and mononuclear lymphocytic was first reported on the East Coast of the United States
cuffs around bronchioles and blood vessels is seen on in 196973 and is now prevalent throughout the
histopathologic examination. Alveoli contain exudate country.74,75 It has been isolated in several countries in
consisting mostly of macrophages and few neutrophils. A ovine and caprine species and is associated with low mor-
characteristic feature is the presence of nodular hyaline tality rates.76
“scars” in the bronchiolar walls. Pleuritis may occasionally
occur with this disease. The characteristic lesions seen on Pathogenesis. Asymptomatic lactating does act as car-
necropsy and histopathology confirm the diagnosis. An riers, shedding the organism in their milk.75 In one out-
immunoperoxidase staining of formalin-fixed, paraffin- break, as many as 1  107 to 1  108 colony-forming
embedded sections for detection of either antigen has units of the organism were shed in each milliliter of
been described.61 Culture of the organism in broth me- colostrum or milk, resulting in the death of 200 kids.76
dia is diagnostic, as is detection of antibodies by an The organism is transmitted orally to the kids through
ELISA.62,63 However, cross-reactivity among different Myco- the ingestion of contaminated milk or colostrum. Trans-
plasma species has created concern about the ELISA’s mission among adults is thought to involve the external
specificity.64 auditory meatus, which has been determined to be a
source of numerous Mycoplasma organisms, of which
Treatment. Treatment with oxytetracycline (20 mg/kg Mmm was the predominant isolate.74 Ear mites
SC every 48 to 72 hours), tilmicosin (10 mg/kg SC), and (Psoroptes species) are thought to serve as vectors for My-
florfenicol (20 mg/kg IM every 48 hours) can be effective coplasma organisms.77 Experimentally, infected fleas of
in eliminating the infection. Some in vitro studies also in- the order Siphonaptera have been reported to transmit
dicate that enrofloxacin may be effective.65 Mmm to susceptible kids. M. mycoides subspecies mycoides
small colony, the causative organism of contagious bovine
Prevention. Prevention and control rely on reducing pleuropneumonia, has been isolated from the milk of
the density of housed lambs, ensuring adequate ventila- goats showing clinical signs of pneumonia.78 Interstitial
tion, and separating batches of assembled lambs. No pneumonia lesions were observed on necropsy, with pri-
vaccine is available. mary lesions occurring at the apical, cardiac, and di-
M. ovipneumoniae and Mycoplasma arginini have been aphragmatic lobes. Hypertrophy of the mesenteric lymph
isolated from young lambs with a chronic “coughing syn- nodes was evident. Experimental studies demonstrate the
drome.” It is thought that failure of the immune response hematogenous spread of the organism and the severe
and chronic persistence of M. ovipneumoniae may play a pathogenicity of Mmm (regardless of the route of inocu-
role in this condition.66 A large number of lambs with the lation), suggesting that natural infection may occur by
disease had autoantibodies in their serum that reacted any route. Occasionally, M. capri has been isolated from
with cilia of the upper respiratory tract.66 A syndrome of cases of caprine pneumonia, although its significance is
severe paroxysmal cough leading to rectal prolapse and uncertain.71,79 Experimental inoculation of goats with M.
poor weight gain is widespread in the midwestern United capri isolates from natural pneumonia and pleuropneu-
States; it produces variable severity and morbidity.64 monia cases resulted in severe respiratory disease and
 Chapter 5 Diseases of the Respiratory System • 117

death.28 Experimental inoculation of kids with M. capri- results. Infected does may be culled or isolated and
colum subspecies capricolum resulted in diffuse interstitial milked separately or last. In clinically normal carrier does,
pneumonia, congestion, and edema, but no signs of pleu- environmental stress (weather changes) appears to be an
ropneumonia.29 M. capri, M. capricolum subspecies capri- important factor in the predisposition to clinical disease.
colum, and Mmm were administered by different routes to Kids born to infected does should be separated immedi-
12 kids, and although the former two organisms are not ately after birth, fed heat-treated colostrum, and then fed
present in the United States at this time, all three pro- pasteurized goat milk, cow milk, or milk replacer. Trans-
duced mycoplasmosis and severe lesions detectable by mission also may occur among does at milking; therefore
immunohistochemistry; Mycoplasma antigens were estab- teat dipping of does and the wearing of gloves by milkers
lished as the cause.80,81 are essential. Milkers should use individual paper towels
to dry teats. A killed vaccine has been reported to prevent
Clinical signs. Adult goats typically display fever, pleu- experimental infection.87 In the midst of an outbreak the
ropneumonia, mastitis, and polyarthritis, whereas com- use of chlortetracycline or tetracycline as a feed supple-
mon signs in kids include septicemia, meningitis, and ment may minimize the spread of the disease.
arthritis.82,83 One outbreak was characterized by increas-
ed cases of mastitis and increased morbidity and mortality
of kids up to 2 months of age. Affected kids suffered from
Contagious Caprine Pleuropneumonia
pyrexia and acute death, neurologic disease and death, or The causative organism of contagious caprine pleuro-
pyrexia and pneumonia, with most dying within 3 to 5 pneumonia (CCPP) is the F38 biotype of Mycoplasma,
days of respiratory signs.61 Pyrexia, leukopenia, and coag- recently reclassified as M. capricolum subspecies capri-
ulopathies are observed with septicemia in goats.82 In pneumoniae.67,88-90 This specific Mycoplasma is very con-
herds with endemic infection, the primary complaint may tagious in housed goats. Morbidity is usually 100% and
be of increased kid morbidity with pneumonia and poly- mortality may range from 60% to 100%. Only goats are
arthritis. Milking herd exposure may result from the pur- naturally infected.
chase of an infected doe and may produce mastitis and
abortions before the kids exhibit problems.84 Clinical signs. Clinical signs include pyrexia, cough,
dyspnea with accompanying grunting, wide-based fore-
Diagnosis. Diagnosis is made by the discovery of limb stance, anorexia, and listlessness. Death may occur
lesions at necropsy. These include acute fibrinous pneu- within 2 days.91
monia and pleuritis, suppurative polyarthritis, periarthri-
tis, osteomyelitis, myocarditis, renal infarction, and Diagnosis. On necropsy the lung lobes (unilateral or
lymphadenitis.71 bilateral) are enlarged, firm, and variegated with red,
yellow, white, and gray foci.92 A fibrinous pleuritis and
Treatment. Treatment may help decrease clinical signs pleural effusion are generally present, with occasional
of the disease, but the prognosis is poor and treatment may pericarditis.71 Although it is occasionally seen in North
not eliminate the carrier state. Recovered animals gener- America, the disease is prevalent in Africa, Asia, and
ally continue shedding the organism for life. The My- eastern Europe. In North America the disease is inappro-
coplasma organisms are generally sensitive to tetracyclines priately diagnosed as other mycoplasmal pneumonias
(oxytetracycline 10 mg/kg IV BID or long-acting oxytet- of the goat. A latex agglutination test has been developed
racycline 20 mg/kg SC or IM every 48 to 72 hours) and to diagnose CCPP in the field, whereas conventional
macrolides (20 mg/kg IM BID), but not beta-lactams. methods or PCR and restriction enzyme analysis may be
used in the laboratory.93,94
Prevention. Maintenance of a closed herd is the sim-
plest way to avoid introducing Mycoplasma into a flock or Treatment. Treatment early in the course of the disease
herd.85,86 After it is present in a herd, preventive practices consists of the administration of tylosin (20 mg/kg IM
should focus on milking practices and management of every 12 hours), enrofloxacin (5 mg/kg IV or IM SID),
kids. Routine culturing of milk to identify infected does is lincomycin (10 to 20 mg/kg IM every 12 to 24 hours), or
imperative to prevent further infection. Initially, bi- tetracycline (20 mg/kg SC every 48 to 72 hours).95 Goats
monthly cultures should be taken from each doe until no that survive the acute phase may have chronic lesions, but
new cases are discovered for two consecutive cultures. a carrier state does not appear to exist among long-term
After that, monthly samples can be taken for 2 to 3 survivors.96
months, followed by pooled samples for 6 months. Tank
samples should be collected and frozen weekly; the Prevention. Prevention may be afforded through the
keeper or clinician should investigate any increase in use of vaccines and the maintenance of closed herds.97,98
somatic cell counts or California mastitis test (CMT) In the midst of an outbreak, the use of chlortetracycline
118 • Sheep and Goat Medicine
or tetracycline as a feed supplement may help minimize Clinical signs. Clinical signs are usually seen in 2- to
the spread of the disease. 4-year-old sheep, although the virus may infect younger
sheep. Progressive respiratory distress and weight loss are
the common clinical signs.107 When infected sheep are
Chlamydia forced to exert themselves, auscultation of the respiratory
Pneumonia caused by Chlamydia psittaci, an obligate in- tract reveals harsh respiratory sounds on inspiration and
tracellular bacterium, is relatively rare in sheep and expiration and occasionally crackles and wheezes. Tachy-
goats.99 Its occurrence is generally linked to animals that pnea is a consistent finding, whereas coughing is incon-
have or have had polyarthritis or abortions. The incidence sistent. Lowering the head or raising of the rear limbs of
of pneumonia caused by Chlamydia in goats was found to the sheep usually produces a flow of accumulated fluid
be only 6.4% (14 of 218) in a study from India.79 In from the nostrils. Most animals are not febrile and con-
calves, chlamydial infection is reported to enhance the tinue to eat unless a secondary bacterial pneumonia
severity of P. haemolytica.100 exists. The course of the disease is progressive and death
usually occurs within weeks or months of the appearance
Clinical signs. Clinical signs may include depression, of clinical signs.108
pyrexia, a dry hacking cough, nasal discharge, dyspnea,
and diarrhea.101 Chlamydia may be identified by observ- Diagnosis. Necropsy of animals with OPC, SPA, or
ing the organism in stained impression smears or fixed jaagsiekte reveals heavy lungs that exude clear fluid from
tissue sections by indirect immunofluorescence, Gimenez the cut surface and clear, foamy fluid from the trachea.109
stain, or yolk sac inoculation and isolation.33,102 Antibody Large, firm, gray masses may be identified in the cran-
titers to Chlamydia may be assessed by either an ELISA ioventral lobes, with smaller ones in the caudodorsal
or a complement fixation test. Indirect immunofluores- lobes.110 The OPC tumor is well-differentiated and arises
cence also may be used to identify the organism. from alveolar type II or nonciliated bronchiolar cells.108
Metastasis may occur to the bronchial or mediastinal
Diagnosis. Reported lesions include consolidation of lymph nodes in as many as 10% of cases.108,109
cranial lobes with interstitial changes and intracytoplas-
mic elementary bodies within alveolar macrophages ob- Prevention. No treatment or vaccine exists for this
served on histopathologic examination. Edematous septa disease. Eradication efforts in some countries are based
and thickened bronchioles that yield a turbid exudate on extensive slaughtering of large numbers of animals
when compressed also have been described.101 because of the lack of an antemortem diagnostic test.
Nevertheless, sheep can still spread the virus to others
Treatment. In most cases, chlamydial infections re- through nasal or lung fluid. After a diagnostic test for use
spond to treatment with oxytetracycline (20 mg/kg SC or on lung or nasal fluid is developed, prevention or even
IM every 48 to 72 hours). In the midst of an outbreak the eradication of this disease may be possible.
use of tetracycline or chlortetracycline in the diet of
normal, unaffected animals may be beneficial.
Ovine Progressive Pneumonia
Ovine progressive pneumonia (OPP), as it is called in the
Ovine Pulmonary Carcinoma United States, or maedi, as it is called in Europe, is a
Sheep pulmonary adenomatosis (SPA), ovine pulmonary chronic progressive pneumonia or atypical pneumonia of
carcinoma (OPC), or jaagsiekte are contagious, slow, sheep that is caused by a nononcogenic, single-stranded
viral infections that affect the respiratory system. Suscep- RNA lentivirus of the family Retroviridae. Economically,
tibility seems to be age-related, with neonates and lambs OPP is one of the most important diseases affecting
younger than 10 weeks being more likely to develop sheep in North America. Losses resulting from sick
OPC.103,104 Incidence of the natural disease is low in animals, reduced production, and decreased sales can all
goats, although OPC has been experimentally transmit- be attributed to ovine lentivirus (OvLV) infection.
ted in kids.105 The disease is found as a sporadic or However, one report demonstrated that subclinical infec-
endemic condition in sheep or goats of all continents of tion with OvLV had no apparent negative effect on the
the world except Australia.105,106 Lung fluid and nasal number of lambs produced or grease fleece weight com-
exudate of affected sheep contain high concentrations of pared with seronegative sheep in the same flock,111 and
the infectious virus. Viruses from lung wash fluid from a another reported no difference in milk production
sheep with jaagsiekte were purified and sequenced, reveal- between seropositive and seronegative ewes with regard
ing that the capsid sequence is most related to a type D to OvLV.112 Nevertheless, flocks that have eradicated
retrovirus and the envelope region is most related to a type OvLV report fewer ewe losses, increased weaning
B retrovirus. Reports indicate that the disease coexists weights, no indurative mastitis, and a lower incidence of
with ovine progressive pneumonia in some animals.103 pregnancy toxemia.47 Although the results of studies of
 Chapter 5 Diseases of the Respiratory System • 119

indirect losses are variable, it seems likely that the degree Nasal discharge and coughing may be observed, but aus-
of economic loss caused by OvLV infection is associated cultation of lungs is usually not remarkable. As the
with the level of sheep production, breed type, local hus- disease progresses, affected animals demonstrate open-
bandry practices, and flock variations. Therefore general- mouth breathing, flaring of the nostrils, forced expira-
izations about the appearance and behavior of flocks with tions, and more coughing. The signs may last 3 to 6
seropositive ewes are not useful or accurate.113,114 months or persist for years. Chronic nonsuppurative
arthritis, vasculitis, mastitis, encephalitis, and rarely pos-
Pathogenesis. The OvLV persists within infected terior paresis may be observed.127,128 The indurative
monocytes and macrophages115,116 and may exist in a mastitis (“hardbag”) is characterized by a large (symmet-
latent state for an undetermined period. It infects goats ric or asymmetric), hard udder with no abnormal secre-
infrequently.117 OvLV is closely related to the caprine tions. Ataxia, stumbling, and unilateral proprioceptive
arthritis-encephalitis (CAE) virus. Because of its long in- deficits may be the first signs noticed with posterior neu-
cubation period (2 to 4 years), the disease is usually seen in rologic manifestations. These signs can slowly progress
older ewes.The seroprevalence of OvLV varies from as low over weeks to months to rear limb paralysis or quadriple-
as 0.5% of 2040 sheep in west Texas to as high as 49% of gia.114,128 A moderate, hypochromic anemia and leuko-
sheep in the Rocky Mountain region; seroprevalence pro- cytosis may be observed, as well as hypergammaglobu-
gressively increases with age.118, 119 Direct or colostral or linemia in advanced disease.109,128 After signs appear, the
milk transmission are the most likely routes, whereas verti- mortality rate is 100%, with the animals dying or being
cal transmission is rarely observed.120,121 A recent report culled within a year.128
indicates that OvLV may be present in semen contami-
nated by leukocytes.122 Blood has not been demonstrated Diagnosis. Diagnosis is by use of an ELISA employing
to be a source of transmission. Animals frequently become a recombinant transmembrane envelope protein.129 This
infected as lambs, with the outcome of infection influenced test is more sensitive than the commonly used agar gel
by viral phenotype, infectious dose, colostral antibodies, immunodiffusion (AGID) and more economical than the
age, and host genetic factors.113,123 OvLV has a strong whole-virus ELISA or Western blot.130 PCR testing is a
ability to mutate and the resultant antigenic drift produces more sensitive and economical way to detect viral nucleic
new strains of the virus.This accounts for the different pat- acids than actual virus isolation.131 In addition, PCR can
terns of disease associated with different strains of be used to test kids before maternal antibody levels
OvLV.113 Close confinement and the duration of exposure decline. Sensitivity of the AGID and PCR are about 95%
also play significant roles in transmission. Many sheep to 96%, with both missing a few positive animals. For
remain asymptomatic carriers for life.124 In flocks with eradication purposes the use of both tests is recom-
both infected and uninfected ewes, approximately 40% of mended, as is repeating tests two or three times over
the offspring of infected ewes and 20% of the offspring of several months. Necropsy of dead ewes reveals large (two
uninfected ewes become seropositive within 1 year.125 to three times normal weight), heavy lungs, possibly with
After sheep have become infected, they remain in- vertical rib impressions because of their swelling (Figure
fected and persistently viremic, even though they may 5-7). The lungs are firm, do not collapse after removal,
produce antibodies. The virus localizes in the lungs, and are gray-blue or gray-yellow. Evidence of secondary
central nervous system (CNS), and hematopoietic tissue. bacterial pneumonia may be present. The tracheo-
In the lung, OvLV stimulates reticular cells and lympho- bronchial and mediastinal lymph nodes are greatly en-
cytes to proliferate, causing thickening of the interalveo- larged, bulge on cut surfaces, and have a gray-white
lar septa and producing adenomatosis of the alveolar color.109 Arthritis commonly affects the appendicular
lining. Regional lymphadenopathy also is common. In joints, with extensive proliferation of the synovium, fibro-
addition, indurative lymphocytic mastitis, proliferative
arthritis, and (less frequently) nonsuppurative encephali-
tis may be caused by OvLV.

Clinical signs. Clinical signs of OvLV often appear

after periods of stress, exertion, or inclement weather.
The clinical course is characterized by an insidious,
slowly progressive malaise resulting in chronic degenera-
tive disease.126 Initially the sheep become listless; pro-
gressive emaciation (thin ewe syndrome) and dyspnea, es-
pecially after exercise, occur later. Despite this the sheep
maintain their appetites and normal temperatures in the
absence of secondary bacterial pneumonia, although they Figure 5-7 A set of lungs of a sheep with ovine progressive
may exhibit tachypnea (80 to 120 breaths per minute). pneumonia. Note the distended appearance.
120 • Sheep and Goat Medicine
sis of the joint capsule, and degeneration of the articular 10. Cutlip RC, Brogden KA, Lehmkuhl HD: Changes in the lungs
cartilage and bone.132 Gross examination of the spinal of lambs after intratracheal injection of lipopolysaccharide from
cord and brain is generally normal. Histopathologic exam- Pasteurella haemolytica A1, J Comp Path 118:163, 1998.
11. Porter JF et al: Predisposition of specific pathogen-free lambs to
ination is distinct, with a chronic diffuse interstitial pneu-
Pasteurella haemolytica pneumonia by Bordetella parapertussis in-
monia, hyperplasia of lymphoid cells around airways and
fection, J Comp Path 112:381, 1995.
blood vessels, and accumulation of mononuclear cells in 12. Davies DH, Herceg M, Thurley DC: Experimental infection of
the interstitium. Lymphocytic meningitis, choroiditis, and lambs with an adenovirus followed by Pasteurella haemolytica, Vet
leukoencephalitis have been reported in some sheep.133,134 Micro 7:369, 1982.
13. Zamri-Saad M et al: Experimental infection of dexamethasone
Prevention. Control of the disease can be difficult. treated goats with Pasteurella haemolytica A2, Brit Vet J 147:565,
Closing the flock, testing, and culling can eliminate the 1991.
virus from a flock within several years. Seropositive 14. Debey BM et al: A comparison of the intratracheal intravenous
animals and offspring less than 1 year old can be removed and intratonsillar routes of inoculation of goats with Pasteurella
from the premises and raised in a separate facility. haemolytica, Vet Res Commun 16:247, 1992.
15. Thomas LH et al: Evidence that blood-borne infection is in-
Feeding OvLV-free colostrum or milk replacer or graft-
volved in the pathogenesis of bovine pneumonic pasteurellosis,
ing to seronegative ewes may be an alternative. The
Vet Path 26:253, 1989.
keeper or clinician should test the flock twice annually 16. Young JD, Griffith JW: Spontaneous Pasteurella pneumonia in
until two consecutive negative herd tests are obtained; adult laboratory goats complicated by superinfection with
positive animals should be culled. The size of the flock Corynebacterium pseudotuberculosis and Muellerius capillaris, Lab
may help determine the most effective approach. After a Anim Sci 35:409, 1985.
flock is established as negative for OvLV, all additions 17. Sargison ND, Scott PR: Evaluation of antibiotic treatment of
must test negative before joining the flock. Antibody respiratory disease, including suspected septicemic pasteurellosis
titers may be low just before and after parturition because in five-week-old lambs, Agri-Pract 16:25, 1995.
of the sequestering of antibodies in colostrum. A vaccine 18. Jakab GJ: Viral-bacterial interactions in pulmonary infection,
will most likely never be available because of the muta- Adv Vet Sci Comp Med 26:155, 1982.
19. Hansen DE, McCoy RD, Armstrong DA: Six vaccination trials
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in feedlot lambs for the control of lamb respiratory disease
must be directed toward decreasing transmission and re-
complex, Agri-Pract 16:19, 1995.
ducing the prevalence of seropositive animals within a 20. Black H, Donachie W, Duganzich D: An outbreak of Pasteurella
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to aetiology, Br Vet J 136:507, 1980. Smith BP, editor: Large animal internal medicine, St Louis, 1996,
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contagious caprine pleuropneumonia (CCCP) in Kenya, Vet Rec 110. DeMartini JC, York DF: Retrovirus-associated neoplasms of the
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for the Mixed Animal Practitioner, Western Veterinary Conference, 112. Snowder GD et al: Effect of ovine progressive pneumonia on ewe
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93. Rurangirwa FR et al: A latex agglutination test for field diagnosis 113. Brodie SJ, Snowder GD, DeMartini JC: Ovine progressive pneu-
of contagious caprine pleuropneumonia, Vet Rec 121:191, 1987. monia: advances and prospects for control, Sheep Res J 8:116, 1992.
 Chapter 5 Diseases of the Respiratory System • 123

114. Watt NJ, Scott PR, Gessert M: Maedi visna ovine progressive
ATYPICAL PNEUMONIAS
pneumonia virus infection: a comparative study of the disease in
the United Kingdom and the United States, Agri-Pract 16:29, Verminous Pneumonia
1995.
Of the parasites known to cause bronchitis in sheep and
115. Knowles DP et al: Evaluation of agar gel immunodiffusion serol-
goats, Dictyocaulus filaria is the most pathogenic, Muel-
ogy using caprine and ovine lentiviral antigens for detection of
antibody to caprine arthritis-encephalitis virus, J Clin Micro
lerius capillaris (Figure 5-8) is the most common and least
32:243, 1994. pathogenic, and Protostrongylus rufescens is intermediate
116. Cheevers WP, McGuire TC: The lentiviruses: maedi/visna, in pathogenicity.
caprine arthritis-encephalitis, and equine infectious anemia, Adv Dictyocaulus usually appears as a full infection of 2- to
Virus Res 34:189, 1988. 18-month-old sheep. These animals generally have
117. Cutlip RC et al: Seroprevalence of ovine progressive pneumonia chronic fever, cough, nasal discharge, tachypnea, anorexia,
virus in various domestic and wild animal species, and species and weight loss. At necropsy the parasites may be ob-
susceptibility to the virus, Am J Vet Res 52:189, 1991. served in the bronchi, especially in the diaphragmatic
118. de la Concha-Bermejillo A et al: Seroprevalence of ovine pro- lobes (Figure 5-9). Pulmonary edema, emphysema, and
gressive pneumonia in Texas, Sheep and Goat Res J 14(15):127,
atelectatic and pus-filled lobules also may be evident.
1998.
P. rufescens can cause serious disease in domestic sheep,
119. Cutlip RC et al: Seroprevalence of ovine progressive pneumonia
virus in sheep in the United States as assessed by analyses of vol-
although infestation is rarely reported in North America.1
untarily submitted samples, Am J Vet Res 53:976, 1992. The life cycle requires an intermediate host of either a snail
120. Brodie SJ et al: Maternal factors associated with prenatal trans- or slug, and the adult nematodes live in the bronchioles.
mission of ovine lentivirus, J Infect Dis 169:653, 1994. The first-stage larvae are best diagnosed in fecal samples
121. Cutlip RC et al: Effects on ovine fetuses of exposure to ovine by use of the Baermann technique, but they also may be
progressive pneumonia virus, Am J Vet Res 43:82, 1982. found in nasal secretions. Clinical signs in a recent report
122. de la Concha-Bermejillo A et al: Venereal shedding of ovine
lentivirus in infected rams, Am J Vet Res 57:684, 1996.
123. de la Concha-Bermejillo A et al: Pathologic responses of lambs to
experimental inoculation with Acholeplasma laidlawii, J Vet Diagn
Invest 8:115, 1996.
124. Froeling J: Review and case report on ovine progressive pneumo-
nia, Agri-Pract 13:35, 1992.
125. Smith C: Ovine lentivirus: a real or imagined threat, J Am Vet
Med Assoc 200:139, 1991.
126. DeMartini JC et al: Pathogenesis of lymphoid interstitial pneu-
monia in natural and experimental ovine lentivirus infection, Clin
Infect Dis 17(suppl. 1):S236, 1993.
127. Cutlip RC et al: Mastitis associated with ovine progressive pneu-
monia virus infection in sheep, Am J Vet Res 46:326, 1975.
128. Knowles DP, McGuire TC, Cheever WP: Ovine progressive
Figure 5-8 A light micrograph of first-stage larvae of Muellerius
pneumonia (visna/maedi). In Knowles DP, McGuire TC,
capillaris recovered by the Baermann technique. (Courtesy Dr. Byron
Cheever WP, editors: Veterinary diagnostic virology: a practitioner’s L. Blagburn, Auburn, Alabama.)
guide, St Louis, 1992, Mosby.
129. Kwang J et al: Evaluation of an ELISA for detection of ovine pro-
gressive pneumonia antibodies using a recombinant transmem-
brane envelope protein, J Vet Diagn Invest 5:189, 1993.
130. Kwang J, Cutlip RC: Detection of antibodies to ovine lentivirus
using a recombinant antigen derived from the env gene, Biochem
Biophys Res Commun 183:1040, 1992.
131. Barlough J et al: Double-nested polymerase chain reaction for
detection of caprine arthritis-encephalitis virus proviral DNA in
blood, milk, and tissues of infected goats, J Virol Meth 50:101,
1994.
132. Cutlip RC et al: Ovine progressive pneumonia (maedi-visna) in
sheep, Vet Micro 17:237, 1988.
133. Cutlip RC, Jackson TA, Lehmkuhl HD: Lesions of ovine pro-
gressive pneumonia: interstitial pneumonitis and encephalitis, Am
J Vet Res 40:1370, 1979.
134. Brodie SJ et al: Current concepts in the epizootiology, diagnosis, Figure 5-9 A set of lungs infested with Dictyocaulus filaria. Note
and economic importance of ovine progressive pneumonia in the larvae in the trachea. (Courtesy Dr. Byron L. Blagburn, Auburn,
North America: a review, Small Rum Res 27:1, 1997. Alabama.)
124 • Sheep and Goat Medicine
foreign material result in dyspnea, abnormal lung sounds
such as crackles and wheezes, signs of septicemia, foul
breath odor (which initially may smell like the fluid aspi-
rated), and nasal discharge that may contain some of the
aspirated material. A gangrenous pneumonia generally
develops and most affected animals die within a week.

Diagnosis. The diagnosis is based on clinical signs and

history. Radiographs may demonstrate a severe cran-
ioventral bronchopneumonia. A CBC demonstrates
Figure 5-10 A set of lungs infested with Muellerius capillaris. acute inflammation with leukopenia, left shift of neu-
Note the light-colored, raised nodules over the dorsal aspect of the trophils, and elevated fibrinogen. Sampling of tracheal
caudal lobes. (Courtesy Dr. Byron L. Blagburn, Auburn, Alabama.) fluid may reveal numerous cell types and debris, with
culture of the fluid revealing a mixture of organisms
including Corynebacterium, Fusobacterium, Bacteroides,
included diarrhea, weight loss, mucopurulent nasal dis- Escherichia coli, Klebsiella, Pseudomonas, Staphylococcus
charge, tachypnea, and increased respiratory sounds.1 aureus, and Streptococcus. Necropsy of dead animals veri-
M. capillaris causes few clinical signs. However, fies the presumptive diagnosis, revealing cranioventral
necropsy of infected animals reveals gray or greenish pneumonia, food material in the airways, gangrenous
subpleural granulomas in the caudal lobes. Goats are re- lesions, and possibly pleuritis.
ported to have widespread interstitial pneumonia without
nodular lesions (Figure 5-10).2,3 M. capillaris may predis- Treatment. The treatment is lengthy and requires
pose animals to secondary infections and reduce general broad-spectrum antibiotics (penicillin, tetracycline, flor-
health.2,4 fenicol), NSAIDs, and supportive care. Nasal oxygen may
be beneficial.
Treatment. Treatment is with either ivermectin (200
mg/kg SC) or fenbendazole (7.5 mg/kg by mouth [PO]). Prevention. Most cases can be avoided with preventa-
Refractory cases of M. capillaris may require larger doses tive measures. Especially with extremely sick animals the
of either fenbendazole (15 mg/kg at 35-day intervals to clinician should ascertain the correct placement of the
30 mg/kg at 30-day intervals) or ivermectin (300 mg/kg) stomach tube by blowing into it while another person aus-
because immature stages of Muellerius may survive lower cultates over the left paralumbar fossa. When drenching
doses or single treatments.5,6 Larval stages of M. capillaris animals, clinicians and keepers should avoid holding the
may survive in the pasture from one season to the next, so head too high or administering liquid too fast. The
goats may be reinfected.7 overzealous use of fluids in treating choke cases should be
avoided. Specific neurologic diseases such as lead toxicity
Prevention. Prevention by eliminating the intermedi- and rabies may all result in aspiration pneumonia or meta-
ate host mollusk is helpful, but most difficult. bolic disturbances such as hypocalcemia. Withholding
water and food for an appropriate period before anesthesia
is crucial; also, maintaining recumbent animals in a sternal
Aspiration Pneumonia position helps prevent the aspiration of foreign materials
Pathogenesis. Aspiration pneumonia is caused by the (see Chapter 16).
entry of foreign material into the lower respiratory tract,
resulting in pulmonary necrosis. This condition usually
results from errors when using stomach tubes or drench-
PLANT TOXICITIES
ing equipment. It also may be a sequela to neurogenic or
pathologic damage of the pharynx, cleft palate, or anes-
Atypical Interstitial Pneumonia
thesia (see Chapter 16). Ingestion of Perilla mint (Perilla frutescens), a common
weed in the Southeastern United States, results in respi-
Clinical signs. Clinical signs depend on the amount of ratory toxicity. This weed, also known as purple mint, wild
material that enters the respiratory tract. Large quantities coleus, and beefsteak plant, has a pneumotoxin in its leaves
of fluid often produce sudden death from asphyxia. and seeds. The plant is purple-tinged at maturity and has
Coughing; shallow, rapid respirations; and frothing from square stems; the flower and seed stage (occurring from
the nose and mouth may be observed before the animal August to October) is the most toxic. After being ab-
collapses and dies. Gurgling or fluid sounds may be aus- sorbed by the rumen, the toxin is thought to be metabo-
cultated over the trachea. Aspiration of smaller volumes of lized by a mixed function oxidase system, resulting in
 Chapter 5 Diseases of the Respiratory System • 125

toxic intermediates that damage type I pneumocytes and

bronchiolar epithelial cells. This causes hyaline mem-
brane formation and proliferation of type II pneumo-
cytes, leading to adenomatosis.

Clinical signs. The clinical signs of toxicity include an

acute onset of dyspnea and tachypnea, extension of the
head and neck, open-mouth breathing, frothing at the
mouth, and sudden death. Exertion may exacerbate signs
and precipitate death.8
Figure 5-11 Perilla mint toxicity. Interstitial pneumonia in sheep.
Note the distended appearance of the lungs.
Diagnosis. Necropsy reveals distended lungs (some
with rib impressions) that fail to collapse on opening
of the chest. The lungs are wet, heavy, emphysema-
tous, and edematous; emphysematous bullae and froth
in the airways are often observed (Figure 5-11). Diagnosis. The diagnosis is made by observation of
Histopathologic examination reveals interstitial edema clinical signs and a history of access to toxic plants. The
and emphysema, congestion, and alveolar epithelial diagnosis may be confirmed by identifying 1.4 and 10 mg
hyperplasia.8 of HCN/g of liver and rumen contents, respectively.10
Rapid intake of 2 to 4 mg HCN/kg of body weight is
Treatment. Treatment is supportive and relies on min- generally lethal.10
imizing stress.
Moldy sweet potato ingestion can result in a similar Treatment. Treatment includes administration of so-
condition. 4-Ipomeanol is a furanoterpene mycotoxin dium nitrate (16 mg/kg IV) followed by methylene
produced by Fusarium solani growing on moldy sweet po- blue or sodium thiosulfate (30 to 40 mg/kg IV).
tatoes. The pathogenesis, clinical signs, lesions, and treat- The drugs must be given soon and may need to be
ment are similar to that for Perilla mint. repeated.
Ingestion of Brassica species plants (rape, kale, turnip
tops, beet tops) also may result in atypical interstitial
pneumonia. These plants contain large amounts of D,L-
Nitrate-Nitrite Toxicity
tryptophan, which is converted in the rumen to 3-methyl Pathogenesis. Nitrate toxicity may be observed in both
indole, which is absorbed and metabolized by a mixed sheep and goats because of the conversion of nitrate to
function oxidase system in the respiratory tract, produc- nitrite in the rumen. Nitrite binds to iron ions (Fe 2),
ing toxic intermediates. Increased rates of morbidity and and hemoglobin is converted into methemoglobin, which
mortality are observed. Clinical signs and treatment are has a greatly decreased ability to transport oxygen. This
similar to those for intoxication with moldy sweet potato results in hypoxia. When levels of methemoglobin exceed
and Perilla mint. 30%, the blood appears brown.

Clinical signs. Clinical signs include dyspnea, tachyp-

Hydrogen Cyanide Toxicity nea, weakness, exercise intolerance, and sudden death.
Hydrocyanic acid (HCN) toxicity is caused by the inges- Spontaneous recovery may be observed in mildly affected
tion of plants containing cyanogenetic glycosides. sheep and goats.
Damage to the plant (wilt, frost, drought) results in the
release of cyanide, which blocks cellular respiration by de- Diagnosis. Diagnosis is confirmed by assessing the
activating the cytochrome oxidase enzyme of oxidative nitrite levels of the blood, urine, or aqueous humor. High
transport. As a result, blood in the affected animals is nitrate levels in feed or water also may be diagnostic.
bright red because hemoglobin cannot release oxygen to
the tissues. This only occurs when the detoxification ca- Treatment. Treatment is with methylene blue (1 to 2
pabilities of the liver and kidney are exceeded. All live- mg/kg of a 1% solution IV every 6 to 8 hours).
stock are susceptible to the effects of HCN, but sheep
and cattle are at the greatest risk.9 Prevention. Keepers can prevent nitrate-nitrite toxi-
city by ensuring that nitrate comprises no more than
Clinical signs. Clinical signs include dyspnea, saliva- 0.6% of the diet.11 Drought, recent fertilization, and
tion, anxiety, staggering, tremors, and terminal convul- retarded growth of plants increase the risk of nitrate
sions. Sudden death is common in affected animals. toxicity.
126 • Sheep and Goat Medicine
OTHER DISEASES CAUSING
Clinical signs. Clinical signs include weight loss and
RESPIRATORY SIGNS mild signs of respiratory disease because the primary
focus of the disease is generally the lung. A deep, moist,
Caprine Arthritis-Encephalitis chronic cough may be heard in the early stages, with
CAE virus (CAEV) causes a persistent lentiviral infec- tachypnea, dyspnea, and abnormal lung sounds identified
tion of goats that produces several progressive, debilitat- in the latter stages. Enlarged local lymph nodes may con-
ing diseases. It is caused by a C-type retrovirus of the sub- tribute to stridor, dysphagia, and bloat.
family Lentivirinae, as is OPP. The most common route
of transmission for CAEV is by a kid ingesting milk or Diagnosis. Necropsy lesions include granulomatous
colostrum from an infected doe. Horizontal transmission lymph nodes that are more prevalent in the respiratory
also may occur, but only after prolonged contact. The nodes but also occur in the liver and mesenteric lymph
virus infects mononuclear cells, which are then infected nodes. The granulomas are encapsulated and filled with
for life. yellow to orange, creamy to caseous, purulent material
Although the most common manifestation of CAEV and gritty foci. Histologically, lesions consist of central
infection is arthritis, an interstitial pneumonia has calcification and caseation surrounded by zones of ep-
been reported in infected kids and adults. It produces ithelioid cells and Langhans’ giant cells enclosed in
chronic pneumonia, weight loss, and dyspnea.12 Lesions fibrous capsules.14 Acid-fast organisms may be present.
occur predominantly in the caudal or cranioventral lobes. These lesions should be differentiated from those of
The lesions of CAEV interstitial pneumonia closely re- caseous lymphadenitis.
semble those of OPP. Experimentally, the chronic intersti-
tial lesions have not been reproduced with inoculation Prevention. Suspected cases should be tested by intra-
of CAEV. dermal skin testing with 0.1 ml of mammalian tuberculin
Other causes of pneumonia should be considered purified protein derivative injected in the caudal tail fold;
because numerous agents may be responsible for the clini- the injections are assessed in 66 to 78 hours as negative,
cal presentation. Serologic testing using either an AGID suspect, or reactor. Keepers should have suspect animals
or ELISA test may help identify the cause of infection. further tested by federal veterinarians using the compara-
Using the AGID test in conjunction with PCR testing is tive cervical test. Depending on governmental regulations,
best for eradication and control purposes.12a Virus isola- reactors are quarantined, appropriately identified, and sent
tion is not routinely performed, but histopathologic ex- to an approved slaughter plant or disposed of under regu-
amination of tissues may provide a diagnosis. No treat- latory supervision.16 False positive results may occur as a
ment or vaccine is available for CAEV. Prevention is crucial result of concurrent M. paratuberculosis, M. avium, or M.
for maintaining CAEV-negative herds. Separation and tuberculosis infection. When all animals older than 12
testing of new animals before mixing with the preexisting months have tested negative consecutively two times an-
population are important, as is routine testing of animals nually, they should be declared free of tuberculosis.
to decrease the incidence of seroconversion. Kids from in-
fected or suspicious does should be removed at birth and
fed heat-treated colostrum, cow colostrum, and pasteur-
Caseous Lymphadenitis
ized milk until they are weaned (see Chapters 9 and 14).13 Caseous lymphadenitis is a chronic insidious disease of
sheep and goats caused by a gram-positive rod, Coryne-
bacterium pseudotuberculosis, often found in manure, soil,
Tuberculosis on the skin, and in infected organs.18,19 The organism has
Pathogenesis. Tuberculosis is a more serious problem two subspecies, one responsible for caseous lymphadenitis
in goats than in sheep. Mycobacterium bovis is widespread in small ruminants and the other causing ulcerative lym-
in some goat flocks but is reported rarely in sheep.14,15 phadenitis in horses and cattle. Although the disease is of
Close proximity to infected cattle herds and wildlife is great importance economically to the sheep and goat in-
thought to play a role in increased prevalence. Occasion- dustry because of carcass condemnation, it is known pri-
ally M. avium or M. tuberculosis may produce disease.16 marily for causing a peripheral lymphadenopathy. Preva-
Spread of the organism is usually by respiratory secre- lence rates may reach 50% to 60% or greater.20 The
tions, feces, milk, urine, vaginal discharge, semen, and organism most often gains entrance to the body through
draining lymph nodes.17 The route of entry in ruminants contamination of superficial wounds or mucous mem-
is the respiratory tract. The organism then invades local branes or indirectly through fomites such as shearing
lymph nodes, where it causes necrosis surrounded by a blades, feeders, grooming equipment, and bedding.
granuloma. The abdominal cavity is sometimes involved, Transmission also may occur by inhalation or ingestion.
suggesting ingestion as a possible route of infection, pos- The organism may survive in the environment for long
sibly as a result of the coughing and subsequent swallow- periods. After it gains entrance to the body, the organism
ing of lung fluid.14 follows lymphatic vessels and migrates to regional lymph
 Chapter 5 Diseases of the Respiratory System • 127

nodes, where it may then disseminate to other parts of the tumors may be identified in the respiratory tracts of sheep
body. and goats.28 OPC has been discussed previously in this
chapter. Thoracocentesis and radiography can be used for
Clinical signs. When the infection affects the respira- preliminary diagnosis of pulmonary tumors; the diagnosis
tory system, clinical signs include weight loss, dyspnea, is confirmed at necropsy.
tachypnea, and a chronic cough.21
Coccidioidomycosis
Diagnosis. Pulmonary radiographs may reveal one or
more masses, but a definitive diagnosis may be obtained The agent that causes coccidioidomycosis, Coccidioides
by culture of a transtracheal wash. In the authors’ and immitis, is a soil fungus whose spores may infect sheep and
others’ experiences, serologic tests using a synergistic he- goats through inhalation and possibly ingestion or cuta-
molysis inhibition method are not reliable.22 Various neous abrasion. The disease is not contagious but is en-
ELISA tests have been developed with varying specifici- zootic in the southwestern United States. The disease
ties and sensitivities, yet few laboratories run these tests manifests as chronic weight loss and a persistent cough.
routinely.23 Involvement of the mandibular, retropharyn- Affected sheep are febrile and have abscesses in peripheral
geal, prescapular, prefemoral, and supramammary lymph lymph nodes.29 Necropsy of affected animals reveals gran-
nodes is common. In the thoracic cavity, abscesses occur ulomas with creamy purulent material, most commonly in
in the lung parenchyma, mediastinal lymph nodes, and the bronchial and mediastinal lymph nodes. Intradermal
bronchial lymph nodes. The number of lung abscesses and complement fixation tests use coccidioidin, an extract
may range from a few to 20 or 30.20 Lymph nodes in the of the fungus, for diagnosis. Culture or histopathologic ex-
abdominal viscera and skeletal tissue are less likely to be amination and identification of the spherules also are di-
involved.24 Involvement of internal nodes is more likely agnostic. No effective treatment is available.
in older animals because morbidity rates increase with
age; as much as 70% of an infected flock may be in-
Pneumocystis carinii Pneumonia
fected.25 Internal involvement is thought to contribute to
the “thin ewe” or “fading goat” syndromes20,26 (see Pneumonia and sudden death in goats has been reported
Chapter 14). to be caused by the sporozoan Pneumocystis carinii.30 Af-
fected animals generally have had a history of chronic
Prevention. Identification of affected animals should disease that allowed them to become immunocompro-
result in culling and a greater attempt to identify affected mised and infected.
individuals and prevent contamination of others and the
environment. Good hygienic practices during lambing or Clinical signs. Clinical signs include fever, weight loss,
kidding, docking, and shearing may all help to prevent tachypnea, mucopurulent nasal discharge, chronic cough,
exposure to the organism.19 Vaccination has produced weakness, tachycardia, and death. The diagnosis is made
equivocal results but may reduce the number of lesions by observing the organisms in tracheal wash fluid silver-
and the severity of the disease. Anecdotal reports suggest stained sections from lung biopsy. A diffuse and locally
reactions may be encountered when using sheep vaccines extensive interstitial pneumonia is observed on necropsy.
for caseous lymphadenitis in goats. The clinician should rule out caseous lymphadenitis and
tuberculosis in affected animals. Treatment of animals is
generally not effective.
Diaphragmatic Hernia
Herniation may be congenital or acquired. In ruminants
Pneumothorax
the reticulum usually herniates through the diaphragm
after parturition, breeding (males), or a traumatic incident. Although it is uncommon in sheep and goats, pneumo-
Increased intraabdominal pressure may be responsible for thorax should be considered in animals with inspiratory
the herniation in cases that have no association with a dyspnea and an abdominal component to breathing.
foreign body.27 Affected animals may demonstrate signs Rupture of an emphysematous bulla as a result of persist-
of dyspnea, weakness, and possibly weight loss.27 Radiog- ent coughing or straining may produce this condition.
raphy can be helpful in diagnosing suspected cases. If diag- Animals with these clinical signs and a history of attack
nosed early, surgical correction may be curative. Surgical by predators also may exhibit subcutaneous emphysema
approaches are similar to those used in other species. and bite wounds. Usually the mediastinum is complete in
sheep and goats, so this condition presents unilaterally,
thus enhancing survival. Reduced lung sounds are auscul-
Neoplasia tated on the affected side and a difference in resonance is
Although they are uncommon, lymphosarcomas, pleural noted between sides on percussion. Radiographs may
mesotheliomas, adenocarcinomas, and squamous cell confirm the diagnosis. Removal of air through a one-way
128 • Sheep and Goat Medicine
suction catheter results in substantial improvement of the 7. Helle O: The efficacy of fenbendazole and albendazole against the
case. Because pleuritis is a possible complication, these lungworm Muellerius capillaris in goats, Vet Parasitol 22:293, 1986.
animals should receive antibiotics for at least 1 week. 8. Smith JA: The interstitial pneumonias. In Smith BP, editor: Large
animal internal medicine, St Louis, 1996, Mosby.
9. Galey FD: Disorders caused by toxicants. In Smith BP, editor:
Pleuritis Large animal internal medicine, St Louis, 1996, Mosby.
10. Diseases of the respiratory system. In Kimberling CV, editor:
Pleuritis is rare in sheep and goats and almost always oc- Jensen and Swift’s diseases of sheep, Philadelphia, 1988, Lea &
curs as a sequela to another disease process such as pas- Febiger.
teurellosis, extension of peritonitis, liver abscesses, tuber- 11. Radostits OM et al: Veterinary medicine, Philadelphia, 2000, WB
culosis, traumatic injuries to the chest, hypoproteinemia, Saunders.
and septicemia. 12. Ellis TM, Robinson WF, Wilcox GE: The pathology and aetiol-
ogy of lung lesions in goats infected with caprine arthritis-en-
Clinical signs. Clinical signs attributable to pleuritis cephalitis virus, Aust Vet J 65:69, 1988.
include weight loss, decreased milk production, fever, de- 12a. James K. Collins, personal communication, June 2000.
13. Rowe JD, East N: Risk factors for transmission and methods for
pression, reluctance to move, extended head and neck,
control of caprine arthritis-encephalitis virus infection, Vet Clin
dyspnea, restricted respiratory movements, soft and sup-
North Am 13(15):35, 1997.
pressed cough, pain on percussion of the chest with an 14. Davidson RM, Alley MR, Beatson NS: Tuberculosis in a flock of
identifiable fluid line, and friction rubs or silence on aus- sheep, N Z Vet J 29:1, 1981.
cultation because of increased fluid in the pleural space. 15. Cordes DO et al: Observations on tuberculosis caused by Mycobac-
terium bovis in sheep, N Z Vet J 29:60, 1981.
Diagnosis. Clinical diagnosis may be enhanced by a 16. Gutierrez M, Garcia Marin JF: Cryptococcus neoformans and My-
CBC indicating anemia of chronic disease or an acute in- cobacterium bovis causing granulomatous pneumonia in a goat, Vet
flammatory response with hyperfibrinogenemia. Hyper- Pathol 36:445, 1999.
globulinemia may occur in more chronic cases. Ultra- 17. Baker JC: Ruminant respiratory system. In Smith BP, editor: Large
sound of the chest or thoracocentesis can confirm the animal internal medicine, St Louis, 1996, Mosby.
18. DeMartini JC et al: Pathogenesis of lymphoid interstitial pneumo-
diagnosis.
nia in natural and experimental ovine lentivirus infection, Clin
Infect Dis 17(suppl. 1):S236, 1993.
Treatment. If possible, the clinician should drain and 19. Ellis JA: Ovine caseous lymphadenitis, Comp Cont Ed Pract Vet
culture fluid from the pleural space. If the protein level is 5:S505, 1983.
less than 2.5 g/dl or the cell count is less than 3000 cells/ 20. Pugh DG: Caseous lymphadenitis in small ruminants, Prac North
mm3 in the pleural fluid, a transudate is present, most Am Vet Conf 11:982, 1997.
likely caused by hypoproteinemia, right heart failure, 21. Jones SL, Schumacher J: What is your diagnosis? Mineralized
neoplasia, or acorn toxicity. The clinician should therefore retropharyngeal mass (3  5 cm) compressing the pharynx ven-
treat the underlying problem. Broad-spectrum antibi- trally, J Am Vet Med Assoc 197:395, 1990.
otics, analgesics, and supportive care are indicated. 22. Brown CC et al: Serodiagnosis of inapparent caseous lymphadeni-
However, the prognosis is generally guarded. tis in goats and sheep, using the synergistic hemolysis-inhibition
test, Am J Vet Res 47:1461, 1986.
23. Ter Laak EA et al: Double-antibody sandwich enzyme-linked im-
Acknowledgments munosorbent assay and immunoblot analysis used for control of
caseous lymphadenitis in goats and sheep, Am J Vet Res 53:1125,
Special thanks to Rachel Eddleman and Carolyn Zorn 1992.
of Auburn University, Auburn, Alabama, for technical 24. Stoops SG, Renshaw HW, Thilsted JP: Ovine caseous lym-
assistance. phadenitis: disease prevalence, lesion distribution, and thoracic
manifestations in a population of mature culled sheep from

R EFERENCES
1. Mansfield LS et al: Lungworm infection in a sheep flock in Mary-
western United States, Am J Vet Res 45:557, 1984.
25. East NE: Common infectious conditions, Small Ruminants for the
Mixed Animal Practioner, Western Veterinary Conference, 1998, Las
land, J Am Vet Med Assoc 202:601, 1993. Vegas, NV.
2. Nimmo JS: Case report: six cases of verminous pneumonia (Muel- 26. Ashfaq MK, Campbell SG: Experimentally induced caseous lym-
lerius sp.) in goats, Can Vet J 21:49, 1979. phadenitis in goats, Am J Vet Res 41:1978, 1980.
3. Kanwar NS, Paliwal OP, Ram K: Verminous pneumonia in goats, J 27. Ahmed SS, El Hamamsy H: Diaphragmatic hernia in a sheep, Vet
Vet Parasitol 12:139, 1998. Rec 115:441, 1984.
4. Kazacos KR et al: Fenbendazole for the treatment of pulmonary 28. McCullagh KA, Mews AR, Pinsent PJN: Diffuse pleural
and gastrointestinal helminths in pygmy goats, J Am Vet Med Assoc mesothelioma in a goat, Vet Pathol 16(15):119, 1979.
179:1255, 1981. 29. Radostits OM et al: Diseases caused by algae and fungi. In Rados-
5. McCraw BM, Menzies PI: Treatment of goats infected with the tits M et al, editors: Veterinary medicine, Philadelphia, 2000, WB
lungworm Muellerius capillaris, Can Vet J 27:287, 1986. Saunders.
6. Bliss EL, Greiner EC: Efficacy of fenbendazole and cambendazole 30. King JM: Sudden death in sheep and goats, Vet Clin North Am
against Muellerius capillaris in dairy goats, Am J Vet Res 46:1923, 1985. 5(15):704, 1983.
 Chapter 6

Tandheriogenology
Goats
of Sheep

SEYEDMEHDI MOBINI, ALAN M. HEATH, AND D.G. PUGH

Sheep and goats are very fertile animals. On a percent two crura that join before leaving the pelvis. The entire
body weight basis, very few species rival the testicular size penis is surrounded by the tunica albuginea. The two
of the ram or buck. The ewe and doe also have reproduc- paired retractor penis muscles arise from the coccygeal
tive potential far superior to that of most other domestic vertebrae and pass around the anus to become two dis-
animals. Before beginning an examination of the repro- tinct muscles that attach to the ventrolateral surface of
ductive system, the clinician should examine the animal the penis at the distal bend of the sigmoid flexure. The
as a whole. The old saying, “Sex (reproductive potential) penis is normally held in a S-shaped bend (sigmoid
is a luxury” is true. Animals need to be productive (i.e., flexure) except during erection and ejaculation by the re-
healthy) before they are able to be “reproductive.” The ex- tractor penis muscles1 (Figure 6-1).
amining clinician also should understand the animal’s The testicles are suspended away from the body by the
utility. A single range ewe usually does not undergo the pendulous scrotum. The scrotum is composed of undulat-
same sort of reproductive manipulation performed on a ing epidermis that may or may not be covered by wool,
donor animal used in an embryo transfer program. Re- depending on the breed and husbandry practices. A rich
productive medicine, or theriogenology, of sheep and plexus of blood vessels, lymphatics, and sweat glands lies
goats is covered in this chapter. In some portions of the beneath the skin. The dartos, a smooth muscle layer, is
chapter sheep and goats are discussed separately, but connected to the vaginal tunics of the testicle by the
when applicable the two species are discussed together. scrotal fascia. The scrotal fascia is the connective tissue
that is typically broken down when the clinician separates
the skin from the testicle during routine castration. The
MALE REPRODUCTION vaginal tunics are outcroppings of the peritoneum and
form a protective covering over the testicles. The space
Anatomy and Physiology of the Male between the two layers of vaginal tunic (parietal and vis-
The anatomy of the reproductive organs of the ram and ceral) as it reflects around the testicle normally contains a
buck is similar to that of other ruminants. The penile small amount of peritoneal fluid. The scrotal septum,
urethra is surrounded by the corpus spongiosum penis composed primarily of the dartos muscle, divides the
(CSP) throughout its length. The urethra terminates as a scrotum into two halves.2
vermiform appendage. Blood enters the CSP proximally The testicle itself is surrounded by a thick fibrous con-
and exits through two exhaust veins located on the free nective tissue known as the tunica albuginea. The
portion of the penis. Contractions of the urethralis and parenchyma of the testicle is composed of seminiferous
bulbospongiosus muscles force blood rhythmically tubules that contain the germ cells and their supporting
through the CSP, producing the characteristic pulses of cells (Sertoli cells). The seminiferous tubules drain into
urine observed during normal micturition. The most the rete testes, which in turn is drained by 10 to 12 ef-
prominent structure of the penis is the corpus caver- ferent ducts. These ducts drain into the head of the epi-
nosum penis (CCP). It consists of cavernous space sup- didymis, which is located on the dorsal craniolateral
ported by fibrous trabeculae. This cavernous tissue is aspect of the testicle. The body of the epididymis curves
located on the dorsal surface and partially surrounds the around the lateral portion of the testes and ends caudo-
CSP. At its origin in the pelvis the CCP is composed of medially as the tail. The tubular structure is reflected dor-
• 129 •
130 • Sheep and Goat Medicine
tonin can alter the breeding season of rams, but the prac-
ticality of these procedures is debatable.7
A change in the sexual attitude of the ram toward the
ewe as day length decreases defines the onset of the
breeding season. He becomes more sexually interested in
the female, and courtship behavior occurs more fre-
quently. Rams display a typical flehmen response to
females in estrus after sniffing the vulva region and urine
from the estrus female. He often strikes out at the female
with one front leg before mounting her.6 The physiologic
changes in testicular size, mating behavior, and semen
quality are caused by the activation of the hypothalamus
and a decrease in the effectiveness of testosterone on the
negative inhibition of gonadotropin-releasing hormone
(GnRH). Significant differences are seen between the
breeding and the non-breeding season with respect to the
pattern of GnRH and luteinizing hormone (LH) pulses
Figure 6-1 Gauze strip wrapped around the penis at the junction and the response of the pituitary gland to GnRH.
of the free portion of the penis and the prepuce to prevent retraction
into the sheath. Note the prominent villiform appendage. Buck. Breed, age, and nutrition contribute to the onset
of sexual maturity in the buck.8 The age at puberty
depends on the breed, varying from 2 to 3 months in
sally and becomes the vas deferens.2 Rams and bucks pygmy breeds to 4 to 5 months in Nubian and Boer bucks.
have a full complement of accessory sex glands. The Most breeds of goats raised in the temperate environment
small bulbourethral glands are located caudally in the of the Northern Hemisphere possess sperm in the ejacu-
pelvic cavity on either side of the pelvic urethra; they can late at 4 to 5 months. However, at this age their semen
be palpated rectally. They also have lobulated vesicular quality is poor and they are not suitable for breeding.9
glands, disseminate prostates, and a widening of the vas Nubian and Boer bucks begin exhibiting libido at 10 to
deferens known as the ampulla.3 Spermatogenesis re- 12 weeks and start producing quality semen at about
quires about 49 to 60 days from the start of germ cell di- 8 months.8,9 Natural adhesions of the urethral process and
vision until the sperm are released from the seminiferous glans penis to the prepuce make the immature buck inca-
tubules. Another 10 days to 2 weeks are required for the pable of copulation. This attachment begins to separate at
sperm to pass from the seminiferous tubules through the 3 months, and fertile mating is possible at 4 to 5 months.8,9
epididymis.4 Fast-growing, well-fed, and well-managed kids are able to
breed sooner than starved males of equal age.
Whether bucks are truly seasonal breeders is contro-
Puberty and Seasonality
versial. Many bucks have depressed libido, reduced
Ram. Puberty typically occurs in the ram at 6 months. pheromones, decreased scrotal circumference (SC), lower
It is defined as the point at which the ram develops an in- semen freezability, and a larger number of abnormal sper-
terest in sexual activity and produces spermatozoa in suf- matozoa outside of the breeding season. All these
ficient numbers to achieve pregnancy in ewes. The exact changes reflect lower levels of LH and testosterone. LH
age of puberty depends somewhat on breed and time of and testosterone concentration, libido, and odor presence
birth. Rams born early in the spring are older at puberty in the buck peaks in the fall.10,11 Sexual behavior of the
than late-born lambs. Moreover, rams that are periodi- buck includes actively seeking does in estrus, courtship
cally exposed to cycling ewes tend to reach puberty (kicking, pawing, muzzling, grunting, and flehmen),
earlier.5 Rams are seasonal breeders; the sperm quality, mounting, intromission, and ejaculation. Ejaculation
daily sperm output, and sexual activity are modulated by occurs spontaneously and is characterized by a strong
the increased periods of darkness that typically occur in pelvic thrust with a rapid backward movement of the
the fall (Northern Hemisphere). This seasonality in the head.9 After ejaculation the buck dismounts and shows
ram also is manifested by an increase in the testicular cir- no sexual arousal for a few minutes to several hours.
cumference.6 Melatonin is secreted from the pineal gland
during the dark hours. The increase in this hormone that
occurs as day length shortens is responsible for many of
the physiologic mechanisms associated with the ram in
R EFERENCES
1. Beckett SD, Wolfe DF: Anatomy of the penis, prepuce, and
transition from the non-breeding to the breeding season.6 sheath. In Wolfe DF, Moll HD, editors: Large animal urogenital
Manipulation of light-dark intervals and the use of mela- surgery, ed 2, Baltimore, 1998, Williams & Wilkins.
 Chapter 6 Theriogenology of Sheep and Goats • 131

2. Heath AM, Purohit RC: Anatomy of the scrotum, testes, epi- tests are the most reliable predictor of an animal’s libido.
didymis, and spermatic cord (bulls, rams, and bucks). In Wolfe DF, Ewes used for libido tests may be synchronized to estrus,
Moll HD, editors: Large animal urogenital surgery, ed 2, Baltimore, or ovariectomized and administered estrogen. Compared
1998, Williams & Wilkins.
with low-libido rams, rams that are identified as high-
3. Ashdown RR, Hancock JL: Functional anatomy of male reproduc-
performing or having a high degree of libido have a
tion. In Hafez ESE, editor: Reproduction in farm animals, ed 4,
Philadelphia, 1980, Lea and Febiger.
higher lambing percentage and more live lambs born per
4. Pineda MH, Faulkner LC: The biology of sex. In McDonald LE, exposed ewe. Serving capacity tests also may be used to
editor: Veterinary endocrinology and reproduction, ed 3, Philadelphia, determine proper ram-to-ewe stocking ratios.1,6 These
1980, Lea and Febiger. tests of flock reproduction can produce a shorter, more
5. Price EO, Borgwardt R, Dally MR: Heterosexual experience dif- uniform lambing season.3 Adult rams achieving four to
ferentially affects the expression of sexual behavior in 6- and 8- six or more breedings during 30 minutes are preferred.
month old ram lambs, Appl Anim Behav Sci 46:193, 1996. Rams achieving two or three breedings during 30
6. Fitzgerald J: Applied reproductive physiology of the ram. In minutes are acceptable. Rams that appear sexually inac-
Youngquist RS, editor: Current therapy in large animal theriogenol- tive can be tested twice. If they still appear to be sexually
ogy, Philadelphia, 1997, WB Saunders.
inactive, the keeper can paint the rumps of the tested
7. Nett TM: Controlling seasonal reproduction: emphasis on the
ewes with different colors of ink and leave the rams
male, Proceedings of the Society for Theriogenology, 1991, Nashville,
TN.
overnight in the pen with them. The next day the keepers
8. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea should examine the rams’ chests for the colored ink.5
and Febiger. Still, fertility is maximized if only acceptable groups of
9. Goyal HO, Memon MA: Clinical reproductive anatomy and rams are kept for breeding.
physiology of the buck. In Youngquist RS, editor: Current therapy Selection of rams from high-producing ewes as meas-
in large animal theriogenology, Philadelphia, 1997, WB Saunders. ured by the number of lambs born, the weight of lambs
10. Hill J: Goat reproductive management, Proceedings of the Sympo- weaned, and a history of having lambs early in the season
sium on Health and Diseases of Small Ruminants, Nashville, TN, also may have a positive relationship with fertility.7 It
1996, American Association of Small Ruminant Practice. appears that rams born co-twin to male siblings have
11. Wilddeus S: Reproductive management for meat goat production,
higher serving capacities than those born co-twin to
Proceedings of the Southeast Region Meat Goat Producers Symposium,
females.8 Rams also should be selected for structural
Tallahassee, FL, 1998, Florida A & M University.
soundness and for the genetics they can pass on to their
offspring because they contribute approximately 60% to
SELECTION AND 80% of the genetics of the average flock.1 Rams should be
maintained on a good nutritional, vaccination, and de-
MANAGEMENT worming program. Their body condition scores before
breeding season should be 3.5 to 4. Obesity minimizes
Ram willingness to breed. Rams should be sheared and their
A ram with good-quality semen, adequate testicular size, feet trimmed before breeding season. During breeding
and good libido can breed 100 ewes in a 17-day breeding season, free access to shelter or shady areas should be pro-
season.1 However, most producers in North America use vided to minimize heat stress–associated infertility.
3 to 3.5 rams per 100 ewes. Yearlings and mature rams Special care should be taken during the initial examina-
can be expected to service 35 to 50 ewes, whereas ram tion of rams to eliminate those that have diseases of the
lambs should only be expected to service 15 to 25 ewes.2 reproductive tract.
Adjustments should be made for multiple sire breeding
units. It is desirable to always have more than three rams
to a multiple sire unit because this tends to alleviate some
Buck
of the territorial fighting among rams. A number of breeds of goats are well established in North
Libido serving capacity and testing can provide useful America. Some of the dairy breeds are Alpine, Nubian,
information regarding how many ewes a ram can be ex- Saanen, Toggenburg, and Lamancha. Angora and cash-
pected to service or even if a ram should be retained.3 mere are the predominant fiber-producing goat breeds.
Serving capacity tests are performed to measure how Meat goat breeds include Spanish (brush goat), Ten-
many times a ram services ewes during a defined period. nessee stiff-legged, pygmy, Boer, Kiko, and Genemaster.
One report suggests that the test serving pen should be Bucks are chosen based on individual performance or
approximately 3 m by 5 m and in clear view of rams that progeny testing for traits such as milk production, meat
are to be tested.4 However, larger or smaller pens may be traits, adaptability, and twinning rate. Prolific bucks are
used. Typically the ram is placed in a pen with two to four preferred. Birth, weaning, and yearling information is
cycling, unrestrained ewes for a period of 20 to 40 valuable in establishing the superiority or inferiority of a
minutes. The keeper monitors and records all sexual be- potential sire. Selection for growth rate and meat produc-
havior, with emphasis on the number of breedings. Such tion should be a high priority for meat goats. Bucks
132 • Sheep and Goat Medicine
should have good conformation and be large and muscu- extended by pressing down around the external preputial
lar. Selection based on testicle size is important; bucks orifice and grasping the protruding penis with a gauze
with the largest testicles usually produce the highest- pad. Occasionally the sigmoid flexure may need to be
quality sperm. straightened to assist in extending the penis. The clini-
The same serving capacity tests used for rams are ap- cian should carefully examine the penis for evidence of
plicable to bucks. Bucks with apparent defects in posture active lesions or old scars. The penis can be held in ex-
and genital tract abnormalities should be avoided. tension by wrapping a strip of gauze around the junction
Because the intersex condition has been linked to the between the free portion of the penis and the prepuce.
polled gene, the use of phenotypic polled bucks should be This method also is helpful when collecting semen by
avoided. Changing bucks every 2 years prevents loss of electroejaculation. The penis is generally easier to extend
vigor and reduces inbreeding in the herd. Bucks should when the animal is being held up on his rump than when
be kept separate from does in a group on pasture or in he is in lateral recumbency.
single housing. They should be introduced with females
only during the established mating season, after which
their job for the year is finished. Bucks require proper nu-
Scrotal Circumference
trition, routine foot care, vaccination, deworming, and The clinician should pull both of the ram’s testicles ven-
exercise. trally into the scrotum and measure it at its largest cir-
cumference using a tape measure marked in centimeters.
BREEDING SOUNDNESS Care must be taken with breeds that have heavy scrotal
wool because wool may falsely enlarge the measured cir-
EXAMINATION IN THE RAM cumference. Taking the average of several measurements
A breeding soundness examination (BSE) should be per- can increase the accuracy of the SC measurements. The
formed on all rams before the beginning of the breeding tape should be snug on the scrotum and barely indent the
season. With the ram being expected to breed as many as skin so that the tape does not slide on the scrotum
100 ewes during a season, his individual worth far out- (Figure 6-2). SC in the ram is highly heritable, and al-
weighs the cost of a BSE. A proper BSE consists of a though controversy exists regarding its importance, it
thorough physical examination with special attention to appears to be related to sperm output, age of puberty, and
the scrotum and testicles, as well as an evaluation of the the propensity for multiple births in his female
semen quality. Most BSEs do not routinely include an offspring.1 During the selection of ram lambs the testicu-
evaluation of the ram’s libido or his physical ability to lar diameter at 170 days provides a long-range prediction
make intromission. The veterinarian should communi- of postpubertal testicular size and sperm output.9 SC is a
cate clearly with the client regarding the limitations of major criterion in selecting replacement rams. Minimum
the BSE performed and the need for some sort of libido accepted SCs of 30 cm for ram lambs weighing more
testing. This testing can often be accomplished by di-
rectly observing the animal in the first part of the breed-
ing season. Large sheep producers may be encouraged to
keep an extra 10% more rams that have been deemed sat-
isfactory according to a veterinary examination to ensure
adequate ram power.

Physical Examination
A complete physical examination should be performed
on all rams, with particular emphasis on the eyes and
feet. The ram can be restrained by placing him on his
rump in a sitting position. The scrotum should be pal-
pated to ensure that both testicles are present, approxi-
mately equal in size, and of firm consistency; the clinician
should note any localized swellings or areas of indura-
tion. The head and tail of the epididymis is palpated for
swelling, pain, and signs of inflammation. Epididymitis is
a relatively common problem in rams. Any ram exhibit-
ing signs of epididymitis should be considered infected Figure 6-2 Measuring the scrotal circumference of a ram. The
procedure is the same for bucks. The tape measure should slightly
with Brucella ovis until proven otherwise. The clinician indent the skin, and the examiner should firmly push the testicles into
should examine the spermatic cord for deformities in the the scrotum with the free hand. Care should be taken to read the
vascular plexus and vas deferens. The penis can usually be measurement at the correct location on the measuring tape.
 Chapter 6 Theriogenology of Sheep and Goats • 133

than 150 lb, 33 cm for 12- to 18-month-old rams, and 36 The clinician then dips the corner of a coverslip into the
cm for rams weighing more than 250 lb have been sug- drop of raw semen and mixes it with the drop of warmed
gested.1 Based strictly on age, rams from 8 to 14 months saline. The resultant mixture should allow the examiner
should have 28 to 36 cm of SC to be classified as satisfac- to watch the motion of individual spermatozoa. If the
tory and more than 36 cm to be classified as exceptional semen mixture is too concentrated to allow identification
(Table 6-1). Rams older than 14 months should have 32 of individual spermatozoa, a new preparation should be
to 40 cm of SC to be classified as satisfactory and more made with less semen. With experience the observer will
than 40 cm to be classified as exceptional.10 Scrotal size is be able to determine the amount of semen to place on the
usually greatest from August to October. Smaller testicu- coverslip to make an adequate slide. The examiner should
lar measurements (0.5 to 1.5 cm smaller) are to be ex- visually estimate the number of progressively motile
pected when rams are tested outside of the normal breed- sperm. A common error is to overestimate the percentage
ing season (February to April) or during periods of of progressively motile sperm. The observer can minimize
extreme sexual activity.1 errors by mentally “freezing” the microscopic image
before making the motility estimate. One technique to
Semen Evaluation
The penis is extended as described previously. The ram is
then placed in lateral recumbency to collect semen by elec-
troejaculation. The same electroejaculators (EEs) de-
C
scribed for use in bucks are used for rams (Figure 6-3).The
clinician inserts the tip of the ram’s penis and the urethral
process into the warmed glass or plastic tube. Some rams
ejaculate at this point of the examination. The rectum is
cleared of feces and a lubricated electric rectal probe is
carefully inserted.The clinician massages the accessory sex
glands by moving the probe back and forth in a cranial to B
caudal direction 8 to 10 times while gently forcing the tip
of the probe ventrally. Mild electrical stimulation is then
applied for 5 seconds. The ram typically vocalizes during
this procedure and attempts to escape. After the ram
relaxes, the massage and electrical stimulation are repeated
until the ram ejaculates into the tube.The spiraled urethral
process straightens during the ejaculatory process. The A
collected semen is evaluated for motility, morphology, and
the presence of inflammatory cells.
Figure 6-3 The two electroejaculators shown here are the Bailey
Motility. A drop of raw semen is first examined under (A) and Lane (B) electroejaculators. Both contain batteries and require
low power (100) to estimate the concentration and no external power source. Other models are available. An artificial
motility. A drop of warmed saline is placed on the slide. vagina also is shown (C).

TABLE 6-1

SCROTAL CIRCUMFERENCE AND BREEDING SOUNDNESS EVALUATION BY AVERAGING THREE MEASUREMENTS

FOR RAMS

8 to 14 Months Older Than 14 Months

SIZE* RATING SIZE* RATING

Smaller than 28 cm Questionable Smaller than 32 cm Questionable

28 to 36 cm Satisfactory 32 to 40 cm Satisfactory
Larger than 36 cm Exceptional Larger than 40 cm Exceptional
From Yarney TA, Sanford LM: Pubertal development of ram lambs: physical and endocrinological traits in combination as indices of postpubertal
reproductive function, Therio 40(4):735, 1993.
*Testicles may be 2 to 3 cm smaller in the off season.
134 • Sheep and Goat Medicine
TABLE 6-2

MOTILITY AND MORPHOLOGY PERCENTAGES REQUIRED TO PLACE RAMS INTO DIFFERENT CATEGORIES

EXCEPTIONAL SATISFACTORY UNSATISFACTORY

Motility Greater than 70% Greater than 30% Less than 30%
Morphology Greater than 90% Greater than 50% Less than 50% normal
From Yarney TA, Sanford LM: Pubertal development of ram lambs: physical and endocrinological traits in combination as indices of postpubertal
reproductive function, Therio 40(4):735, 1993.

make the estimate easier is to determine whether more or

less than 50% of the spermatozoa are motile. After
making that determination, the observer can try to arrive
at the nearest 25%, then the nearest 10%. The observer
also should record the number of round cells present in
each image. If more than two round cells are seen in each
medium power field, a smear of the semen should be
made for cytologic evaluation (e.g., Wright’s stain). The
presence of white blood cells indicates inflammation
and/or infection. The presence of early nucleated round
germ cells indicates an aberration of spermatogenesis.
Rams should have more than 30% progressively motile
cells to obtain a satisfactory rating and more than 70% to
have an exceptional rating11 (Table 6-2). Motility is
usually depressed outside the breeding season.

Morphology. A slide is next prepared for examination

of spermatozoa morphology. A small drop of semen is
placed on the edge of a slide, and a ribbon of eosin-
nigrosin stain is placed slightly closer to the center of the
slide. The corner of a second slide is dipped into the
semen drop and the resultant “hanging drop” of semen is
mixed with the ribbon of stain. The second slide is then Figure 6-4 A, A normal spermatozoon; B, a spermatozoon with a
pulled across the first slide in a manner similar to creating primary abnormality—tightly coiled tail and midpiece; C, a
a blood smear. The amount of semen placed on the edge spermatozoon with a primary abnormality—microcephalia, or small
head; D, a pear-shaped head, which is a primary abnormality; E, a
of the second slide is determined by experience. The re- spermatozoon with a distal cytoplasmic droplet, which is a secondary
sultant smear should have an even distribution of cells. abnormality; F, a spermatozoon with a proximal cytoplasmic droplet.
Spermatozoa should be spaced so that individual cells are
easily distinguished but each field should have approxi-
mately 10 cells. The slide is allowed to dry and then ex- testicular degeneration. Droplets also can occur in
amined at 1000 with an oil-immersion lens. The ob- samples taken from rams out of season. At least 50% to
server should count at least 100 cells and determine a 70% of the observed spermatozoa should be morphologi-
percentage of normal spermatozoa. Abnormalities are cally normal for the ram to be considered a satisfactory
usually recorded as either primary or secondary. Primary breeder; more than 80% to 90% is considered
abnormalities involve the head and midpiece of the sper- exceptional11 (see Table 6-2).
matozoa, whereas secondary abnormalities involve the
tail (Figure 6-4). The type of abnormality can be used to
Breeding Soundness Prediction
estimate the severity of problems in rams with an exces-
sive number of abnormal cells. Abnormalities of the head The SC, progressive motility, and percentage of normal
and the acrosome are associated with severe testicular spermatozoa can be combined to classify rams into cate-
aberrations. Tail abnormalities are often associated with gories to help predict their usefulness in a breeding flock.
less severe problems or diseases of the epididymis. Round Rams that are classified as satisfactory in all categories
droplets of cytoplasm on the tail are usually seen in young can be expected to impregnate about 50 ewes in a 60-day
rams and are associated with overuse, immaturity, or mild breeding season. Rams that receive exceptional ratings
 Chapter 6 Theriogenology of Sheep and Goats • 135

Serologic screening for B. ovis should be performed

on all rams at the time of the BSE.12

BREEDING SOUNDNESS
EXAMINATION IN THE BUCK
All breeding bucks need to be evaluated for breeding
soundness 3 to 4 weeks before mating season. As in the
ram, the examination of the buck should include a physi-
cal examination, reproductive examination, measurement
of SC, and semen collection and evaluation. BSEs are
only able to evaluate the physical soundness and semen
quality of the buck. A satisfactory finding cannot guaran-
tee the buck’s ability to produce live offspring.14 At-
tempts to assess libido in the buck greatly aid in a com-
plete reproductive evaluation. The libido measurement
Figure 6-5 Ultrasonography of the ovine testicle (sagittal or described for the ram can be adapted for the buck.
longitudinal plane). The hyperechoic mediastinum is seen here as a
distinct line on the image (large arrow). The vaginal tunic can be best
visualized in the field opposite the transducer (small arrow). Physical Examination
Physical examination of the buck must include a general
examination for health, with particular attention to as-
sessment of body condition and musculoskeletal condi-
can be expected to impregnate 100 ewes during a 60-day tion (feet and legs). To be a satisfactory breeder, a buck
breeding season. Any ram that does not receive at least a should be in good body condition. Thin or excessively fat
satisfactory rating in all categories should either be culled animals should be avoided (see Chapter 2).14,15 The buck
or retested in 60 days. The decision to cull or retest should be free of known genetic defects such as hernias,
should be based on the severity of observed lesions and jaw malformation, cryptorchidism, supernumerary teats,
the economic value of the individual animal.9,10 and intersex condition. Bucks should not be phenotypi-
cally polled.
Ancillary Tests
Ultrasonography can be used to evaluate the testicles of
Examination of the Reproductive Tract
rams (or bucks). Changes from the normal homogeneous Reproductive evaluation includes examination of the
testicular parenchyma such as hyperechoic and hypoe- testes, epididymis, spermatic cord, and penis. Testis
choic areas are indicative of fibrotic changes or cystic should be examined for size, symmetry, and consistency.
structures. The examiner should not confuse the normal A buck should have two large, oval testes of equal size;
hyperechoic mediastinum that is found in the center of they are firm during the breeding season and slightly
the testicle for a fibrotic lesion. The mediastinum appears softer during the non-breeding season. If only one testicle
as a distinct round area in the center of transverse images is present, the male should be disqualified as a potential
of the testicle and as a hyperechoic line on longitudinal breeder. Ultrasonography may be useful in aiding detec-
images (Figure 6-5). The epididymis and spermatic cord tion or confirmation of abnormalities.14-16 Gross changes
also can be examined for fibrosis and cystic structures. in the epididymis are fairly rare in goats. The clinician
Areas of fibrosis or degeneration and testicular abscesses should examine the penis for abnormalities when collect-
can usually be visualized. ing a semen sample. The penis must be manually ex-
Testicular biopsies using a 14-gauge biopsy needle tended from the sheath so that a careful examination can
can allow a direct examination of the testicular architec- be made. The urethra extends beyond the tip of the penis
ture. Testicular biopsies are useful in determining for about 2 to 3 cm, forming the urethral process. When
atrophy, degeneration, and hypoplasia. This technique is bucks have a history of urinary calculi, the urethral
usually relegated to use in valuable animals. The clinician process is usually removed during treatment because it is
aseptically prepares the testicle and anesthetizes an area a common area of obstruction. The loss or removal of the
of skin. He or she then inserts the biopsy needle into the urethral process appears to have no detrimental effect on
dorsum of the testicle, avoiding the epididymis and the buck’s fertility.15 Because of its high correlation of
taking care not to penetrate the mediastinum. Tissue can testicular size and capacity for sperm production, SC is
be fixed in either Bouin’s solution or 10% formalin for important in the buck. However, its use in the evaluation
routine histopathologic analysis.13 of breeding soundness is not well defined. SC is measured
136 • Sheep and Goat Medicine
in the buck as described in the ram. SC in 45-kg dairy BOX 6-1
goats has been reported to be 25 to 28 cm, with larger
bucks having SCs of 34 to 36 cm.14,15 No age and breed
standards exist for SC in meat goats. In 1999, during the
M INIMAL A CCEPTABLE L EVELS
Georgia and Southeast Meat Goat Buck Performance
Test, SCs in 45-kg, 7-month-old Kiko and Boer bucks
FOR A S ATISFACTORY P OTENTIAL B REEDER B UCK

averaged 26 to 29 cm.16 Volume—0.5 ml

Motile sperm—70%
Semen Collection Concentration—2 billion
Morphology—80% normal
Semen may be collected with an artificial vagina (AV) in
a trained buck or by electroejaculation.13 The Bailey
Adapted from Memon MA, Mickelsen WD, Goyal HO: . In
Ejaculator (Western Instrument Company, Denver, CO) Youngquist RS, editor: Current therapy in large animal theriogenology,
and Lane Ejaculator (Lane Manufacturing Inc., Denver, Philadelphia, 1997, WB Saunders.
CO) are the two most commonly used EEs (Figure 6-4).
EEs should be 25 to 30 cm long and 2 to 3 cm in diame-
ter. An AV can be built from a polyvinyl chloride (PVC) matozoa per milliliter; it can vary from “whey-like” to
pipe or radiator hose with an inner liner made of a cut “milky” to “creamy.” Gross motility is measured as de-
section of bicycle inner tube. An AV also can be pur- scribed for the ram. Even though concentration is not rou-
chased. The length of the AV should be 18 to 22 cm, and tinely assessed in field conditions, it is advisable to include
its outside diameter should be 6 cm. It should be filled it in the evaluation. Two of the authors (Drs. Mobini and
with warm water to maintain proper turgor and warmth Pugh) have evaluated meat bucks with very low sperm
(38° to 40° C). A semen collection cone should be placed concentrations but with other satisfactory examination
at one end. A nonspermicidal lubricant is placed in the parameters.16 Concentration can be easily assessed using a
open end. For electroejaculation bucks are restrained in hemocytometer and a commercial Unopette system for
chutes or held against the wall. The rectum is cleaned of white blood cell count.15 Morphology can be determined
feces and a well-lubricated probe is inserted. The prostate by examination. An eosin-nigrosin–stained smear is eval-
is massaged five to six times, electrical current is applied uated using a 1000 objective; the examiner measures
through the probe for 4 to 6 seconds, and then the probe primary or secondary abnormalities in 100 to 200 sperma-
turned off for 3 to 4 seconds. This pattern is maintained tozoa per slide, as described for the ram (see Figure 6-4).
until ejaculation occurs (usually four to five cycles). Normal values for a buck to be classified as a satisfactory
Libido cannot be assessed when collecting semen by an potential breeder are shown in Box 6-1. A questionable
EE. During and after collection, semen should be pro- potential breeder may require reevaluation after 8 weeks or
tected from direct sunlight and temperature shock, and need to be culled. The classification of unsatisfactory po-
sperm motility should be evaluated within 10 minutes. tential breeder may be given for reasons other than semen
quality (e.g., cryptorchid, lameness) Bucks showing de-
pressed libido, slightly decreased SC, and increased sperm
Semen Evaluation abnormalities should be identified and culled.14,15
The volume of normal buck ejaculate is 0.5 to 1.5 ml
(with an average of 1 ml). Semen is evaluated for color,
gross and progressive mortality, morphology, and concen-
tration.15 Both semen quality and quantity may vary with
R EFERENCES
1. Burfening PJ, Rossi D: Serving capacity and scrotal circumference
age, season, temperature, breed, and even between indi- of ram lambs as affected by selection for reproductive rate, Small
viduals within the same breed. Normal semen values in Rumin Res 9:61, 1992.
the buck are as follows15: 2. Grotelueschen DM, Doster AR: Reproductive problems in rams,
NebGuide (http://www.ianr.unl.edu), Lincoln, NE, 2000, Coopera-
Volume—1 ml (with a range of 0.5 to 1.5 ml) tive Extension, University of Nebraska.
Motility—80% (with a range of 70% to 90%) 3. Fitzgerald J: Applied reproductive physiology of the ram. In
Concentration—4 billion (with a range of 2 to 5 Youngquist RS, editor: Current therapy in large animal theriogenol-
billion) per ml ogy, Philadelphia, 1997, WB Saunders.
Normal morphology—80% (with a range of 70% to 4. Katz LS: Sexual performance tests in sexually inexperienced rams.
90%) In Dziuk PJ, Wheeler M, editors: Handbook of methods for study of
reproductive physiology in domestic animals, Urbana, IL, 1991, Uni-
Minimally acceptable values are shown in Box 6-1. versity of Illinois.
Volume is measured directly from the graduated collec- 5. Fitzgerald J, Perkins A: Serving capacity tests for rams. In Dziuk
tion vial. Volume is of some value in evaluating semen col- PJ, Wheeler M, editors: Handbook of methods for study of reproduc-
lected using an AV, but of limited value when EEs are tive physiology in domestic animals, Urbana, IL, 1991, University of
used. The color of semen depends on the number of sper- Illinois.
 Chapter 6 Theriogenology of Sheep and Goats • 137

6. Perkins A, Fitzgerald JA, Price EO: Sexual performance of rams in otherwise. This is especially true of older rams that have
serving capacity tests predicts success in pen breeding, J Anim Sci been actively breeding in multiple sire units. However,
70(9):2722, 1992. one case report involving an outbreak of B. ovis in a group
7. Fitzgerald JA, Perkins A: Ram sexual performance: a relationship
of virgin ram lambs suggests that the disease may be
with dam productivity, Sheep Res J 7(1):7, 1991.
spread in utero or neonatally, before any known sexual ac-
8. Fitzgerald JA, Perkins A, Hemenway K: Relationship of sex and
number of siblings in utero with sexual behavior of mature rams,
tivity.2 The primary means of spread is thought to be
Appl Anim Behav Sci 38:283, 1993. through contact with mucous membranes, which results
9. Yarney TA, Sanford LM: Pubertal development of ram lambs: in bacteremia. The organism localizes in the epididymis
physical and endocrinological traits in combination as indices of and secondary sex glands. Contact can occur among rams
postpubertal reproductive function, Therio 40(4):735, 1993. and from recently infected ewes; venereal and oral-nasal
10. Kimberling CV, Marsh DJ: Breeding soundness evaluation and transmission also are possible.3 Swelling of the epi-
surgical sterilization of the ram. In Youngquist RS, editor: Current didymis is the primary presenting sign, occurring about 3
therapy in large animal theriogenology, Philadelphia, 1997, WB weeks after the initial exposure. Grossly, there is localized
Saunders. inflammation followed by hyperplasia and obstruction of
11. Bulgin MS: Ram breeding soundness examination and SFT form,
the epididymal ducts. This obstruction causes a backup of
Nashville, Proceedings of the Society for Theriogenology, 1992,
spermatozoa, the development of sperm granulomas, and
Nashville, TN.
12. Pugh DG: Examination of the ram for breeding soundness, Proc
pressure necrosis. The seminal vesicles also are commonly
Hudson-Walker Therio Conf 7:19, 1996. affected, which may account for the large number of in-
13. Carson RL et al: Examination and special procedures of the fected rams that show no palpable signs of epididymitis.3
scrotum and testes. In Wolfe D, Moll HD, editors: Large animal Semen collected from infected rams usually contains a
urogenital surgery, Baltimore, 1997, Williams & Wilkins. large number of polymorphonuclear neutrophils that can
14. Pugh DG: Breeding soundness examination in male goats, Proc be seen on the motility preparations or on Wright’s
Hudson-Walker Therio Conf 7:29, 1996. stained specimens. Serology for B. ovis should be consid-
15. Memon MA, Mickelsen WD, Goyal HO: Examination of the re- ered a routine part of a BSE. Both enzyme-linked im-
productive tract and evaluation of potential breeding soundness in munospecific assay (ELISA) and complement fixation
the buck. In Youngquist RS, editor: Current therapy in large animal
(CF) tests are available. Herd infections with B. ovis can
theriogenology, Philadelphia, 1997, WB Saunders.
result in a 15% to 30% reduction in lambing rate depend-
16. Mobini S: Reproductive management in goats, Proceedings of the
North American Veterinary Conference, vol 14, 2000, Orlando, FL.
ing on the chronicity of the herd problem. This decrease
in reproductive efficiency results from lowered fertility in
the rams, failure of the ewes to conceive, reabsorption of
embryos, abortions, stillbirths, and weak lambs.5
DISEASES OF THE MALE Recommendations outlined by Bulgin4 include the
following:
Varicoceles
• Buying virgin rams that have been serologically
A varicocele is defined as a localized dilatation and
tested for brucellosis
thrombosis of the internal spermatic vein and is recog-
• Keeping newly purchased rams separate until all
nized as a fluctuant to hard swelling in the spermatic
rams are tested free from Brucella
cord. Varicoceles are more common in rams than in
• Performing palpation and culling all rams with
bucks. This condition is often manifested as rear limb
epididymitis before the breeding season
lameness and awkward posture as the ram tries to relieve
• Culling all B. ovis–positive rams
pressure on the swollen cords. Affected animals may
• Retesting all rams in the flock 60 days after any
become weak and susceptible to other diseases as a result
rams are found positive
of debilitation brought on by an unwillingness to walk to
• Performing BSEs yearly on all rams
obtain food and water. Varicoceles can be diagnosed by
palpation and diagnostic ultrasound. Abnormalities such If a large number of serologically positive rams is
as decreased total sperm count, reduced sperm motility, found after a year of adherence to these guidelines, efforts
and morphologic abnormalities of the sperm are often as- should be made to determine whether a serologically neg-
sociated with varicoceles. The exact etiology of the condi- ative carrier ram is present in the flock by culturing semen
tion is not known but a genetic predisposition is sus- from all rams.
pected. No easy treatment is available, and affected rams
or bucks should be culled.1
Epididymitis in Young Males
In younger rams, and less commonly in bucks, epididymi-
Epididymitis in Older Males
tis can be caused by a number of organisms such as
Epididymitis is a rare condition in the buck but a clini- Histophilus, Actinobacillus, and Haemophilus species, as
cally important disease in rams. Epididymitis in rams well as Corynebacterium pseudotuberculosis. Lamb epi-
should be considered to be caused by B. ovis until proven didymitis can be spread from ram to ram by the oral or
138 • Sheep and Goat Medicine
nasal route. The organisms responsible for lamb epi- the ducts become distended and may rupture, resulting in
didymitis can frequently be cultured from the preputial a severe inflammation. As fluid accumulates, pressure
cavity of rams younger than 2 years of age and are com- continues to build and testicular degeneration may occur.
monly found in the mucous membranes of the prepuce, Some animals are initially fertile but lose fertility after the
penis, mouth, and nasal cavity.5 Colonization and subse- efferent ducts become completely occluded. Granulomas
quent disease of the reproductive tract may depend on the are firm swellings found in the head of the epididymis.
hormonal changes that occur during maturation and On palpation the testicles may be initially edematous, but
puberty, along with other unknown differentiating factors they eventually become hard. The testicles may eventually
that allow most animals to eliminate the bacteria sponta- become small and atrophic. Ultrasonographic evaluation
neously while causing others to develop clinical signs.6 may reveal mineralization of the testicles or the granu-
Diagnosis of lamb epididymitis is made by palpation of loma itself. No treatment is available for sperm granulo-
the enlarged epididymis and by ruling out B. ovis infec- mas, and the clinician should be cognizant of the poten-
tion. Semen from infected lambs is characterized by a large tial association with the intersex condition.
number of neutrophils and by the morphologically abnor-
mal spermatozoa typical of epididymal disease. Although Testicular Hypoplasia and Degeneration
the signs of most cases of lamb epididymitis are restricted
to the reproductive tract, occasionally an associated fever Testicular hypoplasia and degeneration are difficult to
and hind limb lameness also occur. Lamb epididymitis can differentiate during an initial examination.8,10 In rams
be treated with long-acting oxytetracycline (20 mg/kg in- and bucks out of season, testicular size and palpation
tramuscularly [IM] or subcutaneously [SC]) injections for characteristics may be difficult to differentiate from
three treatments at 3-day intervals.6,7 Inclusion of tetracy- subtle cases of testicular atrophy. More extreme differ-
cline (20 mg/kg by mouth [PO] daily) products in the ences are encountered in rams than in goats, but in
ration may be appropriate in herds experiencing a high in- general the testicle in the non-breeding season is smaller
cidence of lamb epididymitis. Treatment should be re- and lacks normal resiliency.8 True hypoplasia can be asso-
served for valuable lambs and cases diagnosed in the early ciated with the intersex condition in bucks and a specific
stages because most lambs develop scar tissue in the epi- chromosomal abnormality in rams8,10 (Figure 6-6).
didymis that prevents functional recovery. Other causes of testicular atrophy include zinc defi-
ciency, hypothyroidism (iodine deficiency, ingestion of
goitrogenous plants), starvation diets, systemic disease,
Orchitis and heat and cold stress. Iodine-induced hypothyroidism
Orchitis is a common occurrence in the ram and is occa- has been associated with decreased testicular weight, de-
sionally seen in the buck.8-10 Scrotal abscesses may be pressed spermatogenesis, and decreased libido. Atrophic
caused by trauma or may be an extension of epididymitis. or degenerated testicles become elongated, small, and
Whenever testicular trauma or infection is encountered, either softer or harder. Normal testicles usually have a ho-
it should be considered a medical emergency in breeding mogenous echogenicity on ultrasound. Atrophic or de-
animals. Excessive heat from one testicle can result in generative testicles tend to have a heterogenous pattern
possibly irreversible thermal injury to the germinal ep- and more hyperechoic areas. Testicular biopsy can be of
ithelium of the contralateral testicle. All the organisms value in diagnosis. Many cases of atrophy and degenera-
discussed in the section on epididymitis can cause orchi- tion are not treatable; the exceptions are cases caused by
tis. The signs include a hot, swollen scrotum (usually uni- diet or certain diseases. In treating diet-related atrophy,
laterally); inability to move the affected testicle freely in
the scrotum; and pain on manipulation of the affected
testicle and the scrotum. Some animals may show signs of
systemic disease, pain on walking, and decrease in
libido.10 In cases affecting valuable animals, hemicastra-
tion in the acute phase may prevent permanent infertility.

Sperm Granulomas
Although testicular tumors are rare in rams and bucks,
granulomatous swellings are occasionally encountered.
Sperm granulomas are more common in goats than in
sheep, and unlike abscesses or other forms of orchitis,
they usually occur bilaterally. Sperm granulomas are often Figure 6-6 These small, thin, hard, hypoplastic testicles are from
caused by a partial or complete blockage of the efferent a polled yearling buck.
ducts draining into the epididymis.10 As pressure builds,
 Chapter 6 Theriogenology of Sheep and Goats • 139

ensuring adequate protein-energy intake and free access ovaries) but they may be partially or totally descended.
to a good-quality trace mineral supplement is essential. If Partially descended testes may be mistaken for udders, es-
zinc deficiency is suspected, reducing the legume content pecially when they begin to enlarge during puberty.11
of the diet and adding a chelated form of zinc (zinc me- Hypospadias (opening of the urethral orifice on the
thionine) to the diet or trace mineral mixture is useful. If ventral aspect of the penis), sperm granulomas, and hy-
iodine-induced hypothyroidism is diagnosed, the inclu- poplastic testicles should all be considered part of the in-
sion of iodine in a trace mineral mixture and the removal tersex complex.10
of goitrogenous plants from the diet should be under- The principal hormone produced by the gonads in
taken; males should be kept off pastures with goitroge- caprine intersexes is testosterone, which accounts for
nous plants before and during breeding. masculine behavior. Intersex goats can be used as teaser
animals because they do not produce sperm.12 Gonadec-
tomy is generally required if the animal is to be used as a
Intersex pet. Identifying intersex animals with normal or nearly
Caprine intersexes are referred to as male pseudohermaph- normal external genitalia is difficult. Failure to exhibit
rodites because a majority of them have testes. True her- estrus, development of male behavior during the breeding
maphrodites have testicular and ovarian structures and season, a shortened vagina on speculum examination, and
generally constitute a much smaller proportion of inter- smaller than normal teats may be the first signs of the in-
sexes.11 Intersex is more prevalent in polled dairy goats tersex condition.12 The breeding of phenotypically polled
(Saanen, Toggenburg, alpine, and Damascus breeds). The bucks should be avoided.
polled intersex condition is rare or not reported in some
breeds (Nubian and Angora).12 Cytogenetic evaluations
of caprine intersexes clearly show that most polled inter-
Penile Abnormalities
sexes are karyotypically female (XX), and the breeding Several penile abnormalities may occur, albeit rarely in
histories of the parents indicate that intersexes are ho- sheep and goats. Both hypospadias and short penile
mozygous for the polled trait.10 length are associated with intersex in goats. Such animals
Affected animals are genetically female but may exhibit should be culled. Careful examination of the penis in the
male, female, or mixed external characteristics.12 Gener- fully extended state may reveal existing abnormalities.
ally they are female-appearing at birth, but as they reach Occasionally urethral rupture (as a sequela to urethral
sexual maturity they become larger than normal females, stones), balanoposthitis (see Chapter 10), injuries to the
with masculine heads and erect hair on their necks.10 An villiform appendage, hair rings, and other abnormalities
enlarged clitoris in a doe-like animal or a decreased are identified.
anogenital distance in a more masculine individual is Both phimosis (inability to extend the penis) and
typical of intersex12 (Figure 6-7). Intersexes may start to paraphimosis (inability to withdraw the penis into the
smell and may act aggressively toward other goats and prepuce) are occasionally seen in rams and bucks; both
people during the breeding season. Some dribble urine or conditions can cause significant loss of libido and fertility.
stretch out with a concave back and urinate forward If they are not quickly diagnosed and treated, affected
between the legs.11 Whenever bilateral cryptorchidism is animals may be rendered infertile. These two conditions
encountered, intersex should be suspected. The testes are may be associated with hair ring, trauma, and bal-
generally intraabdominal (in the normal location of the anoposthitis. In cases associated with a hair ring on the
glans of the penis, inspecting the penis allows the clini-
cian to identify the problem and remove the “ring” of hair.
Shearing the wool or mohair just anterior to the sheath
can minimize the incidence of this problem.8,10 Phimosis
also may occur as a sequela to trauma, balanoposthitis,
and congenital abnormalities. In cases of trauma an adhe-
sion may form in the sheath or in the sigmoid region, re-
sulting in an inability to extend the penis. As a general
rule these cases may be difficult to treat. In cases in which
inflammation and scarring result in posthitis, the treat-
ment is the same as that described for balanoposthitis.
The clinician can attempt to “break down” the adhesions
manually. The use of nonsteroidal antiinflammatory
drugs (NSAIDs; flunixin meglumine 1 to 2 mg/kg
Figure 6-7 This intersex goat had two ovo-testes in the inguinal twice a day [BID]) or antibiotics (procaine penicillin
region. The vulva is positioned very ventrally and joins to an enlarged 22,000 IU/kg BID) and lavage of the sheath with mild
clitoris at its termination. antiseptics may be of value (see Chapter 10). In cases of
140 • Sheep and Goat Medicine
phimosis most animals experience a loss of libido and ceration, infection, rupture or tearing of the ureter, and
should be culled because the prognosis is poor.10 tetanus.The clinician should administer tetanus toxoids or
Paraphimosis also is associated with trauma, infection, antitoxins when castrating animals. Lambs and kids
and balanoposthitis. It is slightly more common in bucks should receive 150 to 250 units of tetanus antitoxin; adults
than in rams, but it is rare in both. In cases of paraphimo- of unknown vaccination history should receive 500 to 750
sis, applying antibiotic cream with or without cortico- units of antitoxin. Previously vaccinated adults should
steroids, replacing the penis, and placing a purse-string receive a tetanus toxoid booster. In some instances antibi-
suture into the preputial orifice may be of value. The in- otics may be of value. Evisceration may occur at any age
clusion of a tube in the sheath, exiting through the orifice, but appears more common in young goats; some breed
allows urine drainage. The clinician should take care to predisposition (pygmy, Spanish meat) is possible. Routine
ensure proper urine flow. Flushing the sheath and penis castration of lambs and kids is usually done during the first
with a mild antiseptic solution, providing penile hy- week of life. However, if the lamb or kid is to be a long-
drotherapy, and covering the penis with medicated oint- term pet, it is advisable to wait until the animal is at least 5
ments are valuable treatments for this condition. The to 6 months old to allow for growth of the penis and
penis should be extended at least every third day so the urethra and detachment of penile adhesions.
keeper or clinician can monitor healing. Sexual rest
should be enforced throughout recovery. However, the Surgical castration. Surgical removal of the testes is
prognosis in these cases is poor, particularly if the condi- superior to all other forms of castration. During the sur-
tion is more than 2 weeks old and the animal makes no gical removal of the scrotum and testicles, animals may be
attempt to retract the penis.10 lightly sedated, anesthetized, or held by a helper or tech-
nician. Young lambs or kids 2 to 4 days old are often cas-

R EFERENCES
1. Kimberling CV: Disease of rams. In Kimberling CV, editor: Dis-
trated by this method without anesthesia. However, seda-
tion can be beneficial because of their vocalization and
their greater tendency to develop hypotensive shock.
eases of sheep, ed 3, Philadelphia, 1988, Lea and Febiger. Anesthesia can be achieved by local infiltration of lido-
2. Bulgin MS: Brucella ovis epizootic in virgin ram lambs, J Am Vet caine hydrochloride in smaller animals. A 1% solution is
Med Assoc 196(7):1120, 1990. recommended to prevent lidocaine toxicity (see Chapter
3. Kimberling CV: Sheep flock fertility, Proceedings of the Society for 16). Large bucks and rams should be sedated with xy-
Theriogenology, 1990, Nashville, TN. lazine hydrochloride (0.05 to 0.3 mg/kg IM) because
4. Bulgin MS: Epididymitis caused by B. ovis, Proceedings of the they are susceptible to shock associated with the stress
Society for Theriogenology, 1991, Nashville, TN.
and pain of castration. In young kids or lambs the lower
5. Walker RL, Leamaster BR: Prevalence of Histophilus ovis and Acti-
nobacillus seminis in the genital tract of sheep, Am J Vet Res 47:1928,
third of the scrotum is removed by a scalpel blade to
1986. expose both testicles. In weanlings and adult bucks or
6. Bulgin MS: Ram lamb epididymitis, Proceedings of the Society for rams, the surgeon makes an incision over each testis or
Theriogenology, 1991, Nashville, TN. removes the distal third of the scrotum. The scrotal fascia
7. Ley WB: Ram epididymitis, Agri-Pract 14(5):34, 1993. is then stripped away from the testicles. The surgeon pulls
8. Bruer AN: Examination of the ram for breeding soundness. In the testicles ventrally by steady traction while breaking
Morrow DA, editor: Current therapy in theriogenology, ed 2, the cremaster muscle and the scrotal fascia away from the
Philadelphia, 1986, WB Saunders. remaining spermatic cord. The spermatic cord should be
9. Pugh DG: Breeding soundness evaluation in male goats, Proc torn in such a manner that it breaks dorsal to the
Hudson-Walker Therio Conf 7:29, 1996. pampiniform plexus.
10. Mickelsen WD, Memon MA: Infertility and diseases of the repro-
When castrating rams or bucks older than 4 months of
ductive organs of bucks. In Youngquist RS, editor: Current therapy
in large animal theriogenology, Philadelphia, 1997, WB Saunders.
age and when castrating during the breeding season, the
11. Basrur PK, Yusoff RBH: Sex anomalies in goats. In Youngquist clinician may need to use an emasculator or place a trans-
RS, editor: Current therapy in large animal theriogenology, Philadel- fixation ligature cranial to the pampiniform plexus to
phia, 1997, WB Saunders. prevent or control hemorrhage. In cases in which hemor-
12. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea rhage appears to be clinically significant, the bleeding
and Febiger. vessels should be located, cleaned, and ligated. If the
bleeding vessel cannot be identified, the clinician should
pack the scrotum with sterile gauze, antiseptic-soaked
SPECIAL PROCEDURES gauze (iodine), or epinephrine-soaked gauze and then
suture the scrotum closed. If gauze is not available and
Castration the bleeding vessels cannot be located, the surgeon can
Castration is the most common surgical procedure per- close the scrotum with a purse-string suture or a through-
formed in small ruminant practice. Some of the complica- and-through suture pattern to obliterate any “dead space.”
tions that can occur include excessive hemorrhage, evis- The scrotum should be reopened and the gauze removed
 Chapter 6 Theriogenology of Sheep and Goats • 141

12 to 18 hours after the surgery. These animals may

Hemicastration
benefit from antibiotic therapy (penicillin 20,000 IU/kg) A decision may be made to remove a diseased testicle to
for 1 to 4 days. On rare occasions, when the testicles are prevent the spread of disease or heat-induced testicular
pulled to allow the cord to rupture above the pampini- degeneration (such as that caused by inflammation) to
form plexus, the testicular artery may be avulsed from the the healthy testicle. The ram or buck should not eat for
aorta, resulting in fatal or near-fatal hemorrhage. Exces- 48 hours and not drink for 24 hours before being put
sive tension can occasionally tear the ureter from the under general anesthesia; the clinician should administer
urinary bladder.1 a broad-spectrum antibiotic 2 to 4 hours before surgery.
Complications are rare with this method. It is easy to The animal should be anesthetized (see Chapter 16),
perform, and if done quickly, it appears to be associated placed in right lateral recumbency, and have the entire
with limited stress. Animals need exercise after castration scrotum and surrounding areas clipped and prepared
to reduce postoperative swelling. aseptically. The surgeon makes an elliptical skin incision
on the lateral surface of the scrotum, starting near the
Elastrator. Elastrator castration is the simplest and base of the affected testicle and extending to near the
most common technique used by producers. Lambs and apex. This incision should include the tunica dartos
kids younger than 1 to 3 weeks of age are the most muscle. The surgeon should take care not to extend the
suitable candidates for this technique. A very heavy incision into the normal hemiscrotum. This elliptical in-
rubber ring is placed around the neck of the scrotum cision should be wide enough to remove any excess skin
with a special applicator. Care must be taken to ensure after the testicle is removed; however, the surgeon should
that the entire scrotum is included within the band. The be careful to leave enough skin to close the wound. The
penis should be palpated to ensure that it is not trapped testicle and its associated tunics are bluntly dissected
within the band. Placing the band over the testicular away from the scrotum. The vaginal tunics should be
cord and not directly against the abdominal wall helps excised to expose the testicle and spermatic cord. The
prevent the trapping of any portion of the penis (sigmoid spermatic artery and vein should be ligated with a trans-
flexure). The rubber band method may initially appear to fixation suture (0 gut) at a level above the pampiniform
be less traumatic and stressful, but it is considered plexus. The cremaster muscle should also be ligated at a
inhumane by some if it is performed on animals older point proximal to the vascular ligature. A separate ligature
than 3 weeks of age.1 The scrotal sac and the trapped should be placed around the entire spermatic cord. A
testicles become ischemic, die, and drop off within 2 clamp or suture is placed around the cord approximately 5
weeks. No hemorrhaging occurs because no open wound to 6 cm distal to the vascular suture, and the cord is tran-
is formed, but the risk of tetanus is increased compared sected. The remaining vaginal tunic is transected far
with other techniques.1 Occasionally the blood supply to enough distally to allow the tunics to be closed over the
one or both testicles does not become occluded, and the remaining cord. An inverting suture pattern (Connell or
testicles continue to elaborate testosterone.1 Parker-Kerr) is used with an absorbable material (0 gut).
The tunica dartos muscle is closed over the wound with a
Burdizzo emasculatome. A third method that may be simple continuous pattern. The longitudinal skin incision
used in older sheep and goats is castration by emascu- should be closed, and if excess skin is present it should be
latome. The main advantage of this technique is the trimmed so that no dead space remains. The scrotum can
absence of an open wound and the decreased risk of be bandaged immediately after surgery if bleeding is ex-
tetanus (compared with elastrator bands). Anesthesia is pected. This bandage should be left in place no longer
usually not required or used. A Burdizzo emasculatome than 12 hours to avoid thermal damage to the remaining
crushes the spermatic cord and its blood vessels above testicle. Routine presurgical antibiotics (penicillin or
each testis. The operator holds each cord tightly against tetracycline) should be continued postsurgically as
the lateral aspect of the scrotum with one hand while ap- needed. NSAIDs may be indicated for control of pain,
plying the instrument twice on each side to crush the swelling, and other signs of inflammation.
cord. The crushes are made 2 cm apart, ensuring that the
midline of the scrotum is not crossed. The testicular cords
may be clamped together or separately as previously de-
Teaser Preparation
scribed. When employing an emasculatome, the operator Teaser rams and bucks greatly facilitate estrus detection
should ensure that both testicular cords are completely for artificial insemination (AI) and embryo transfer pro-
clamped. The complications of this method include tes- grams, particularly if they are used in conjunction with
ticular survival, scrotal sloughing, extreme scrotal marking harnesses. In goats, one of the simplest teasers to
swelling, tetanus, and undue suffering. One author of this attain is an intersex animal. Temporary teasers can be
chapter (Dr. Pugh) considers this the most inhumane created hormonally. A wether, doe, or ewe that is not to
method of castration. As with the banding method, the be used for breeding can be given testosterone propionate
devitalized tissue is allowed to slough. (100 mg every third day or 150 mg weekly), beginning 3
142 • Sheep and Goat Medicine
Epididymectomy
weeks before intended use and continuing through the
season.2 A male used for estrus detection should be An alternative approach is to remove the entire tail of the
healthy and have good libido. A young postpuberal male epididymis. This technique, similar to vasectomy, does
is best, particularly if he is not so large that he injures not prevent intromission but does result in infertility. Bi-
females during mounting. The male should be incapable lateral caudal epididymectomy is the simplest surgical
of intromission to minimize the spread of venereal procedure for teaser buck or ram preparation.4 Although
disease. Moreover, in AI programs the introduction of it is a “field procedure,” the surgery should be performed
bacterial pathogens into the anterior vagina before breed- under aseptic conditions. The clinician clips the scrotal
ing should be avoided, which is another reason why males wool, cleans the scrotum, aseptically prepares the area,
incapable of intromission are preferred teasers. The and infiltrates a local anesthetic in the skin over the tail of
estrus-detecting male should not be able to ejaculate but the epididymis. He or she then grabs the testis and forces
should maintain a good libido. it to the distal segment of the scrotum. The tail of the
epididymis bulges out on the ventral side of the scrotum.
The clinician makes a 3-cm skin incision directly over the
Vasectomy tail of the epididymis and continues it through the
A properly performed vasectomy renders the male inca- common vaginal tunic until the tail of the epididymis has
pable of ejaculation but does not prevent intromission. extruded. He or she grasps the tail of the epididymis with
The authors prefer mild sedation (xylazine 0.05 mg/kg a pair of towel forceps and, using a combination of blunt
IM) and local infiltrative anesthesia with lidocaine. The and sharp dissection, separates it from the testicle (Figure
skin around the area proximal to the scrotum and the skin 6-9). Enough of the epididymis should be isolated so that
on the proximal scrotum is prepared for surgery. The sutures can be placed proximally on the body of the epi-
surgeon identifies the vas deferens by palpation with one didymis and distally on the tail of the epididymis. Alter-
hand and cuts through the skin over the vas deferens. A natively, a pair of forceps can be clamped across the loop
combination of blunt and sharp dissection is used to of epididymis that has been created and crushed. The
isolate the vas deferens from the other structures of the loop of epididymis is now removed. If sutures were placed
spermatic cord (Figure 6-8). Two ligatures are placed 4 on the epididymis, and the procedure was performed
cm apart, and a 2-cm section of the vas deferens is under aseptic conditions, the skin may be closed. In less
removed. The skin is closed with sutures, staples, or by a sterile conditions the skin wound may be left open to
subcuticular closure.3 The procedure is then repeated on granulate. Advantages of epididymectomy over vasec-
the other testicle. A surgeon can perform a bilateral va- tomy include its technical ease and the fact that it can
sectomy through a single, very “cranial” incision over the performed under less than ideal conditions. A minimum
spermatic cord. The ram or buck should be rested for 30 of 30 days of sexual rest should be enforced before the
days before use. animal is used in a teaser program.4

Penile Translocation
One method of preventing intromission is to “free” the
penis and move it over to the left flank. This method is
Place sutures here
useful in some teaser systems. The surgery prevents intro-
mission, but not ejaculation. Therefore if penile transloca-

Incise vas deferens

at this point

Figure 6-8 Isolation of the vas deferens away from rest of the Figure 6-9 The tail of the epididymis is pulled away from the
testicular cord in preparation for vasectomy. As the vas deferens is testicle. The scalpel is being held where the tail of the epididymis is to
lifted out of the incision, sutures are applied (at the Xs) and the vas be cut. A hemostat can be placed proximal to the testicle and the
deferens is cut. epididymis cut distal to it.
 Chapter 6 Theriogenology of Sheep and Goats • 143

tion is attempted, a vasectomy (epididymectomy) also The penis should now be at a 45° angle to the long axis of
should be performed. The clinician should give the buck the body1 (Figure 6-10). The penis should not be re-
or ram a systemic antimicrobial agent 2 or more hours stricted at any point through the tunnel, and the penis and
before surgery. With the animal standing, the clinician prepuce should not be torsed. The reference suture should
marks an area 1 cm cranial to the flank fold.1 The buck or be used to align the cranial aspect of the preputial orifice to
ram is then heavily sedated, anesthetized with injectable the dorsal portion of the circular flank incision.1,5
anesthetics, intubated and maintained on gas anesthesia, The circumferential incision should be sutured with a
or administered a lumbosacral epidural (see Chapter simple interrupted pattern using absorbable material. The
16).1,5 The animal is placed in right lateral recumbency, subcutaneous tissue of the transposed prepuce should be
the ventral abdomen and left flank are clipped, and the sutured to the cutaneous trunci and followed with closure
surgical site is aseptically prepared.1,5 The clinician excises of the skin. The clinician then closes the longitudinal in-
a 4- to 7-cm circle of skin and cutaneous trunci muscle cision, attempting to diminish all open dead space with
above the fold in the left flank. The lower edge of the cir- absorbable material. The authors prefer either a single in-
cular incision should be 1 cm above the flank fold, just terrupted or horizontal mattress type suture pattern. The
cranial to the mark made on the left flank. Hemostasis is skin over the longitudinal incision is closed by a simple
achieved and the area is covered with saline-moistened interrupted pattern in all areas except the most cranial
gauze. The clinician then makes a circumferential incision aspect of the original preputial incision. To allow for
1 to 2 cm caudal to the preputial orifice through the skin ventral drainage, this area is not sutured.1,5 Fly control
around the sheath and extends the incision longitudinally should be maintained, and tetanus prophylaxis should be
along the ventral penile shaft, two thirds of the way to the provided (using tetanus toxoid or antitoxin). The clinician
scrotum.9 The penis is left inside the prepuce, and the two then performs a bilateral epididymectomy, continues ad-
structures are freed of all subcutaneous tissue by blunt dis- ministering antibiotics for 5 to 7 days (procaine penicillin
section, avoiding large vessels. A single “reference” suture 22,000 IU/kg BID), and removes the sutures in 14 days.
is placed in the skin at the most cranial aspect of the The male is ready for use in 1 month.
preputial orifice and a sterile glove is placed over the
orifice.1 From the circular incision in the flank to the most SEMEN COLLECTION
caudal aspect of the longitudinal incision, the clinician
creates a tunnel using scissors and blunt dissection. The AND STORAGE
penis (along with the sterile glove covering the preputial
orifice to maintain asepsis) is pulled through the tunnel. Rams
Semen from rams may be collected and used fresh or
frozen for future use. Typically the rams are trained to
service an AV (described in the section on buck evalua-
tion) in the presence of females in estrus or treated
ovariectomized females (i.e., females that have been given
1 mg estradiol benzoate per week or prepared as de-
scribed in the section on libido testing). The semen is col-
lected into a warm (39° C) AV and handled carefully to
avoid exposure to any contaminants or ultraviolet rays.
Temperature control is of utmost importance in the suc-
cessful freezing of semen. The semen should be placed in
an incubator or water bath (30° C).6 Semen intended for
freezing should have a concentration of more than 3 
109/ml and a motility of more than 70% of the ejaculate.
Semen should be extended in a warmed extender (30°
C).7 This extender can be as simple as whole milk or
Dulbecco’s phosphate-buffered saline (PBS) with 10%
fetal calf serum. Other homemade or commercially pre-
pared extenders containing antibiotics, tris, fructose, and
egg yolk may be used. Many methods of semen freezing
are used. Only a few are described here.

Straws. The ejaculate is normally diluted to a ratio

Figure 6-10 This view of the ventral abdomen shows the original
site of the penis (a) and the translocated site (b) to the left flank. With between 11 and 14, with extenders added slowly by
this procedure the penis is moved 45° to one side to prevent constant slow mixing.6,7 The diluent is usually hyper-
intromission. tonic; therefore rapid mixing may cause osmotic shock in
144 • Sheep and Goat Medicine
Cooled Semen
TABLE 6-3
Ram semen also may be collected and chilled for same or
EXAMPLES OF EGG YOLK–BASED SEMEN next day AI. This provides producers with the opportu-
EXTENDERS nity to use semen shipped from other farms.8,9

INGREDIENT EXTENDER* FREEZE BUFFER† Bucks. No established health requirements exist for AI
sires in goats. The health of the individual buck and the
Tris (hydroxy methyl) herd of origin should be evaluated. Two common semen
amino methane (g) 3.634 24.2 collection methods are used in the buck: AV and EE.
Fructose (g) 0.50 10.0 Dairy bucks are handled more often and are more easily
Citric acid trained to use an AV. Semen from meat bucks is more
(monohydrate) (g) 1.99 13.6 commonly collected by EE. The AV method is preferred
Egg yolk (ml) 14 200 because it is quicker, not stressful to the male, and results
Distilled water (ml) 100 1000 in the collection of better-quality semen.7 Semen col-
From Evans G, Maxwell WMC: Salmon’s artificial insemination of
lected by EE is generally of larger volume but lower con-
sheep and goats, Sydney, 1987, Butterworth Publishing. centration than that collected by AV. The frequency at
*Used for both fresh, cooled semen and the initial extender in which semen may be collected depends on the age, condi-
freezing. tion, and temperament of the animal. Bucks can be col-
†pH at 6.8. lected two to three times daily on alternate days. Intervals
of 30 minutes to 1 hour are advisable between daily col-
lections to obtain good-quality semen.7 Labeled ejacu-
lates are placed in a water bath at 35° C until they can be
spermatozoa.6 The extended semen is slowly cooled to evaluated. An immediate 1:1 extension with a diluent
around freezing (4° to 5° C) over a 1.5- to 2-hour period. provides energy and buffer. The semen is evaluated for
The cooled, extended semen should be diluted (usually at volume, motility, concentration, and morphology as de-
a ratio of 11) with an additional freeze buffer containing scribed previously. Accurate determination of the concen-
an energy source, a protein, an antibiotic, and a cryopro- tration of the semen is important; the dilution ratio
tectant (glycerol) before being placed into labeled serum depends on it. Semen can be processed to be used fresh or
straws. The extended semen is then rapidly chilled to frozen in straws in a similar fashion as described for rams.
between 80° and 100° C by placing the filled straws
in liquid nitrogen vapors 4 cm over the surface of liquid COOLED OR FRESH SEMEN: The diluents commonly
nitrogen for 10 minutes. The semen is then rapidly used to dilute buck semen contain either tris or citrate as
cooled to its final storage temperature of 196° C by sub- the buffer, glucose or fructose as the energy source, and
mersing the straws in liquid nitrogen. Formulas for egg yolk to protect the spermatozoal cell membranes
mixing extenders and freeze buffers may be obtained by against cold shock. The concentration of egg yolk should
consulting the references. Some extenders are available be reduced to 2% to avoid it reacting with the coagulating
commercially. An example of an extender with and enzyme present in the seminal plasma.7 This enzyme
without the cryoprotectant is shown in Table 6-3. occurs in greater concentrations when semen is collected
by EE. To overcome any problems with the coagulating
Pellets. Semen also may be frozen into pellets by drop- enzyme, a low-concentration egg yolk diluent or skim
ping cooled semen into depressions drilled or scratched milk can be used or the seminal plasma can be removed
into dry ice. This is a convenient method for freezing, but by centrifugation immediately after collection.7,10 Under
semen treated this way is more difficult to thaw and use. field conditions the most readily available semen diluent
In this method collected semen can be diluted by volume is skim milk. The ultra–heat-treated milk is sterile and
to contain 4% glycerol and 12% egg yolk in a slightly hy- may be used directly as a diluent without any further
pertonic, buffered solution.6,7 Evans6 described an treatment.7 When does are inseminated with fresh sper-
example of 1 volume of semen to 4 volumes of diluent, matozoa by laparoscopic technique, PBS with the addi-
with a diluent of 3.63 g tris (hydroxy methyl) amino tion of 1000 IU of sodium penicillin and 1 mg of strepto-
methane, 0.50 g glucose, 1.99 g citric acid (monohy- mycin per ml can be used as an extender.7 The extended
drate), 15 ml egg yolk, and 5 ml glycerol extended to 100 semen can be inserted by pipette into 0.5-ml straws and
ml with distilled and deionized water. In a cooled, venti- cooled gradually over 1 to 2 hours from 30° C to the
lated room the examiner makes several small circular cuts storage temperature of 5° C. This semen should be used
(0.5 to 0.8 cm diameter) on a flat piece of solid carbon within 6 to 8 hours.7 The semen should be cooled gradu-
dioxide (dry ice). Cooled pipettes (4° C) are used to drop ally over 1 to 2 hours.
0.1 to 0.3 ml into the cut surface of the dry ice. The
semen is allowed to dry for 2 to 3 minutes before the FROZEN SEMEN: Many of the same principles de-
frozen pellets are transferred to the liquid nitrogen.6 scribed for the storage of frozen ram semen are applicable
 Chapter 6 Theriogenology of Sheep and Goats • 145

to goats. Buck semen can be placed in plastic straws and the straw to be thawed with tweezers or forceps. The cane
frozen in liquid nitrogen vapor by either slow or fast is immediately dropped back into the canister, and the
methods. Diluents for freezing buck semen should have canister is immersed in the liquid nitrogen.11,12 Straws
similar properties to diluents used to extend fresh semen. should not be touched by the handler’s hands.11 The cli-
In addition, they should contain an agent to protect the nician should shake the straw (to remove any liquid nitro-
cell membrane during cooling (usually egg yolk) and a gen), quickly identify whether it is the correct straw, and
cryoprotective agent (usually glycerol) to protect the sper- then immerse it in a water bath (33° to 35° C). Straws
matozoa against membrane damage during freezing.7,10 should be thawed based on manufacturers’ recommenda-
Dilution of semen can be performed in two ways. The tions, but generally thawing requires only 40 seconds for
two-step dilution method is similar to that used for bull 0.5-ml straws and 20 seconds for 0.25-ml straws.11 Only
semen. The semen is diluted at 30° C shortly after collec- as many straws as can be used in 10 to 15 minutes should
tion to half of the final diluted volume with a diluent con- be thawed at one time. If possible, the clinician should
taining no glycerol.7 After cooling at 5° C for 1.5 to 2 thaw no more than three straws at one time to avoid low-
hours, the semen is extended to the final volume with a ering the thaw water temperature.11
diluent containing glycerol.7 For one-step dilution the As goblets are emptied, they should be discarded to
semen is gradually diluted to the final pre-freezing expedite the retrieval of straws in the lower goblets.
volume at 5° C in 1.5 to 2 hours in a refrigerator or cold However, if straws are to be retrieved from lower goblets,
room. The two-step dilution method has no advantage the cane is raised until the straws are even with the other
over the one-step method for buck semen. Therefore the cane tops, and then the straw to be used is removed.11,12
one-step method is preferred because it simplifies diluent If pellets are used, the clinician removes the pellets
preparation and reduces the handling of semen before from liquid nitrogen storage and places two or three di-
freezing. rectly in a dry, sterile tube. The tube is kept in a warm
After dilution the semen is loaded in 0.5-ml labeled water bath (37° C). The thawed semen should be pulled
plastic straws and sealed for freezing. The straws are into a pipette and used for AI immediately.6 Alterna-
placed horizontally on a cold rack (5° C) and lowered into tively, some processing techniques may require the addi-
liquid nitrogen vapor 3 to 4 cm above the surface of the tion of a warm diluent to the frozen pellets.
liquid nitrogen in a Styrofoam or other suitable container.
After 7 to 8 minutes the frozen straws are immersed in
liquid nitrogen, carefully packaged into goblets of appro-
priate size, and transferred into liquid nitrogen storage
R EFERENCES
1. Hooper RN: General surgical techniques for small ruminants:
tanks.7 small ruminants for the mixed animal practitioner, Proceedings of
the Western Veterinary Conference, 1998, Las Vegas, NV.
FROZEN SEMEN HANDLING 2. Smith MC, Sherman DM: Goat medicine, Philadelphia, Lea &
Febiger, 1994; pp 411-463.
Frozen semen for bucks and rams is stored in liquid ni- 3. Kimberling CV, Marsh DJ: Breeding soundness evaluation and
trogen (196° C). Any changes in this storage tempera- surgical sterilization of the ram. In Youngquist RS, editor: Current
ture can seriously alter semen quality.11 Semen is most therapy in large animal theriogenology, Philadelphia, 1997, WB
commonly packaged in 0.25- or 0.5-ml straws. The straw Saunders.
is placed in a holding goblet, with two goblets attached to 4. Wolfe DF, Baird AN: Urogenital surgery in goats. In Youngquist
RS, editor: Current therapy in large animal theriogenology, Philadel-
a cane. Multiple canes are set inside a canister, which is
phia, 1997, WB Saunders.
immersed and maintained in a liquid nitrogen tank. The 5. Riddell MG: Prevention of intromission by estrus-detector males.
liquid nitrogen tank lid should be kept closed and the In Wolfe DF, Moll HD, editors: Large animal urogenital surgery,
liquid nitrogen level checked and maintained at an ade- Baltimore, 1999, Williams & Wilkins.
quate level. A schedule of tank maintenance should be set 6. Evans G: Freezing sheep semen. In Dziuk PJ, Wheeler M, editors:
up and followed. A record of where particular semen is Handbook of methods for study of reproductive physiology in domestic
stored (goblet, cane, canister) helps expedite semen trans- animals, Urbana, IL, 1991, University of Illinois Press.
fer and retrieval.12 The tank should be kept in a cool, 7. Evans G, Maxwell WMC: Salmon’s artificial insemination of sheep
well-ventilated room. Straws should not be removed from and goats, Sydney, 1987, Butterworth Publishing.
the tank unless they are to be used; they should not be 8. Buckrell BC et al: Reproductive technologies in commercial use
transferred from tank to tank unless the procedure takes for sheep, goats, and farmed deer, Proceedings of the Society for
Theriogenology, 1997, Nashville, TN.
less than 2 seconds.
9. Mylne MJA, Hunton JR, Buckrell BC: Artificial insemination of
To thaw the straws, the clinician should identify the sheep. In Youngquist RS, editor: Current therapy in large animal
canister holding the cane. The canister is raised until theriogenology, Philadelphia, 1997, WB Saunders.
the cane tops can be seen (5 to 7 cm below the mouth of 10. Cehmineau P et al: Training manual on artificial insemination in
the tank). Straws should be maintained below the frost sheep and goats, Rome, 1991, FAO of the United Nations.
line in the neck of the tank at all times. Using a light 11. Buckrell BC: Guelph system for transcervical AI (user manual),
source to identify the correct cane, the clinician removes Georgetown, Ontario, Canada, Small Ruminant Genetics.
146 • Sheep and Goat Medicine
12. Marshall CE: Handling of frozen semen straws. In Dziuk PJ, artificial manipulation of light to mimic shorter days
Wheeler M, editors: Handbook of methods for study of reproductive hastens the onset of estrus in ewe lambs. Melatonin im-
physiology in domestic animals, Urbana, IL, 1991, University of Illi- plants can cause a similar effect.5,6 Differing reports
nois Press.
about the effect of light manipulation and melatonin im-
plants can be found in the literature.7-9 The sex of sib-
lings in multiple-birth lambings does not seem to affect
FEMALE REPRODUCTION the age of puberty in the ewe10; however, exposure to
intact rams can decrease the time required for the ewe
Ewe
lamb to achieve her first estrus.4 The attainment of
Anatomy. The reproductive tract of the ewe and doe is puberty depends on the interaction of the juvenile hypo-
similar to that of other domestic animals. It is composed thalamus, the anterior pituitary, and the ovary. Estradiol
of the external genitalia (vulva, clitoris), vagina, cervix, secreted by developing follicles has a negative feedback
uterus, oviducts, and ovaries. The vulva has two labia, on LH secretion. As puberty approaches this inhibitory
which are composed of adipose tissue and portions of influence becomes less important and GnRH pulses from
constrictor vulvae muscle covered with skin. The labia are the hypothalamus and subsequent pituitary pulses of LH
marked by dorsal and ventral commissures. On parting become more frequent. This stimulates further follicular
the vulvar lips, the inner surface is easily visualized. The development. As the follicle develops, it produces more
clitoris is homologous to the penis and has some erectile estradiol until a threshold is reached, causing a positive
tissue. The vestibule is located cranial to the clitoris. It is feedback on LH secretion.11 The resultant LH surge
lined with stratified squamous epithelium, rich in mucous induces the luteinization of the follicle and usually ovula-
glands. The vestibule of the ewe contains paramedian tion. The life span of the resultant corpus luteum (CL)
glands that exist along the urethral orifice; the doe lacks is usually shorter than that of subsequent cycles. This
these glands. first ovulation in the sheep is not associated with behav-
The tubular portion of the tract (vagina, cervix, uterus, ioral estrus. The second and subsequent cycles of follicu-
oviducts) is composed of an outer serosal surface, a double lar growth, LH secretion, and CL development appear
layer of muscular tissue, submucosa, and a mucosal layer. more normal and result in behavioral estrus. Follicle-
The vagina is located cranial to the vestibule. In the stimulating hormone (FSH) also is released from the an-
normal position the vaginal walls are collapsed into folds. terior pituitary gland in response to GnRH.12
The vaginal lumen is composed of stratified squamous Sheep are considered short-day breeders because their
epithelium. The cervix is located at the most cranial breeding season is regulated by the length of the day or,
portion of the vagina and is found in a subtle depression more specifically, by the increased duration of night.13
near the vaginal floor. The canal of the cervix has 5 to 6 Light duration and timing affect not only the induction
and 5 to 8 irregular overlapping rings in the ewe and doe, of estrus, but short daylight regimens also can affect the
respectively. This tortuous, narrow, cervical lumen causes length of the breeding season.14 Seasonality is controlled
great difficulty in transcervical AI, particularly in the ewe. by the visual perception of light that is transmitted by the
The cervix of the ewe and doe, unlike the vagina, is not superior cervical ganglion to the pineal gland. The pineal
easily dilatable. The cervix opens cranially into the gland produces melatonin and secretes it during the
uterine body. The bicornate uterus is composed of a short night. Alteration in melatonin secretion provides cues to
body and two horns that, in the nongravid state, are the hypothalamus in its pulse generations of GnRH.12
slightly coiled and lie in the pelvic canal. The serosal The hypothalamus also changes in its sensitivity from a
surface of the uterus is slung in the abdominal cavity by strictly negative feedback response to estrogen (from the
the highly vascular broad ligament. The endometrium is a developing follicles) to a positive feedback from increas-
pink-gray structure with folds that have convex caruncles. ing concentrations of estrogen.15 The increased pulses of
Melanin pigmentation is found in these caruncular GnRH appear responsible for the induction of estrus
regions in some breeds of sheep (Hampshire). This during the breeding season.16 In seasonally breeding
pigment is rare in goats. animals a similar scenario occurs during puberty as is ob-
The two oviducts attach the uterine horns to the served in the yearly transition from anestrus to the sea-
ovarian bursa. The small (1.5 by 1 to 2 cm) oval ovaries are sonal cycle. However, much variation occurs among
partially covered by the ovarian bursa. The ovarian surface breeds with respect to the occurrence and length of the
is usually rough. During the breeding season or during breeding season. Dorset, Merino, Rambouillet, and
gestation, the ovary can have two or more progesterone- Finnish-Landrace sheep tend to have longer breeding
secreting corpus lutea. seasons, whereas the Southdown, Shropshire, and Hamp-
shire breeds respond to day length and adhere to the
Physiology. Age, nutritional status, and season of the short-day breeding season. Sheep living near the equator
year all play roles in the development of sexual maturity (or breeds that originated there such as the Barbados) are
in the sheep.1-4 The approach of the breeding season or usually less sensitive to the effects of the seasons.
 Chapter 6 Theriogenology of Sheep and Goats • 147

Estrus cycle. Estrus in the ewe lasts between 15 and 45 limits antibodies moving from the maternal to the fetal
hours (with an average of 30 hours), and the interval circulation, necessitating the ingestion of colostrum by
between estrous activity is between 14 and 19 days (with the neonate for antibody transfer. After day 75 the con-
an average of 17 days)—3 to 5 days of metestrus, 7 to 10 centration of progestin in the peripheral blood markedly
days of diestrus, and 2 days of proestrus). Ewe lambs, increases. This increase results from the placental produc-
ewes cycling outside of the normal breeding season, and tion of progestin and is of major clinical significance
transitional ewes tend to have shorter estrus periods. As because luteolytic agents cannot guarantee abortion after
estrus approaches, the larger follicles of the FSH-induced day 75 of gestation. Parturition occurs as a result of a
follicular wave begin to produce more estradiol. This complex set of interactions involving the uterine muscu-
signals the hypothalamus to secrete GnRH, which results lature and fetus. As the fetal hypothalamus matures, it
in the release of LH by the anterior pituitary gland. This begins producing increasing amounts of corticotropin-
LH surge typically occurs about 9 hours after the onset of releasing hormone, which stimulates the pituitary gland
estrus. The high estradiol concentration is partially re- to produce and release corticotropin. This in turn stimu-
sponsible for the ewe showing signs of estrus. However, lates the fetal adrenal glands to produce and release corti-
the sheep also must have been recently exposed to proges- sol. Endogenous cortisol results in an increase in the
terone. Sheep ovulate toward the final third of estrus or estradiol, PGF2a, and prostaglandin-E2 (PGE2) concen-
occasionally after the end of behavioral estrus.17 Ovula- trations. This in turn decreases progesterone production
tion typically occurs 14 to 26 hours after the LH surge. and relaxes the cervix. Uterine responsiveness to oxytocin
This coincides with about 21 to 45 hours after the begin- also increases because of the estrogen-induced recruit-
ning of estrus. The length of estrus may vary depending ment of oxytocin receptors. Normal parturition occurs
on the breed, with wool breeds generally having a longer over a period of 3 to 8 hours. The first stage of parturition
estrus than meat breeds. Signs of estrus include vulvar (initiation of organized contractions) lasts from 1 to 4
swelling and anorexia in the ewe. The ewe may secrete hours. The second stage (active labor and delivery of the
small amounts of mucus, much less than that secreted by fetus) lasts as long as 2 hours. The final phase of parturi-
the cow. tion is the delivery of the placenta and should occur
After ovulation the follicle becomes luteinized and within 8 hours after the fetus is delivered.12
begins producing progesterone. The progesterone con-
centration remains elevated for about 12 to 13 days. In
the absence of a conceptus the ovaries produce oxytocin
Doe
and the uterine endometrium begins to secrete Physiology. From a pure physiologic standpoint, sheep
prostaglandin F2a (PGF2a). The PGF2a is transported and goats have great similarities. Nevertheless, they are
away from the uterus by the uterine veins and is trans- dissimilar in length of the estrus cycle and maintenance
ferred directly to the ovarian arteries that run adjacent to of pregnancy. Goats in a temperate region are polyestrous
the veins. The increased concentration of PGF2a in the and breed efficiently when day lengths are short (August
ovarian arteries leads to the regression of the luteal tissue to March), with a peak breeding season of October
and diminished progesterone secretion. The cycle begins through December.19 The transitional periods are ap-
again with a decrease in serum progesterone, concurrent proximately 2 months before and after breeding season,
development of the follicle, and a subsequent increase in with deepest anestrus in April and May.20,21 In tropical
serum estrogen concentrations. Ovum transport to the areas near the equator, native breeds show less seasonality
uterus takes 2 to 4 days in ewes. Approximately 12 days and breed year-round (as do sheep). Variation in season-
after conception, signals are sent to the endometrium and ality occurs among and within breeds, which allows for
ovaries to prevent lysis of the luteal tissue and to maintain selection of out-of-season breeders.20,22 For example,
the pregnancy. The substance that inhibits uterine pro- pygmy and Tennessee stiff-legged meat goat breeds tend
duction of estrogen receptors is interferon-t; the decrease to cycle year-round in North America, whereas Nubian,
in estrogen receptors in turn inhibits oxytocin receptors. Spanish, Boer, and Kiko goats show more seasonality.21
This breaks a link in the production of luteolytic amounts Producers can use this seasonality to their advantage in a
of PGF2a.18 Attachment of the embryo to the uterine en- synchronization program by introducing bucks during
dometrium is a slow process, beginning around day 18. the summer transitional period to induce estrus in does.
This “buck effect” is lessened when males live year-round
Gestation. The normal gestation length of the ewe is with does.
145 to 150 days. Sheep have a cotyledonary, epitheliocho-
rial placenta. The placental cotyledon and the maternal Puberty. Does reach sexual maturity and begin to cycle
caruncle together form a placentome. In the pregnant at 6 to 8 months.19 In pygmy goats, puberty may occur as
ewe, 90 to 100 cotyledons are dispersed over the chori- early as 3 months. Generally a single-born doe has her
onic membrane. Around day 16 the chorion begins at- first ovulation in the fall after her birth. Breeding should
taching to the uterine caruncles. This type of placenta be delayed until a doe has attained 60% to 70% of her
148 • Sheep and Goat Medicine
predicted adult weight (or 60 to 70 lb in meat goats and
70 to 90 lb in dairy breeds).21
R EFERENCES
1. Mukasa-Mugerwa E, Kasali OB, Said AN: Effect of nutrition and
endoparasitic treatment on growth, onset of puberty and reproduc-
Estrus cycle. The length of the estrus cycle in the doe tive activity in Menz ewe lambs, Therio 36:319, 1991.
is 21 days (with a range of 18 to 22 days). Although vari- 2. Forcada F, Abecia JA, Zarazaga L: A note on attainment of
ations exist, estrus tends to be longer in does than in puberty of September-born early-maturing lambs in relation to
level of nutrition, Anim Prod 53:407, 1991.
ewes. Short cycles of 5 to 7 days are more common at the
3. McCann MA et al: Effect of rapid weight gain to puberty on re-
beginning and end of the breeding season in does.19 After
production, mammary development and lactation in ewe lambs,
midsummer, the decreasing day length causes increased Therio 32:55, 1989.
melatonin release from the pineal gland, and the sequence 4. Kassem R, Owen JB, Fadel I: The effect of pre-mating nutrition
of hormonal events is similar to that seen in the ewe. and exposure to the presence of rams on the onset of puberty in
During estrus and seasonal anestrus, plasma progesterone Awassi ewe lambs under semi-arid condition, Anim Prod 48:393,
concentrations are less than 1 ng/ml, whereas proges- 1989.
terone levels during the luteal phase are 4 to 8 ng/ml19,20 5. Rajkumar RR, Argo CM, Rodway RG: Effect of melatonin on
(Figure 6-11). pulsatilla release of luteinizing hormone in female lambs, Horm
Estrus varies from 24 to 72 hours, with most does ex- Metab Res 24:229, 1992.
hibiting estrus for 36 hours. Does in estrus are restless, 6. Fitzgerald JA, Butler WR: Sexual maturation of ewes raised
without ram exposure in a controlled lighting environment, Therio
wag their tails, vocalize, and have swollen vulvas with
29:811, 1988.
clear mucous discharge that changes to cloudy toward the
7. Kennaway DJ et al: Pituitary response to LHRH, LH pulsability
end of estrus. These behaviors may be pronounced in the and plasma melatonin and prolactin changes in ewe lambs treated
presence of a buck. Milk production and appetite may de- with melatonin implants to delay puberty, J Repro Fert 78:137, 1986.
crease during estrus in dairy goats. Well-fed, healthy, 8. Nowak R, Rodway RG: Effect of intravaginal implants of mela-
mature does average two to three ovulations per cycle, tonin on the onset of ovarian activity in adult prepuberal ewes, J
which results in a high proportion of multiple births. Repro Fert 74:287, 1985.
9. Sunderland SJ et al: Effect of photoperiod before and after birth
Gestation. Twins or triplets are more common than on puberty in ewe lambs, Bio Repro 53:1178, 1995.
single kids. Oviductal transfer of the embryo(s) requires 3 10. Meridith S, Kiesling DO: Age of puberty in ewes which developed
to 4 days in goats. The average duration of gestation is 5 prenatally with either a ram or a ewe fetus, Small Rumin Res
20:137, 1996.
months, with a range of 147 to 155 days.19 Similar to
11. Kinder JE et al: Endocrine basis for puberty in heifers and ewes, J
ewes, does have epitheliochorial, cotyledonary placentae.
Repro Fert-Suppl 49:393, 1995.
Pregnancy is maintained by progesterone, which is pro- 12. Stellflug JN, Weems YS, Weems CW: Clinical reproductive phys-
duced entirely by the CL of pregnant does and not by the iology in ewes. In Youngquist RS, editor: Current therapy in large
placenta. This is different from ewes, which maintain suf- animal theriogenology, Philadelphia, 1997, WB Saunders.
ficient progestogen output from their uteroplacental 13. Sweeny T, O’Callaghan D: Physiology of seasonal reproductive
units. The plasma concentration of progesterone remains transitions in the ewe—regulation by photo period and other envi-
high until about 4 days before parturition. ronmental cues, Repro Domestic Anim 30:178, 1995.

Estrus Progesterone Estrus

Ovulation Ovulation
Relative levels

Estradiol
Estradiol

Luteinizing hormone

18 20 21 1 4 6 8 10 12 14 16 18 20 21 1 4
Day of cycle

Figure 6-11 A schematic diagram of the caprine estrus cycle showing a follicular stage of the cycle.
Plasma progesterone levels decline, removing the negative feedback from the pituitary and permitting the
increased release of LH, which in turn acts on the follicle to subtly increase estrogen production and
ovulation. Note that the LH and estradiol levels are highest when progesterone levels are lowest. The
ewe’s cycle is very similar, with one major exception: it is 3 to 4 days shorter.
 Chapter 6 Theriogenology of Sheep and Goats • 149

14. O’Callaghan D et al: Role of short days in timing of onset and du-
BREEDING MANAGEMENT
ration of reproductive activity in ewes under artificial photoperi-
ods, Bio Repro 44:23, 1991. Ewe
15. Karsch FJ et al: Seasonal changes in gonadotropin-releasing
To maximize reproductive potential, keepers should
hormone secretion in the ewe: alteration in response to the nega-
maintain ewes in a healthy and disease-free state with a
tive feedback action of estradiol, Bio Repro 49:1377, 1993.
16. Barrel GK et al: Seasonal changes of gonadotropin-releasing
body condition score between 2.5 and 3.5 at the initiation
hormone secretion in ewe, Bio Repro 46:1130, 1992. of the breeding season. Ewe lambs should be bred so that
17. Keisler DH: Endocrine control of reproduction in the ewe and they go through parturition earlier in the season than
ram: a review. Small ruminant short course, Proceedings of the older ewes. Ewes require at least one cycle of increasing
Society for Theriogenology, p 2, 1994, Nashville, TN. day length before the decreasing day length that signals
18. Spencer TE, Becker WC, George P: Ovine interferon-tau regu- the breeding season in order to cycle. Replacement lambs
lates expression of endometrial receptors for estrogen and oxytocin should be chosen from a pool of lambs born early in the
but not progesterone, Bio Repro 53:732, 1995. previous lambing season. Ewe lambs should weigh ap-
19. Smith MC: Clinical reproductive anatomy and physiology of the proximately 70% of their projected mature weight at the
doe. In Youngquist RS, editor: Current therapy in large animal the-
time of breeding.
riogenology, Philadelphia, 1997, WB Saunders.
20. Hill J: Goat reproductive management, Proceedings of the Sym-
posium on Health and Disease of Small Ruminants, American As- Doe
sociation of Small Ruminant Practice, p 114, 1996, Nashville,
TN. Replacement doe kids should be selected at weaning (4 to
21. Mobini S: Reproductive management in goats, Proceedings of the 5 months). Selection of meat does should emphasize traits
North American Veterinary Conference, vol 14, p 219, 2000, Orlando, such as reproduction and soundness. Milking does are se-
FL. lected based on production traits such as soundness of the
22. Wilddeus S: Reproductive management for meat goat production, udder and teats, adequate body size, and good body condi-
Proceedings of the Southeast Region Meat Goat Production Sympo- tion. Female goats that were born as twins or triplets, those
sium, Tallahassee, FL, 1996, Florida A & M University. born early in the season, and those whose dams gave birth
more than once each year are preferable replacement does.
BREEDING SOUNDNESS All females of breeding age should be maintained in a
single group. Breeding should be delayed until a doe has
EXAMINATION OF THE FEMALE attained 60% to 70% of its adult weight at a body condi-
History is an essential component of a BSE of a doe or tion score of 3 to 3.5. Does that do not kid by the time they
ewe because of the inaccessibility of the majority of the are 2 years old should be culled. Breeding does should not
reproductive tract to palpation or visual inspection. His- be allowed to become too thin or too fat. Thin does may
torical information of significance includes duration of fail to conceive, have low twinning rates, and produce kids
heat, interestrous intervals, reaction to the male, and with low weaning rates. Obese does can suffer from preg-
breeding and kidding history. A general physical exami- nancy toxemia and/or decreased milk production if they
nation emphasizing body condition, femininity, confor- are allowed to become fat before the onset of puberty.
mation of the mammary glands, and determination of
whether the female is polled or horned is important in
the evaluation of breeding soundness.
Control of the Estrus Cycle
External genital examination should include evalua- With the increasing use of AI and the desire of produc-
tion of the anogenital distance and whether the clitoris ers to concentrate their efforts around lambing, control of
is visible without parting the lips of the vulva. The the estrus cycle of the female is necessary. Estrus syn-
vulva should be examined for abnormalities. A clear chronization programs useful in goats and sheep are
AI speculum or an endoscope can be used to evaluate shown in Box 6-2. Producers often request estrus syn-
the vagina and cervix. The clinician should note any chronization during the fall breeding season and to
discharges from the cervix or vagina. A normal, clear induce estrus during the winter anestrous period (non-
mucous vaginal discharge in early standing estrus that breeding season) and summer transitional period. To
turns into a cloudy or creamy mucous discharge late in maintain a continuous milk supply from dairy goats and
standing estrus is common, particularly in does. Trans- sheep, the flock should be divided into four equal breed-
abdominal ultrasonography can be used to examine ing groups. This necessitates some form of estrus syn-
the uterus for pregnancy and pseudopregnancy. Pseudo- chronization. In the Northern Hemisphere, these groups
pregnancy is a more common problem in does than should be assigned to breedings in late August, mid-
in ewes. Transrectal probes often allow visualization October, mid-November, and late December. Ade-
of the non-pregnant uterus and ovaries and early quate nutrition, estrus detection, and adequate sire or
pregnancy. insemination capabilities are essential components of a
150 • Sheep and Goat Medicine
BOX 6-2

M ETHODS OF E STRUS C MYCLE ANIPULATION U SED IN S

HEEP AND G OATS IN THE U S NITED TATES

EWE DOE
BREEDING SEASON BREEDING SEASON
• Prostaglandins (single or double injections 9 to • Prostaglandins (single or double dose)
11 days apart) • Progestins (PO or SC) for 14 days
• Progesterone implants for 14 days used alone • Progestins for 14 days plus 4 ml of PG 600 24 to 48
or in conjunction with PG 600* hours before or at the time of implant removal
• Oral melengestrol acetate (MGA, 0.125 mg/
ewe/day BID for 14 days)
TRANSITIONAL SEASON TRANSITIONAL SEASON
• Ram effect • Buck effect
• Progestin (MGA, implants, or pessary) for 8 • Progestin for 14 days plus 5 ml of PG 600 48 hours
to 14 days plus PG 600 up to 48 hours before before progestin removal
progestin removal
OUT OF BREEDING SEASON OUT OF BREEDING SEASON
• Selection of breeds and individuals that cycle • Progestin for 14 days plus 5 ml of PG 600 48 hours
out of season or early in breeding season before progestin removal
• Progestin (MGA, implants, or pessary) for 8 • Lighting programs
to 14 days plus PG 600 up to 48 hours
before progestin removal
• Ram effect
• Light manipulation
• Melatonin administration

*PG 600 (400 IU eCG and 200 IU hCG/5 ml vial), Intervet, Millsboro, NC.

synchronization program. Because any form of stress can with estradiol cypionate (2 mg IM) for 2 weeks before
affect the efficacy of a synchronization program, stress using him to breed. Males that have undergone vasectomy
should be minimized as much as possible. or epididymectomy and castrated males treated with
testosterone (100 mg weekly for 3 weeks) may be used. Re-
Ram or buck effect. Introducing a buck or ram into a gardless of the type of teaser male used, he should be intro-
group of transitional period does or ewes is a powerful tool duced to the females for 2 to 3 weeks to bring them into
to induce estrus.5-7 Introducing a ram into a ewe herd heat before the desired breeding male is brought in. The
induces estrus in most ewes within 6 days. The females first estrus after introduction of the male is usually silent.
should have no contact with the males for 3 to 4 weeks
before their introduction. Suddenly placing the male with Prostaglandins. PGF2a can be used to lyse the CL
females induces an LH surge and ovulation within a few and bring diestral females into heat. Goats and sheep are
days. Similarly, fence line contact by males can be used to generally susceptible to prostaglandin-induced luteolysis
achieve a ram or buck effect for hand mating. The use of after days 5 to 6 of the estrus cycle. This method of estrus
high-performing rams, as defined by serving capacity synchronization should be used if the producer is sure
tests, has been shown to be more effective in inducing early that a significant number of ewes and does are actively
ovulation than the use of low-fertility rams.6 The response cycling; it is most effective during the middle to late fall
to male stimulation can be quite variable and is influenced (October and November in North America). One shot of
by breed, previous isolation, depth of anestrus, nutrition, PGF2a can be expected to result in 60% to 70% of the
and length of time since parturition.This technique can be females in the flock exhibiting estrus within 30 to 60
used in combination with pharmacologic out-of-season hours. Ewes or does that do not show estrus after a prop-
breeding programs and appears to enhance their efficacy. erly administered prostaglandin injection have either
Males should be isolated from females for 30 to 60 days been in estrus recently or are anestrous. A two-treatment
before introduction. When using the ram or buck effect in method involving a second injection 9 to 11 days after the
out-of-season breeding, producers should expose the male first results in tighter synchrony within the flock. An al-
to a cycling female or an ovariectomized female treated ternative is to observe the flock actively for 4 days, breed
 Chapter 6 Theriogenology of Sheep and Goats • 151

all females that come into estrus during this time, admin- of eCG and human chorionic gonadotropin (hCG) while
ister PGF2a on the fourth day, and breed all females that removing the progestin can help tighten synchrony in the
come into estrus during the next 3 days. This should herd.1 Administering prostaglandins 24 hours before
result in most females being bred within a 7-day period. progestin removal, followed by eCG 24 to 48 hours
Both PGF2a (10 to 20 mg) and cloprostenol (75 mg per before or at the time of progestin removal may further
45 kg of body weight) are used for estrus synchroniza- tighten estrus synchrony. The use and removal of these
tion.1 Producers should ensure that none of the ewes or progestin products also may hasten estrus in the non-
does are pregnant at the time of administration of breeding season.3
prostaglandins because abortion may be induced.
Seasonal manipulation. Seasonal manipulation of the
Progestins. Progestins are used to synchronize estrus by female cycle can be used to hasten the onset of estrus to
delaying its onset. Exogenous progestin can be used obtain more than one breeding per year. Seasonal manip-
during the breeding season to control the length of the ulation also can change the time of lambing and kidding
luteal phase artificially. The use of progestins is the most and lactation to better match forage availability. Dairy
common method of estrus synchronization in goats for AI goats should be more than 120 days into the lactation
or embryo transfer. The most common route of applica- period before the producer attempts an out-of-season
tion of progestin is transvaginal. After the progestin prod- breeding program.8 All animals should be examined with
ucts are removed, estrus should occur within a few days. real-time ultrasonography equipment to determine
Placing sponges that contain progesterone into the vagina whether any reproductive abnormalities exist that may
(controlled intravaginal drug-releasing devices, or CIDRs) preclude the effectiveness of an out-of-season breeding
is becoming a popular method of estrus control in some program (e.g., pregnancy, hydrometra).8 Artificial light-
countries.2 Several progesterone concentrations are avail- ing, either by itself or in conjunction with exogenous
able in CIDRs. However, devices containing 366 mg melatonin can be used for effective manipulation of the
appear to yield the most reproducible responses in the ex- breeding season. The sudden introduction of the male
perience of one of the authors (Dr. Pugh). Occasionally maximizes the efficacy of light-melatonin programs. Ar-
CIDRs may be difficult to remove if the string is not tificial lighting is mostly employed to mimic a long day.
visible from the vulvar lips or the sponge has adhered to During the Northern Hemisphere winter, long days (ap-
the vaginal wall. In both cases the examiner should restrain proximately 20 hours of light) can be simulated for 2
the female, introduce a gloved finger into the vaginal vault, months (in a barn) and then stopped on March 1.
identify the CIDR, and carefully remove it after separating Animals are then exposed to natural daily sunlight. After
it from the vaginal wall. The use of norgestomet implants 6 weeks of natural daylight exposure, males are intro-
(1⁄2 to 1 implant, or 3 to 6 mg) inserted between the skin duced and a fertile estrus occurs within 10 to 20 days.
and cartilage of the dorsal aspect of the ears’ pinnae also Does undergoing this type of estrus manipulation have a
are commonly used. Synchronization rates after feeding short breeding season of around 60 days. Bucks and rams
melengestrol acetate are similar to those encountered with also may benefit from this type of treatment to increase
norgestomet implants.4 The feeding of oral melengestrol libido and quality of semen. Light manipulation, al-
acetate (0.22 mg/ewe or doe for 14 days, or 0.125 mg/ewe though effective, is rarely practical (see Box 6-2).
or doe twice daily for 14 days) also is of value in control- Some producers combine hormones and lighting for
ling estrus. However, it is generally recommended that out-of-season breeding. Lighting manipulation is used
breeding be delayed until the second heat after the mel- successfully in many dairy goat operations. Exogenous
engestrol acetate feeding is discontinued.1 Also, if proges- melatonin can be administered to supplement the en-
terone is added to the feed, a continuous adequate intake is dogenous release and thereby mimic the short days asso-
imperative. This may be a problem in goats and some ciated with the onset of breeding season. Exogenous
sheep, particularly if inadequate feeder or bunk space is melatonin can be given as a slow-release implant, repeat-
available. All of these methods require the removal of the edly as an injection, or orally over 30 to 60 days to accel-
progestin after 9 to 14 days in the ewe, and 12 to 14 days erate the onset of breeding. After the cessation of mela-
in the doe. The removal of the progestin source can be tonin administration, females begin to cycle in 40 to 70
used to synchronize the entire flock at one time. The flock days. The lack of availability of this drug limits its use.
can be divided, and the progesterone source removed daily, Exogenous melatonin should be combined with the in-
so that one ram can be used for breeding or the AI troduction of the male. Melatonin works most efficiently
program can be spread out. Estrus can be expected about in dairy goats when combined with artificial lighting for
24 to 48 hours and 24 to 36 hours after the removal of the out-of-season breeding.
progesterone sources in ewes and does, respectively. The most commonly used program for out-of-season
Introducing a teaser male 24 hours after progestin breeding is a combination of progestin (delivered as an
removal enhances synchrony. Administering equine implant in the ear [norgestomet] or vaginally [CIDR])
chorionic gonadotropin (eCG, 250 IU) or a combination and pregnant mare serum gonadotropin (PMSG) or
152 • Sheep and Goat Medicine
eCG. The progestin should be injected, fed, or implanted sources, decrease some parasite burdens, and improve lamb
for 14 days. A gonadotropin, either FSH or PMSG, is or kid supplies for some seasonal markets. Ewes and does
administered 48 hours before progestin removal. PMSG can be selected to begin a fall lambing or kidding flock.9
(400 IU) is most commonly used because it requires only Selected females should be highly prolific and should have
one injection. In areas where PMSG is not available for given birth early in the traditional lambing or kidding
use, a product containing both hCG and PMSG can be season. If they are normal, ewe lambs or doe kids from
substituted. Variable results have been reported with the these reproductively efficient females should be saved as re-
use of these products depending on the timing and placements. The producer should plan on retaining 30% to
dosage of administration. The introduction of a buck or 40% more lambs or kids than are needed to select for out-
ram enhances the synchronization of these programs. of-season breeding potential.9 This process should be re-
peated over several years to identify animals that will serve
well in off-season breeding programs. Producers who do
Increasing Twinning Rates not have record systems to identify superior females should
Most successful sheep-rearing enterprises depend on the expose the flock to superior rams or bucks in the spring and
number of lambs raised and sold per ewe per year. Genetic retain any females that become pregnant to create a fall
selection for prolific ewes can be slow because of the low lambing flock. Females that do not lamb or kid can be
heritability of the trait (10%), but some breeds tend to exposed to males in the fall to follow traditional breeding
have this predisposition (Finnish-Landrace sheep). programs. Males should be selected using a similar ap-
However, large variation occurs among flocks with regard proach. Males born to the more prolific females should be
to this trait. This variation allows for the selection of supe- selected as replacement males and older rams or bucks that
rior animals with a good potential for genetic progress.9 A have a proven history of superior fertility should be used.
review of several studies suggests that an annual improve- Good record-keeping systems and individual identifica-
ment of 1.3 lambs per 100 ewes can be obtained. Although tion of females are essential in any selection program.
this number may seem small, when results are compiled Females born early in the lambing season as twins should
over several years, a sizable influence on flock revenues is be selected as replacements. With respect to growth traits,
apparent. The ability to select prolific females depends twins should be compared with other sets of twins because
highly on accurate records. The more information that is early selection based on size alone may discriminate against
collected on each individual ewe or doe, the more accurate them compared with singletons. Ewe lambs of most meat
the selection becomes. Replacement females should be se- breeds should weigh about 100 lb by the time they are 7
lected from lambs or kids born to females that consistently months old. Selected lambs should be bred at about 10
produce a larger than average number of young per year. months so they will lamb at 15 months early in the spring.
The management practice of providing supplemental Ewes that bear twins early during lambing should be se-
feeding to ewes 2 to 3 weeks before breeding (commonly lected for the accelerated fall lambing flock.10-12
known as flushing) can result in increased ovulation rates
(see Chapter 2). The most demonstrative response to sup-
plemental feeding is seen in flocks that are experiencing a
Sheep
low lambing rate and whose nutritional status is not ade- A similar program for sheep, termed the STAR manage-
quate. Flushing has little benefit if the ewes are already in ment program, has been developed at Cornell University.
good body condition. Ewes can be flushed by feeding 1 lb The STAR program’s unique feature is that it allows for an
of a high-energy supplement (e.g., corn, oats, barley, or a almost continuous supply of market lambs. This is a good
combination) per day. An increase in numbers of twins and fit with the year-round niche market that many producers
triplets requires a concomitant increase in the ovulation have developed. A chart of the calendar year is made using
rate; the embryos also must be in an acceptable environ- a 5-pointed star. The time lag between each point on the
ment for survival. Stressors that may be associated with star is 73 days, which is also approximately half of the
decreased embryonic survival include the female’s age, normal gestation length of the ewe. Therefore an individ-
body temperature of both the male and the female, lacta- ual ewe exposed to the ram at the time corresponding to
tion status during breeding, and overall nutritional status.9 one point on the star will lamb at the time corresponding
Females bred outside of the normal breeding season may to the third point on the star (146 days later). She can then
not be as prolific as those bred during it. be exposed to the ram at the fourth point on the star (216
days after the first breeding). This spreads lambing
ALTERNATIVE BREEDING throughout the year, and provides five lambings in 3 years.
The use of this system is contingent on the selection of
PROGRAMS highly prolific ewes that have the ability to cycle and con-
Certain sheep breeds (Rambouillet, Dorset, Finnish- ceive out of season. Accelerated breeding programs place
Landrace) and goat breeds (pygmy, Tennessee stiff- demands on the producer to improve management of the
legged) can be encouraged to breed outside of the tradi- flock’s nutritional program and ensure that rams have ex-
tional breeding season. This may be done to match forage cellent potential reproductive ability. These complex
 Chapter 6 Theriogenology of Sheep and Goats • 153

breeding schemes also demand the accurate identification 12. Keisler DH, Buckrell BC: Breeding strategies. In Youngquist RS,
of individual animals so that ewes capable of out-of- editor: Current therapy in large animal theriogenology, Philadelphia,
season breeding can be identified and replacement animals 1997, WB Saunders.
13. Karatzas G et al: Fertility of fresh and frozen-thawed goat semen
can be chosen from these females.12
during the non-breeding season, Therio 48:1049, 1997.

Goats
In a controlled accelerated kidding program in which
NATURAL BREEDING SYSTEMS
three kid crops every 2 years is desired, out-of-season Natural breeding is more commonly used in meat and
breeding is necessary. This requires intense management, fiber sheep or goat production systems, whereas AI or
early weaning, and hormonal manipulation of does for in- hand mating is the most common means of breeding in
duction and synchronization of estrus. Seasonal effects on dairy goats or sheep and the method most commonly
reproductive characteristics also have been documented in used by purebred breeders. In a meat production system,
bucks. Buck libido and ejaculate quality and quantity productivity is largely a function of the number of off-
appear highest in late summer and fall, which coincides spring born and weaned and the frequency with which
with the seasonal breeding patterns of the does. Distinct they are produced. The desired date of parturition in a
behavior changes and odors also occur in the males in the given farm dictates the breeding date and the manage-
fall to trigger the buck effect in bringing the female into ment of the breeding male. Females are usually bred in
heat. Bucks can be used successfully for out-of-season the fall for spring kidding or lambing. Bucks should be
breeding without any additional treatment.13 However, kept separate from the does until they are to be used for
they will benefit from winter light treatment to increase breeding. After establishing a mating time, the producer
libido and quality of semen. Producers also can accomplish should leave the bucks with the does for 32 days 11⁄2 re-
this by administering 50-mg GnRH injections three times productive cycles) and the rams with the ewes for 27 days.
daily for 4 days to boost testosterone production.3 This ensures that all kids or lambs are born within about
1 month of one another, reducing the amount of supervi-
sion required at kidding time. The male-to-female
R EFERENCES
1. Rowe JD: Reproductive management of sheep and goats, Proceed-
mating ratio depends on the age and SC of the male, the
size of the mating area, and whether one or more rams or
bucks are to be used. Meat goat production systems
ings of the Annual Meeting of the American Veterinary Medicine Asso-
should have 1 buck per 30 does. A buck may breed 50 to
ciation, p 616, 1998, Schaumburg, IL.
2. Wheaton JE et al: CIDR: a new progesterone releasing intravagi-
200 does in a single breeding season, but 3 to 4 bucks
nal device for induction of estrous and cycle control in sheep and should be put with 100 does.1 Most sheep producers
goats, Anim Repro Sci 33:127, 1993. should keep 3 to 5.5 adult rams per 100 ewes. A marking
3. Bulgin MS: Increasing reproductive performance of the ewe flock, harness should be used on the males to identify which
Proceedings of the Society for Theriogenology, p 244, 1990, Nashville, females have been bred. In commercial flocks, males
TN. should be changed at least every 2 years to prevent in-
4. Quispe T et al: Estrous synchronization with melengestrol acetate breeding. Bucks or rams of high libido and good semen
in cyclic ewes. Insemination with fresh or frozen semen during the quality can be used in a staggered breeding program in
first or second estrous post treatment, Therio 41:1385, 1994. which seven or eight synchronized ewes or does exhibit-
5. Cushwa WT et al: Ram influence on ovarian and sexual activity in
ing estrus at the same time are placed with the male for
anestrous ewes: effect of isolation of ewes from rams before joining
breeding. Hand mating of males can be used as a modifi-
and date of ram introduction, J Anim Sci 70:1195, 1992.
6. Perkins A, Fitzgerald JA: The behavioral component of the ram
cation of staggered breeding, with the same female ratio
effect: the influence of ram sexual behavior on the induction of of 71 to 81. Table 6-4 outlines a proposed male-to-
estrous in anovulatory ewes, J Anim Sci 72:51, 1994. female ratio.
7. Haresign W: Manipulation of reproduction in sheep, J Repro Fert
45(suppl.):127, 1992.
8. Rowe JD, East NE: Reproductive management—estrous cycles,
ARTIFICIAL INSEMINATION
synchronization, artificial insemination, pregnancy diagnosis: The goat and sheep industry has used AI commercially in
small ruminants for the mixed practitioner, Proceedings of the North America for many years.The cervix of the doe is less
Western Veterinary Conference, p 137, 1998, Las Vegas, NV. of an obstacle to insemination than the cervix of the ewe.
9. Thomas DL: Improving reproductive performance of sheep
As a result, commercial AI programs using fresh or frozen
through selection, Proceedings of the Society for Theriogenology, p
semen have been developed and are used most commonly
178, 1996, Nashville, TN.
10. Robinson JJ: Embryo survival in the sheep, Proceedings of the
in goats. Advantages of AI include the following2:
Society for Theriogenology, p 270, 1995, Nashville, TN.
11. Fitch GQ: A breeding program for fall lambing, OSU extension • Maximal use of outstanding sires
facts, no 3801, Stillwater, OK, 2000, Cooperative Extension • Elimination of the need for rams and bucks on the
Service, Oklahoma State University. farm
154 • Sheep and Goat Medicine
TABLE 6-4 producer may inject eCG (200 to 500 IU) when removing
the progestin.
RECOMMENDED MALE-TO-FEMALE RATIOS Because no uniform standards are available for freez-
FOR RAMS AND BUCKS ing goat or sheep semen, any frozen semen to be used
should be evaluated before an AI program is begun.
ANIMAL COMMENT MALE-TO-FEMALE RATIO Optimal timing of insemination is an important factor in
the success of AI programs. Females do not ovulate until
1-year-old In a paddock late estrus or shortly after the end of standing estrus.
or confined Therefore recognizing the signs of standing heat is im-
pasture 120 to 125 portant. However, the optimal timing of insemination is
Adult In a paddock or best determined by changes in cervical mucus. As the doe
confined pasture 140 to 150 progresses through estrus, the mucus turns from clear and
Adult Range 125 to 130 thin at the beginning of standing heat to cloudy and
Adult Synchronized stringy at middle to late heat. Insemination should be
females performed in does before or at the time the mucus turns
in season 115 to 125 cloudy, usually 12 to 15 hours after the onset of estrus.3 If
Adult Synchronized the doe continues to exhibit heat after insemination, she
females should be inseminated again after 12 hours, particularly if
out of season 15 to 110 the program uses cooled or frozen semen.
Adapted from Menzies PI: Reproductive health management. In
Timed insemination of synchronized meat goats and
Youngquist RS, editor: Current therapy in large animal theriogenology, ewes tends to work well. Fixed-time insemination using
Philadelphia, 1997, WB Saunders; Pugh DG: Breeding soundness fresh semen 50 to 55 hours after removal of the proges-
evaluation in male goats, Proc Hudson Walker Therio Conf 7:29, 1996. terone source is an excellent labor-saving technique. If a
laparoscopic AI is to be performed, sheep and goats
should be inseminated 55 to 60 hours and 52 to 60 hours
• Relatively inexpensive semen cost
after progesterone removal for frozen and thawed or fresh
• Decreased potential for venereally transmitted
semen, respectively.4 Australian workers suggest that ob-
diseases
servation for estrus before breeding has no advantage over
• Improved herd management
timed insemination (laparoscopy) in the ewe.5 In dairy
Disadvantages of AI include the following2: goats, does should be observed for heat using a teaser
animals and inseminated accordingly, whereas meat
• Cost for AI equipment and liquid nitrogen
animals are usually synchronized in groups. Techniques
• Increased labor for estrus detection and
that place the semen into the uterus should be used for
insemination
frozen semen.
• Lack of standardization procedures for packing and
quality control for goat semen
• Lack of suitable sire proofs for production traits Vaginal Insemination
• Potential for spread of less desirable traits
The vulva is wiped clean with dry cotton or paper towels.
The success of an AI program depends on many The practitioner carefully advances a pipette into the
factors (fresh versus frozen semen, number and time of cranial vagina by sliding it along the dorsal vaginal roof to
inseminations, insemination method, quality and quan- avoid entering the urethral orifice. A cleaned, lubricated
tity of semen, semen handling practices, and the manage- speculum may afford better visualization for pipette
ment of the animals to be inseminated). placement. The equipment needed is shown in Figure
Females selected for AI should be in good health, have 6-12. Insemination with 4  109 and 3  109 progres-
a body condition score of 2.5 to 3, and be put on an im- sively motile, fresh, spermatozoa close to the cervix max-
proved nutrition plan for 2 to 5 weeks before breeding. imizes fertility with vaginal insemination in ewes and
They also should be free of disease and have a history of does, respectively.2,6-9 The conception rate with this
giving birth to live, healthy young and raising those kids method ranges from 15% to 30%; experienced techni-
or lambs to weaning. Preference should be given to cians may achieve better rates.
females that conceive early in the breeding season, those
that lambed or kidded during poor weather conditions,
and those that gave birth to and raised multiple young.
Cervical Insemination
AI is usually performed in conjunction with estrus Cervical insemination is more time consuming and re-
synchronization. Progestin implants or intravaginal quires greater skill than vaginal insemination. In this
devices are favored over prostaglandin regimens because method the ewe’s or doe’s hindquarters (not its abdomen)
of their tighter synchrony of estrus and ovulation. The are elevated and its legs are held over a table or more
 Chapter 6 Theriogenology of Sheep and Goats • 155

commonly a bale of hay. The operator gently introduces a restrained on her back with the hind limbs pulled forward.
lubricated vaginal speculum approximately 12 cm Special cradles designed for foot trimming or a V-shaped
through the cleaned vulva and into the vagina. With the wooden trough can be used. A specially designed Plexiglas
help of a good light source such as a transilluminator the vaginal speculum that has a 1-cm opening running along
cervix is visualized through the speculum. At this point its entire length is introduced into the vagina and the
the operator introduces an insemination pipette through cervix is identified. A wand-type light source that can be
the speculum and attempts to atraumatically pass the partially introduced into the speculum with a retaining
pipette as far into the cervix as possible. The long (7 to 8 clip can be used to provide a light for this procedure
cm) cervix and the 6 to 8 rear-directed cervical rings (Figure 6-13). The clinician inserts a pair of 25-cm
make completely traversing the cervix difficult in the ewe. Bozeman forceps into the speculum and grasps tissue near
Therefore semen is usually deposited into the caudal the cervical os. Any mucus preventing visualization of the
cervix. A 12-gauge tube attached to the semen delivery cervical os can be aspirated with a syringe infusion pipette.
system allows deeper penetration of the cervix. The doe’s The slit-like opening in the speculum allows the introduc-
cervix has a smaller luminal size but is slightly easier to tion of the forceps; after grasping the cervical tissue the
pass. Approximately 1  109 sperm cells from fresh operator can retract the cervix caudally and slide the
semen are needed to ensure good lambing and kidding forceps partially through the slit to allow better visualiza-
rates using this method.2,6-9 If cooled or frozen and tion of the cervix. Holding the speculum and forceps with
thawed semen is used, these numbers may need to be ex- one hand, the clinician next introduces a special bent-
panded by a factor of 1.5 and 2, respectively.2,6-9 The tipped insemination rod into the cervical os and attempts
conception rate with this method ranges from 35% to to traverse the cervical rings. Manipulating the AI rod and
50% (and occasionally higher). the cervix with the grasping forceps facilitates the place-
ment of semen directly into the uterus. The tip of the in-
Transcervical insemination. The more invasive semination gun can be used to locate the cervical canal. By
methods of insemination are designed to place semen di- turning the gun, most of the cervical rings can be traversed
rectly into the uterus. With these methods a much (Figure 6-14).
smaller number of progressively motile sperm are needed. Proper attachment of the forceps to the cervical os is
Transcervical insemination of dairy and meat goats is a crucial for maximal cervical penetration. If the AI pipette
relatively common procedure and one that can be easily tip can be moved without resistance, it is in the cervical
mastered with some practice. The necessary speculum, lumen or uterine body. The closer to the uterine body the
light source, and insemination equipment are readily semen is deposited, the higher the conception rate. This
available through goat supply companies (Figure 6-13). procedure requires 50 to 100 million progressively motile
All items that come into contact with the internal repro-
ductive tract of the doe should be sterile. Dairy goats are
usually restrained on a milking stand. Meat goats are not
usually cooperative on stands and should be restrained by
an assistant lifting the hindquarters and holding both
hindlegs. A

SHEEP: The most commonly used technique in sheep

is known as the Guelph system for transcervical AI,7 but
variations of this technique also are available. The ewe is B

A C
B
C D
D

Figure 6-12 Equipment for intravaginal insemination and Figure 6-13 Equipment used for transcervical AI in sheep. A,
laparoscopic semination in sheep and goats. A, Laparoscopic Wand-type light source with retaining clip; B, Bozeman forceps; C,
insemination gun; B, needle to be attached to a syringe for speculum; D, insemination pipette with special adaptor that allows
laparoscopic insemination. Both can be successfully used in movement into the cervix. This equipment is part of the Guelph AI
laparoscopic procedures. The needle (B) is useful when fresh semen system.
is to be inseminated laparoscopically. C and D, Equipment used for
intravaginal and intracervical insemination of goats. Cassou guns are
designed to use semen frozen in straws. C is a standard Cassou gun,
whereas D has a longer plunger and is better adapted for intracervical
or transcervical insemination.
156 • Sheep and Goat Medicine

Figure 6-14 Cervical or transcervical insemination. The practitioner inserts an AI pipette (a) through
a speculum (b) and into the ewe’s cervix (c) and uterus (d). Inset, The tip of the pipette (t) is moved slowly
through the cervix, traversing the cervical rings. The cervix of the ewe is tortuous, with five or six cervical
rings. These anatomic barriers make insemination difficult.

sperm cells. It also requires much experience and the re- tion and forward movement, slowly depositing the semen
ported results (40% to 70% lambing rates) are variable. in the interior cervix or uterine body. After insemination
Operators report a higher pregnancy rate when they can the doe is allowed to stand and relax for a few minutes.
enter the uterus with the insemination pipette instead of Conception rates between 50% and 85% have been re-
depositing the semen into the cervix. Pregnancy rates ported, depending on the skill of the operator and the
may be similar to those achieved in laparoscopic methods quality of the semen used. Fresh extended semen produces
when the semen is placed into the uterus.10 better fertility than frozen semen.2,8,9 In the doe the
desired number of motile sperm per insemination for fresh
GOATS: For AI of goats, the perineal area is washed liquid semen is 150 million; 200 million sperm are re-
with soapy water, rinsed, and dried with a paper towel. A quired in frozen semen.8,9 Both fresh and frozen semen
lubricated clear AI speculum is inserted into the doe’s should be evaluated for quality before insemination.
vagina and directed dorsally first and then slightly ven-
trally to pass over the ischial arch. The AI light is inserted
into the speculum and the cervix is visualized. After locat-
Laparoscopic Insemination
ing the cervical opening, the clinician places pressure The use of a laparoscope (0°) allows visualization of the
on the speculum to lock the cervix into the lumen of uterus so that semen can be placed directly into the
the speculum. An assistant should hold the speculum in lumen. The ewe and doe should be held off feed and
the vagina while the inseminator prepares the semen. The water for 24 hours before surgery. The animals are
frozen semen straw is placed in water based on the proces- sedated and positioned in dorsal recumbency, with the
sor’s recommendation (usually 30 to 60 seconds in 35° C head tilted down at a 45° angle or more to allow the
water). The clinician dries the straw with a paper towel, urinary bladder to fall away from the uterus as the proce-
cuts it, and places it in the AI gun.The insemination gun is dure proceeds. The abdomen should be clipped and pre-
manipulated through the cervical opening by gentle rota- pared for aseptic surgery. Local anesthetics are infiltrated
 Chapter 6 Theriogenology of Sheep and Goats • 157

reported in sheep and goats. The success of insemination

depends largely on the quantity and motility of spermato-
zoa being inseminated.11 An experienced operator re-
quires only 3 to 8 minutes to perform this procedure, and
the females should recover uneventfully. Ewes and does
may be laparoscopically inseminated many times
throughout their lives.

EMBRYO TRANSFER
Traditional cross-breeding programs using AI focus on
the male to produce offspring. Breeding programs using
multiple ovulation and embryo transfer (ET) use geneti-
cally superior females to contribute to this genetic diver-
sity. The limited economic value of most sheep and goats
precludes the widespread use of ET for the average pro-
duction unit. Also, the invasive procedure required makes
ET less practical in goats than in cattle. Nevertheless, ET
is an efficient method for moving genetics between
flocks, across countries, and among continents. ET is less
Figure 6-15 Sites for placement of trocars for laparoscopic practical in ewes than in cows because surgical collection
insemination. The trocar and cannula for the optic instruments are
placed at 1, and the trocar and cannula for the insemination and transfer are usually required. A successful ET
instruments are placed at 2. program requires advanced planning and lots of attention
to detail in donor and recipient selection, superovulation,
synchronization of donor and recipient, and successful re-
at two sites, both of which are 5 cm cranial to the udder covery and transfer of high-quality embryos. ET can be
and 4 cm to either side of the midline. A trocar or carried out in or out of season, but the best response is at-
cannula is placed at the site of local anesthetic infiltration tained during the breeding season when donors and re-
on one side of the midline and the abdominal cavity is cipients are cycling normally.13-17
distended with 1 to 2 L of carbon dioxide. A second
cannula is placed opposite the first (Figure 6-15). The
laparoscope (6.5 to 10 mm diameter, 0° telescope) is in-
Donor and Recipient Management
serted into the first cannula, and the uterus is visualized. Donor and recipient selection and management are
The clinician inserts the insemination pipette into the crucial to the success of an ET program. Recipient and
second cannula and inseminates each horn using a special donor ewes must be synchronized to cycle together.
needle on the end of the pipette. Alternatively, an insem- Donors respond most successfully to estrus synchroniza-
ination gun fitted with a brass injection tip (see Figure tion and superovulation when they are young, healthy,
6-12) or an aseptic needle (0.5 to 0.7 cm) is inserted and cycling normally. Does and ewes 2 to 5 years of age
through the other cannula into the abdominal cavity. An respond best to synchronization and superovulation pro-
avascular area at the anterior uterine horn is identified grams. Unfortunately, does and ewes presented as poten-
and the needle is inserted into the uterine lumen at a tial donors may often be older animals, and therefore past
right angle to the uterine wall. The clinician should place their peak reproduction performance. Donors should be
the needle in the center of the horn, taking care to ensure in good body condition (with a body condition score of 3
that the needle is in the lumen of the uterus. The authors to 3.5) and good general health. They should be vacci-
prefer to make a quick, controlled thrust into the uterine nated against any infectious diseases prevalent in the area
lumen. The semen should easily flow through the insem- and kept in separate groups for 2 to 4 months before the
ination device and into the uterus. If it does not, the beginning of the ET program. This helps acclimatize the
needle is likely in the wall of the uterus and should be donors and prevents stress.15 Any changes in environ-
redirected. After insemination the laparoscope and ment, feeding, and handling should occur well in advance
cannula are removed and the puncture sites are sutured, of the initiation of an ET program. Premature luteal re-
stapled, or covered with an antibiotic ointment. Ewes and gression, a syndrome common in some breeds (Boer),
does should be moved to a recovery area and left undis- appears to be caused by stress.
turbed for 1 to 2 hours. The desired number of motile Recipients should be healthy animals with proven re-
sperm for laparoscopic AI using fresh or frozen semen is productive ability that are in good body condition (with a
20 million (both horns) for does and 50 million for body condition score of 3 to 3.5) and cycling normally.
sheep.7,8,11,12 Conception rates of 20% to 90% have been Does 2 to 4 years of age with good mothering character-
158 • Sheep and Goat Medicine
istics and adequate potential for milk production are pre- The clinician or a helper anesthetizes the female, clips
ferred. Recipients also should be current on their vaccina- and prepares the abdominal area cranial to the udder for
tions against diseases prevalent in the area. aseptic surgery, and positions the animal in dorsal recum-
bency. The uterus and ovaries are exposed through a small
caudal ventral midline laparotomy beginning in front of
Synchronization the mammary gland. The clinician should examine the
Most ET programs rely on exogenous hormones to ovaries to determine the response to superovulation. This
induce and synchronize estrus in donors and recipients as can also be accomplished with a laparoscope before
described in the section on control of estrus cycle. Syn- laparotomy to minimize ovarian handling. The uterus is
chronization is commonly achieved using progestin elevated out of the laparotomy incision. The clinician
sponges, CIDR, or half of a norgestomet ear implant. Ac- uses a 20-gauge, blunt needle to pierce the uterine wall
curate detection of estrus can be achieved using a teaser near the uterotubal junction; he or she then inserts a “tom
buck or ram. The method of estrus synchronization cat” catheter into the uterine horn. The tip of a small
should be the same for both donor and recipient, with the artery forceps is used to cut a small hole through the
exception that superior results are obtained if progestin uterine wall for insertion of a 8- to 10-inch Foley catheter
sources are removed from recipients 12 hours before they at the base of the uterine horn. The cuff is inflated with 5
are removed from donors. cc of saline, and 20 ml of flushing media (Dubecco’s PBS
solution containing 100 IU/ml penicillin and 100 mg/ml
streptomycin supplemented with 2% heat-activated goat
Superovulation serum) is infused through the catheter to lavage the
Superovulation of the donor is accomplished by injecting uterus. The fluid should drain through the Foley catheter
PMSG and pituitary extracts of FSH. PMSG has a and into a collection bowl or Petri dish. The procedure is
longer half-life (about 72 hours). It is associated with repeated on the opposite uterine horn. The uterine punc-
overstimulation of the ovaries, resulting in the release of ture sites are left unsutured. PGF2a should be adminis-
large numbers of eggs; an increased proportion of unfer- tered postoperatively to lyse all luteal tissue. If embryos
tilized embryos; and poorer-quality embryos. PMSG are to be collected before the fourth day after breeding,
(1000 to 1500 IU) is administered in a single dose 48 oviductal flushing (through a cannulated oviduct near the
hours before the progesterone source is removed. The fimbria) is necessary. The collection media is flushed in a
donor also can be superovulated using an FSH product retrograde direction through the oviduct using a catheter
alone or in combination with eCG 2 days before the end placed at the uterotubular junction.
of the artificially created luteal phase.17 FSH has a half-
life of about 6 hours and requires twice-daily injections Nonsurgical. Nonsurgical or transcervical embryo col-
beginning 48 hours before progestin removal. FSH is su- lection techniques avoid the risk of postsurgical adhesions
perior to PMSG in ovulation and fertilization rates and and maintain the value of genetically superior donors
production of good-quality embryos. Does and ewes gen- after multiple embryo collections. Several reports of suc-
erally exhibit estrus 24 to 36 hours after progestin cessful nonsurgical collection in sheep and goats have
removal. Frequent observation of does for estrus with the been published.18 However, no practical technique is
aid of a teaser animal is needed to ensure accurate record- available yet that can be recommended for field use. In a
ing of the time of estrus. Donors can be hand mated 12 to recent report,19 embryos were collected transcervically
24 hours after estrus detection. Laparoscopic deposition from 38 standing unanesthetized Boer goats. In this
of frozen and thawed semen into the uterine horns 24 study the clinician inserted a duck-billed speculum into
hours after the animal is first seen in estrus yields ade- the vagina and grasped the external os of the cervix with
quate results. If donors are to be naturally bred, one buck Allis tissue forceps. The speculum was removed and the
or ram should be kept with one or two superovulated does external os was carefully pulled caudally until it almost
or ewes.16 reached the vulvar opening in a similar fashion as that
used for transcervical AI in sheep. A 3.2-mm outside di-
ameter, #10 Rusch flushing catheter was passed through
Embryo Recovery the cervix and directed into the left or right uterine horn
Embryos are usually recovered from the donor’s uterus on with a finger in the vaginal fornix. The clinician per-
day 5 or 6 after breeding. In most instances, surgical col- formed 24 flushings, with a 2-hour pause between the
lection may be employed. However, alternative tech- first and last 12 flushings. The embryo recovery rate
niques such as laparoscopic and nonsurgical embryo col- appears to be comparable to that achieved with surgical
lection have been developed.13-16 collection.19

Surgical. For surgical collection of embryos, does or Laparoscopic. Laparoscopic-assisted collection can be
ewes are taken off feed and water 36 hours before surgery. performed to exteriorize the tip of the uterine horn, with
 Chapter 6 Theriogenology of Sheep and Goats • 159

the flushing being performed in the same manner de- identify the horn suitable for the ET. The tip of the
scribed for surgical collection. This method reduces the uterus is grasped with forceps and gently elevated
severity of adhesions that result from the handling re- through the incision to the exterior. The tip of the uterus
quired in a laparotomy approach.14 Laparoscopy also can is punctured with a blunted needle and the embryos are
be used to collect the embryos within the abdomen introduced as previously described. The small incision in
without performing laparotomy. This technique requires the midline is sutured.
considerable skill and is not practical for routine field use. Although the laparoscopic collection of embryos re-
A laparoscope-assisted procedure can be used to enhance quires considerable expertise, laparoscopic transfer of
this technique and decrease the risk of adhesion forma- embryos is relatively easy and recommended for large ET
tion.8 The laparoscopic method allows the operator to vi- programs. However, laparoscopic-assisted transfer and
sualize the ovary, locate the CL, and more easily exterior- surgical transfer are the techniques used most often for
ize the uterine horn. Advantages include reduced surgical ET in goats.
time and a smaller abdominal incision.8 For laparoscopic transfer the recipient animals are pre-
pared as described for laparoscopic-assisted ET. The cli-
nician examines the ovaries through the laparoscope and
Embryo Handling identifies the horn ipsilateral to the CL for transfer of the
The flush medium is searched under a dissecting micro- embryos. The embryos are loaded in a 0.5-ml straw and
scope, and the embryos are retrieved and placed in a inserted into an AI insemination gun fitted with a brass
holding dish after washing. Before freezing or transfer, injection tip. The Cassou gun is inserted into the abdom-
they are carefully assessed for quality and stage of devel- inal cavity through the cannula, an avascular area at the
opment. Morula and blastocyst stages are expected when tip of the uterine horn is identified, and the needle is in-
embryos are collected at day 5 or 6. Embryos should be serted into the uterine lumen at a right angle to the
held in Dubecco’s PBS with 5% to 20% fetal calf serum. uterine wall. The clinician depresses the plunger of the
The International Embryo Transfer Society (IETS) has AI gun gently to expel the embryos.
defined handling procedures to reduce the risk of disease Many factors can affect the success of an ET program.
transmission during ET. An average of 8 to 10 transferable embryos can be ex-
Embryos are pulled into the tip of a small-bore intra- pected per flush, with expected pregnancy rates of 60% to
venous (IV) catheter attached to a 1-ml syringe for im- 80% for the transfer of two fresh embryos per recipient.20
mediate transfer into recipients.7 Alternatively, the Pregnancy rates from the transfer of frozen embryos are
embryos may be processed for freezing. much lower.

Embryo Transfer IN VITRO FERTILIZATION

Most transfers are done surgically. Recipients are selected In vitro fertilization (IVF) and culture technology offer
for transfer based on the greatest synchrony of estrus to the the advantage of producing embryos from animals when
donor doe. This synchrony is one of the most important other techniques for producing embryos might be more
factors in the success of ET programs.The recipient is pre- difficult or impossible. In addition, efficient IVF proce-
pared as for surgical embryo collection, and a small ventral dure is important for the development of biotechnologies
midline incision is made in front of the mammary gland. such as embryo sexing, nuclear transfer (cloning), and
The ovaries are examined for a CL, and the uterine horn gene transfer. Recent progress in embryo biotechnologies
ipsilateral to the CL is exteriorized. Embryos are trans- has resulted in increased efforts in practical and commer-
ferred to the oviducts via the fimbria using a tom cat cial applications of IVF for the ET industry. Sheep and
catheter or Pasteur pipette if the embryos are in an early goat oocytes can be successfully matured during the
stage of development (earlier than day 4). Older embryos breeding and non-breeding seasons.21,22
(those collected after day 4) are transferred to the uterine Oocytes for in vitro maturation (IVM) and IVF are
horns through a small stab incision made with a rounded usually obtained from superovulated does or ewes by as-
20-gauge needle or with the “eye” of a suture needle. pirating follicles on the ovaries using midline laparotomy
Before closing the abdominal incision, the clinician should or laparoscopy. Ovariectomized ovaries or ovaries col-
examine the catheter used to make the transfer microscop- lected at slaughter also may be used. Oocytes can be aspi-
ically to ensure that no embryos are retained in it. rated from 2- to 6-mm follicles with a 20-gauge needle
Recipient animals undergoing laparoscope-assisted attached to a 5-ml syringe. The immature oocyte with
transfer are prepared and placed on a surgical table or surrounding cumulus cells is then washed in Dubecco’s
cradle as described for laparoscopic AI. Two cannulas are PBS in a Petri dish and incubated for 27 hours in tissue
placed in the abdominal cavity, each 2 to 3 cm from the culture medium 199 (TCM-199) supplemented with
midline and approximately 10 cm cranial to the udder. 20% goat serum, 100 mg FSH/ml, and 1 mg estradiol
The ovaries are examined through the laparoscope to 17B/ml. The in vitro matured oocytes are incubated in
160 • Sheep and Goat Medicine
100 ml droplets of medium under paraffin oil in a humid- 16. Hill J: Maximizing the results of goat embryo transfer programs,
ified 5% CO2, 5% O2, and 90% N2 atmosphere at 38.5° Proceedings of the American Association of Small Ruminant Practi-
C.21 IVF is commonly performed with frozen and tioners, Research Symposium on Health and Disease, p 120, 1996,
Nashville, TN.
thawed spermatozoa after a process of sperm swim-up in
17. Husein MQ et al: Effect of eCG on the pregnancy rate of ewes
Tyrode’s albumin lactate pyruvate (TALP) medium with transcervically inseminated with frozen-thawed semen outside the
added heparin.23 This procedure aids in both sperm se- breeding season, Therio 49:997, 1998.
lection and capacitation. Oocytes are incubated with 18. Flores-Foxworth G: Reproductive biotechnologies in the goat. In
sperm for 24 hours as described for IVM. Fertilized ova Youngquist RS, editor: Current therapy in large animal theriogenol-
are then cultured in TCM-199 and 10% goat serum and ogy, Philadelphia, 1997, WB Saunders.
monitored for development every 24 hours. Embryos 19. Pereira RJTA, Shohnery B, Hollz W: Nonsurgical embryo collec-
reach the 4- to 8-cell stage at 48 to 72 hours and the tion in goats treated with prostaglandin F2a and oxytocin, J Anim
morula to blastocyst stage at around 120 hours.21,22 The Sci 76:360, 1998.
reader interested in pursuing IVF and other advanced re- 20. Rowe JD: Reproductive management in sheep and goats, Proceed-
productive technologies should read and study as much of ings of the American Association of Small Ruminant Practitioners, Re-
search Symposium on Health and Disease, p 39, 1998, Nashville, TN.
the current scientific literature on the subject as possible.
21. Keskintepe L et al: Term development of caprine embryos derived
from immature oocytes in vitro, Therio 42:527, 1994.

R EFERENCES
1. Alford A, Strickland J: Meat goat production in Georgia, Athens,
22. Samake S et al: In vitro fertilization of goat oocyte during the non-
breeding season, Small Rumin Res 35:49, 2000.
23. Keskintepe L, Simplicio AA, Brackett BG: Caprine blastocyst de-
GA, 1998, UGA Extension Bulletin. velopment after in vitro fertilization with spermatozoa frozen in
2. Nuti L: Techniques for artificial insemination of goats. In different extenders, Therio 49:1265, 1998.
Youngquist RS, editor: Current therapy in large animal theriogenol-
ogy, Philadelphia, 1997, WB Saunders.
3. Mobini S: Reproductive management in goats, Proceedings of the
PREGNANCY DETERMINATION
North American Veterinary Conference, vol 14, p 219, 2000, Early pregnancy diagnosis and determination of the
Orlando, FL. number of fetuses are of considerable value in goat and
4. Karatzas G, Karagiannidia A, Varsakeli K: Fertility of fresh and sheep reproductive herd health management. Goat
frozen-thawed goat semen during the non breeding season, Therio
owners frequently use clinical signs such as failure to
48:1049, 1997.
5. Moses D et al: A large-scale program in laparoscopic intrauterine
return to estrus after breeding, enlarging abdomen, and
insemination with frozen-thawed semen in Australian Merino developing mammary glands to make a presumptive diag-
sheep in Argentine Patagonia, Therio 48:651, 1997. nosis of pregnancy. However, pathologic conditions of the
6. Mylne MJA, Hunton JR, Buckrell BC: Artificial insemination of uterus and ovaries, physiologic anestrus late in the breed-
sheep. In Youngquist RS, editor: Current therapy in large animal ing season, and out-of-season breeding may cause post-
theriogenology, Philadelphia, 1997, WB Saunders. breeding anestrus in non-pregnant does.1,3 Many does
7. Buckrell B et al: Reproductive technologies in commercial use for and some ewes exhibit estrous behavior during pregnancy.
sheep, goats, and farmed deer, Proceedings of the Society for Ultrasonography, hormonal assays, and radiography are
Theriogenology, p 185, 1997, Nashville, TN. the most useful methods of pregnancy diagnosis. Abdomi-
8. Evans G, Maxwell WMC: Salmon’s artificial insemination of sheep nal palpation or ballottement and rectal-abdominal palpa-
and goats, Sydney, 1987, Butterworth Publishers.
tion with a rod have limited use or have been abandoned.
9. Chemineau P et al: Training manual on artificial insemination in
sheep and goats, Rome, 1991, FAO of the United Nations.
The value of pregnancy determination lies in the iden-
10. Halbert GW, Walton JS, Buckrell BC: Evaluation of a technique tification of nonproductive females and ewes bearing
for transcervical artificial insemination of sheep, Proceedings of the multiple fetuses; early identification allows appropriate
Society for Theriogenology, p 293, 1990, Nashville, TN. nutritional and management programs to be imple-
11. Rodriquez F et al: Cervical versus intrauterine insemination of mented. The ability to divide the flock into groups of
ewes using fresh or frozen semen diluted with aloe vera gel, Therio animals based on pregnancy status and fetal numbers not
30:843, 1988. only improves the health care of these animals by reduc-
12. Eppleston J, Maxwell WMC: Sources of variation in the reproduc- ing the incidence of some disease, but also decreases pro-
tive performance of ewes inseminated with frozen-thawed ram duction costs.
semen by laparoscopy, Therio 43:777, 1995. Ultrasonographic techniques for pregnancy determi-
13. Buckrell BC, Pollard J: Embryo transfer in sheep. In Youngquist
nation include amplitude modulation (A-mode),
RS, editor: Current therapy in large animal theriogenology, Philadel-
phia, 1997, WB Saunders.
Doppler, and real-time (B-mode) imaging.2 A-mode ul-
14. Scudamore CL et al: Laparoscopy for intrauterine insemination trasonography can be used to detect pregnancy between
and embryo recovery in super ovulated ewes at a commercial 60 and 100 days’ gestation. Detection of a fluid density is
embryo transfer unit, Therio 35:329, 1991. interpreted as pregnancy. Because of this hydrometra or a
15. Ishwa AK, Memon MA: Embryo transfer in sheep and goats: a large bladder may give a false positive result. Therefore
review, Small Rumin Res 19:35, 1996. A-mode ultrasound is an unreliable method for diagnos-
 Chapter 6 Theriogenology of Sheep and Goats • 161

ing pregnancy. Doppler ultrasonography can be used to finding a fetus, placentomes, or, less reliably, numerous
detect movement that may indicate pregnancy (blood fluid-filled uterine luminal sections. The placentomes
flow in the middle uterine artery or umbilical arteries, appear as round “doughnuts” or C-shaped structures
fetal heart beat, and fetal movements). The external (Figure 6-16). Transabdominal ultrasonography can be
Doppler technique has an accuracy of 100% during the used as early as 30 days and as late as 120 days. After day
second half of gestation but is not as effective at 50 to 75 90 to 120 reliable identification of the number of fetuses
days or earlier.2 The intrarectal technique for Doppler becomes difficult because their individual size fills the
ltrasound may be attempted as early as 25 to 30 days after screens; one fetus may be mistaken for two, or two differ-
breeding, but waiting until day 35 to 40 produces better ent fetuses may be mistaken for one.
results.2,3 False-negative and false-positive results are Twin pregnancies can often be determined between 45
common, and determining fetal numbers is difficult. and 90 days of gestation. Sector scanning units provide a
Pregnancy detection in the ewe is now performed wider visual angle or view of the abdomen.1 This allows
almost entirely with real-time ultrasonography. Linear more of the uterus to be seen in the visual field, improv-
array real-time ultrasound transducers can be used ing the accurate identification of multiple fetuses. The
transrectally to diagnose pregnancy as early as 18 days clinician should shear the belly wool just cranial to the
and as late as 60 days. A homemade plastic extension can udder and scan the abdomen slowly to make a mental
easily be fashioned from PVC pipe to allow easy intro- image of all abdominal contents. Generally, the C-shaped
duction of the transducer into the rectum. A 5- or a 7.5- placentomes can be seen “pointing” their concave por-
MHz transducer is recommended for rectal scans. After tions toward the fetus. The fetal bones form “shadows,”
60 days the gravid uterus is pulled down into the and the fetal ribs produce a characteristic striated appear-
abdomen and may be difficult to visualize transrectally. ance. Careful attention to a complete and thorough ex-
Table 6-5 shows age of gestation and associated ultra- amination helps minimize errors, but viewing a single
sonographic findings for pregnant sheep and goats. fetus too long can result in a false diagnosis of twins.
Transabdominal ultrasonography with a 3.5- or 5- After 120 days the fetal bones can produce a very dis-
MHz linear or sector scanner is used after 30 days of ges- torted image, but a diagnosis can be made with some
tation. The transducer is placed on a fiberless area of the effort. To maximize the usefulness of ultrasound, ewes
abdomen high in the inguinal region, preferably in the should be scanned between 45 and 60 days so producers
right flank.1 A bland fluid (e.g., vegetable oil, methylcel- can implement any management changes indicated by
lulose) should be used to couple the ultrasound trans- pregnancy status or number of fetuses. Clinicians also can
ducer to the skin. The clinician aims the transducer’s
beam toward the pelvis and scans the abdomen by slowly
“sweeping” the transducer cranially. In goats, shearing the
inguinal region increases the accuracy and speed of exam-
ination. Identification of the bladder (typically triangular
in appearance) provides an excellent landmark. The
uterus is normally located dorsal or cranial to the bladder.
Pregnancy at this point can be diagnosed on the basis of

TABLE 6-5

ULTRASONOGRAPHIC FINDINGS WITH PREGNANCY

DAYS COMMENTS

17 to 25 Transrectal; embryo visible after 24 days

26 to 35 Transabdominal; hypoechoic amnion
and hyperechoic fetus
30 to 75 Transabdominal; doughnut-shaped to
C-shaped placentomes
45 to 90 Best time for twin detection; mid-
Figure 6-16 Real-time, linear array ultrasound using a 5-MHz
abdomen in front of udder transducer reveals positive signs of pregnancy (placentomes) at the
90 to term Determination of number of fetuses is top of the image. The hypoechoic area at the bottom of the picture is
less accurate close to term amnionic fluid, and the hyperechoic region at the bottom of the image
is a fetus.
162 • Sheep and Goat Medicine
use ultrasonography to stage pregnancies by measuring and commercial laboratories offering the test are limited.2
the biparietal diameter of the fetus.2-4 Multiple fetuses result in higher levels of PSPB.1
Abnormal ultrasonographic findings include hy-
drometra, pyometra, fetal mummy, and macerated fetus.
Progesterone
Hydrometra appears as an anechoic, fluid-filled uterus,
often with membranous strands visualized in the lumen Progesterone analysis is not a test for pregnancy, and it
of the uterus. The uterus also does not have the typical more accurately detects non-pregnant rather than preg-
placentomes characteristic of pregnancy. Hydrometra is nant females. Goats depend on progesterone from the
often seen in does with apparently normal reproductive CL to maintain pregnancy throughout gestation. Plasma
histories.2,3 Pyometra also is manifested as a fluid-filled or serum progesterone concentrations below 1 to 2 ng/ml
uterus with more hyperechoic densities and a swirling 21 days and 18 to 19 days after breeding in the doe and
appearance. ewe, respectively, indicate non-pregnancy based on the
Assessment of fetal viability may be crucial in cases absence of a functional CL. An elevated progesterone
such as pregnancy toxemia.1 Fetal mummification may be concentration may indicate pregnancy, hydrometra,
identified as hyperechoic areas without any identifiable pyometra, early embryonic death, fetal mummification, or
body parts within a relatively fluid-free placentome-less irregular estrus cycle.2 The accuracy of blood proges-
uterus. The fetal heartbeat can be easily recognized by 30 terone level analysis is reported as 80% to 100% for non-
to 35 days after breeding.2 Early fetal death may be rec- pregnancy and 67% to 100% for pregnancy. In some
ognized by finding free-floating fetal masses along with management scenarios, particularly in dairy goats, serum
ribbon-like placental membranes.4 These ribbon-like or milk progesterone is collected on day 19 to 22 after
membranes may be found contralateral to a normally de- breeding. Serum or plasma progesterone concentrations
veloping fetus. Lack of fetal movement, amniotic fluid, more accurately reflect the true endocrine status of the
heartbeat, and blood coursing through the umbilicus can doe and are more accurate than milk progesterone analy-
easily differentiate a dead lamb fetus from a living one sis. Commercial on-farm cattle progesterone test kits can
with real-time ultrasonography. Soon after fetal death the be used in goats with good accuracy.1,2
placentomes lose their “crisp” margins.1
Radiography
Hormone Assays Abdominal radiography is useful for detecting pregnancy
Measurement of hormones in blood, milk, or urine pro- and fetal numbers in the individual pet goat brought to a
vides an alternative method of pregnancy diagnosis when clinic. It also provides an accurate alternative when ultra-
ultrasound equipment is not available. The estrone sulfate sound equipment is not available. This procedure is appli-
test, pregnancy-specific protein B (PSPB), and proges- cable but rarely used in ewes. Radiography is not practical
terone measurement are examples. for examining large numbers of animals. The fetal skele-
ton may be seen as early as 58 days after breeding and
may be radiopaque after day 65. Radiography is probably
Estrone Sulfate best performed 90 days or later after breeding in goats to
Estrone sulfate is a pregnancy-specific hormone pro- avoid false negative results.2
duced by the fetal placental unit. It can be detected in the
urine, serum, or milk after day 50 of pregnancy. When GENERAL FEMALE
performed any time after day 50 after breeding, this test
has been characterized as almost 100% accurate in the MANAGEMENT
detection of pregnancy. A positive test indicates a viable Pregnant ewe and doe flocks should be intensely
fetus. False positive results may occur if hemolyzed managed to control disease and lessen the chance of re-
serum samples are assayed. False negative results may productive failure. A review of records provides the vet-
occur if samples are collected before day 50 of gestation. erinarian the opportunity to look at the reproductive per-
Commercial laboratories offering this test are limited and formance of the flock over the past several years. This can
expensive.1 help in the implementation of management changes to
enhance productivity. Particular attention should be paid
to lambing percentages and dystocia rates to determine
Pregnancy-Specific Protein B whether more aggressive monitoring and intervention
PSPB is produced by binucleate giant cells of the placenta may be necessary around the time of birthing. Some basic
throughout gestation. It can be used in sheep and goats to guidelines should be followed with respect to control of
detect pregnancy any time after day 25 after breeding. infectious disease. Producers should attempt to keep
Both false positive and false negative results are possible, flocks closed during gestation and should be vigilant for
 Chapter 6 Theriogenology of Sheep and Goats • 163

potential fomite transmission among flocks. Biosecurity tion of myometrial contraction, which lasts from 2 to 12
should be extended to include pest and stray cat control. hours. In the first stage the female may leave the flock and
act uncomfortable. The female is restless, lies down and
gets up, and urinates frequently. During the first stage the
Pregnant Female Care cervix relaxes and releases the cervical seal. The second
Females should be maintained at a body condition score stage is delivery of the fetus, which is fairly quick, lasting
of 2.5 to 3 and should be allowed free access to an accept- about 1 to 2 hours. Does and ewes may prefer lateral re-
able mineral salt mixture (see Chapter 2) and clean water. cumbency during this stage, but some older, more experi-
All causes of stress should be avoided. Deworming, hoof enced females may remain standing for delivery. Initially
trimming, shearing, vaccination, moving, and other the amnion protrudes from the vulva, which should be
stressful procedures should be minimized for 1 month followed shortly by the forefeet and the head. The lamb
before the ewes and does give birth.1 Producers should or kid should be in a position such that the dorsum of the
determine the animals’ pregnancy status and number of lamb or kid is aimed toward the sacrum of the ewe or doe.
fetuses and sort and feed them accordingly. Females NOTE: Any female that fails to continue progressing
should be monitored and assessed for body condition through parturition should be examined.
score every 2 to 3 weeks throughout gestation. Basic Some lambs and kids are born in posterior presenta-
feeding programs and herd health recommendations are tion, which is normal if both legs are extended and deliv-
covered elsewhere in this text (see Chapters 2 and 17). ery occurs rapidly after the feet are delivered. In the case
of multiple kids or lambs, the female may rest between
R EFERENCES
1. Rowe JD, East NE: Reproductive management—Part I: estrous
deliveries or the deliveries may occur in quick succession.
If a female strains without producing any kid or ewe for
longer than an hour, intervention is indicated.
cycles, synchronization, artificial insemination, pregnancy diagnosis, The third stage is characterized by delivery of the pla-
Small Ruminants for the Mixed Animal Practitioner Western Veteri- centa within 6 hours and involution of the uterus. In the
nary Conference, p 137, 1998, Las Vegas, NV. absence of septicemic or toxic signs, failure to deliver the
2. Buckrell BC: Guelph system for transcervical AI (user manual),
placenta should be of no cause for concern until 12 to 18
Georgetown, Ontario, Canada, 1999, Small Ruminant Genetics.
3. Mastas D: Pregnancy diagnosis in the goat. In Youngquist RS,
hours. Involution of the uterus is complete by day 28 after
editor: Current therapy in large animal theriogenology, Philadelphia, birth. Lochia (a nonodorous, reddish-brown discharge) is
1997, WB Saunders. normally discharged for as long as 3 weeks.
4. Haibel GK: Use of ultrasonography in reproductive management of
sheep and goat herd, Vet Clin North Am: Food Anim Pract 6:597,
1990. INDUCTION OF PARTURITION
AND PREGNANCY
PARTURITION TERMINATION
Normal parturition requires the functional maturation of Termination of pregnancy in the doe can be achieved at
the fetal adrenal cortex. Parturition is triggered by activa- any time because she depends on progesterone from the
tion of the fetal pituitary-adrenal axis. Adrenocorti- CL to maintain pregnancy throughout gestation.
cotropic hormone (ACTH) is released by the fetal pitu- Therefore intentional or accidental administration of
itary gland, stimulating the release of corticosteroids by prostaglandins induces abortion or parturition at any
the fetal adrenal glands. An increase in fetal corticos- stage of gestation. The typical reason for a client’s request
teroids stimulates placental estrogen biosynthesis, which for early termination of pregnancy is mismating. The
in turn stimulates the synthesis and release of PGF2a drug of choice to induce abortion or parturition in the
from the placenta and endometrium. PGF2a causes lute- doe is PGF2a (5 to 10 mg) or cloprostenol (75 to 100
olysis, which results in a decrease in progesterone. An in- mg/45 kg). The ewe is similar to the cow in that PGF2a
crease in estrogen and decrease in progesterone stimulates may not induce abortion throughout gestation. To allow
myometrial activity, stimulating oxytocin release.1 the CL to mature and become receptive to the effect of
Birth is much more likely to occur during the daylight prostaglandin, the doe or ewe should not be treated
hours than at night; it is most frequent around midday. earlier than 5 to 7 days after breeding. Successfully
When the female is close to birthing, the udder fills up aborted does typically show estrus in 3 to 5 days.1
rapidly, the pelvic ligaments relax, and the vulva enlarges
and shows small amounts of colorless mucous discharge.
The cervical plug is often shed just before parturition, but
Ewe
it may be lost as much as 1 week prepartum. Parturition Farm personnel can use induction of lambing as a man-
can be divided into three stages. The first stage is initia- agement technique to ensure proper attention to the
164 • Sheep and Goat Medicine
delivery process. Lambing can be reliably induced in ewes uterus or birth canal. Some females with dystocia may
after day 137 of gestation with dexamethasone (15 to 20 have a complicating uterine inertia because they have
mg IM), but better lamb survival rates may be expected if become fatigued; signs of pain and panting may occur.
induction is initiated within 1 week of the expected due Hypocalcemia (both primary or secondary to respiratory
date.2,3 Lambing can be expected within 36 to 48 hours alkalosis) contributes to poor uterine contractility. Ad-
after the injection. ministration of a caudal epidural analgesic facilitates cor-
rections in fetal alignment and helps decrease the associ-
ated straining and pain. The area over the first two caudal
Doe vertebrae should be clipped and aseptically prepared. A
The gestation age of a kid should be at least 144 days at 18- to 21-gauge, 4-cm needle is directed ventrally into
induced parturition for the animal to be viable. Therefore the junction between the first two caudal vertebrae per-
accurate breeding records are very important. Females pendicular to the slope of the tail head. In small goats a
with enlarged udders filled with milk are the best candi- 25- to 27-gauge needle may be required. After penetrat-
dates for induction. A doe induced in the morning at the ing the skin the clinician should fill the hub of the needle
correct stage of gestation can be expected to kid by the with 2% lidocaine (0.5 ml/45 kg body weight) and
next afternoon. Prostaglandins may be given all at once (5 advance the needle slowly in a ventral direction. When
to 10 mg of PGF2a or 75 to 100 mg/45 kg of clo- the needle is in the proper position the lidocaine should
prostenol) or in a step-wise fashion (100 mg cloprostenol flow into the space because of the negative pressure in the
followed in 10 hours by 50 mg). This allows owners to epidural space. Location of the site can be enhanced by
plan the time and day of kidding so that assistance is moving the tail up and down. Epidural administration
available. Unlike cows, does seldom retain placentas after provides approximately 1 hour of analgesia. Ideally, the
induced parturition. If does are to be induced because of area around the vulva should be clipped of wool and thor-
pregnancy toxemia, administering a glucocorticosteroid oughly cleansed before any obstetric maneuvers. The cli-
(10 to 20 mg dexamethasone IM) 6 to 12 hours before in- nician should next attempt to palpate the fetus and deter-
duction may enhance fetal maturation and improve mine the cause of the dystocia. The use of copious
postinduction survivability.4 amounts of lubricant should be encouraged when per-
forming obstetric maneuvers in the ewe. Disposable
gloves should be worn by all people participating in the
DYSTOCIA MANAGEMENT birth process because of the potential for zoonotic disease
Dystocia can be a major cause of economic loss in sheep transmission. Common causes of dystocia include devia-
and goat flocks. The most common cause of dystocia is tions from normal presentation, position, or posture;
fetal postural abnormalities. Other causes include incom- flexion of the neck, carpus, and shoulder; fetal-maternal
plete cervical dilation, simultaneous presentation of disproportion; and more than one fetus attempting to exit
lambs or kids, cervicovaginal prolapse, uterine inertia, and the vaginal canal at the same time.5 However, not all
occasionally fetal-maternal size disproportion. Cases of cases of abnormal fetal presentation, position, or posture
fetal-maternal size disproportion are usually associated result in dystocia. Some does and ewes may give birth
with singleton births and overly finished ewes or does.5 normally if only one forelimb is presented with the head.
Most birthing problems are handled by owners, and only In dystocia caused by a relatively large head or fetus
the more difficult cases are submitted for veterinary assis- blocking the vaginal canal, one of the forelimbs may be
tance. Most kids or lambs are born in cranial, longitudinal repositioned into shoulder flexion, allowing room to pass
presentation. All manipulative procedures should follow the head and remaining forelimb; the kid can then be de-
general principles of veterinary obstetrics such as cleanli- livered by traction. In cases in which just the head is pre-
ness, lubrication, and gentleness. Practitioners with small sented and both shoulders are in a flexed position, trac-
hands tend to have an advantage. tion of the head with a snare may be sufficient for delivery
When a ewe or doe is presented for dystocia manage- if the vaginal canal has been well lubricated.
ment, the clinician should first assess her overall condi- Carpal and shoulder flexions are corrected digitally by
tion and rule out the presence of concurrent disease. The hooking a figure around the forelimbs below the flexed
3-30 rule is employed by many practitioners. That is, the carpus and straightening the limb.
ewe or doe should be examined 30 minutes after contrac-
tions begin or after the breaking of the chorioallantoic
membrane. If the female is normal and parturition is pro-
BREECH PRESENTATION
gressing normally, the clinician should wait at least 30 A true breech presentation implies that the fetus is in
minutes before beginning any treatments or manipula- posterior presentation in a dorso-sacral position with
tions. Females should be examined 30 minutes after de- both back limbs retained beneath the fetal body. Breech
livery to determine whether another fetus is still in the fetuses are handled similar to those with carpal flexion by
 Chapter 6 Theriogenology of Sheep and Goats • 165

straightening each flexed hindlimb. In these cases the ported in goats. This condition is referred to as ringwomb
rear quarters of the fetus and the tail are felt on vaginal and is considered to be a heritable condition. A similar
examination. If the veterinarian’s hands are small enough clinical condition occurs when the natural birth process is
he or she may be able to correct this dystocia. The fetus disrupted and the cervix is not properly stimulated for
should be pushed cranially and to one side. Raising the normal dilation to occur. If the veterinarian’s hand can fit
female’s hindquarters can make this maneuver much into the pelvis, he or she can attempt manual dilation of
easier. The clinician next should try to pull a hock back the cervix. Oxytocin can be administered to induce
into the pelvic canal. After one hock is in the pelvis, it uterine contractions; pushing against the closed cervix
should be rotated laterally in relation to the long axis of may aid in the dilation process. However, a Cesarean
the fetus while the foot is pulled ventrally and medially section is usually required. A fetotomy knife can be used
out through the vulva. The veterinarian should take care to open the cervix if the animal’s value does not warrant
not to injure the ewe’s vagina with the fetal hooves. The surgery and the fetuses are still viable. Euthanasia should
same procedure is then repeated on the contralateral be considered after this procedure depending on the con-
limb, and the fetus is extracted from the ewe. dition of the cervix and uterus.

HEAD MALPOSITION CESAREAN SECTION

OR LATERAL DEVIATION Because of the small size of ewes and does relative to
other farm animals, the veterinarian often cannot effec-
OF THE HEAD tively perform vaginal manipulation of fetuses. Therefore
Repulsion should be attempted to gain enough room to Cesarean section is recommended if vaginal delivery is
pull the head back around in normal position. If this not possible and the animal’s value does not preclude the
cannot be accomplished the clinician can place a snare- cost of this procedure. Mild sedation with acepromazine
type device over the laterally retained head and legs to in conjunction with leg restraints and local anesthetic in-
keep the head of the fetus as tight against its body as pos- filtration is usually sufficient for most sheep. If deeper se-
sible and then extract the fetus by pulling on the dation is needed, Telazol (6.6 mg/kg IV) and ketamine
forelimbs. (6.6 mg/kg IV) may be used (see Chapter 16). An
inverted-L type block with 10 to 20 ml of 2% lidocaine
provides good regional anesthesia (Figure 6-17). Al-
FRONT LEG MALPOSITION though other approaches are possible, a simple recum-
One or both front legs can be retained. If both front legs bent, left flank approach has the advantage of easy re-
are retained the head is usually in the pelvis or can be straint, and it is a familiar approach for most large animal
found protruding from the vulva. If the fetus is still viable practitioners. The ewe or doe can be placed in right
it should be repulsed into the pelvic canal to create the lateral recumbency with the front and rear legs restrained
room necessary to extract both legs one at the time. in extension with soft cotton ropes. The owner or an as-
Lambs can be delivered with only one foot forward if re- sistant can hold the head to minimize stress. A rolled
peated efforts to extend the second leg are unsuccessful. towel can be placed under the spine to tilt the ewe to a
Care should be taken to ensure that the legs pulled into 30° angle to the surgeon. The paralumbar fossa is clipped
the pelvic canal are from the same fetus as the head. If no and prepared for aseptic surgery. The clinician makes a
response is elicited from the fetus by pinching or pulling
on the tongue and if the veterinarian is confident the
fetus is dead, he or she can remove the head with a
guarded wire saw or a fetotomy knife. This may allow for
easier correction of the retained legs. The same basic pro-
cedure can be done if only one leg is retained. When both
legs and the head present at the same time (i.e., the legs
do not present before the head), the elbows often lodge
against the inner entrance of the pelvic canal, creating an
elbow lock. This can often be corrected by mild repulsion
of the head followed by traction on one limb at a time.

RINGWOMB Figure 6-17 Cesarean section. The solid lines indicate the
location for a local anesthetic block. The clinician injects 10 to 20 ml of
Failure of the cervix to dilate properly is a relatively 2% lidocaine both superficially and deep into the muscle along the
common occurrence in the ewe that also has been re- solid lines.
166 • Sheep and Goat Medicine
15- to 25-cm skin incision near the center of the left par- pelvic canal. If two fetuses are wedged into the pelvic
alumbar fossa. Depending on the size of the ewe the inci- canal and repulsion of one or both is not possible, partial
sion should start 5 cm ventral to the lateral processes of fetotomy may be beneficial. Partial fetotomy is warranted
the lumbar vertebrae and continue in a slight ventrocra- when the fetus has been dead for some time and the
nial direction to compensate for the bulging rumen and female’s uterus is very friable. In such cases pretreatment
uterus. The external and internal abdominal oblique with NSAIDs (flunixin meglumine) and antibiotics
muscles are cut in the same plane as the skin incision. Al- (penicillin) may be indicated.
ternatively the oblique muscles may be cut in the direc-
tion of their fibers to provide a grid-type entry. The clini-
cian must be careful because the distended abdominal
PREPARTURIENT DISEASE
walls of sheep and goats are fairly thin compared with A variety of periparturient conditions such as pregnancy
cows. A small nick incision can be made through the toxemia, vaginal prolapse, milk fever, and uterine inertia
transverse abdominal muscle and peritoneum. This entry may interfere with normal parturition or adversely affect
can be extended by inserting fingers into the incision and the health and fertility of the ewe or doe after parturition.
pulling dorsally and ventrally to separate the muscle With the exception of pregnancy toxemia, these condi-
along the direction of its fibers. tions are more frequently encountered in sheep than in
The uterus is located and exteriorized. The clinician goats.
should be aware that the ovine uterus is more fragile than
that of the doe or cow. Sterile towels or laparotomy pads
can be packed around the exposed uterus to decrease the
Fetal Hydrops
chance of abdominal contamination. The uterus should be Consumption of legumes with high concentrations of es-
incised in a longitudinal plane over the greater curvature of trogenic compounds, hypothyroidism secondary to iodine
the horn in a relatively avascular area. The incision should deficiency, and ingestion of goitrogens are all associated
be made long enough to guarantee easy removal of the with hydrops uteri. Hydrops also may result from placen-
fetus without risking uterine tears. Separate incisions may tal or uterine disease. Retention of large quantities of
be needed in the case of multiple fetuses. The incision fluid may result in rupture of the prepubic tendon. Induc-
should be closed with an inverting incision pattern (e.g., tion of parturition should be considered in cases of fetal
Utrecht pattern). In general a one-layer closure of the hydrops.
uterus is sufficient; however, the incision should be
checked closely to ensure that a good seal has been ob-
tained. If not, the entire incision can be oversewn in a
Rupture of the Prepubic Tendon
second inverting pattern.The clinician generally closes the Rupture of the prepubic tendon is occasionally seen in
transverse abdominal wall and peritoneum with a simple sheep and goats pregnant with multiple fetuses, pregnant
continuous pattern using #1 absorbable suture. The inter- females with fetal hydrops, and pregnant females that
nal and external abdominal oblique muscles may be closed have experienced abdominal trauma. If the owner chooses
together, after which the skin is closed. The authors prefer to keep the female until parturition, applying a home-
an interrupted suture pattern (cruciate) for skin closure. made canvas girdle (for added abdominal support), re-
Antibiotics are generally not necessary unless abdominal ducing rumen fill (increasing concentrate and decreasing
contamination is suspected. However, in field conditions forage intake), and reducing salt or trace mineral intake
many clinicians administer a broad-spectrum antibiotic may all be effective treatments. Surgical correction is
before the surgery. NSAIDs (flunixin meglumine) may be usually cost-prohibitive and may be unsuccessful. If an
used for postoperative pain management. accurate breeding date exists, the clinician may consider
performing an elective Cesarean section or inducing par-
turition. If parturition is induced, the clinician should
FETOTOMY closely observe the female in case she requires help to
A complete fetotomy, such as that performed in cows, is deliver. Preventing stress and trauma (e.g., deworming,
rarely practiced in either goats or does. Before performing shearing) in late-term females and selecting for animals
a fetotomy the clinician should clean the animal’s per- that do not give birth to quadruplets may help prevent
ineal area and lubricate the entire reproductive tract well; rupture of the prepubic tendon. Females that survive par-
he or she should exercise extreme caution to avoid uterine turition should be culled.
rupture and cervical or vaginal damage. Partial fetotomy
of the head in most cases is sufficient to allow enough
room in the vagina for further manipulation or passage of
Vaginal Prolapse
the remaining fetal parts. In both sheep and goats, percu- Vaginal prolapse is a relatively common problem in the
taneous fetotomy to remove the front legs may help ewe. It typically occurs during the last 3 weeks of gesta-
reduce size so the fetus may be manipulated through the tion in multiparous ewes. Vaginal prolapse is relatively
 Chapter 6 Theriogenology of Sheep and Goats • 167

uncommon in goats but is occasionally encountered in of umbilical tape placed lateral to each side of vulva,
dairy breeds. The ventral vaginal floor is usually the area works well. The owner can loosen the lacing and check on
that protrudes from the vulva lips. Many different theo- the progress of parturition. If the female is 1 month from
ries have been advanced regarding the etiology of vaginal parturition, a Buhner suture can be used, with the clini-
prolapse. The consumption of low-quality forage results cian substituting a standard cadaver needle for a Buhner
in increased abdominal filling, which may lead to the needle. The Buhner method results in a suture that may
vagina being forced out of the vulva. The estrogen last longer and will rarely tear out.
content of some legumes also has been incriminated. A retention harness also has been described. A rope or
Other nutrition-related problems include over- and stout cord is placed over the back so that half of the rope
under-conditioning and poor bunk management result- is on either side of the body. The rope is then crossed
ing in overcrowding. Other physical factors that have under the front legs and then brought back dorsally to be
been implicated include obesity, persistent cough causing crossed over the back legs. The rope is then passed ven-
repeated episodes of high intraabdominal pressure, and trally and under the rear limbs on either side of the udder
improper or close tail docking in sheep. The tails of sheep and crossed again as it is brought dorsally over the per-
should be docked beyond the sixth coccygeal vertebrae or ineal area. The two ends are now tied to the rope that is
left just long enough to cover the anus when pulled ven- crossed over the back. This configuration discourages
trally (see Chapter 9). Unfortunately show animals are straining and secures the perineum.
often docked closer than this to improve the look of the
rump area in the show ring.
Because of a possible genetic component the offspring
Uterine Prolapse
of ewes or does that have experienced vaginal prolapse Uterine prolapse generally occurs within 12 to 18 hours
should not be kept as breeding stock.7 An epidural (2% after lambing or kidding and may be associated with any
lidocaine 0.5 ml/45 kg) helps prevent straining. Alterna- condition that weakens the ewe or causes difficult deliv-
tively, a combination of xylazine (0.07 mg/kg) and lido- ery. Hypocalcemia may contribute to the flaccidity that
caine (0.5 mg/kg) can be used to provide as much as 24 predisposes to uterine prolapse. The prolapsed uterus is
hours of relief from straining, although they may cause usually atonic and is slowly expelled from the vulva lips
some pelvic limb ataxia.8 The prolapsed vagina should be rather than being forcefully expelled by straining. The
cleaned with a mild soapy solution before replacement. prolapsed tissue should be gently washed and well lubri-
Occasionally the urinary bladder is found inside the pro- cated before replacement into the abdomen. The admin-
lapsed tissue. Real-time ultrasonography is beneficial in istration of a caudal epidural (lidocaine 2%, 0.05 ml/45
determining the location of the urinary bladder. If the kg) before replacement decreases straining by the ewe or
bladder is within the prolapsed tissue, it can usually be doe. The replacement procedure can be aided by raising
drained by locating the urethral orifice beneath the pro- the hindquarters off the ground. This allows the abdomi-
lapsed tissue (caudal to the vulvar commissures), inserting nal contents to fall away from the pelvic canal and pro-
a finger into the orifice, and lifting the prolapse. A 12 motes correct intraabdominal replacement of the
French catheter can be inserted through the urethra and prolapsed uterus.
into the bladder if draining is required. The prolapsed Closure of the vulvar opening is accomplished using a
tissue should be well lubricated with a water-soluble lu- Buhner or shoelace suture as described for vaginal pro-
bricant (methylcellulose), gently massaged, and carefully lapse. If hypocalcemia is suspected, the female should be
forced cranially to its natural position. Picking up the ewe given a calcium solution. Oxytocin is indicated to aid
by her hindlegs can facilitate the replacement of the pro- uterine contraction. The prognosis is normally good.
lapse. In the event that the prolapse has swollen and re- Lacerated and severely soiled prolapses may be
placement is difficult to impossible, either a hydroscopic complicated by infection.
agent (e.g., Epsom salts, sugar) or steady pressure can be
applied to the prolapse to decrease edema and reduce
size.
Retained Fetal Membranes
A popular method of retaining the prolapsed tissue is The placenta should be expelled by 6 hours after parturi-
through the use of a specially designed plastic prolapse tion. In the absence of toxemia, septicemia, or abnormal
retainer. This retainer has a broad spoon-shaped end that vaginal discharge, the clinician should take no action to
pushes down on the replaced vaginal floor and two reten- remove the placenta until 12 to 18 hours postpartum. Re-
tion arms that are tied into the wool or sutured to the skin tained fetal membranes (RFMs) may be caused by defi-
on either side of the rump. These can be successfully used ciency in selenium or vitamin A, infectious abortions
in some goats. (e.g., toxoplasmosis, chlamydiosis, listeriosis), obesity of
Various types of purse-string and mattress-type the dam, hypocalcemia, dystocia, and possibly other
sutures also have been used. Making a shoelace pattern factors.9,10 RFMs are uncommon in goats but appear to
across the vulva with soft rolled gauze, using small loops be a problem in some sheep flocks. A higher incidence of
168 • Sheep and Goat Medicine
RFM has been reported in dairy goats and in does or open cervix, broad-spectrum antibiotics can be infused
ewes whose young have died or been removed. A retained through the cervix and into the uterus. Uterine infusion is
placenta with no other concurrent clinical signs is of little controversial, and clinicians performing it should take
significance, except that the RFM may be associated with care not to damage the cervix, puncture the uterus, and
certain diseases or deficiencies. Occasionally a vaginal ex- cause greater uterine scarring or damage. A 12 to 14 Fr
amination can reveal the placenta if it is not visible Foley catheter can be passed carefully through the cervix
externally. for uterine lavage and infusion. Uterine evacuation with
prostaglandins (PGF2a, 5 to 10 mg; cloprostenol, 75 to
Treatment. If the ewe or doe appears clinically normal, 100 mg/45 kg body weight) or oxytocin (5 to 10 IU), re-
treatment should entail only the removal of the placenta. hydration as needed, and NSAIDs (e.g., flunixin meglu-
Manual removal should not be attempted. Instead, the mine 1 mg/kg) should be included in the therapeutic
doe or ewe can be given oxytocin (5 to 10 IU two to six plan. If the placenta is retained, it should be removed, but
times a day) or prostaglandins (PGF2a, 5 to 10 mg; clo- not manually. Because of the potential for clostridial in-
prostenol, 75 mg/45 kg body weight). One of the authors fections, particularly in animals with dystocia-induced
(Dr. Pugh) prefers PGF2a or its analogues and avoids uterine trauma, macerated fetuses, or uterine bacterial
using oxytocin in females with nursing young. contamination, clostridial disease prophylaxis should be
undertaken. Previously vaccinated females can be given a
booster that includes C. tetani. In animals with no history
Metritis and Endometritis of clostridial prophylaxis, antitoxin is indicated.9,10
Metritis is uncommon in sheep and goats but is encoun-
tered in dairy goat breeds and in association with RFM;
dystocia; retained dead lambs or kids; abortion caused by
Pyometra
toxoplasmosis, chlamydiosis, and listeriosis; and possibly Pyometra can occur as a sequela to cases of metritis in
other diseases.9,10 A retained placenta may serve as a which the cervix has been damaged; it also occurs in
“wick” between the environment and the uterus. females that cycle after parturition during the anestrous
season (Nubians, dwarf goats). The late cycle can result in
Clinical signs and diagnosis. Clinical signs include a an ovulation and retention of the resultant CL for a pro-
thin, watery, brown to red, possibly purulent, malodorous longed period. Pyometra is a very uncommon disorder.
vaginal discharge. Infected females may be relatively Signs include anestrus, occasionally sustained elevated
normal or extremely ill and toxic. They may be febrile and serum progesterone, ultrasonographic evidence of varying
exhibit decreased rumen motility, dehydration, increased amounts of echogenic intrauterine fluid, and occasionally
scleral injection, and possibly depression. In severe cases a purulent vaginal discharge.
animals can become infected with Clostridium tetani,
other Clostridium species, or other toxin-producing bac- Treatment. Treatment should include prostaglandins
teria. Peritonitis may develop as a result of severe uterine (PGF2a, 5 to 10 mg; cloprostenol, 75 to 100 mg/45 kg
infection or postpartum uterine tears or ruptures. Uterine body weight) and/or oxytocin (5 to 10 IU BID).9,10
tears are more common after dystocia, but they also may
occur spontaneously.11 As expected, a CBC indicates
toxemia or septicemia. Abdominocentesis may reveal in-
Pregnancy Toxemia
creased protein, increased number of leukocytes, and pos- Pregnancy toxemia typically occurs during the final
sibly toxic leukocytes. Ultrasonographic examination trimester of gestation in ewes and does. The condition is
usually reveals an enlarged fluid-filled uterus containing usually seen in females carrying multiple fetuses and may
hyperechoic fluid. Both goats and ewes normally have a result from their inability to consume enough energy.
thick, nonodorous, brown to reddish brown vaginal dis- Conditions that increase energy demands or decrease
charge (lochia) for as long as 4 weeks after birth. This energy intake also can predispose to this disease. Ewes and
normal lochia requires no treatment. New, relatively inex- does carrying multiple fetuses have a decreased dry matter
perienced sheep or goat owners, particularly those with intake compared with ewes carrying a single fetus. This
pet animals, may interpret this normal discharge as a sign decreased dry matter intake results from a decrease in
of illness (e.g., metritis). rumen volume because of the enlarging uterus, an increase
in heat production from the fetuses, and changes in free
Treatment. Any underlying disease that is resulting in fatty acid concentrations.12 Obese or extremely thin
metritis should be treated. Affected ewes or does should females may be more prone to developing the condition.
be given broad-spectrum antibiotics (oxytetracycline 10 Gestating ewes carrying twins require 180% more energy
to 20 mg/kg once a day [SID] to BID) or antibiotics with than those carrying singletons, and those carrying triplets
good efficacy against anaerobic bacteria (penicillin 20,000 require 240% more than ewes carrying singletons. Ewes
IU/kg BID). If a vaginal speculum examination reveals an and does may not be capable of consuming enough to meet
 Chapter 6 Theriogenology of Sheep and Goats • 169

these demands, resulting in a negative energy balance. fleece coat increases the workload for the ewe. Ewes in
Ewes and does perform little net glucose absorption from late pregnancy carrying multiple fetuses also tend to be
the gastrointestinal tract, but instead synthesize it in the larger and more awkward than their flock mates. Man-
liver.4,12 A negative energy balance in late gestation results agement must ensure that these animals are being
in changes in the insulin-glucagon ratio and activates allowed to eat and that adequate bunk space is available
lipases that mobilize fatty acids and glycerol from body for them. Serum beta-hydroxybutyrate concentrations
energy reserves. The liver uses these fatty acids and glyc- have been used as indicators of the nutritional status of
erol as energy for fetal growth. If the energy demands are ewes within a herd. Values greater than 0.7 mmol/L indi-
greater than the supply, the liver cannot produce enough cate that the herd is in a negative energy balance; the pro-
glucose and may become overwhelmed with free fatty ducer should take immediate steps to prevent pregnancy
acids, resulting in the production of ketones. toxemia and not wait for clinical cases to appear. Ultra-
sonography is used to separate ewes that are carrying
Clinical signs and diagnosis. Pregnancy toxemia is twins so that owners or caretakers can meet their addi-
characterized by depression and recumbency progressing tional nutritional needs.
to tremors, stargazing, incoordination, circling, and
grinding of the teeth. Ketones and low glucose concen-
trations result in the observed clinical signs.13 The diag-
Hypocalcemia
nosis is confirmed by detecting an increase in urine and Hypocalcemia is typically seen during the last 2 weeks of
blood ketone concentrations. Urine concentrations are gestation. Twin-bearing ewes require as much as 8 g of
more sensitive and specific than blood concentrations. calcium and 4 g of phosphorus per day.
Other findings may include decreased serum calcium and
potassium, increased blood urea nitrogen, elevated free Clinical signs and diagnosis. The clinical signs can
fatty acid concentrations (more than 500 mg/ml), and ele- overlap the signs seen with pregnancy toxemia because
vated beta-hydroxybutyrate concentrations (more than 1 the two diseases are often seen concurrently. Hypocal-
mmol/L).13 Necropsy findings include a pale, swollen cemic ewes are initially ataxic and hyperactive but soon
liver. become recumbent. Other clinical signs include bloat and
failure of pupillary light responses. The initial hyperactiv-
Treatment. Treatment of pregnancy toxemia must be ity results from a lack of membrane stabilization by
immediate and aggressive. The fetuses must be removed calcium. The subsequent paralysis occurs because little to
as soon as possible. In critical cases a Cesarean section no calcium is available to release acetylcholine at the neu-
should be performed. If the animal is not critically ill or romuscular junction and influence muscle contractility.
if its value does not warrant surgery, parturition should be Calcium concentrations can be measured to confirm
induced. Glucose should be given to control the in- hypocalcemia. The serum calcium concentration is less
creased ketone production by the liver. A single injection than 7 mg/dl in clinical cases.
of 50% (100 to 250 ml IV) dextrose may be effective, de-
pending on the size of the ewe or doe. More frequent ad- Treatment. Clinical cases are treated with 1 g of
ministration may result in a rebound hypoglycemia. If the calcium per 45 kg body weight, and the response is dra-
animal’s value warrants the expense, a slow drip of 5% matic. Ewes should have a good supply of calcium in their
dextrose can be used after the initial bolus. B vitamins diets during the final 6 weeks of gestation. Alfalfa hay
can be given to stimulate the appetite and provide some provides a good source of calcium, as does a mineral mix
of the necessary precursors for the liver to produce containing calcium.9
glucose. If hypocalcemia is suspected, the slow adminis-
tration of 50 ml of calcium borogluconate (20 mg
calcium/ml) is warranted. If the animal has been anorexic
NEONATAL CARE
for several days, transfaunation with the rumen liquor
from a healthy ruminant can produce a more favorable
Lambing Management
rumen environment. Propylene glycol can be given (15 cc Ewes should be managed to ensure they have a body con-
BID) to treat the hypoglycemia.14 dition score of 3 to 3.5 at lambing. Producers should
monitor body condition throughout gestation so that the
Prevention. Prevention of pregnancy toxemia entails ewes are not forced to try to create body reserves during
providing a good nutrition plan and decreasing any stres- the final few weeks of gestation. A good herd health
sors such as increased workloads and parasitism. The ad- program should be planned and implemented to decrease
dition of niacin and ionophores may provide an addi- the incidence of disease in the prepartum ewe. Monitor-
tional means of combating this disease (see Chapter 4).12 ing of blood calcium, phosphorus, magnesium, and sele-
Shearing of pregnant sheep also is beneficial because it nium concentrations is warranted if a history of deficien-
increases dry matter intake.12,13,15 The weight of the cies has occurred in the geographic region. The ewe’s
170 • Sheep and Goat Medicine
energy balance also can be monitored by measuring beta- commercial supplements. If possible the colostrum donor
hydroxybutyrate concentrations in serum. A clean, dry should be from the same general location as the dam and
lambing area that is protected from severe cold and wind be vaccinated against the clostridial diseases.6
should be provided for the ewe. She should be sheared
before lambing and have her mammary glands examined PERIPARTURIENT CARE
to ensure that the lambs will be physically able to nurse
and that no severe teat and udder lesions are present.16 OF THE DOE
After lambing the ewes and lambs should be placed to- Prepartum care of does prevents most postpartum prob-
gether in claiming pens for at least 24 hours. This allows lems. Does should be examined with ultrasonography to
the manager to observe the nursing behavior of the lamb confirm pregnancy status and the stage of gestation. The
and thereby enhances the opportunity to intervene. clinician or producer should determine their body condi-
Newborn lambs should attempt to stand and nurse tion scores. Dairy does should be “dried off ” 60 days
within 30 minutes of birth. Dipping the navel with an before the expected due date. During the final 4 weeks of
iodine solution (7% tincture), a weak iodine solution, or a the dry period, does should be supplemented with con-
chlorhexidine solution is recommended. The chlorhexi- centrates or good-quality pasture. They should be
dine solution appears to have a more residual antibacter- watched closely for signs of ketosis, hypocalcemia, hypo-
ial effect, and the strong iodine solutions may be associ- magnesemia, or abortion diseases.16 Where possible,
ated with umbilical abscesses or patent urachus. Still, the females should receive their annual vaccinations and be
“test of time” suggests that all of these solutions are safe dewormed during the final month of pregnancy. Vaccina-
and useful if used judiciously. Neonatal lambs are espe- tion of females for enterotoxemia, tetanus, and other
cially prone to hypoglycemia and hypothermia, so careful endemic diseases optimizes the presence of immunoglob-
observation of newborns is mandatory. The newborn ulins in the colostrum. Dairy does should be brought into
lamb should be up and nursing within the first 2 hours of a kidding pen, and the hair around their udders, tails, and
life. If the lamb does not seem satiated after nursing or if perineal areas should be clipped. Meat does should have
the ewe has udder pathology with a potential for inade- access to a clean shelter for kidding and should be ob-
quate milk production, colostrum should be supple- served regularly.
mented. Table 6-6 shows how to make and use a sodium At birth, kids should be observed for abnormal respi-
sulfate solution that can be used to assess the success or ration and other evidence of fetal distress such as meco-
failure of passive transfer of colostral antibodies. Recom- nium staining. Mucus and fluids should be removed from
mendations for the supplementation of colostrum are 50 the nose and mouth immediately. Normal kids attempt to
ml/kg in the first 2 hours after birth, and a total of 200 stand within a few minutes of birth and nurse vigorously
ml/kg in the first day. Lambs can be supplemented with within the first few hours. The kid’s respiration is stimu-
ovine or caprine colostrum. Fresh or frozen colostrum lated by the doe licking it or the owner vigorously
from animal sources is generally considered superior to rubbing it with a towel. The umbilicus should be in-

TABLE 6-6

A METHOD OF ASSESSING THE SUCCESS OR FAILURE OF PASSIVE TRANSFER IN THE NEONATAL LAMB OR KID

Sodium Sulfate Test for Passive Transfer

• Place 14, 16, and 18 g of powdered sodium sulfate into labeled containers filled with 100 ml of distilled water.
• Place 1.9 ml of each of these solutions (14%, 16%, 18%) into three separate sterile tubes.
• Add 0.1 ml of serum to each container, then mix thoroughly.
• Allow the mixture to stand undisturbed at room temperature for 1 hour to permit maximal precipitation. Assess the
tubes for clarity. A cloudy appearance (manifested by the inability to read newsprint through the tube) is associated
with immunoglobulin precipitation.
IMMUNOGLOBULIN 14% 16% 18% COMMENT CONCENTRATION (MG/DL)

More than 1500 Cloudy Cloudy Cloudy Successful passive transfer

More than 1000 Clear Cloudy Cloudy Successful to partially successful passive transfer
500 Clear Clear Cloudy Partial failure of passive transfer
Less than 500 Clear Clear Clear Failure of passive transfer
 Chapter 6 Theriogenology of Sheep and Goats • 171

spected for hemorrhage or herniation, and the umbilical 8. Scott PR et al: The use of combined xylazine and lidocaine
stump should be disinfected with 7% tincture of iodine or epidural injection in ewes with vaginal or uterine prolapse, Therio
another suitable iodine or chlorhexidine solution. The 43:1175, 1995.
9. Rowe JD: Reproductive management—Part III. Small ruminants
way kids are raised and handled after birth depends on
for the mixed animal practitioner, Small Ruminants for the Mixed
the type of goat and owner’s preference. Meat and fiber
Animal Practitioner Western Veterinary Conference, p 147, 1998, Las
goats raise their kids on pasture, whereas dairy kids Vegas, NV.
are removed before they have a chance to nurse. Kids 10. Braun W: Periparturient infection and structural abnormality. In
need to receive adequate colostrum within the first Youngquist RS, editor: Current therapy in large animal theriogenol-
4 hours of birth. Dairy kids are bottle fed heat-treated ogy, Philadelphia, 1997, WB Saunders.
goat colostrum (at 56° C for 1 hour) to prevent caprine 11. Pugh DG, Hardin DK: Ovine uterine rupture, Agri-Pract 7:15,
arthritis-encephalitis virus (CAEV) transmission. Weak 1986.
kids should receive colostrum by an oral stomach tube or 12. Gessert ME: The use of niacin and other energy modifiers of
a lamb feeder. Kids should be fed 10% of their body energy metabolism for the prevention of pregnancy toxemia in
weight in colostrum the first day, divided into three or ewes, Proceedings of the Society for Theriogenology, p 296, 1995,
Nashville, TN.
four feedings. Colostrum substitutes are not suitable for
13. Scott PR et al: Cerebrospinal fluid and plasma glucose concentra-
kids and do not increase their immunoglobulin levels.
tion of ovine pregnancy toxemia cases in apparent ewes, Br Vet J
Delayed colostrum intake, inadequate colostrum inges- 151:39, 1995.
tion, and ingestion of poor-quality colostrum are 14. Marteniuk JV, Herdt TH: Pregnancy toxemia and ketosis of ewes
common reasons for failure of passive transfer16 (see Table and does, Vet Clin North Am: Food Anim Pract 4:307, 1988.
6-6). In meat and fiber production herds, adequate 15. Austin AR, Young NE: The effect of shearing pregnant ewes on
colostrum intake can be assessed by observing kids lamb birth weights, Vet Rec 100:527, 1977.
nursing and palpating their abdomens. Serum im- 16. Menzies PI, Bailey D: Lambing management and neonatal care.
munoglobulin levels can be assessed using a sodium In Youngquist RS, editor: Current therapy in large animal theri-
sulfate test, zinc sulfate turbidity test, or other commer- ogenology, Philadelphia, 1997, WB Saunders.
cially available screening test. Levels higher than 1600
mg/dl are desirable; levels below 600 mg/dl may indicate
failure or partial failure of passive transfer.12 IV transfu-
REPRODUCTIVE DYSFUNCTION
sion of 20 to 40 ml/kg of caprine plasma from the dam or
Reproductive Failure
another adult goat in the herd may be indicated for a valu-
able neonate exhibiting failure of passive transfer. Kids During an investigation of reproductive failure in rumi-
born in selenium-deficient areas should be injected with nants, the infectious causes always seem to garner the
selenium at birth. Finally, kids are at greatest risk of hy- most attention. However, noninfectious causes can often
pothermia and hypoglycemia during the first few days of be more problematic to diagnose but easier to treat. Defi-
life. They should be protected from rain and cold weather ciencies in iodine, copper, and other nutrients can result
and treated for hypoglycemia with glucose solution. in reproductive failure in sheep and goats. These and
other nutritional problems are covered in more detail in
Chapter 2.
R EFERENCES
1. Thomas JO: Survey of causes of dystocia in sheep, Vet Rec 127:574, Plant Toxicity
1990.
2. Peters AR, Dent CN: Induction of parturition in sheep using dex- Veratrum californicum. Members of the Veratrum genus
amethasone, Vet Rec 131:128, 1992. are associated with numerous congenital abnormalities in
3. Owens JL et al: A note on the effects of dexamethasone-induced lambs. V. californicum, commonly known as false hellebore,
parturition on ewe behavior and lamb survival in prolific Booroola contains a teratogenic alkaloid (cyclopamine) that is re-
Merino ewes, Anim Prod 41:417, 1985. sponsible for a number of congenital defects in lambs de-
4. Rowe JD: Reproductive management of sheep and goats. Proceed- pending on the stage of gestation when they are con-
ings of the American Association of Small Ruminant Practitioners, Re- sumed. Exposure to V. californicum during the first 10
search Symposium on Health and Disease, p 39, 1998, Nashville, TN. days of gestation is associated with early embryonic
5. Brawn W: Parturition and dystocia in the goat. In Youngquist RS,
death. The classic, demonstrable conditions associated
editor: Current therapy in large animal theriogenology, Philadelphia,
with V. californicum ingestion—severe facial abnormalities
1997, WB Saunders.
6. Majeed AF, Taha MB: Preliminary study on treatment of ring-
such as a cyclops-like appearance, anophthalmos, and
womb in Iraqi goats, Anim Repro Soc 18:1999, 1989. cleft palate—occur when exposure takes place between
7. Menzies PI, Bailey D: Diseases of the periparturient ewe. In day 12 and 14. Exposure between day 25 and 36 results in
Youngquist RS, editor: Current therapy in large animal theriogenol- hypoplasia of the metacarpals and metatarsals. Exposure
ogy, Philadelphia, 1997, WB Saunders. has also been reported to cause inadequate development
172 • Sheep and Goat Medicine
TABLE 6-7

PLANTS THAT AFFECT REPRODUCTION

PLANT COMMENT

Fusarium • Found in moldy corn and wheat

• Produces the estrogenic substance zearlenone
• Signs include a decreased lambing and kidding percentage
Clovers (subterranean, • Produce estrogen-like substances
crimson, red, white, • Signs include cystic hyperplasia of the cervix and hydrops uteri
alsike) • White clover also has cyanogenic ergotalkaloids
• Alsike also can cause photosensitization, liver disease, and stomatitis
Ponderosa pine • Signs include stillbirths, last-trimester abortions, renal tubular necrosis, pulmonary
congestion, weak uterine contractions, and poor cervical dilation
Cottonseed • Toxic substance is gossypol
• Signs include testicle and spermatozoa abnormalities
• Signs occur most often in young preruminants
Broomweed, Monterey
cypress, jumpweed
Veratrum californicum • All parts of plant are toxic
• Signs include salivation, diuresis, muscular weakness, incoordination,
• Preventive measures include delaying grazing until after the first frost and breeding ewes
5 weeks before putting on range containing Veratrum
DAYS OF GESTATION EFFECT
0 to 10 Failure to implant
12 to 14 Cyclopia
12 to 34 Motor nerve paralysis
22 to 30 Cleft palate
25 to 36 Hypoplasia of metacarpals and tarsals
Tobacco • Toxic effects are more common in swine
Poison hemlock • Toxic effects are more common in cattle
Lupine • Can cause arthrogryposis
Locoweed • Can cause arthrogryposis
Sudan grass • Can cause arthrogryposis and contracted tendons

of the fetal pituitary glands. This can result in prolonged Broomweed. Broomweed (Gutierrezia microcephala,
gestations, abnormally large fetuses, and an increased in- Xanthocephalum lucidum) ingestion can cause abortions
cidence of dystocia. V. californicum is an erect herb with an and small, weak, premature lambs because of the toxic
unbranched stem. Large, wide, alternate, clasping effects of an ecbolic toxin in these plants (triterpenoid
leaves with prominent spiraling parallel veins are saponin). Other clinical signs include gastrointestinal
characteristic1,2 (Table 6-7). upset, hematuria, and death. Broomweed is a shrub found
in arid regions of the western United States.4
Locoweeds. Members of the genera Astragalus and
Oxytropis are commonly referred to as locoweeds; they have Ergot alkaloids and ergot. The consumption of fescue
been implicated as causing abortions, small weak lambs, (Festuca arundinacea) infected with the fungus Nety-
and bent legs in newborns. The incidence of abortion and phodium coenophialum is associated with decreased repro-
small weak lambs has been reported to be as high as 75% ductive efficiency.4 The ergot alkaloids produced by the
in exposed ewes. The toxin affects the fetal-placental fungus have been shown to affect prolactin production in
unit, causing delayed placentation, decreased placental ewes and increase the interval from introduction of the
vascularization, fetal edema, and altered development of ram until conception.5 Ergot concentrations greater than
the cotyledons. It also is associated with decreased sper- 0.1% to 0.7% of the diet can reduce the number of live
matogenesis in the ram.3 births in sheep.6
 Chapter 6 Theriogenology of Sheep and Goats • 173

Estrogen-producing plants. Sheep appear to be sensi- cells). Angora goats have a decreased ability to respond to
tive to the effects of phytoestrogens from plants such as heat stress compared with other breeds of goats. Sheep
subterranean clover (Trifolium subterraneum), white can tolerate external temperatures higher than 110° F if
clover (T. repens), and alfalfa (Medicago sativa). Clinical the humidity is less than 65%, but they will pant if the
signs associated with phytoestrogen consumption include rectal temperature is higher than 106° F. Secondary bloat
infertility, irregular and prolonged heat cycles, lowered and acidosis can occur if high-energy feed is made avail-
conception rates, and early embryonic death.7 Physical able at night or if a break in the weather occurs because
changes that may be seen in ewes include vaginal pro- animals may engorge themselves.
lapse, cystic glandular hyperplasia of the cervix and
uterus, enlarged teats, and inappropriate lactation. Dysto- Diagnosis. Diagnosis is based on the clinical signs.
cia and uterine inertia also are observed.6 Plants associ- Necropsy findings include cerebral edema, rapid pu-
ated with depressed reproduction are shown in Table 6-7. trefaction, and large, distended veins. CBC results are
unremarkable.
Nutritional Abnormalities Treatment. Treatment should include lowering the
Poor body condition, depressed energy intake, and de- body temperature with cold water submersion, cold water
creased mineral and vitamin intake all suppress reproduc- enemas, ice applications, or alcohol rubs. Affected
tive activity in ewes and does. Lower overall nutritional animals should be sheared. Non-pregnant animals can be
intake results in poor or weak signs of estrus, depressed given glucocorticoids (dexamethasone 1 to 2 mg/kg IV).
ovulation, abnormal estrus cycle length, and delayed Normal hydration should be maintained. If animals are
puberty. Deficiencies in energy, protein, vitamins A and more than 10% dehydrated, IV fluids should be adminis-
E, phosphorus, and many trace minerals are most com- tered, but if animals are less than 10% dehydrated, fluids
monly seen. Deficiencies in vitamin A, copper, man- can be administered orally. Keepers should place affected
ganese, and iodine are associated with irregular estrus animals in the shade and attempt to improve air circula-
cycles. tion around them. Bucks and rams should undergo a BSE
after periods of heat stress. If spermatic abnormalities are
noted, the examination should be repeated in 49 to 60
Heat Stress days.
Heat stress depresses reproductive ability and causes fetal
wastage. Causes of heat stress include decreased water Prevention. Prevention is aimed at keeping animals
intake, obesity, exercise, and fatigue during hot weather. cool. Woolly or hairy animals should be sheared before
Both very young and very old animals are susceptible to periods of hot weather. Long scrotal wool also should be
heat stress. High ambient temperatures and high humid- shorn. Animals should be maintained at a good body
ity result in poor or compromised cooling. As the condition score. Providing shade at feed bunks and spray-
ambient temperature approaches body temperature, skin ing water on the animals’ backs around the lounging areas
vasodilation no longer aids in heat dissipation. In sheep are helpful in prevention. Spraying or misting at the feed
the respiratory passages are important in cooling, so bunks can increase feed intake. On hot, humid days,
animals will pant when they are hot. Unsheared Angora animals should only be worked or handled in the early
goats and heavily wooled sheep, particularly young sheep, morning. Trace mineral salt and cool water should be
are especially susceptible to heat stress. provided free choice. Animals should be fed in the early
morning or late afternoon. Toxins and plants that de-
Clinical signs. Common clinical signs include de- crease peripheral vasodilation should be avoided (fescue).
creased fertility and depressed signs of estrus in females as Ventilation across the animals’ backs and an open-ridge
well as an increased number of abnormal spermatozoa barn with a high ceiling help keep animals cool.
and depressed libido in males. Angora goats experience For dairy goats or sheep, sprinklers and good ventila-
high embryonic mortality if the heat stress occurs during tion in holding pens helps minimize heat stress, but these
the first 3 to 6 weeks of pregnancy. However, all breeds measures may be contraindicated for the prevention of
and both species can experience high embryonic losses. mastitis. Increasing the energy concentration of feed may
Other clinical signs include dullness, depression, rapid improve production after a period of reduced intake.
respiration, open-mouth breathing, congested conjunc- Feeding bypass protein (blood meal, fish meal, corn
tiva, dilated pupils (early), constricted pupils (late), de- gluten meal, roasted soybeans, extruded soybeans) im-
creased feed intake, increased heart rate, weak rapid proves production, particularly if fat has been added to
pulse, hyperthermia, acid-base alterations, dehydration, the feed. The addition of sodium bicarbonate (0.85% to
excessive loss of potassium and sodium from sweat, and 1%) may enhance milk production in hot weather. Less
increased packed cell volume (greater than 60% red blood heat is generated from good-quality forage than from
174 • Sheep and Goat Medicine
poor-quality forage. The acid-detergent fiber (ADF) ruled out. Other causes of vaginitis include caprine
content of the diet can be dropped to 21% of the dry herpes vulvovaginitis (edema and cloudy gray discharge),
matter intake for short periods. The addition of granular vulvovaginitis caused by Mycoplasma and Achole-
ionophores improves productivity and decreases intake plasma, and Actinomyces pyogenes and Staphylococcus infec-
for many animals, but may not benefit lactating females. tions.6 Lavaging the vagina with mild antiseptic solutions
The feeding of long-stem hay should be implemented. If (commercial chlorhexidine) may be all that is required. If
green or wet feeds are fed, the bunks should be checked animals are in a lot of pain, NSAIDs are useful.
for spoilage on a routine basis on hot days. Ectopic mammary tissue on the vulva is occasionally
encountered. It appears as vulvar swelling before parturi-
tion. Because outflow tracts for milk are rare, this glandu-
Pseudopregnancy lar tissue usually undergoes pressure atrophy. The glandu-
Pseudopregnancy (mucometra, hydrometra, cloudburst) lar tissue can be surgically removed, but this form of
is caused by a prolonged luteal phase in goats. The inci- therapy is rarely required.
dence in dairy goats may be as high as 3% to 5% on some
farms,8 with the highest incidence occurring in Novem-
ber through December. It is much less common in fiber
Cystic Ovarian Disease
or meat breeds of goats and sheep. The cause of this con- Cystic ovaries appear to be more common in goats than in
dition is poorly understood, but possible modes of action sheep. In one study, 2.4% of more than 1000 female goats
that have been proposed include out-of-season breeding, examined at slaughterhouses had ovarian cysts.9 Owners
sheep and goat hybrid pregnancy, and the overuse of hor- often make the diagnosis based on short cycles or
monal manipulation of the reproductive cycle. Some nymphomania,8 so cystic ovarian disease is probably over-
cases probably occur as sequelae to abortion or early em- diagnosed. Graafian follicles larger than 12 mm may be
bryonic loss with a retained CL. Spontaneous CL reten- considered cystic, but few studies have been performed to
tion outside of pregnancy, which may result from hor- document a standard size.8 The normal follicle diameter
monal manipulation for superovulation or out-of-season size of sheep (15 to 19 mm) is larger than that reported in
breeding, also has been proposed as a cause of pseudo- the doe.6 The use of some superovulation protocols
pregnancy.6,8 The condition may occur numerous times (PMSG), possibly phosphorus deficiency, and the feeding
during the life of a doe, or it may occur only once. of estrogenic compounds may be associated with the for-
mation of cystic ovaries. Treatment with hCG (750 to
Clinical signs and diagnosis. Some females may show 1000 IU) or GnRH (50 to 100 mg) may be effective.8 Does
signs of parturition, udder development, and a bloody that habitually develop cystic ovaries can be treated with
vaginal discharge. Pseudopregnancy also is characterized hCG or GnRH, watched for signs of estrus, bred, and then
by anestrus, occasionally increased abdominal size, and retreated with hCG or GnRH 24 hours after breeding.
external and behavioral signs of pregnancy. Blood proges-
terone concentrations may be consistent with pregnancy
and remain elevated for as long as 5 months. Real-time
Ovarian Tumors
ultrasonography may reveal a uterus with varying Ovarian tumors are rarely reported in sheep and
amounts of fluid that is either clear, slightly cloudy, or goats.6,10,11 A granulosa theca cell tumor is shown in
clear with some flecks. The uterus usually appears thin- Figure 7-5. This is the most common type of ovarian
walled, and no placenta or fetus can be visualized. In tumor occurring in ewes and does. Animals with these
females that undergo ultrasound examination before pla- tumors may exhibit nymphomania, virilism, and inappro-
centomes are visible (before day 30 of gestation), this priate lactation syndrome. Ovarian ultrasonographic ex-
condition may be falsely diagnosed as pregnancy. There- amination, either per rectum or transabdominal, usually
fore careful ultrasonographic examination with attention reveals an enlarged ovary that is either solid or cystic. The
to the stage of pregnancy and positive signs of pregnancy contralateral ovary is devoid of structures and lacks a CL.
(e.g., fetus, placenta, umbilicus) is imperative. A tentative diagnosis can be based on elevated concen-
trations of testosterone or estradiol, diagnostic ultrasound
Treatment. The most common treatment for pseudo- findings, and clinical signs. The treatment is ovariectomy.
pregnancy is the injection of PGF2a (10 to 20 mg) or clo- The authors and others have suggested that does with
prostenol (75 to 100 mg/45 kg). granulosa cell tumors may have elevated concentrations
of testosterone and estradiol.10
Vaginitis
Vaginitis has several causes (see Chapter 10). Whenever
Ovariectomy
either nonparturient or parturient vaginitis is encoun- The animal should be heavily sedated and the flank
tered, particularly in sheep, contagious ecthyma should be blocked with a local anesthetic, or anesthetized (see
 Chapter 6 Theriogenology of Sheep and Goats • 175

Chapter 16). Animals should be given antibiotics up to 4 8. Braun W: Noninfectious infertility in the doe. In Youngquist RS,
hours preoperatively, and the clinician should adhere to editor: Current therapy in large animal theriogenology, Philadelphia,
aseptic technique. Either a flank or ventral midline ap- 1997, WB Saunders.
9. Lyngset O: Studies on reproduction in the goat. V. Pathological
proach is acceptable. For the removal of ovarian tumors,
conditions and malformations of the genital tract of the goat, Acta
a flank approach made by positioning the animal with
Vet Scand 9:364, 1968.
the affected ovary side up is preferred. For bilateral 10. DeWalque J: Tumeur ovarienne et masculinization chez une
ovariectomy the authors prefer a ventral midline ap- chamoisee de Alpas, Annales de Med Vet, p 322, 1963.
proach. Regardless of the approach selected, the 11. Lofstedt RM, Williams R: Granulosa cell tumor in a goat, J Am
abdomen should be entered as far caudally as possible. Vet Med Assoc 189:206, 1986.
The technique to open and close the abdomen is the 12. Riddell MG: Ovariectomy. In Wolfe DF, Moll HD, editors: Large
same as that described in the sections on Cesarean animal urogenital surgery, Baltimore, 1999, Williams & Wilkins.
section and surgical ET. After locating the ovaries, the 13. Katz LS: Sexual performance tests in sexually inexperienced rams.
clinician should identify the pedicle and exteriorize the In Dziuk PJ, Wheeler M, editors: Handbook of methods for study of
ovary and pedicle out of the incision. Slow tension reproductive physiology in domestic animals, Urbana, IL, 1991, Uni-
versity of Illinois Press.
usually enhances visualization of the ovary. A crushing
hemostat is placed on the ovarian pedicle, and a transfix-
ation ligature is placed through the pedicle on the side of
the hemostat, opposite the ovary. The ovarian pedicle is
ABORTION
transected next to the hemostat opposite the suture. The Abortion (fetal loss or fetal wastage) is the loss of the
clinician then releases the hemostat and examines the conceptus anytime during gestation, but it is most com-
pedicle for hemorrhage. If only one ovary is to be monly observed during the final 2 months. Fetal losses in
removed, the abdomen can then be closed. If the second early to middle gestation often go undetected. The ewe
ovary is to be removed, a hemostat may be placed around and doe are both normally very fertile animals but may
the pedicle of the removed ovary for easy retrieval in case have a high incidence of abortion compared with other
of excessive bleeding. The second ovary is removed in the farm animals.1,2 Abortion rates of 5% for these two
same manner as the first, after which the pedicles of both species are commonplace; rates less than 5% are consid-
should be examined and the abdomen closed.12 Bilateral ered good, and a less than 2% abortion rate is considered
ovariectomy is performed to produce females for semen excellent.3,4 Many infectious agents, stressors, pharma-
collection and libido testing of males. These ovariec- ceuticals, nutritional deficiencies, and toxic plants have all
tomized females should be given estradiol (100 mg) 24 to been indicated as causes of pregnancy loss.2 Infectious
48 hours before use.13 causes are common and may be major sources of eco-
nomic loss. During an abortion outbreak the safest ap-
proach is to assume that all causes of abortion are infec-
Others tious in nature.5,6 Several microbial agents have been
Freemartins are rare in sheep and goats compared with incriminated as causes of abortion in sheep and goats, but
cattle because both sheep and goats are adapted to multi- the most common are Chlamydia psittaci, Toxoplasma
ple births. gondii, and Campylobacter species.3,7-9
In a study of western North America sheep abortion
and stillbirth specimens submitted during a 10-year
R EFERENCES
1. Kampen KR, Ellis LC: Prolonged gestation in ewes ingesting Ver-
period, T. gondii, Campylobacter species, and C. psittaci
were diagnosed in approximately 25% of all cases.9 Many
atrum californicum: morphological changes and steroid biosynthe- of the organisms that cause abortion in sheep also are
sis in the endocrine organs of cyclopic lambs, J Endocrin 52:549, common causes of abortion in goats. Campylobacteriosis
1972. is the exception, as it appears to be rare in goats in North
2. James LF: Teratological research at the USDA-ARS poisonous America.10
plant research laboratory, J Nat Toxins 8:63, 1999. The most consistent finding in most cases of infectious
3. James LF: Effect of locoweed feeding on fetal lamb development, abortion is placentitis (placental disease), which results in
Can J Comp Med 40:380, 1976. retarded fetal growth or death and occasional septicemia
4. Putman MR: Toxicologic problems in livestock affecting repro- of the ewe or doe.6 Regardless of the type of flock (com-
duction, Vet Clin North Am: Food Anim Pract 5:325, 1989.
mercial, hobby farm, pet), midterm and late abortions are
5. Porter JK, Thompson FN: Effects of fescue toxicosis on reproduc-
of great concern to the owner from both an economic and
tion in livestock, J Anim Sci 70:1594, 1992.
6. Roberts SJ: Veterinary obstetrics and genital diseases (theriogenology),
emotional standpoint. When fetuses are lost, the unpro-
North Pomfret, VT, 1986, David and Charles. ductive females must be fed and cared for until the next
7. Adams NR: Organizational and activational effects of phytoestro- breeding season or sold, both of which result in economic
gens on the reproductive tract of the ewe, Proc Soc Exp Biol Med losses. In case of infectious abortion a prolonged period
208:87, 1995. of uterine disease and infertility may follow.10 Fetal
176 • Sheep and Goat Medicine
BOX 6-3

G ENERIC A BORTION P REVENTION P ROGRAM

• Institute a biosecurity program to quarantine all herd additions for as long as 30 days before introduction to the
flock.
• Maintain good body condition scores and offer a complete, good-quality trace mineral–salt mixture free choice.
Maintain a source of supplemental energy and protein for use during emergency situations.
• In endemic areas, vaccinate 4 and 2 months prepartum for Chlamydia and Campylobacter (and possibly other
diseases) for animals not previously immunized; only one vaccination is required for those with a history of
vaccination.
• Feed chlortetracycline (200 to 400 mg/head/day) and monensin (15 mg/head/day) or decoquinate (2 mg/kg body
weight) during gestation. These can be included in a grain supplement or mineral mixture.
• Avoid exposure to cows or hogs
• Keep feed and water sources free of fecal-urine contamination
• Reduce numbers of rats, birds, and cats. Keep only spayed adult cats in barns.
• Do not place feed on the ground.
• Submit fetal samples (including placenta) to a diagnostic laboratory promptly.
• Keep first lambing and purchased ewes in separate areas from the rest of the flock.
• Keep postpartum and prepartum females in separate pastures.
• Respond aggressively to any abortions in a flock (diagnose, dispose of aborted tissue, separate aborting females,
treat remaining animals).
• Maintain flock in a stress-free, sanitary, uncrowded environment.

mummification is not a common finding in sheep or nancy will abort or produce lambs with developmental
goats. However, when fetal mummification occurs, toxo- defects (hydranencephaly). Goats are frequently infected
plasmosis, chlamydiosis, border disease, and Coxiella in- in endemic regions as evidenced by serology, but clinical
fection should be at the top of a differential list.10 signs are rarely recorded. Bluetongue is an unlikely cause
Box 6-3 describes a generic abortion prevention of abortions in goats.7
program. Because of the zoonotic potential of many abor-
tifacient conditions, pregnant women, persons with Diagnosis. Bluetongue viruses can be isolated from the
cancer, and those who are immunosuppressed should blood, semen, brain, and spleen of aborted fetuses. Viral
probably avoid handling aborted fetuses and placentas. In isolation is enhanced if blood is collected during febrile
this discussion, causes of abortion or fetal wastage are dis- periods (see Chapters 4 and 14).
cussed in terms of those that result in fetal deformities
and those that do not. Prevention. Vaccination against bluetongue is of ques-
tionable value because of the large numbers of serovars.
ABORTION ASSOCIATED WITH Housing sheep away from low-lying areas during gnat
season, particularly at night, may help prevent the disease.
DEFORMITIES
Bluetongue Akabane Virus Disease
Bluetongue is an infectious, noncontagious disease of ru- Akabane viral abortion has been reported in sheep and
minants, especially sheep, that is caused by an orbivirus. It goats.2,10,11 Akabane virus is an arbovirus that is trans-
is transmitted by a Culicoides gnat (or midge), and cattle mitted by gnats and mosquitoes.5 It has been reported in
may serve as reservoirs for infection.3 Abortion associated Australia, Japan, South Africa, the Middle East, and Ar-
with bluetongue occurs seasonally and is tied to the life gentina, but it is rare in North America.2,8,9
cycle of the gnat.3
Clinical signs. Clinical disease has been observed in
Clinical signs. Infected ewes may become febrile; have both sheep and goats. Infection of non-pregnant animals
a swollen tongue, ears, or face; exhibit an ulcerated mouth is subclinical. Pregnant animals may remain healthy but
or nose; and become lame.3 Ewes infected during preg- abort, deliver stillborn fetuses, or have mummified
 Chapter 6 Theriogenology of Sheep and Goats • 177

fetuses. Dystocia is common, particularly when arthro- ewe is infected before day 85 of gestation, her fetuses are
gryposis is present.5 aborted, macerated, or mummified. Surviving lambs may
have disturbances in the normal formation of the cere-
Diagnosis. The diagnosis of Akabane disease is made bellum and hair follicles. Some of these lambs may be
on the basis of arthrogryposis and/or hydranencephaly in born persistently infected. Lambs infected after 85 days
the newborn. The identification of a positive antibody of gestation may be born normal, weak, or stillborn; they
titer to this virus in live-born or aborted fetuses also is may be negative for the virus or have viral antibody
diagnostic. titers.3

Prevention. Akabane viral infection is untreatable and Clinical signs and diagnosis. Signs of infection
prevention is difficult. However, effective vaccines have include increased numbers of open females, mummified
been developed and are used before breeding season in or macerated fetuses, stillbirths, and weak lambs with
epizootic areas.7 hairy fleece and tremors.12 Fetal anomalies include cere-
bellar hypoplasia, hydranencephaly, and others. The hairy
fleece of affected lambs is usually darkly pigmented and
Cache Valley Virus most prominent around the head and shoulder.3 These
Cache Valley virus is similar to Akabane virus and is an “hairy shaker” lambs tend to grow poorly and may
arthropod-borne disease. Mosquitoes are likely carriers of develop polyarthritis. Cotyledons are small or dysmature,
this virus. It is endemic in parts of the United States. with focal necrosis.12 The virus can usually be isolated
from fetal blood (buffy coat).3
Clinical signs. Clinical signs in sheep include aborted
fetuses with arthrogryposis, brachygnathia, hydranen- Prevention. All animals suspected of infection should
cephaly, and microencephaly, as well as hypoplasia of the be culled. Any replacement lambs should be screened (by
spinal cord in live-born lambs.3,7 It appears to have a BDV titers and/or viral isolation) before they are added to
predilection for nervous tissues. The more severe the re- the flock.3 Any flock additions should be quarantined for
sultant lesion, the earlier in gestation the infection oc- 30 days and tested for the presence of this and other dis-
curred. Early infection (between day 28 and 32 of gesta- eases before being placed into the flock. Cattle and sheep
tion) may result in mummification or embryonic loss.3 It should be separated, and the use of common water sources
is likely that goat fetuses also are susceptible to Cache should be minimized. Modified live cattle vaccines should
Valley virus. be avoided.The use of killed vaccines for BDV in cattle are
of questionable efficacy but have been used.
Diagnosis. The diagnosis is aided by the detection of
antibodies in fetal fluids or precolostral serum, concurrent
with characteristic congenital abnormalities. Absence of
Others
titers from the dam also is significant, but absence from Teratogenic changes and abortion have been associated
the lamb does not preclude diagnosis.3 with several plant species, including Gutierrezia (broom-
weed), Lupinus formosus (arthrogryposis), Conium macula-
Prevention. In areas in which vaccines are available, tum, Nicotiana tabacum, and Veratrum californicum (skunk
their use 1 or 2 months before breeding may help prevent cabbage). Astragalus (locoweed; causes arthrogryposis),
the disease.3 Natural immunity derived from infection Lathyrus, Sophora, and Sudan grass (ankylosis, contracted
may be for life.3 Reducing insect populations, fencing tendons) have been reported to cause congenital defects
boggy low-lying areas with high insect populations, and in sheep and goats similar to the malformations observed
using insect repellents are all potential preventative meas- with Akabane virus and Cache Valley virus infections7
ures, but they are difficult to implement. (see Table 6-7).
Iodine deficiency may be a problem in certain loca-
tions around the world. Affected lambs are born with
Border Disease greatly enlarged thyroid glands, a condition commonly
Border disease virus (BDV) infection, or hairy shaker known as goiter. Late-term aborted fetuses with no wool
disease, is closely related to bovine viral diarrhea. BDV and weak newborns are commonly seen. Flocks grazing
causes abortion and congenital abnormalities of sheep in on plants that are members of the Brassica family (e.g.,
North America, Britain, Australia, New Zealand, and rape, kale, turnips) and animals of certain breeds (polled
possibly other areas.3,12 Goats appear fairly resistant to Dorsets) are more susceptible to iodine deficiencies.
this disease. Iodine should be supplied at a rate of 0.10 to 0.80 mg/kg
of dry matter of feed intake. Supplementation with
Pathogenesis. The ewe is infected by ingesting or in- iodine in iodine-deficient areas has been associated with
haling the virus. Viremia ensues for 7 days. If a pregnant increased lambing rates and decreased lamb mortality.
178 • Sheep and Goat Medicine
Copper deficiency causes a condition in newborn dogs, and some birds. The organisms can be shed by the
lambs known as enzootic swayback. Lambs are typically intestinal tract and through the gallbladders of carrier
normal at birth but develop rear-limb paresis or paralysis sheep and occasionally guard dogs (that have ingested
within a few weeks. The neurologic deficits are caused by aborted fetuses). Infection occurs through ingestion of
a dystrophic demyelination of the white matter in the the organism by the pregnant female. After ingestion the
spinal cord. This lesion begins during gestation and organism enters the bloodstream through the intestinal
cannot be corrected after diagnosis. Therefore the focus lining, with a resultant bacteremia.
of attention should be on the gestating ewes and does.
Pygmy goats appear to be the most susceptible of the Clinical signs. Late-gestation abortions, stillbirths,
goat breeds. Infertility problems also have been blamed and weak lambs are common. Aborted fetuses and pla-
on copper deficiencies. Copper supplementation in ewes centas are expelled with little or no autolysis, but fetal re-
should be done with caution because copper toxicity can tention may occur. Aborting does usually show no signs
result from oversupplementation and also may cause of systemic illness but may have diarrhea. A mucopuru-
abortions and other systemic disease. Copper should be lent vaginal discharge is reported in most aborting does.14
fed to ewes at a rate of 5 ppm (mg/kg) of the diet on a In South Africa, where Campylobacter abortion is
dry-matter basis. Copper is commonly supplemented in common in goats, as many as 30% of aborted kids have
salt mixtures. These salt mixtures should contain between grossly visible liver necrosis. The placenta is often edema-
0.0625% to 0.13% copper in the form of copper sulfate, tous, with necrosis or swelling of the cotyledons.7 The
which would be between 0.25% and 0.50% copper sulfate fetus may have some subcutaneous edema, pleuritis, hep-
in the salt mix. Important interactions occur between atitis, and peritonitis. Necrotic areas on the livers of
copper and molybdenum and copper and sulfur. High aborted lambs may occasionally look like “gray targets.”
concentrations of molybdenum (1 to 2 ppm) and sulfur Although abortion storms may occur in as much as 70%
(more than 2000 ppm) in feed and water sources can de- to 90% of a flock, they usually affect less than 20% of
crease copper availability.2 Interaction with other miner- ewes in enzootically infected sheep flocks.2 Ewes that
als such as iron (more than 400 ppm), cadmium (more become infected abort and then become immune.
than 3 to 7 ppm), and zinc (more than 100 to 400 However, some become persistently infected and shed the
ppm) also can negatively affect copper absorption and organism in their feces. Ewes usually recover uneventfully
metabolism.2 but occasionally may die from retained dead fetuses,
Manganese deficiency during gestation can result in metritis, and possibly peritonitis.
abortion or weak, small, paralyzed, or deformed
neonates.2 As with other deficiencies, the addition of a Diagnosis. Definitive diagnosis of Campylobacter abor-
palatable trace mineral salt mixture offered free choice, tion is through isolation of the organism. Direct micro-
year-round, is usually preventative (see Chapter 2). An- scopic examination (dark field or contrast) and isolation
thelmintics in the benzimidazole class (albendazole and of Campylobacter species from placenta, fetal abomasal
cambendazole) given to pregnant females during the first contents, and maternal vaginal discharge is the preferred
trimester have been associated with fetal abnormalities diagnostic procedure.15 Stained cotyledonary impression
and abortions.7 smears are useful in identifying the organism.3 A sero-
logic test can be done at a few specialized laboratories.
Whenever the organism is isolated, culture and antibiotic
ABORTION NOT ASSOCIATED sensitivity patterns are useful for guiding possible flock
WITH DEFORMITIES, treatment.
INFECTIONS Treatment and prevention. The antibiotic regimen of
penicillin or streptomycin injections or tetracycline in
Campylobacter feed (300 mg/head/day) may be useful in the face of a
Campylobacter (vibriosis) is the most significant cause of disease outbreak.13,14 Tetracycline in the feed (200 to 300
abortion in sheep in North America, particularly in mg/head/day) before and during lambing or kidding
western regions. However, it has rarely been documented season appears to decrease the incidence of abortion, as
in cases of goat abortion.5,7,13,14 It also is an important does the use of injectable long-acting oxytetracycline (20
cause of abortion in other areas of the world (Britain, mg/kg every 48 hours) during an outbreak. However,
New Zealand, Africa).7,12 penicillin- and tetracycline-resistant strains have been
Campylobacter jejuni and C. fetus (formerly Vibrio fetus identified.3 In cases of apparent tetracycline resistance,
intestinalis) have been identified as the causative sulfamethazine (110 mg/kg PO), or tylosin (30 mg/kg
species.7,14 C. jejuni is the most common of the two in IM SID) may be given.
North America. These organisms are gram-negative, mi- A combined killed bacterin of C. fetus and C. jejuni is
croaerophilic rods that live in the intestines of sheep, available for use in sheep. In a confirmed outbreak, vacci-
 Chapter 6 Theriogenology of Sheep and Goats • 179

nation of all pregnant ewes and does with an ovine at conception (cotyledon formation), resulting in both
Campylobacter bacterin is advisable.7 The vaccine is ini- abortion and immune response. Inflammation and necro-
tially administered before breeding, with a booster in 2 to sis of the placenta caused by multiplication of the organ-
3 months. Revaccination annually shortly before or just ism prevent normal transfer of nutrients across the pla-
after breeding is recommended.16 If an immunologic centa, resulting in fetal death and abortion.7 Aborting
agent for Escherichia coli is combined with C. fetus or C. females shed large numbers of the organism in the
jejuni, it should be avoided in early gestation because it uterine discharge, fetus, and placenta, particularly during
has been anecdotally associated with fetal wastage. On the first 3 weeks after abortion. After aborting the dam
farms where Campylobacter is a confirmed cause of abor- develops a good immune response, and elimination of
tion, autogenous bacterins that are strain-specific are Chlamydia from her uterus usually occurs within 3
valuable. Because of the probable oral route of infection, months of the abortion.24,25 However, some ewes that
maintaining sanitary conditions, avoiding fecal contami- have aborted as a result of C. psittaci infection may shed
nation of feedstuffs, and isolating aborting animals are the organism in vaginal secretions during estrus,3 and
recommended.14 The placentas and aborted fetuses susceptible females exposed for the first time in the last
should be burned or buried and never fed to guard dogs. half of pregnancy may abort in the subsequent preg-
Occasionally Flexispira rappini is identified in suspected nancy.18,20,26 These females may serve as sources of infec-
cases of vibriosis. Obviously, in these cases vaccination for tion by shedding the organism from their vaginal secre-
Campylobacter is of no value.3 tions, feces, or expired air.3,18,20 Regardless of the time of
infection in the female, the organism does not proliferate
Zoonotic potential. C. jejuni has been recognized as a and attack the placenta until about day 90 of gestation.27
cause of mild gastroenteritis and a possible cause of some Chlamydia has been isolated from the semen of experi-
neuromuscular disease in human beings. Domestic mentally infected rams for as long as 29 days after inocu-
animals and unpasteurized milk are thought to be sources lation.22,23 Still, the primary modes of transmission are
of C. jejuni infection in human beings. Aborted fetuses from vaginal or uterine secretions of aborting females and
infected with C. jejuni should be handled carefully. Shep- from females shedding the organism the following year.
herds giving artificial resuscitation to infected lambs have During the subsequent breeding season the does show
reportedly acquired the disease.14 no signs of infertility, and the natural immunity after an
abortion lasts about 3 years. Outbreaks of abortion
among goats by dual infection with Chlamydia and Cox-
Chlamydia iella burnetii also have been reported.28
C. psittaci is a gram-negative, intracellular organism that
contains both ribonucleic acid (RNA) and deoxyribonu- Clinical signs. In newly infected flocks, 25% to 60% of
cleic acid (DNA).5 Chlamydial abortion is one of the ewes or does may abort.17 In flocks in which the disease is
most common causes of infectious abortion in sheep and epizootic, abortion rates tend to drop to between 1% to
goats in North America.6,17,18 It also has been diagnosed 15%, with abortions predominately occurring in flock ad-
in other areas (Britain, Europe).19 Chlamydial infections ditions.3 Abortions often occur in the last month of ges-
also can produce pneumonia, keratoconjunctivitis, epi- tation but may occur as early as day 100 of gesta-
didymitis, and polyarthritis in sheep and goats.10,11,13,18 tion.6,10,24,25 Does and ewes may become anorexic and
This organism was established as the causative agent of febrile and may show a bloody vaginal discharge 2 to 3
enzootic abortion of ewes (EAE) in the late 1950s.20 The days before aborting. The fetus may be delivered in a
antigenic strains found in sheep and goats appear to be fresh state, but if it is retained in the uterus for 1 or 2
closely related. At least nine immunotypes and possible days, it will be autolyzed. Some weak newborns may
more have been identified.3 Antigenic type 1 is impli- survive, and a few females may retain the placenta.6,17
cated in abortions, stillbirths, weak kids and lambs, and Occasionally, pneumonia may be seen in young animals
neonatal chlamydial pneumonia. Type 2 isolates cause during an abortion storm. Pathologic changes in the fetus
polyarthritis and conjunctivitis in adults.21,22 However, are nonspecific. Regional to generalized placentitis in-
serotype 2 has recently been reported as an abortion- volving the cotyledons and intercotyledonary space are
inducing strain in ruminants as well.18 Little or no cross- usually noted.6,17 The placenta may be thickened with
protection occurs between these two antigens.21 white, gray, yellow, or red cotyledons.

Pathogenesis. Pigeons and sparrows may serve as Diagnosis. Diagnosis is by history of abortion, clinical
reservoirs for the organism, and ticks or insects may play signs, and demonstration of the characteristic inclusion
a role in the transmission of this disease.22,23 C. psittaci bodies in impression smears of placenta, fetal tissue or
can infect a non-pregnant female and remain dormant, uterine discharge. Stained cotyledonary impression
eliciting little or no immune response. The organism can smears (Gimenez or modified Ziehl-Neelsen stain)
stay dormant, probably in the intestine, until it multiplies and identification of elementary bodies also are good
180 • Sheep and Goat Medicine
diagnostic indicators.3 A definitive diagnosis is made by the vaccine should be given IM or SC 8 weeks before
culturing the organism from the placenta or fetal breeding and followed in 4 weeks with a booster.16 Even
tissue.6,11,13,17 Serological testing also is a valuable aid in though trials in sheep have demonstrated that protection
diagnosis. Ewes and does have significant increases in an- against abortion lasts for about 3 years, annual revaccina-
tibodies against chlamydial antigens after abortion.29 tion is recommended.16,31 Vaccination helps prevent
Paired serum samples taken 2 to 3 weeks apart from the abortion but may not eliminate infection and should
aborting female or the presence of antibodies in fetal therefore not be considered 100% effective.7
serum can aid in diagnosis.6,13,20 The tests of choice for Aborting females should be removed from the herd for
Chlamydia are the enzyme-linked immunospecific assay at least 3 weeks, and fetuses and placentas should be
(ELISA) and the indirect inclusion fluorescence antibody burned or buried. Producers should take care to prevent
(IIFA) tests.29 A four-fold increase in antibody titers the contamination of feed and water. No feedstuffs
between paired serum samples or titers in the range of should be offered directly on the ground, and feeders
1:32 to 1:256 are highly suggestive of chlamydial infec- should be designed to prevent animals from crawling into
tion, but not diagnostic. When chlamydiosis is suspected, and contaminating feed.19
the following samples should be submitted to a diagnostic
laboratory: Zoonotic potential. C. psittaci is contagious to human
beings. During lambing and kidding season, pregnant
1. Fresh placenta and fetus packed in ice women assisting with parturitions may become infected
2. A vaginal swab taken within 3 days of abortion (if and miscarry. An influenza-like syndrome also has been
the placenta is not available) described in people assisting with lambing of infected
3. Paired serum samples from both aborting and animals.7 Veterinarians and others assisting with normal
non-aborting females parturition, dystocia, and abortion should wear masks
and latex gloves and try to limit exposure to uterine fluids.
Treatment. Success has been reported in controlling an The same precautions apply when collecting fetuses or
outbreak by treating all females with tetracycline during placentas for disposal or diagnostic evaluation. Pregnant
the final 4 to 6 weeks of gestation.6,13,17 Tetracycline (400 women should avoid contact with the flock during the
to 500 mg/head/day) mixed into the feed for 2 weeks can kidding and lambing season.7
prevent the disease.7,30 This is a reasonable approach for
fiber-producing animals. However, in dairy herds it is
customary to treat individual nonlactating does or ewes
Q Fever
with injections of long-acting oxytetracycline (20 mg/kg Query or Queensland fever (Q fever) is a zoonotic infec-
IM or SC) every 10 to 14 days.7 Others have given the tion affecting a variety of animal species as well as human
drug twice a week during the final 4 to 6 weeks of gesta- beings. It can cause abortion in sheep and goats7,32 and
tion.6,13,17 Considering the management difficulties and has been reported in North America and many other
cost associated with this mode of prevention, the most ef- countries.6,7,10,32,33 Q fever is caused by Coxiella burnetii,
fective protocol appears to be one injection of long-acting an obligate, intracellular, rickettsial organism that can
oxytetracycline 6 to 8 weeks before parturition, followed survive in a dried condition for extended periods.3 Cattle,
by a second injection 3 weeks after parturition.22 The sheep, goats, and wildlife may carry the organism, which
authors prefer to include tetracycline in the feed or is shed in large numbers in placentas, uterine fluids,
energy-protein supplement when possible. Regardless of colostrum, and milk.7,33 Cows may be a source of infec-
the route of administration, suppression of the organism tion for sheep and goats when they share pastures, water,
with antibiotics may prevent additional placental damage feed sources, and handling equipment. Animals and
and reduce shedding of Chlamydia. Tylosin (20 mg/kg human beings can be infected by inhaling contaminated
IM SID or BID) also may be an effective treatment. dust. Contact with aborted material, vaginal discharge,
and mucous membranes of infected animals also are
Prevention. Enzootic abortion is of such serious eco- modes of contamination. This organism may be sexually
nomic concern in some countries that compulsory vacci- transmitted. Grazing contaminated pastures and tick
nation programs have been implemented.19 Killed vac- bites are other sources of infection.7
cines for sheep are available in certain locales. These
vaccines may be used in goats but have been associated Clinical signs. The primary significance of this disease
with local and systemic reactions (marked soreness and is its zoonotic potential. In livestock the disease is usually
stiffness).8,16 Vaccines are usually available only in combi- subclinical. However, occasional abortion outbreaks
nation with Campylobacter bacterin or Campylobacter and caused by C. burnetii have been reported in goats and, less
E. coli bacterin.8,16 Anecdotal evidence suggests that commonly, in sheep.8,34 Susceptible pregnant females
these three-way vaccines may result in fetal wastage if ad- develop placentitis, whereas non-pregnant females do not
ministered during the first month of pregnancy. If used, develop clinical signs.3 Clinical signs are infrequent, but
 Chapter 6 Theriogenology of Sheep and Goats • 181

abortion and stillbirth may occur late in gestation as a pasteurization but is readily transmitted in nonpasteur-
result of severe damage to the placenta, necrosis of the ized milk. All persons should wear masks and gloves
cotyledons, and thickening of the intercotyledonary when removing manure from the barn, assisting with
areas.6,33,34 Some does abort without apparent clinical lambing and kidding, and handling aborted fetuses.7
signs, whereas others show anorexia and depression 1 to 2
days before aborting. After the initial abortions or infec-
tions, animals become immune.
Brucellosis
Brucellosis is an infectious disease of goats characterized
Diagnosis. Diagnosis is based on placental findings, by abortion, weak kids, mastitis, and the formation of lo-
serology, and isolation of the organism.6,33 Although iso- calized lesions in various tissue.36 In sheep, brucellosis
lation of C. burnetii is the ideal means for diagnosis of the rarely causes abortion but it can cause epididymitis in
disease, it is usually not feasible because of the contagious rams. The incidence of brucellosis caused by Brucella
and zoonotic potential of the organism. Some diagnostic melitensis in goats has historically been extremely low in
laboratories are unwilling to handle such organisms North America, but recent sporadic outbreaks have been
because of strict biosafety procedures.34 Ziehl-Neelsen reported in goats in Texas and Colorado.37 It is wide-
staining of histologic sections of cotyledons or fetal spread in goats in the Middle East, India, Pakistan,
abomasa may reveal the organism.3 The fluorescent anti- Africa, Mexico, and parts of South America.2,6,11 B. ovis
body test can be used to identify the organism in frozen is widespread in sheep throughout the western portions
placental sections. Even though a variety of serologic tests of North America.
have been described, a diagnosis of Q fever abortion Both B. ovis and B. melitensis are small, gram-negative
cannot be given solely on the basis of positive test results coccobacillus organisms. Although considered goat-
because symptomatic infections without abortions are specific, B. melitensis may cause abortion in sheep.3 It also
possible.35 Antibody titers of more than 1:20 indicate ex- is the cause of Malta fever in human beings.2,6,11 Occa-
posure to C. burnetii, although the organism may not nec- sionally, B. abortus infection occurs in goats living in close
essarily be the cause of abortions. A four-fold increase in contact with infected cattle or as a result of inadvertent
titers between acute and convalescent samples indicates vaccination of goats with live strains of the organism.36
recent infection.34 A rapid presumptive diagnosis of in-
fection with C. burnetii is possible by identifying a large Pathogenesis. As goats ingest contaminated feed or
number of characteristic organisms in the placental tissue water, the organism enters through mucous membranes
and ruling out other causes of placentitis (Brucella, and becomes localized in the udder, uterus, testes, spleen,
Campylobacter, and Chlamydia).8,31 or lymph nodes.2,36 In sheep the organism appears to be
transmitted orally from ram to ram or ram to ewe, but not
Treatment and prevention. After the infection is es- from ewe to ewe.3 Infected rams, if they remain fertile,
tablished, the female can carry the organism indefinitely, will pass the organism in their semen.3 In pregnant
shedding it in milk and at parturition. Producers should animals, localization in the placenta leads to the develop-
burn or bury placentas and aborted fetuses promptly.33 In ment of placentitis with subsequent abortion. Goats
one outbreak of Q fever abortion in goats, abortions excrete the organism in milk, urine, feces, and placenta
stopped after administration of chlortetracycline (200 mg and for 2 to 3 months in vaginal discharge. If ewes
anally every day) for 19 days.33 The injection of long- become infected and abort, they usually clear the organ-
acting oxytetracycline (20 mg/kg SC or IM) every 3 days ism within 2 to 4 weeks.3 Non-aborting infected females
or every 10 to 14 days has been recommended.8 Preven- often give birth to infected kids or lambs that are capable
tion in sheep to be used in medical research is a major of shedding the organism.2,7,30
problem. No effective vaccine is currently available.
However, using an autogenous produced vaccine and ad- Clinical signs. Sheep and goats with brucellosis often
ministering therapeutic levels of chlortetracycline may abort during the final trimester.36,38 Goat flocks may
control the disease. Removing rodents, cats, and cattle have an abortion storm after the disease is contracted.
that may serve as sources of infection also may aid in The initial flock abortions are followed by a period of
control efforts.8 resistance during which abortions are rare. Again, abor-
tion appears to be more of a problem in goats than in
Zoonotic potential. Q fever can be transmitted to sheep. In goats and rarely in sheep a systemic disease with
human beings by ingesting milk from infected animals fever, depression, weight loss, diarrhea, mastitis, lame-
and having contact with placentas or feces. Disease in ness, hygroma, and orchitis in males can occur.2,36 In-
human beings is characterized by influenza-like symp- fected ewes are rarely ill. On gross examination the pla-
toms, hepatitis, myalgia, and endocarditis.3,11,33 The ma- centa is normal in B. melitensis infection in goats, whereas
jority of human cases have a history of contact with in- B. ovis infection of sheep results in a thickened, necrotic
fected sheep, goats, or cattle.34 The organism is killed by placentitis.
182 • Sheep and Goat Medicine
Diagnosis. Identification of brucellosis as the cause of of goat abortion in Spain, 2.6% resulted from infection
abortion is usually made by isolating the organism from with Leptospira, with the serovar pomona being the
the aborted fetus (abomasal contents), placenta (cotyle- most prevalent (75% of the abortions attributed to Lep-
don), or vaginal discharge. Serologic testing alone may tospira), followed by the serovars sejroe (12.5%) and
lead to a false diagnosis. Various agglutination, precipita- icterohaemorrhagica (12.5%).39
tion, and complement fixation tests are available to detect
carrier animals.7 Clinical signs. Clinical signs include anorexia, fever,
marked jaundice, hemoglobinuria, anemia, nervous man-
Treatment and prevention. No treatment is available ifestations, abortion, and occasionally, death.7,39 Flaccid
for brucellosis in goats or sheep. In countries with a low agalactia may occur in ewes.3 Abortions have been re-
prevalence of infection, slaughter of the entire flock is ported during the final trimester of gestation in goats and
generally the control measure of choice.2,7,38 In other sit- to a lesser extent sheep.39
uations a test and slaughter program may be more appro-
priate. In sheep, palpating the scrotum for epididymitis, Diagnosis. Dark field microscopy, immunofluores-
serologic testing, and vaccinating ram-lambs may help cence testing, and silver stains on placenta, fetal tissue,
control the disease.3 Vaccination of goats is not permitted and fluids are used to confirm the diagnosis.7,39 The or-
in the United States. In many countries in which caprine ganism is difficult to isolate from contaminated speci-
brucellosis is prevalent, the disease is controlled by an in- mens. Paired sera from aborted does and ewes showing a
tensive vaccination program that is very effective. The four-fold increase in titer is suggestive of leptospirosis.7
killed vaccine occasionally used in sheep (B. ovis) appears
to have poor efficacy. Where permitted, a live attenuated Treatment and prevention. Vaccination two to four
strain of B. melitensis can be given SC in kids and lambs 3 times a year with multivalent cattle vaccines containing
to 8 months of age.7,38 This vaccine causes abortion in the serovar endemic to the area is indicated in regions
goats and should therefore be avoided in pregnant where leptospirosis is prevalent. Other control measures
animals or those within 1 month of breeding. Immunity include separating animal species, reducing the number
from a single vaccination for B. melitensis is considered to of rodents, maintaining a clean water supply, and feeding
be lifelong.7 All new animals should be serologically tetracycline (300 to 500 mg/head/day) during middle to
tested before introduction to the flock. Rams and bucks late gestation.7
should be tested yearly before breeding season.2 Placentas
and aborted fetuses should be carefully burned or buried. Zoonotic potential. Producers or clinicians that
suspect leptospirosis should exercise caution to minimize
Zoonotic potential. Goats were the first species associ- human contact with aborted tissues, the urine of affected
ated with transmission of brucellosis to human beings.36 animals, and potentially contaminated ponds and water
Malta fever is caused by B. melitensis and should be con- sources. Human beings are susceptible, and infections can
sidered a serious human pathogen. Often the first indica- result in death.
tion of brucellosis is the occurrence of undulant fever in
humans consuming unpasteurized goat milk or cheese.2,7
Therefore a large percentage of human infections can be
Salmonellosis
prevented by pasteurizing goat dairy products. B. meliten- Salmonella infection can cause abortion, metritis, and sys-
sis and B. abortus infections in sheep and goats should be temic illness in ewes and does.30 The condition appears
handled with precautions to minimize human exposure. to be more of a clinical entity in stressful situations.12
B. ovis is not considered zoonotic, but the clinician should These include overcrowding, shipping, water or feed dep-
still exercise caution when handling suspected cases. rivation, and possibly the inappropriate use of antibiotics.
Salmonella abortus-ovis was first implicated as a cause of
abortion in pregnant females. Only sheep and goats are
Leptospirosis affected by S. abortus-ovis, which is uncommon in North
Sheep and goats appear to be less susceptible to lep- America. S. typhimurium, S. dublin, S. montevideo, and S.
tospirosis than other domestic species. However, goats are arizonae also are associated with infections and abortion
more susceptible than sheep.39 Several serovars of Lep- in persistently infected females.3,7 Sources of infection
tospira interrogans (icterohaemorrhagiae, grippotyphosa, and include birds, cattle, and some wildlife species. Climatic
pomona) have been reported as primary causes of abortion changes, shipping, overcrowded conditions, and other
in goats.33 The common serovars seen in sheep are hardjo, diseases may all predispose to a flock abortion storm. The
bratislava, pomona, and icterohaemorrhagica.3 route of infection is by oral ingestion of the organism.

Pathogenesis. Exposure to environments contami- Clinical signs. Abortion storms affecting as many as
nated by urine from species other than sheep or goats 70% of the females may occur. Infected females may
appears to be the primary source of infection.7 In a study become febrile and depressed and have diarrhea. Metritis
 Chapter 6 Theriogenology of Sheep and Goats • 183

and retained placenta are common findings. A high mor-

tality rate is seen in ewes after abortion. Abortion may
occur throughout gestation but is more common during
the final month.

Diagnosis. A diagnosis can be made by culturing Sal-

monella from aborted fetuses, placentas, and uterine dis-
charge. Specific agglutinins can be demonstrated in the
sera of adults and aborted fetuses.

Treatment and prevention. Prevention and control

measures include treating pregnant females with appro-
priate antibiotics based on culture and antibiotic sensitiv-
ity. Administering two doses of an autogenous vaccine Figure 6-18 These cotyledons are from a goat that aborted as a
result of toxoplasmosis. Cotyledons from such abortions typically have
followed by an annual booster and cleaning the environ- interspersed white foci, as shown here. These white foci are areas of
ment may help minimize this disease.7 coagulative necrosis that are mineralized in many cases. In
Toxoplasma abortion the intercotyledonary space is usually normal.
Zoonotic potential. Salmonella infections should be (Courtesy Dr. JP Dubey, Beltsville, MD.)
considered pathogenic to human beings. These organ-
isms can cause abdominal pain, enteritis, and miscarriage
in human beings. People who are being treated with oral
antimicrobial therapy and those who are immunosup- occur from infections during the latter half of gestation.10
pressed should avoid handling affected sheep or goats.3 Does and ewes are often clinically normal at the time of
abortion.41 The incidence of abortion in a flock is usually
low but can vary from 3% to 50%. Rarely, the pregnant
Toxoplasmosis female becomes febrile; if she is immunosuppressed, she
Toxoplasmosis has a worldwide distribution and is one of may develop the neurologic form of the disease. The in-
the most common parasitic infections in sheep and tercotyledonary areas of the aborted placenta are usually
goats.40-42 The protozoan Toxoplasma gondii is capable of normal, with the cotyledons having gray-white to yellow,
causing abortion, fetal mummification, stillbirth, and the small focal areas of necrosis and calcification (1 to 3 mm
birth of weak lambs and kids.7,40 in diameter). These lesions are clearly visible after the
cotyledons are washed in saline6,10,13,41,42 (Figure 6-18).
Pathogenesis. Cats are vital in the transmission of T. However, C. burnetii and Brucella and Chlamydia species
gondii.43 Cats become infected by ingesting infected also can cause placentitis that includes the intercotyle-
rodents or birds and develop a transplacental infection. donary region.42 Fetal lesions include chalky-white
Kittens infected in utero can shed T. gondii oocytes after necrotic brain lesions.
birth.43 Unless they are immunosuppressed, cats appar-
ently shed the disease only as kittens and rarely show Diagnosis. A presumptive diagnosis can be made from
signs of clinical illness. Cats defecate into and bury feces placental lesions alone. However, because of its rapid de-
in hay and food bins. Ewes and does become infected by composition the placenta is often not available for exam-
ingesting feed or water contaminated with oocytes found ination.44 The preferred diagnostic procedure is to iden-
in the feces of infected cats. After ingestion the organism tify T. gondii antibodies in fetal fluids or presuckling
enters the blood and spreads to other tissues. In the preg- blood. Their presence indicates transplacental Toxoplasma
nant ewe or doe, Toxoplasma can invade and multiply in infection.45 The absence of T. gondii antibodies within 7
the placenta, spread to the fetus, and cause fetal death, days of an abortion tends to rule out the possibility of in-
abortion, stillbirth, or the birth of weak lambs and kids; fection. Serologic examination of neonates must occur
infected animals also may give birth to normal lambs or before colostrum ingestion.41 High antibody titers in doe
kids.40 Abortion occurs as a result of necrosis of the pla- or ewe serum is not diagnostic of recent infection because
centa, particularly the cotyledons. Although T. gondii is titers may remain elevated from one season to the next.
found in goat semen, venereal transmission is an unlikely However, the absence of antibodies is good evidence that
cause of abortion.41 toxoplasmosis was not the cause of abortion.7,41 The
modified agglutination test (MAT) can be used to detect
Clinical signs. Goats appear to be more susceptible to antibodies in fetal and maternal serum and is more sensi-
Toxoplasma infection than sheep.44 Ewes and does in- tive than other tests.45 The ELISA and IFA tests also are
fected before breeding usually do not abort. Those in- useful in diagnosis.41 Positive diagnosis of toxoplasmosis
fected 30 to 90 days after breeding usually have fetal requires isolation of the organism from the placenta or
death with resorption or mummification. Most abortions the fetal brain, lung, or muscles.45 Samples taken for
184 • Sheep and Goat Medicine
isolation of the organism should be shipped to a diagnos- Clinical signs. Abortion results from infection early in
tic laboratory packed in ice, but not frozen.41 gestation, whereas late gestational infection results in
stillbirth or weak neonates. The abortifacient and en-
Treatment and prevention. Control of toxoplasmosis cephalitic forms of listeriosis do not usually occur simul-
is based on preventing exposure of pregnant females to taneously in sheep, but may occur in goat flocks.8 Abor-
oocyte-contaminated pasture, food, water, and bedding. tion occurs in the final 2 months of pregnancy and is
Fetal membranes and dead fetuses should be buried or in- sometimes preceded by septicemia.6,7 Signs of septicemia
cinerated so they do not serve as sources of infection for include fever, decreased appetite, and reduced milk pro-
cats and other animals.43 Cats should not be allowed near duction. Sheep and occasionally goats that abort may
pregnant sheep and goats.41,43 Spayed cats can be kept in develop metritis. Kids grafted to the aborting female can
the barn because this may help keep pregnant queens contract listeriosis through the milk, develop septicemia,
from nesting there. Attempts should be made to prevent and die.7
cats from defecating in feeders, hay, and other feedstuffs.
Cat litter boxes can be placed in strategic areas; if cats Diagnosis. Culture of the organisms from the fetal
have access to hay, the top layers should be discarded or abomasum or liver, placenta, or uterine discharge is diag-
fed to non-pregnant animals. A vaccine containing tachy- nostic. Unfortunately, fetal autolysis can be so severe that
zoites that do not persist in sheep tissues is available in culture may be difficult. In cases in which the liver can be
some areas of the world (Europe and New Zealand). examined, microabscesses are visible as white pinpoint
Ewes vaccinated with the S48–strain vaccine remain spots. Identification of microabscesses of the liver and
immune for at least 18 months.43 Goats that have been brain aids in diagnosis.3,12
infected by T. gondii are likely to be resistant to reexpo-
sure in subsequent pregnancies.46 Treatment and prevention. Feeding poor-quality or
Feeding decoquinate (2 mg/kg body weight/day) or spoiled silage or grazing on contaminated pastures should
monensin (15 to 30 mg/head/day) throughout gestation be discouraged. The addition of chlortetracycline (300
may reduce the incidence of abortion. Anecdotal reports mg/head/day) to a grain supplement has been reported to
suggest that lasalocid is less effective than monensin in stop abortions during a listeriosis outbreak.49 During
toxoplasmosis control. outbreaks the administration of long-acting oxytetracy-
cline (20 mg/kg of body weight every 48 to 72 hours) is
Zoonotic potential. Aborted fetal membranes and also of value. Vaccination to produce cellular immunity
fetuses should be handled with caution.43 This organism has been investigated. Theoretically, live vaccines should
can cause encephalitis or blindness in human fetuses in- be more effective than killed preparations. The adminis-
fected in utero and in immunosuppressed adults. Toxo- tration of two doses of reduced-virulence live vaccine
plasmosis has been reported in humans after drinking raw before breeding is reported to have provided significant
goat milk. Therefore goat and sheep milk should be pas- protection against experimental challenge in pregnant
teurized or boiled before human consumption. This is does.7
particularly true for goat and sheep milk fed to infants.47
Zoonotic potential. Persons should take care when
handling aborted fetuses because Listeria can cause neu-
Listeriosis rologic disease in human beings.
Listeriosis commonly causes meningoencephalitis, abor-
tion, and septicemia in goats and sheep. Listeria monocy-
togenes and L. ivanovii are gram-positive, non–acid-fast
Mycoplasmosis
facultative microaerophilic organisms. L. monocytogenes Mycoplasma species are significant pathogens of the goat,
causes encephalitis, septicemia, and abortion in sheep and causing mastitis, arthritis, keratoconjunctivitis, and occa-
goats, whereas L. ivanovii causes abortion only in sheep.3 sionally vulvovaginitis and abortion.10,51,52 M. mycoides
and M. agalactia have been reported as the species causing
Pathogenesis. L. monocytogenes can be found in soil, abortion in goats. Mycoplasmosis is uncommon in sheep,
water, plant litter, silage, and the digestive tracts of rumi- but a similar organism, Ureaplasma, has been isolated
nants and human beings.7 The organism can survive in from ewes with a history of infertility and granular vulvi-
soil and feces for extended periods and grows in poorly tis.10,52 Ureaplasma infection also may result in placentitis
fermented silage (with pH levels higher than 5.5).2,6,7,10 and low-birth-weight lambs.3,10 Abortion is not the pre-
Abortion has been attributed to the feeding of contami- dominant clinical finding in an outbreak.
nated silage. Abortions also have been reported in Abortion occurs in does (and rarely in ewes) in the
animals fed only hay or browse.7,48-50 Of the cases ob- final trimester of gestation. Females that abort generally
served by the authors, ingestion of contaminated silage is shed the organism in their milk, amniotic fluids, and pla-
rarely a component, but grazing on boggy, high-pH soils centa. The organism also may be found in the cotyledons
is a consistent finding. and in the liver and spleen of the fetus. Diagnosis of abor-
 Chapter 6 Theriogenology of Sheep and Goats • 185

tion caused by Mycoplasma species is by culture and mineral mixture offered free choice are usually protective
serotyping of the isolate. Treatment with tetracyclines or (see Chapter 2).
tylosin may be of benefit, but identification and culling of Various pharmaceuticals have proven to be abortifa-
all infected animals is the best course of prevention51 (see cients, or at least their use has been reported to be fol-
Chapters 5 and 13). lowed by abortion. A number of anthelmintics such as
phenothiazine and levamisole given in the final months
of gestation may cause abortion.7,52 Anecdotal reports of
Miscellaneous abortion following the use of other dewormers (iver-
Actinobacillus seminis has rarely been associated with abor- mectin, fenbendazole) exist, but are largely unsubstanti-
tion and metritis in ewes. It may be transmitted from ated. Xylazine and high doses of acepromazine in the first
carrier rams (see Chapter 14). This organism is rare in half of pregnancy may cause abortion because of their
North America. adverse effects on uterine contraction and placental per-
Several other organisms are associated with infectious fusion.53 The administration of corticosteroids in late
abortion. Any diseases that result in debility (e.g., internal gestation and estrogen and prostaglandins throughout
parasites, Johne’s disease, caseous lymphadenitis) and in- most of gestation may induce abortion.53 Plants that ac-
fections with significant amounts of endotoxin produc- cumulate nitrate such as sweet clover, Johnson grass,
tion (gram-negative mastitis or septicemia) may result in sorghum, lamb’s quarter, Jimsonweed, sunflower,
fetal loss. Mycotic abortion, although rare, may occur in pigweed, and oat hay can cause abortion as a result of
certain areas of the world. nitrate-nitrite toxicity.53 If nitrate-nitrite toxicity is sus-
pected, diluting the affected forage with other feedstuffs
NONINFECTIOUS CAUSES is a useful treatment. Cutting suspected forage 30 cm
above the ground and avoiding the feeding of drought-
OF ABORTION stressed crops help decrease nitrate concentrations in
Noninfectious causes such as hereditary, stress, nutri- feeds to less than 1000 ppm nitrate as nitrogen, or less
tional deficiencies, pharmaceutical effects, and toxic plant than 0.44% nitrate. Concentrations higher than this
ingestion can result in pregnancy loss. Stress may trigger should be avoided or diluted with other feeds. Feeds con-
a higher percentage of abortions in goats than in sheep taining more than 3500 ppm of nitrate nitrogen, or more
because of the goat’s dependency on the CL for the than 1.76% nitrate, should not be fed to pregnant
maintenance of pregnancy. Predator attack, severe animals.54
weather, or shearing may all trigger early regression of the
CL in the doe, resulting in abortion. Angora goats expe-
rience some forms of abortion not typically seen in other
breeds. Young Angora does are susceptible to stress abor-
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1. Smith MC: Some clinical aspects of caprine reproduction, Cornell
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abortions as a result of adrenal dysfunction.7,53 These 2. Smith MC: Causes and diagnosis of abortion in goats. In Morrow
does are heavier than average and have very fine mohair. DA, editor: Current therapy in theriogenology, ed 2, Philadelphia,
This habitual, familial form of abortion usually starts 1986, WB Saunders.
when the doe is 4 or 5 years old. Abortions occur at ap- 3. Menzies PI, Miller R: Abortion in sheep: diagnosis and control. In
proximately day 100 of gestation.7 Mature Angora does Youngquist RS, editor: Current therapy in large animal theriogenol-
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that abort in this fashion should be removed from the
4. Bulgin MS: Nutrition for the breeding flock, Small Ruminants for
breeding stock, and their offspring should be culled.7 the Mixed Animal Practitioner Western Veterinary Conference, p 5,
Heat stress also may result in early embryonic losses, 1998, Las Vegas, NV.
abortions, stillbirths, or weak kids.10 5. Braun WF: Infectious caprine abortion, Proceedings of the American
Energy and protein deficiencies can result in embry- Association of Sheep and Goat Practitioners, 1983, Springfield, IL.
onic loss, decreased fetal growth, depressed placental 6. Braun WF: Manifestations and aberrations of caprine pregnancy,
growth, fetal mummification, and the birth of weak Proceedings of the Society for Theriogenology, 1986, Nashville, TN.
young. Fetal wastage resulting from nutritional deficien- 7. Smith MC, Sherman DM: Reproductive system. In Smith MC,
cies often occurs between day 90 and 120 of gestation.53 Sherman DM, editors: Goat medicine, Philadelphia, 1994, Lea and
Deficiencies in a number of minerals and vitamins such as Febiger.
iodine, copper, magnesium, manganese, vitamin A, and 8. Bretzlaff K: Problems of reproduction of goats, Proceedings of the
Small Ruminant Short Course, Society for Theriogenology, 1994,
selenium can cause abortion or the birth of weak kids and
Nashville, TN.
lambs.7,53 Some heavy metal toxicities (lead) can cause 9. Kirkbride CA: Diagnosis in 1784 ovine abortions and stillbirths, J
fetal wastage in ewes.10 High concentrations of dietary Vet Diagn Invest 5:398, 1993.
sulfur, particularly sulfate, may result in both selenium 10. Roberts SJ: Veterinary obstetrics and genital diseases (theriogenology),
and copper deficiency.10 Maintaining optimal body con- ed 3, Woodstock, VT, 1986, David and Charles.
dition scores, ensuring adequate protein intake, and sup- 11. Carter GR: Veterinarian’s guide to the laboratory diagnosis of infec-
plementing the diet with a good-quality, complete trace tious diseases, Lenexa, KS, 1986, Veterinary Medicine Publishing.
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12. Fielden ED: Infectious ovine abortion. In Morrow DA, editor: 33. Miller RB, Palmer NC, Kierstad M: Coxiella burnetii infection in
Current therapy in theriogenology, Philadelphia, 1986, WB Saun- goats. In Morrow DA, editor: Current therapy in theriogenology, ed
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13. Kimberling CV: Diseases of reproduction, Proceedings of the First 34. Moore JD et al: Pathology and diagnosis of Coxiella burnetii infec-
National Sheep Reproduction Symposium, Fort Collins, CO, 1989, tion in a goat herd, Vet Path 28:81, 1991.
Colorado State University Press. 35. Zeman DH, Steen PL, Peacock MG: Ovine abortion caused by
14. Anderson KL: Campylobacteriosis. In Morrow DA, editor: Coxiella burnetii. In Kirkbride CA, editor: Laboratory diagnosis of
Current therapy in theriogenology, ed 2, Philadelphia, 1986, WB livestock abortion, ed 3, Ames, IA, 1990, Iowa State University
Saunders. Press.
15. Dennis SM: Campylobacter abortion in sheep. In Kirkbride CA, 36. Padmore CL: Infectious diseases of goats, Proceedings of the Inter-
editor: Laboratory diagnosis of livestock abortion, ed 3, Ames, IA, national Goat Producers Symposium, Tallahassee, FL, 1990, Florida
1990, Iowa State University Press. A & M University Press.
16. Council on Biologics and Therapeutics: Vaccination guidelines for 37. Kahler SC: Brucella melitensis infection discovered in cattle for
small ruminants, J Am Vet Med Assoc 205:1539, 1994. first time, goats also infected, J Am Vet Med Assoc 216:648, 2000.
17. East NE: Chlamydiosis. In Morrow DA, editor: Current therapy in 38. Nicoletti P: Brucellosis. In Howard JL, editor: Current veterinary
theriogenology, ed 2, Philadelphia, 1986, WB Saunders. therapy food animal practice, ed 3, Philadelphia, 1993, WB Saun-
18. Sourian A et al: Differentiation of abortion-inducing and intes- ders.
tinal strains of Chlamydia psittaci isolated from ruminants by the 39. Leon-Vizcaino L, Hermoso de Mendoza M, Garrido F: Incidence
microimmunofluorescence test, Vet Rec 132:217, 1993. of abortions caused by leptospirosis in sheep and goats in Spain,
19. Mobini S: Infectious causes of abortion in the goat, Proceedings of Comp Immun Microbiol Infect Dis 10:149, 1987.
the International Goat Producers Symposium, Tallahassee, FL, 1990, 40. Dubey JP: Transplacental toxoplasmosis in goats. In Morrow DA,
Florida A & M University Press. editor: Current therapy in theriogenology, ed 2, Philadelphia, 1986,
20. Gatewood DM, Spire MF: Chlamydial abortion in domestic rumi- WB Saunders.
nants, theriogenology fact sheet B-5, Hastings, NE, 1990, Society 41. Dubey JP: Toxoplasmosis in goats, Agri-Pract 8:43, 1987.
for Theriogenology. 42. Dubey JP: Epizootic toxoplasmosis associated with abortion in
21. Schachter J et al: Serotyping of Chlamydia isolates of ovine origin, dairy goats in Montana, J Am Vet Med Assoc 178:661, 1981.
Infect Immun 9:92, 1974. 43. Dubey JP: Toxoplasmosis, J Am Vet Med Assoc 205:1593, 1994.
22. Timoney JF et al: Chlamydiaceae. In Timoney JF et al, editors: 44. Dubey JP et al: Toxoplasma gondii-induced abortion in dairy goats,
Hogan and Bruner’s microbiology and infectious diseases of domestic J Am Vet Med Assoc 188:159, 1986.
animals, ed 8, Ithaca, NY, 1988, Comstock Publishing Associates. 45. Dubey JP: Diagnosis of livestock abortion due to Toxoplasma
23. Storz J: Chlamydia-induced diseases of sheep and goats. In gondii. In Kirkbride CA, editor: Laboratory diagnosis of livestock
Howard JL, editor: Current veterinary therapy food animal practice, abortion, ed 3, Ames, IA, 1990, Iowa State University Press.
ed 2, Philadelphia, 1986, WB Saunders. 46. Obendorf DL, Statham P, Munday BL: Resistance to Toxoplasma
24. Hall RF: Infectious abortions in ewes, Comp Cont Ed Pract Vet abortion in female goats previously exposed to Toxoplasma infec-
4:S216, 1982. tion, Aust Vet J 67:233, 1990.
25. Storz J: Chlamydia and Chlamydia induced diseases, Springfield, 47. Dubey JP: Toxoplasmosis: zoonosis update, J Am Vet Med Assoc
IL, 1971, Charles C Thomas. 196:123, 1990.
26. Munro R, Hunter AR: Infection of lambs by orally administered 48. Antic S et al: Frequency of goat abortion and finding of Listeria
ovine abortion strain of Chlamydia psittaci, Vet Rec 109:562, 1981. monocytogenes as probable causative agent, Vet Glas 43:849, 1989.
27. Storz J: Chlamydia-induced diseases of sheep and goats, Proceed- 49. Wiedmann M et al: Molecular investigation of a listeriosis out-
ings of the American Association of Small Ruminant Practitioners, break in goats caused by an unusual strain of Listeria monocyto-
WRCC Forty-Sixth Symposium of the Health and Disease of Small genes, J Am Vet Med Assoc 215:369, 1999.
Ruminants, Kerville, TX, 1991. 50. Johnson GC et al: Epidemiologic evaluation of encephalitic liste-
28. Schopf K, Khaschabi D, Dackau T: Outbreak of abortion among riosis in goats, J Am Vet Med Assoc 208:1695, 1996.
goats caused by dual infection with Coxiella burnetii and Chlamydia 51. East NE: Mycoplasmosis. In Morrow DA, editor: Current therapy
psittaci, Tierarzll Prax 19:630, 1991. in theriogenology, ed 2, Philadelphia, 1986, WB Saunders.
29. Storz J: Chlamydial absorption. In Kirkbride CA, editor: Labora- 52. East NE: Common infectious conditions, Small Ruminants for the
tory diagnosis of livestock abortion, ed 3, Ames, IA, 1990, Iowa State Mixed Animal Practitioner Western Veterinary Conference, 1998, Las
University Press. Vegas, NV.
30. Hungerford TG: Diseases of livestock, ed 9, Sydney, 1990, 53. Braun WF: Pregnancy wastage in the goat, American Association of
McGraw-Hill. Small Ruminant Practitioners, Proceedings of the Symposium on
31. Watson WA: The prevention and control of infectious ovine abor- Health and Diseases of Small Ruminants, 1997, Nashville, TN.
tion, Br Vet J 129:309, 1973. 54. Pioneer forage manual—a nutritional guide, Des Moines, 1995,
32. Behymer D, Riemann HP: Coxiella burnetii infection (Q fever), J Pioneer Hi-Bred International.
Am Vet Med Assoc 194:764, 1989.
 Chapter 7

DSystem
iseases of the Endocrine

DEBRA C. RUFFIN, UNDINE CHRISTMANN, AND D.G. PUGH

The endocrine system is rarely discussed as a separate tions are lowest from late October through late February
entity in textbooks of sheep and goat medicine. This (less than 39 ng/ml) and highest from May through Sep-
chapter presents current data, literary reviews, and avail- tember (200 to 350 ng/ml). Prolactin, unlike other pitu-
able case reports regarding the endocrine systems of these itary hormones, is regulated primarily by hypothalamic
two small ruminant species. It provides an overview of inhibition.7 Dopamine (prolactin-inhibitory hormone)
endocrine function and pathology to aid the clinician in inhibits the release of PRL from the anterior pituitary
treating some of the endocrinologic abnormalities of gland.8
sheep and goats. GH is not only involved in the normal development of
young animals but also influences milk and fiber produc-
tion in adults. Administration of recombinant bovine so-
PITUITARY GLAND matotropin (rBST, a growth hormone) to lactating goats
can increase milk yield,9 as well as milk fat and lactose
Anterior Pituitary Gland content.10 Goats treated with rBST exhibit elevated
The anterior pituitary gland is located in the base of the serum levels of GH, insulin, thyroxine, and insulin-like
skull in the sella turcica, which is the cavity of the sphe- growth factor-1. Studies have found that rBST signifi-
noid bone. It is composed of a variety of cell types: soma- cantly increases the secondary fiber growth rate and
totrophs, which produce growth hormone (GH); mam- weight gain in goats.11 However, in lactating does, no dif-
motrophs, which produce prolactin (PRL); corticotrophs, ference in fiber production was noted between animals
which produce adrenocorticotropic hormone (ACTH); treated with rBST and those that were not.12 Still, the
gonadotrophs, which produce luteinizing hormone (LH) average daily gain of kids nursing from does given rBST
and follicle-stimulating hormone (FSH); and thy- was higher than the average daily gain of kids nursing
rotrophs, which produce thyroid-stimulating hormone from nontreated does.12 This increased gain was seen
(TSH). Somatomammotrophs are unique cells that only during the treatment period, and no posttreatment
secrete both GH and PRL1 in varying proportions de- effect was reported. Sustained-release rBST has been
pending on the action of other hormones such as cortisol shown to increase body weight gain by 22% in castrated
and progesterone.2 These cells have been identified in male goats.13
both sheep3 and goats.4 Hypothalamic hormones regu- Thyrotropin-releasing hormone (TRH), which is se-
late (i.e., stimulate or inhibit) the release of hormones creted by the hypothalamus, stimulates the thyrotrophs of
from the anterior pituitary cells (Table 7-1). Hormones the anterior pituitary to release TSH. TSH stimulates the
from the hypothalamus are transported to the pituitary production of triiodothyronine (T3) and thyroxin from
gland by the hypothalamic-pituitary portal circulation. the thyroid gland. T3 provides negative feedback to pitu-
PRL is a hormone that stimulates udder development itary secretion of TSH. Therefore in the absence of ade-
and subsequent lactation. Serum PRL levels fluctuate sea- quate thyroid hormones, excessive TSH is released, re-
sonally in photoperiodic seasonal breeders such as sheep sulting in enlargement in the thyroid gland (goiter).
and goats.5,6 PRL levels are generally higher during the
anestrous season of the year and lower during the breeding Evaluation of anterior pituitary function. The litera-
season.6,7 In the Northern Hemisphere, PRL concentra- ture contains very few reports of normal pituitary hor-
• 187 •
188 • Sheep and Goat Medicine
TABLE 7-1

HORMONES PRODUCED BY THE HYPOTHALMIC-PITUITARY AXIS

HYPOTHALMIC HORMONE ACTION PITUITARY CELL PITUITARY HORMONE

Thyrotropin-releasing hormone Stimulatory Thyrotroph Thyroid-stimulating hormone (TSH)

(TRH) Mammotroph Prolactin (PRL)
Corticotropin-releasing hormone Stimulatory Corticotroph Adrenocorticotropic hormone (ACTH)
(CRH)
Growth hormone–releasing hormone Stimulatory Somatotroph Growth hormone (GH)
(GHRH) Somatomammotroph
Somatostatin Inhibitory Somatotroph GH
Somatomammotroph
Dopamine (prolactin-inhibiting Inhibitory Mammotroph PRL
hormone, PIH) Somatomammotroph
Prolactin-releasing hormone Stimulatory Mammotroph PRL
Somatomammotroph
Gonadotropin-releasing hormone Stimulatory Gonadotroph Luteinizing hormone (LH)
(GnRH) Follicle-stimulating
hormone (FSH)

mone parameters in small ruminants. Lofstedt et al14

Posterior Pituitary Gland
performed an ACTH stimulation test in a normal and a The posterior pituitary gland (also known as the neurohy-
lactating male. They found that within 10 minutes of the pophysis) is an extension of the hypothalamus. Neuronal
administration of porcine corticotropin hormone (80 IU cell bodies within the supraoptic and paraventricular
intramuscularly [IM]), the blood cortisol rose to more nuclei of the hypothalamus manufacture antidiuretic
than 120 nmol/L.14 Blood cortisol levels in these two hormone (ADH) and oxytocin, which are transported
goats continued to rise throughout the 150-minute sam- along neurons to the posterior pituitary for storage and
pling period, reaching a maximum level of approximately secretion.7
200 nmol/L and 280 nmol/L in the normal and lactating ADH regulates water and sodium balance in the body.
male goats, respectively.14 Secretion of ADH in the dehydrated animal is stimulated
Little controlled research data are available regarding by both the increased plasma osmolality and the de-
the use of the dexamethasone suppression test in sheep creased plasma volume. Either of these conditions alone
and goats. However, this test has been employed in the also can stimulate ADH secretion. ADH is a vital com-
investigation of the endocrinologic status of a lactating ponent in effective recovery from hemorrhage-induced
male goat.5 In one experiment dexamethasone (0.1 hypovolemia.15,16 ADH increases plasma volume, en-
mg/kg IM) was administered and blood samples were hances the permeability of the kidneys’ collection ducts to
then taken at hourly intervals for 10 hours. This dose water, and improves sodium chloride transport in Henle’s
suppressed cortisol to less than 30 nmol/L throughout loop. Without ADH, the animal cannot concentrate its
the sampling period in both a normal male goat and a lac- urine and develops diabetes insipidus. An animal with
tating male goat. The baseline cortisol level in the normal this disease produces very dilute urine with no evidence
goat was reported to be between 40 and 70 nmol/L, of glucosuria. Naturally occurring diabetes insipidus is so
whereas the baseline was 80 to 125 nmol/L in the lactat- rare in sheep and goats that the authors could find no
ing male goat with adrenal neoplasia. The authors of this reports in the scientific literature. However, the authors
chapter have administered the same dosage of dexam- have noted many anecdotal reports of psychogenic poly-
ethasone in eight does and report suppressed cortisol dipsia in sheep and goats. Polydipsia results in polyuria
output to very low levels (less than 14 nmol/L) for at least and could easily be confused with diabetes insipidus. Di-
8 hours. These eight does had baseline cortisol levels abetes insipidus has been experimentally produced in
ranging from 36 to 257 nmol/L before the administration goats by the creation of lesions in the median eminence of
of the dexamethasone. Samples taken 12 to 13 hours after the hypothalamus.16
the dexamethasone injection tended to be erratic, but Oxytocin released from the posterior pituitary gland
samples taken 24 hours after injection were significantly stimulates contraction of the myometrium myoepithelial
suppressed in seven of the eight does (Figure 7-1). cells of the mammary gland. Stimulation of the mammary
 Chapter 7 Diseases of the Endocrine System • 189

350
300

Cortisol (nmol/L)
250
200
150
100
50
0
12 13 18 962 966 968 BW SE

Before drug administration 4 hours after drug administration

8 hours after drug administration 12 to 13 hours after drug administration
24 hours after drug administration

Figure 7-1 Dexamethasone suppression test (0.1 mg/kg dexamethasone) of eight apparently healthy does.

gland by the neonate or by milking causes afferent nerve

THYROID GLAND
impulses to be carried to the hypothalamus by the spinal The thyroid is a bilobed gland that lies just behind the
cord. These impulses stimulate the supraoptic and par- larynx and lateral to the trachea. It is partially imbedded
aventricular nuclei to release oxytocin from the posterior in the thymus in young animals. The lobes are connected
pituitary gland. Oxytocin is responsible for milk ejection by an isthmus. By iodinating tyrosine-containing com-
or “letdown.” The release of oxytocin from the pituitary pounds, the thyroid gland is responsible for manufactur-
each time the neonate nurses stimulates myometrial con- ing thyroxine (T4) and T3. These two hormones are pro-
tractions that aid postpartal uterine involution. Exogenous duced by, stored in, and released by the thyroid gland in
oxytocin may be useful for the treatment of retained fetal response to the anterior pituitary hormone TSH. Both T3
membranes, metritis, and some other uterine diseases (see and T4 help moderate the animal’s metabolic rate.
Chapter 6).
Thyroid Enlargement
Pituitary Gland Tumors Pathogenesis. The most common causes of enlargement
Pituitary gland tumors are rare in sheep and goats. of the thyroid gland (goiter) are deficient iodine intake and
However, acidophilic adenomas of the anterior pituitary the consumption of plants containing goitrogens.20-22
gland have been reported in both sheep and goats.17,18 Thyroid enlargement appears to be associated with in-
The pituitary lesions reported in does consist of dis- creased TSH output by the anterior pituitary resulting
tinct nodules of acidophil-type cells that compress ad- from depressed blood T4 and T3 concentrations. Iodine de-
jacent pituitary tissue. Pituitary adenomas in ewes pro- ficiency–induced goiter is more common in neonates and
trude dorsally into the optic chiasm and erode the has a worldwide distribution. Iodine-deficient soils result
sella turcica ventrally.18 In most of these cases, animals from rain-induced leaching. Iodine is absorbed in the small
have inappropriate lactation. Similar acidophilic adeno- intestine, and any feedstuffs high in nitrates or other min-
mas have been reported in other species in association erals decrease its absorption.22 Because of the widespread
with abnormal mammary development.19 Acidophil- use of iodine supplementation in trace mineral salt mix-
type cells produce GH and PRL, both of which are tures, the incidence of goiter caused by frank iodine defi-
lactogenic.1 Anterior pituitary adenoma should be con- ciency is rare. Still, when treating animals that graze plants
sidered as a differential diagnosis for does with inap- grown on sandy soils, iodine-deficient soils, or heavily
propriate lactation syndrome (ILS). However, no defini- fertilized soils, the clinician should be aware that iodine
tive antemortem diagnostic test is currently available for deficiency is a potential problem. Compared with other
this condition. Several other pathologies have been re- breeds polled Dorset sheep and Boer and Angora goats
ported in does with ILS. Two does with ILS described by appear to be more susceptible to iodine deficiency–induced
Miller et al17 also had concurrent pheochromocytoma hypothyroidism.20,21
and cystic endometrial hyperplasia. Furthermore, one Neonatal hypothyroidism (cretinism) has been de-
of them had thyroid hyperplasia and follicular ovarian scribed in Angora goats.23Adequate levels of selenium are
cysts.17 needed for proper functioning of thyroid hormones in pe-
190 • Sheep and Goat Medicine
ripheral tissue. Therefore if selenium is chronically defi-
cient, decreased production (“ain’t doing right”) may
ensue but not be the result of primary thyroid dysfunc-
tion. Goitrogenic compounds (e.g., thiourea, thiouracil)
can decrease iodine uptake by the thyroid gland and de-
crease the iodination of tyrosine in the metabolic pathway
for thyroxine production. Ruminants that ingest plants in
the Brassica family may exhibit depressed iodine absorp-
tion and metabolism because of the thiocyanates in these
plants. The most common plants that produce antithy-
roid compounds include the mustard family (e.g., kale,
rape), the legume family (e.g., peanuts, soybeans, white
clover), the prune family (e.g., cherries, apricots), and
some grains (e.g., sorghum).
Hereditary, congenital goiter has been described in
Merino sheep and in Dutch, pygmy, and Nubian
goats.24-28 The congenital thyroid goiters studied by Figure 7-2 Congenital goiter in a 1-week-old cross-bred meat
Dutch researchers27 originated from mixed strains of goat. The 4.5-cm swelling in the left thyroid gland was not associated
with any signs of clinical disease. This goiter was noticed by the goat’s
Saanen and dwarf goats. Goiter in Dutch goats was owner at birth.
found to be inherited in an autosomal recessive manner.
Early investigation of the disease indicated it was most
likely caused by defective thyroglobulin synthesis,28 newborns have large thymus glands that can be mistaken
which had previously been described in sheep.25-27 Thy- for the thyroid.31
roglobulin is the iodoprotein necessary for thyroid
hormone synthesis. Diagnosis. Diagnosis of thyroid disease in sheep and
goats is based on the following findings: a swollen thyroid
Clinical signs. Signs of hypothyroidism include goiter, gland, stunted growth, weight loss or obesity, subcuta-
poor quality and quantity of wool or hair, dry skin, tendon neous edema, and rough and matted fleece. Blood analy-
laxity or failure to form normal insertions in bone, and sis of affected animals may indicate decreased plasma
poor reproductive ability (depressed libido, poor semen protein-bound iodine and increased plasma protein,
quality, irregular estrus, depressed conception, abortion, serum triglyceride, cholesterol, and phospholipid.32
and delivery of weak or dead fetuses; fetal hydrops, poor Iodine concentrations in serum, plasma, and milk and thy-
growth rates, and depressed milk production also may be roxin concentrations in serum and plasma are usually de-
seen). Kids born to dams with iodine-deficient diets or pressed. Normal serum thyroxine levels for goats have
those that consume goitrogenic plants may be weak and been reported to be between 5.0 and 7.0 mg/dl23 and
woolless or hairless, have enlarged thyroid glands (swollen between 6.1 and 8.3 mg/dl.33 Normal serum iodine levels
necks), and may show signs of respiratory difficulty. range from 2.1 to 9.3 mg/dl.29,33 Smith21 reported a dou-
Lambs born to iodine-deficient ewes may exhibit an im- bling of serum thyroxine 4 hours after the administration
paired development of wool-producing follicles. All of thyrotrophin (5 IU intravenously [IV]). The level and
animals can be affected, but signs of hypothyroidism are stage of production (meat, fiber, milk) affects blood thy-
more common in young and growing lambs or kids, geri- roxine concentrations; thyroxine levels in does may drop
atric animals, and ewes and does in heavy production. In by as much as 30% between the prepartal period and 1
one study, eight Angora kids from 298 does showed signs week after birth.34 Thyroid function in Angora goats
of retarded growth, shortened heads, droopy eyelids, dull- has been shown to fluctuate with no apparent relation
ness, weight gain, and prognathism.23 Bilateral goiter was to the season.35 Serum lipid concentration in goats is
easily palpable in all cases. These cases were thought to be affected by thyroid status.23,36 Triglyceride, phospholipid,
caused by ingestion of thiocyanate precursors from highly and cholesterol levels steadily fall in a dose-dependent
fertilized forage.23 manner when animals are treated with T3. Elevated serum
Goats with heritable, large, goitrous thyroid glands are cholesterol (higher than 7.0 mmol/L) has been reported in
born with a rough, sparse hair coat, thickened skin, re- goats with congenital hypothyroidism.23 A thyroid
tarded growth, and sluggish behavior29; they respond gland–to–body weight ratio greater than 0.46:1 has been
poorly or not at all to supplemental iodine. Gestation associated with goiter caused by iodine deficiency.37
length in affected does may be increased to 153 days
(with a range of 148 to 158 days ).30 Figure 7-2 shows a Treatment and prevention. Affected young can be
congenital goiter in a 1-week-old cross-bred goat. Heri- treated with Lugol’s iodine (3 to 5 drops) in the milk or
table goiters are probably overdiagnosed because some can be given potassium iodine (20 mg) orally.31
 Chapter 7 Diseases of the Endocrine System • 191

Pregnant does and ewes in their final trimester should normal adult and fetal tissues39 and may act locally to in-
have free access to a trace mineral salt supplement con- fluence the growth and development of some cells. It has
taining iodine; this supplement should be the only source been shown to increase placental calcium transport in
of salt. Iodized salt containing 0.007% to 0.01% iodine,31 sheep,40 and it increases mammary blood flow in sheep41
preferably in the iodate form, is usually protective against and goats.42 High levels of the hormone are secreted into
goiter. In deficient areas the form of iodine used in the milk and have been detected in venous blood in the lac-
mineral supplement is important. Iodine in the iodide tating goat, as well as in the hepatic portal venous plasma
form is less available than that in the iodate form.22 Trace of suckling kids.43 The more often the mammary gland is
mineral salt intake may be depressed by many factors. milked, the greater the concentration of this hormone in
Because the drive or desire to consume trace mineral salt milk.44 PTHrP may even play a role in ILS.
is based on a craving for sodium, if other sources of At least one study has demonstrated that diets rich in
dietary sodium are available (e.g., commercially prepared phosphorus (one to three times the daily requirement)
feeds, free choice sodium bicarbonate) or the “salt carrier” have no adverse effect on bone mineralization in lambs as
for the iodine has additives rendering it unpalatable (e.g., long as the minimum calcium requirement is met.45
dicalcium phosphate, magnesium oxide), a less than Low dietary phosphorus produces significant hypophos-
optimal intake will occur. If this scenario is further com- phatemia with corresponding hypercalcemia in both sheep
plicated by the increased demands of pregnancy com- and goats.46,47 Still, the authors recommend a dietary
pelling ewes and does to consume more than normal calcium-to-phosphorus ratio of between 11 and 21.
amounts of nitrate-containing feeds or goitrogenic feeds Primary hyperparathyroidism or hypoparathyroidism
(e.g., cabbage, kale, peanuts, rape, soybeans, sorghum, is rare, but nutritional secondary hyperparathyroidism is
turnips), iodine deficiency–induced goiter and thyroid occasionally encountered.
dysfunction may occur in their offspring. Therefore,
when any or all of these situations occur, it is imperative
Nutritional Secondary Hyperparathyroidism
to ensure adequate intake through individual iodine sup-
plementation, painting adult animals with iodine (Lugol’s Pathogenesis. Secondary nutritional hyperparathy-
iodine 2 ml weekly), or drenching with potassium iodine roidism occurs when animals are fed a high-grain diet
(200 to 300 mg by mouth [PO] once during late gesta- that is low in calcium and high in phosphorus. Such a
tion).31 Of course, iodine toxicity should be avoided. diet decreases blood pH and increases blood concentra-
Culling, neutering, and removing parents should be con- tions of PTH. Hyperphosphatemia resulting from exces-
sidered to decrease the herd incidence of the heritable sive phosphorus intake lowers blood calcium levels. This
forms of goiter. results in bone calcium mobilization. Chronic mobiliza-
tion of calcium from bone leads to osteoporosis and re-
placement of reabsorbed calcium with fibrous connective
PARATHYROID GLAND tissue (osteodystrophia fibrosa). Excessive consumption
Parathyroid hormone (PTH) is a polypeptide hormone of oxalate-containing plants (see Chapter 10) can de-
produced by the parathyroid glands and released in re- crease calcium absorption. Consumption of such a diet
sponse to low serum ionized calcium. PTH interacts with coupled with excessive cereal grain feeding can result in
osteoblasts, stimulating cytokine release, which in turn nutritional secondary hyperparathyroidism. Young and
activates osteoclasts. Bone resorption by the osteoclasts growing animals are more likely to succumb than adults.
releases calcium and phosphorus from bone into the
blood. The number of functioning osteoclasts increases in Clinical signs. The disease is characterized by inter-
response to PTH, which also acts on the distal renal mittent shifting leg lameness, loose teeth, pathologic
tubules to increase calcium resorption and phosphorus fractures, and enlargement of the bones of the skull.
excretion. Additionally, PTH increases the conversion of
vitamin D to the active form, 1,25-dihydroxycholecacif- Diagnosis. The diagnosis is based on radiographic evi-
erol, which increases calcium and phosphorus absorp- dence of demineralization, increased urinary fractional
tion from the intestine. PTH also has been shown to in- excretion of phosphorus (see Chapter 10), and dietary
crease absorption of calcium and phosphorus from the mineral analysis. Early in the course of the disease hyper-
forestomachs of sheep.38 phosphatemia and hypocalcemia are seen. As the condi-
Another closely related hormone is parathyroid tion progresses, serum levels of calcium and phosphorus
hormone–related peptide (PTHrP). PTHrP acts simi- usually remain within normal limits. Serum alkaline
larly to PTH, with the exception that it decreases the phosphatase (SAP) may be normal, high normal, or high.
serum level of 1,25-dihydroxycholecaciferol. It is pro- The effects of diet-induced changes in blood pH on
duced by some neoplasms and is one of the causes mineral retention have been studied in lambs.48 A diet
of hypercalcemia (pseudohyperparathyroidism) associ- supplemented with excessive ammonium chloride pro-
ated with malignancy. PTHrP also is found in many duces a mild metabolic acidosis and significantly higher
192 • Sheep and Goat Medicine
plasma PTH levels than does a diet supplemented with pheochromocytomas in these does were histologically
sodium bicarbonate.48 The amounts of calcium and similar to those found in other species. Ultrastructural
phosphorus absorbed from the intestine were similar for features corresponded with the classical descriptions of
each diet, but osteoclastic activity increased in animals secretory granules in the adrenal medullas of other
consuming the acid diet. Although the plasma levels of species. Both norepinephrine and epinephrine granules
the two minerals were not significantly altered by the were found within the same cells.50 Two of the does in
diet, the retention of both calcium and phosphorus was this report had coincidental thyroid gland enlargement as
lower in the animals consuming the acid diet because of previously described in association with pheochromocy-
increased urinary excretion of both minerals.48 Ammo- toma in bulls51 and does.17
nium chloride is rarely fed at a rate greater than 0.25% to Adrenal cortical hypertrophy and elevated plasma cor-
0.3% of the diet. However, demineralization of bone is a ticosteroids have been reported in animals that were
potential problem with long-term (years) feeding of am- maintained on a diet deficient in cobalt and vitamin
monium chloride to pet goats. Although an acid diet is B12.52 The animals in this study had plasma cortisol levels
detrimental for growing animals, it can be helpful for three to five times higher than normal (2 to 3 ng/ml).
animals at risk of periparturient hypocalcemia. These investigators asserted that the effect of vitamin B12
deficiency was remarkably similar to the effects of chronic
Treatment and prevention. Maintaining an adequate malnutrition in other species.52
calcium-to-phosphorus ratio (11 to 21) is important in A habitual abortion syndrome described in Angora
prevention, as is not feeding excessive amounts of cereal goats appears to be associated with hypoadrenocorticism.
grains or oxalate-containing plants. Providing a mineral Some Angora does have an impaired ability to respond to
salt mixture for free choice consumption is always benefi- stress during gestation. This impairment grows worse as
cial. Providing a mixture of equal parts trace mineral salt gestation progresses. The affected females may have small
and dicalcium phosphate usually suffices for animals adrenal glands and decreased plasma cortisol levels.53
grazing grass pastures (see Chapters 2 and 9). This heritable hypoadrenocorticism most likely has
genetic linkage to fine mohair production. Stress (e.g.,
nutritional, climatic, physical) may result in abortion.54
ADRENAL GLANDS Most abortions occur between day 90 and 110 of gesta-
The adrenal glands are two small (2 to 4 cm  1 to 2 cm) tion. Because of the dam’s inability to respond to stress,
hormone-producing glands found near the kidneys. These the fetus develops adrenal hyperplasia. This results in in-
glands function in sheep and goats as they do in other creased fetal cortisol output and thereby prematurely
species. The cortex produces cortisol, aldosterone, and induces the parturition cascade. Aborted fetuses are typ-
other steroid hormones, while the medulla secretes epi- ically dysmature and anemic and have adrenocortical
nephrine, norepinephrine, and other vasoactive amines. hyperplasia.53,54
Necropsy of 2500 goats (80% of which were Angora)
older than 5 years of age revealed that 314 of 2104 cas-
trated males and 2 of 208 females had adrenal adenomas.
PANCREAS
No adrenal adenomas were diagnosed in the 188 intact The pancreas of sheep and goats functions similarly to
males in this study.49 The authors of the study theorized that of other ruminant animals. This bilobed gland is
that testosterone inhibits the pituitary gonadotropins that located in the craniodorsal abdomen and attached to the
mediate adrenal proliferation, as had been previously descending duodenum. The pancreas has both exocrine
shown in laboratory rodents.49 Adrenal cortical neoplasia functions (production and release of digestive enzymes)
has been described in a castrated male goat that was lac- and endocrine functions (production and release of
tating.14 Endocrine parameters in this goat consisted of insulin and glucagon). Diabetes mellitus (DM) has been
elevated levels of estradiol 17b, GH, PRL, cortisol, and described as any condition in which there is a permanent
insulin-like growth factor-1. The elevation in the pitu- elevation of blood glucose and glucosuria. Primary DM
itary hormone levels was most likely caused by the lack of involves beta-cell damage (insulin-producing cells) fol-
negative feedback by testosterone, whereas the elevation lowed by decreased insulin levels and hyperglycemia. Sec-
in cortisol levels occurred secondary to pituitary stimula- ondary DM results from a resistance to the effect of
tion. The elevated estradiol 17b was thought be caused by insulin even with normal or elevated plasma insulin
the adrenal neoplasia.14 levels. DM is rare in goats. Only one case report of
Pheochromocytomas have been reported in two does spontaneous DM could be found in the scientific litera-
with aberrant or inappropriate lactation17 and also from a ture.55 Other case reports describe the features of experi-
family of does in Finland.50 The association between ILS mentally induced DM by administration of alloxan56 or
and pheochromocytoma has not yet been determined. streptozocin.57
The Finnish does examined at necropsy had histories Clinical signs of diabetes in goats include weight loss,
of sudden nervous attacks. Gritz50 reported that the poor appetite, and lethargy.56 Polyuria and polydipsia are
 Chapter 7 Diseases of the Endocrine System • 193

invariable findings, with some animals exhibiting two to

three times their normal water intake. A 90% decrease in
milk production has been observed in lactating goats with
experimentally induced DM. Insulin treatment has been
tried in both spontaneous and experimental DM. In
general a response to treatment is observed within 4 days
and results in a partial relief of clinical signs and normal-
ization of laboratory values.55,56 However, improper
insulin dosage can result in life-threatening hypo- A
glycemia. Recurrence of clinical signs is observed with
discontinuation of therapy.

ABERRANT LACTATION,
GALACTORRHEA, PRECOCIOUS
UDDER (INAPPROPRIATE
LACTATION SYNDROME)
Although only a few cases of ILS in goats are described in
the scientific literature, the anecdotal reports of this
problem are seemingly endless. ILS has been reported in
both castrated and intact males, as well as in female
goats.14,17,58,59 It is, however, more common in females
B
than males. Rare in ewes, it appears to be more of a clini-
cal concern in pet does. Does with ILS usually have an
enlarged udder with no history of being bred. A thorough
history, including assessment of possible exposure to a
male and investigation regarding whether the doe is
being nursed or milked, should be taken. Results of a
routine physical examination are generally within normal
limits. The udder may be slightly enlarged or so large that Figure 7-3 Udders of two does with inappropriate lactation. A, A
4-year-old Spanish crossed goat that had given birth to a single kid 3
the animal has difficulty walking and is in danger of sec- years previously. B, An aged pygmy goat that had been displaying ILS
ondary orthopedic disease (Figure 7-3). The udder is for several years.
usually soft, non-inflamed, and non-painful to palpation.
The initial examination of these animals should rule out
impending parturition through the use of ballottement, tion. Although many does are not being nursed, milk
palpation, or real-time ultrasonography. After pregnancy remains in the teat cistern. The teat cisterns of these does
and “milk removal” have been ruled out as causes of lacta- are often abnormally large (“bottle teats”), either as a
tion, a more comprehensive examination should follow. result of prolonged filling or because the enlarged cistern
Examination of mammary secretions usually reveals a prevents the needed back-pressure from occurring.
substance that appears to be milk. However, a thinner, Bruckmaier et al60 described two different patterns of
more translucent to clear fluid also may be found. The ex- milk ejection during machine milking of goats: one with a
pression of milk is generally difficult during the initial ex- sharp peak and the other with a prolonged plateau. Does
amination because of plugged teat orifices. If the teats are with prolonged plateaus had larger teat cisterns than does
plugged and milk is not easily expressed, the animal is producing sharp-peaked ejection patterns. The larger teat
probably not being nursed or milked. The mammary se- cisterns seem to have a permissive effect on lactation.
cretions from does with ILS may look like milk on the Perhaps a bottle teat is so expandable that adequate back-
first milking but later change to a straw-colored fluid pressure cannot be established. Another possibility is that
with continued or intermittent milking. However, con- abnormal apoptosis of mammary gland cells may occur in
tinued milking of these animals may stimulate milk pro- the udders of these does in response to back-pressure.
duction in some does, and a normal lactation may ensue. Pseudopregnancy is one possible cause of ILS (see
The authors of this chapter have noted a mild familial as- Chapter 6). Most practitioners recommend treating these
sociation with ILS. does with luteolytic hormones (prostaglandin F2a
It is a common presumption that milk removal is nec- [PGF2a] 10 mg IM) after pregnancy has been ruled out.
essary to sustain lactation. Without milk removal, in- Although this does not usually result in a cure, it can and
traudder pressure should develop and inhibit milk secre- should be used to rule out pseudopregnancy. The authors
194 • Sheep and Goat Medicine
have not evaluated the fertility of females with ILS condition occurs in winter, when PRL is normally
because most are older animals that are kept as pets. low).6
However, their fertility is most likely impaired by the vast 2. Normal does treated with PRL for 4 days before and
array of endocrinologic and reproductive organ abnor- 4 days after parturition showed prolonged
malities (e.g., pituitary adenomas, adrenal pheochromo- suppression of PRL but resumed lactation within 10
cytomas, cystic ovaries, cystic endometrial hyperplasia) days and produced 32% higher milk yields than the
that have been reported in goats with ILS.14,17 previous year.62
A complete history of dietary intake should be per- 3. Local production of PRL by the mammary gland
formed in all cases of ILS. Possible grazing of estrogenic could be maintaining the inappropriate lactation and
forage such as legumes (e.g., clover) or grains infected would most likely be unaffected by bromocriptine
with Fusarium roseum should be investigated. F. roseum therapy.61
produces the mycotoxin zearalenone, which has the phys- 4. Other hormones such as PTHrP may be playing a
iologic effect of estrogen. Evaluation of the diet also may role.
be of value because adrenal hypertrophy and elevated 5. A defect in normal mammary gland involution may
plasma cortisol levels have been reported with mal- be present in these animals.
nutrition and certain B vitamin deficiencies. Parenteral
vitamin B12 supplementation or the addition of cobalt to Pituitary adenomas (which can be PRL-secreting
the diet may be beneficial if the diet is found to be inade- tumors in other species) have been reported in two does
quate or marginal. with ILS.17 The authors have examined the pituitary
Although most references to ILS in the literature glands of normal does and a doe with ILS (Figure 7-4).
suggest that PRL levels in these animals are elevated,17,58 The pituitary gland of the doe with inappropriate lactation
this may not always be the case. The authors have meas- (Figure 7-4, B) is larger and protrudes further dorsally
ured serum PRL in four does with ILS and found that all than the pituitary gland in the normal doe (Figure 7-4, A).
had low serum PRL. Two of these measurements were Spontaneous lactation of does also has been reported
taken in the winter months, when PRL is ordinarily in association with ovarian abnormalities. DeWalque63
low (less than 39 ng/ml). LeProvost et al61 described described a doe with a granulosa cell tumor that exhibited
the presence of PRL mitochondrial ribonucleic acid virilism concurrent with inappropriate lactation. Lofstedt
(mRNA) in the mammary glands of lactating sheep and
goats, thus demonstrating that de novo synthesis of PRL
is the likely cause of elevated milk PRL levels during the
periparturient period in normal ruminants. Local PRL
production may play a role in the establishment of ILS in
goats.
PTHrP also may be involved with this syndrome.
Thompson et al44 demonstrated that removing milk from A
one mammary gland of a normal doe in late gestation re-
sulted in an increase in PTHrP from the milked gland.
These researchers also demonstrated that the more often
milk was removed from a single gland, the higher the
milk concentration of PTHrP.44 When milking was dis-
continued in the single gland, PTHrP levels declined,44
indicating that PTHrP has a local (autocrine) lactogenic
role in the goat. Goats with tumors may have elevated
levels of PTHrP that could theoretically stimulate lacta-
tion. If this is the case, hypercalcemia of malignancy B
should also be expected.
Bromocriptine mesylate, a dopamine agonist, has been
suggested as a treatment for does with inappropriate lac-
tation. It should inhibit PRL release by the anterior pitu-
itary gland. However, successful use of this drug to stop
inappropriate lactation has not been reported. Failure of
response to bromocriptine mesylate can be anticipated for Figure 7-4 Midsagittal, T1-weighted, post-contrast magnetic
resonance imaging (MRI) of the brain of a normal female goat (A) and
a number of reasons:
a female with ILS (B). The contrast-enhanced area shows that the
pituitary gland (arrows) of the female with ILS is enlarged compared
1. Some of the does with inappropriate lactation may with that of the normal doe, extending dorsally to the dorsal extent of
already have low serum PRL (especially if the the pituitary fossa. (Courtesy John Hathcock, Auburn, Alabama.)
 Chapter 7 Diseases of the Endocrine System • 195

and Williams have reported udder engorgement in a doe observed prolonged labor and poor cervical dilatation in a
6 days after removal of a granulosa cell tumor.58 The female that had a mastectomy and was then inappropri-
authors of this chapter also have seen masculine behavior ately bred.
and granulosa cell tumors in a doe (Figure 7-5) with a
history of ILS (1-year duration) and mastectomy (2.5
years before the onset of masculine behavior). In addi-
tion, one of the does with ILS described by Miller et al17
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iodoproteins which replace thyroglobulin, J Endocrin 71:179, 1976. and on mineral balance in the lamb, Exper Physiol 76:725, 1991.
28. De Vijlder JJM et al: Hereditary congenital goiter with thyroglob- 49. Altman NG, Streett CS, Terner JY: Castration and its relationship
ulin deficiency in a breed of goats, Endocrinol 103:2105, 1978. to tumors of the adrenal gland in the goat, Am J Vet Res 30(4):583,
29. Rijnberk A et al: Congenital defect in iodothyronine synthesis. 1969.
Clinical aspects of iodine metabolism in goats with congenital 50. Gritz BG: Hereditary caprine pheochromocytomas, J Vet Med
goitre and hypothyroidism, Brit Vet J 133(5):495, 1977. Assoc 44:313, 1997.
30. Piosik PA et al: Effect of maternal thyroid status on thyroid hor- 51. Wilke BN, Krook L: Ultimobranchial tumor of the thyroid and
mones and growth in congenitally hypothyroid goat fetuses during pheochromocytoma in the bull, Path Vet 7:126, 1970.
the second half of gestation, Endocrinol 138(1):5, 1997. 52. Mgongo FOK, Gombe S, Ogaa JS: Influence of cobalt/vitamin
31. Bretzlaff K, Haenlein G, Huston E: Common nutritional prob- B12 deficiency as a stressor affecting adrenal cortex and ovarian ac-
lems feeding the sick goat. In Naylor JM, Ralston SL, editors: tivities in goats, Repro Nutr and Develop 24(6):845, 1984.
Large animal clinical nutrition, St Louis, 1991, Mosby. 53. Roberts SJ: Veterinary obstetrics and genital disease (theriogenology),
32. Sreekumaran T, Rajan A: Clinicopathological studies in experi- ed 3, Woodstock, VT, 1986, David and Charles.
mental hypothyroidism in goats, Vet Path 15:549, 1978. 54. Basrur PK, Koykul W, Yusoff RBH: Genetic disorders of the goat.
33. Reap M, Cass C, Hightower D: Thyroxine and triiodothyronine In Youngquist RS, editor: Current therapy in large animal theri-
levels in 10 species of animals, Southwestern Vet 31:31, 1978. ogenology, Philadelphia, 1997, WB Saunders.
34. Emre Z, Garmo G: Plasma thyroxine through parturition and 55. Lutz TA et al: Secondary diabetes mellitus in a pygmy goat, Vet Rec
early lactation in goats fed silage of grass and rape, Acta Vet Scand 135:93, 1994.
26:417, 1985. 56. Nowak J, Dzialoszynski L: Effect of experimental alloxan diabetes
35. Wentzel D, Viljoen KS, Botha LJJ: Seasonal variation in adrenal on the secretion and composition of goat milk, Acta Physiol
and thyroid function of Angora goats, Agroanimalia 11:1, 1979. Polonica 18(4):488, 1967.
36. Ibrahim RE et al: The effect of altered thyroid status on lipid me- 57. Stangassinger M, Peruche T, Giesecke D: Diabetes Mellitus bei
tabolism in Nubian goats, Compar Biochem Physiol 77B(3):507, Zwergziegen: Modellversuche mit Streptozocin, Zentralblatt fur
1984. Veterinaria Medicine A 29:297, 1982.
37. Sargison ND, West DM, Clark RG: An investigation of the possi- 58. Lofstedt RM, Williams R: Granulosa cell tumor in a goat, J Am
ble effects of subclinical iodine deficiency or ewe fertility and peri- Vet Med Assoc 189(2):206, 1986.
natal lamb mortality, New Zealand Vet J 5:208, 1997. 59. Jassim RA, Khamas W: Gynaecomastia and galactorrhea in a goat
38. Dua K et al: Effects of parathyroid hormone and parathyroid buck, Aust Vet J 75(9):669, 1997.
hormone-related protein on the rates of absorption of magnesium, 60. Bruckmaier RM et al: Machine milking of dairy goats during lac-
calcium, sodium, potassium and phosphate ions from the reticulo- tation: udder anatomy, milking characteristics and blood concen-
rumen in sheep, Exper Physiol 79(3):401, 1994. trators of oxytocin and prolactin, J Dairy Res 61:457, 1994.
39. Ratcliffe WA: Parathyroid hormone-related protein: a polyhor- 61. LeProvost F et al: Prolactin gene expression in ovine and caprine
monal enigma, Equine Vet J 29(3):174, 1997. mammary gland, Neuroendocrin 60:305, 1994.
40. Care AD et al: Stimulation of ovine placental transport of calcium 62. Forsyth IA, Lee PD: Bromocriptine treatment of periparturient
and magnesium by mid-molecule fragments of human parathyroid goats: long term suppression of prolactin and lack of effect on lac-
hormone-related protein, Exper Physiol 75:605, 1990. tation, J Dairy Res 60:307, 1993.
41. Thompson GE: Parathyroid hormone-related protein and 63. DeWalque J: Tumeur ovarienne et masculinization chez une
mammary blood flow in sheep, Exper Physiol 78(4):499, 1993. chevre chamoisee des alpas, Annales de Med Vet 107:322, 1963.
42. Prosser CG, Farr VC, Davis SR: Increased mammary blood flow 64. Diamond JM: Mammary gland as an endocrine organ: implica-
in the lactating goat induced by parathyroid hormone-related tions for mastectomy, Nature 295:191, 1982.
protein, Exper Physiol 79(4):565, 1994.
 Chapter 8

DSystem
iseases of the Integumentary

DAVID E. ANDERSON, D. MICHAEL RINGS, AND D.G. PUGH

Disease conditions affecting the skin and hair of sheep The dermis lies immediately beneath the epidermis
and goats are common. These diseases result in signifi- and is composed of collagen, elastin, neurovascular struc-
cant economic losses to livestock producers because of tures, arrector pili muscles, and a variety of cells and cel-
poor growth, weight loss, and loss of fiber and leather lular products such as proteoglycans. The superficial
products. Veterinarians often are consulted for diagnosis dermis is a loosely arranged network of collagen and
and treatment of these diseases but may become frus- elastin fibers. The deep dermis is more structured with
trated because of economic limitations imposed by collagen fibers arranged parallel to the skin surface. Blood
owners. Therefore history, clinical signs, and physical ex- is supplied to the skin by intercommunicating vessels
amination are important in developing an accurate differ- between the plexuses of the deep, middle, and superficial
ential diagnosis. This chapter discusses specific diseases layers. The subcutis is a composite of bundles of collagen
of the skin and hair of sheep and goats with emphasis on and elastin intermixed with adipose tissue.
diagnosis and treatment strategies. In goats, wattles may be present—typically along the
ventral neck caudal to the angle of the mandible. Al-
though the function of wattles is unknown, they contain
ANATOMY extensive neurovascular structures and cartilage. The
The skin functions as a protective barrier to the environ- presence of wattles is controlled by an autosomal domi-
ment. It also aids in thermoregulation, acts as a sensory nant gene.
organ, and communicates through the secretion of chem- Sebaceous (holocrine) scent glands are located caudal
icals.1,2 The skin acts as a barrier to bacteria partly by its and medial to the base of the horn tissues on the head of
acidic surface pH. It is a layered structure made up of the goats. In male goats these glands produce a pungent odor.
epidermis, dermis and hair follicles, and subcutis. The Surgical procedures to remove the scent glands of goats
epidermis is further stratified histologically into four (descenting) involve excising the sebaceous glands caudal
regions. These regions are, from the superficial to the and medial to the horn base. This procedure is easily done
deep layers, the stratum corneum, stratum granulosum, in young buck kids at the time of dehorning. In sheep,
stratum spinosum, and stratum basale. Areas exposed to scent glands are present rostral and medial to the eye and
frequent abrasion (e.g., muzzle, plenum, hoof margin) may produce a pungent odor in rams. Sweat (apocrine)
also have a stratum lucidum or clear layer, which is com- glands are present throughout the body in goats but are
posed of a nuclear, homogenous material containing re- most pronounced around the eyelids, scrotum, udder, and
tractile droplets (eleidin).3 The ability of the skin to heal perineal regions. These glands are not innervated, but
depends on the severity of damage incurred by the cells of respond to heat by producing sweat at a rate as high as
the stratum basale. Skin thickness varies with anatomic 208 g sweat/m2 skin/hour in males and 216 g sweat/m2
regions; it is thicker dorsally and thinner ventrally. skin/hour in females in response to temperatures in excess
Overall, skin thickness in sheep averages 2.6 mm; it is 2.9 of 41° C (106° F).3
mm in goats.2 Specialized cells found in the skin include The hair coat of sheep (wool and hair) and goats
melanocytes, which give color to the hair and skin; (fiber) has variable economic potential based on the
Langerhans’ cells, which process antigens; and Merkel texture of the hair. Two types of hair follicles are found in
cells, which function as mechanoreceptors. the skin of goats: primary and secondary. Primary hairs
• 197 •
198 • Sheep and Goat Medicine
are long and coarse and may occur singly or in groups of herd without confirmatory testing. Specific diagnostic
two or three. Primary hairs often are referred to as guard tests may be performed when diseases fail to respond to
hairs, outer coat, or kemp. Secondary follicles produce fine, seemingly appropriate therapy or when animals are
shorter hairs (undercoat and lanugo hairs in goats are scheduled for sale or show activities.
nonmedullated hairs), creating an undercoat often re- Historical data should include the signalment of the
ferred to as down. Secondary hairs include larger, medul- animal: species, breed, age, gender, weight, and color.
lated hairs (undercoat) and smaller, nonmedullated hairs Some breeds have a higher likelihood of developing spe-
(lanugo). Some fiber breeds of goats are genetically se- cific disease conditions (Table 8-1). Therefore breed in-
lected for down production.1 The ratio of secondary to formation is useful to assess for susceptibility. The clini-
primary hairs ranges from 31 to 251.3 Primary hair fol- cian should note details concerning the origin of and
licles have associated sebaceous and apocrine sweat exposure risks to the animals. Origin of the animal in-
glands and arrector pili muscles. The number of primary cludes whether the animal was born and raised on the
hairs per square centimeter for goats ranges from 175 farm, purchased by farm contracts, purchased through
hairs/cm2 for sexually intact males to 216 hairs/cm2 for sale barns, or imported from another state or country. Ex-
sexually intact females and 259 hairs/cm2 for castrated posure risks include transportation to another farm; com-
males.3 Secondary follicles also have associated sebaceous mingling in sales, shows, or fairs; farm tours involving
glands. children or livestock owners; and diseases that are
Livestock owners specifically interested in wool or endemic to the particular farm. In the latter case the cli-
fiber production are concerned about disease processes nician should also note when the last outbreak occurred.
that damage the quality of the product. They may consult Chronologic data are important in making a differential
veterinarians about pathologies such as fungal dermatitis, diagnosis. The date of the first observation of clinical
lice, and skin mites that cause noticeable lesions in the signs should be determined, the duration of clinical signs
coat. The hair follicle is composed of a bulb of tissue that should be evaluated, and details regarding the progression
produces the hair shaft, an arrector pilus muscle that of the disease within the affected animals should be de-
changes the angle of the hair shaft to the surface of scribed. The region of the body affected and the spread of
the skin, and various sebaceous and sudoriferous glands disease to other regions of the body also are important.
that excrete coatings onto the shaft. The growth of hair Often the current state of disease is so severe that the
follicles is controlled by a variety of factors, including
genetics.4-6
Active hair growth is referred to as the anagen phase. It TABLE 8-1
occurs for variable time periods and is followed by a
resting, or telogen, phase. The telogen phase disrupts the BREED PREDILECTIONS FOR SKIN DISEASES
integrity of the hair shaft; when the anagen phase begins IN SHEEP AND GOATS
again the previous hair shaft breaks away and is shed.
Goats may shed in the spring and fall, but sheep do not BREED DISEASE
undergo a noticeable shedding period and continuously
Border Leicester- Cutaneous asthenia
grow wool. Hair growth in goats can be influenced by
Southdown
ambient temperature, photoperiod, or both; hair growth
cross sheep
is not affected by castration. One study found that wool
Finnish crossbred sheep
growth intensity is greatest in autumn and winter and
Merino sheep
least in spring in sheep.7 Also, sebaceous and sudoriferous
Norwegian Dala sheep
gland volume was greatest in winter and spring and wool
Romney sheep
sulfur content was greater in autumn and winter, corre-
Corriedale sheep Congenitohereditary
sponding to larger diameter hair shafts.
photosensitivity
Southdown sheep
APPROACH TO DIAGNOSIS Dorset sheep Viable hypotrichosis
Merino sheep Hereditary goiter
The diagnosis of skin disease is confirmed in the same
Saanen dwarf cross goat
way as that of diseases affecting other body systems: com-
Scottish blackface sheep Epidermolysis bullosa
plete historical data, including environment and com-
Southdown sheep
mingling risk assessment; detailed clinical signs; thor-
Suffolk sheep
ough physical examination; and diagnostic testing based
Suffolk sheep Scrapie
on differential diagnosis lists. Often skin diseases in
sheep and goats are diagnosed based on risk factors such Adapted from Scott DW: Large animal dermatology, Philadelphia,
as species, clinical signs, age, and exposure risk within the 1988, WB Saunders.
 Chapter 8 Diseases of the Integumentary System • 199

point of origin cannot be determined by physical exami- tunately, these findings are consistent with chronic der-
nation. Assessment of whether the disease has spread matopathy and are not disease-specific. The distribution
from one animal to another within the flock or herd is of lesions may be more important than the actual histo-
particularly important. Finally, the veterinarian may as- logic description in this scenario.
semble a detailed chronology of any treatments applied, Alopecia is hair loss. It may be associated with disease
the dosage and route used for administration, and the du- or other stressors, producing a stress-induced telogen
ration of treatment. phase. This “stress break” in the hair shaft may result in
Clinical signs are important in the development of a generalized hair loss. Stress alopecia usually is associated
differential diagnosis. They can vary widely and depend with normal skin and normally growing hair. Systemic
on the tissues involved in the disease process. Differential disease causing prolonged pyrexia also can disrupt normal
diagnoses are most easily determined early in the course hair and fiber growth and result in easily epilated hair. In
of disease, when the primary lesions are abundant (Table sheep this is referred to as wool break. Nutritional defi-
8-2). As the disease progresses, secondary lesions such as ciencies in zinc, selenium, and vitamin E may cause hair
infection, thickening, crusting, and hair loss may over- loss. A congenital form of alopecia, termed hypotrichosis,
whelm the primary disease and make assessment of skin is well described in cattle and is associated with a reces-
disease extremely difficult. Therefore animals with newly sive genetic trait.8
emerging disease should be selected for examination. Scratching associated with skin disease is termed pru-
Erythema refers to reddening of the skin. It is not a ritus. Assessment of the severity of pruritus can aid in the
disease-specific change but usually indicates the presence formulation of an accurate differential diagnosis. Severe
of inflammation. pruritus typically is seen with ectoparasitism. Mild pruri-
Papules are solid masses, small in diameter (less than 1 tus is more often associated with nutritional deficiency,
cm), that are reddened, raised from the surface of the allergic skin disease, bacterial or fungal skin disease, and
skin, and may be painful to palpation. They are consistent autoimmune disease. It is a common clinical sign associ-
with infection, allergic reaction, and ectoparasites. When ated with scrapie that also is seen in pseudorabies virus
the papule is centered on a hair follicle, bacterial or fungal and rabies virus infections.
folliculitis and ectoparasites such as demodectic mange Changes in skin and hair pigmentation are uncommon
should be suspected. When papules occur independent in most ruminant diseases. Exceptions to this include the
from hair follicles, allergic skin reactions and ectopara- hair pigment lightening seen in cattle with chronic
sites such as scabies mites should be suspected. copper deficiency and molybdenosis and the black wool
Vesicles are similar in size and shape to papules, but pigment that develops in blackfaced sheep after skin
these masses are filled with a serous fluid and are fluctu- injury (abrasions, laceration, chronic irritation). The de-
ant. Vesicle formation may be preceded by a papule. Vesi- velopment of dark pigmentation also has been observed
cles are most often associated with viral skin diseases such in Saanen goats exposed to excessive sunlight.
as poxvirus infections, contact allergies, and autoimmune Lesion location can be used to establish a differential
diseases such as pemphigus. diagnosis (see Table 8-2). Regions commonly affected in
Pustules are similar to vesicles but are purulent in the early stages of skin disease include the face, ears, feet,
nature. Purulent exudate is formed because of migration udder, and perineal region. Fungal skin infections more
of neutrophils either in response to infection or because commonly occur on the face, neck, and ears, whereas bac-
of an autoimmune disease. Vesicles and pustules are rup- terial skin diseases also affect the feet, udder, and per-
tured by abrasion or spontaneous disruption of the over- ineum. Nutritional deficiencies typically involve all
lying membrane. The fluids accumulated on the skin regions to various degrees. Photosensitization is more
surface form crusts, and the underlying skin becomes severe in areas that receive little protection by the hair
thickened in response to the injury. coat and areas with slight or no pigmentation. Ectopara-
Crusts are firm, adherent amalgamations of serum, site lesions are most severe around the feet, face, and ears.
pus, blood, cellular debris, and associated organisms. The
presence of crusts indicates an exudative process but is
not disease-specific. Microscopic examination of crusts
Diagnostic Tests
may reveal infectious organisms such as fungi, bacteria, or Although many skin diseases are diagnosed based on
cells. The term scale simply refers to desquamated stratum clinical signs and intuition, specific diagnosis requires
corneum and is not disease-specific. confirmation by laboratory tests (Table 8-3).
Thickening of the skin (specifically, thickening of the
stratum corneum) often is referred to as hyperkeratosis. Skin scraping. Skin scraping and cytology are easily
The term orthokeratosis is used to describe hyperkeratosis performed under field conditions and may be diagnostic
without the presence of nuclei. Parakeratosis is hyperker- of certain diseases. Observation of bacteria on cytology is
atosis with nuclei present in the keratinized skin. Unfor- not diagnostic because bacteria are ubiquitous on the
200 • Sheep and Goat Medicine
TABLE 8-2

TYPICAL DISTRIBUTION OF LESIONS ASSOCIATED WITH SELECTED DISEASES OF THE SKIN

AREA INVOLVED DISEASE PRIMARY LESION TYPE

Head and neck Dermatophytosis Papulocrustous

Dermatophilosis Pustolocrustous
Demodicosis Papulonodular
Elaeophoriasis Ulcerative
Fly bites Papulocrustous
Actinobacillosis Nodular
Clostridiosis Edematous
Sarcoptic mange Papulocrustous
Contagious viral pustular dermatitis Pustolocrustous
Ovine viral ulcerative dermatitis Ulcerative
Goat pox Pustolocrustous
Sheep pox Pustolocrustous
Pemphigus foliaceous Vesiculopustular, crusts
Zinc deficiency Crusts
Contact dermatitis Variable
Viral papillomatosis Papulonodular
Squamous cell carcinoma Nodular, ulcerative
Ears Dermatophytosis Papulocrustous
Dermatophilosis Pustolocrustous
Sarcoptic mange Papulocrustous
Fly bites Papulocrustous
Pemphigus foliaceous Vesiculopustular, crusts
Ergotism Necrotizing
Fescue toxicosis Necrotizing
Frostbite Necrotizing
Photodermatitis Edematous, necroulcerative
Squamous cell carcinoma Nodular, ulcerative
Mucocutaneous Contagious viral pustular dermatitis Pustolocrustous
Goat pox Pustolocrustous
Sheep pox Pustolocrustous
Bluetongue Erythema, edema
Zinc deficiency Crusts
Bullous pemphigus Vesiculoulcerative
Pemphigus foliaceous Vesiculopustular, crusts
Dermatophytosis Papulocrustous
Dermatophilosis Pustolocrustous
Squamous cell carcinoma Nodular, ulcerative
Dorsum Dermatophilosis Pustolocrustous
Fly bites Papulocrustous
Psoroptic mange Papulocrustous
Contact dermatitis Variable
Ventrum Dermatophilosis Pustolocrustous
Fly bites Papulocrustous
Sarcoptic mange Papulocrustous
Contact dermatitis Variable
Adapted from Scott DW: Large animal dermatology, Philadelphia, 1988, WB Saunders.
 Chapter 8 Diseases of the Integumentary System • 201

TABLE 8-2

TYPICAL DISTRIBUTION OF LESIONS ASSOCIATED WITH SELECTED DISEASES OF THE SKIN—cont’d

AREA INVOLVED DISEASE PRIMARY LESION TYPE

Ventrum—cont’d Goat pox Pustolocrustous

Sheep pox Pustolocrustous
Contagious viral pustular dermatitis Pustolocrustous
Zinc deficiency Crusts
Corynebacterium pseudotuberculosis Abscesses
infection
Trunk Dermatophytosis Papulocrustous
Dermatophilosis Pustolocrustous
Psoroptic mange Papulocrustous
Psorergatic mange Alopecia, pruritus
Keds Alopecia, pruritus
Ovine fleece rot Moist dermatitis
Pemphigus foliaceous Vesiculopustular, crusts
Demodicosis Papulonodular
Caprine viral dermatitis Papulonodular
Scrapie Excoriation, pruritus
Vitamin A deficiency Hyperkeratosis
Iodine deficiency Alopecia, scaling
Biotin, niacin, riboflavin, Alopecia, scaling, crusts
pantothenic acid deficiency
Vitamin C–responsive dermatosis Alopecia, erythema, purpurea
Copper deficiency Depigmentation
Hindquarters Dermatophilosis Pustolocrustous
Chorioptic mange Papulocrustous
Legs and feet Dermatophytosis Papulocrustous
Dermatophilosis Pustolocrustous
Chorioptic mange Papulocrustous
Contact dermatitis Variable
Elaeophoriasis Necroulcerative
Clostridiosis Edema
Sarcoptic mange Papulocrustous
Zinc deficiency Crusts
Vitamin C–responsive dermatosis Alopecia, erythema, purpurea
Ovine viral ulcerative dermatitis Ulcerative
Pemphigus foliaceous Vesiculopustular, crusts
Tail Psoroptic mange Scales, pruritus
Selenosis Alopecia
Coronary band Pemphigus foliaceous Vesiculopustular, crusts
Bluetongue Erythema
Contagious viral pustular dermatitis Pustolocrustous
Ergotism Edema
Fescue toxicosis Edema
Dermatophilosis Pustolocrustous
Zinc deficiency Crusts
202 • Sheep and Goat Medicine
TABLE 8-3 TABLE 8-4

TESTS USED FOR DIAGNOSIS OF SKIN DISEASE NORMAL MICROBIAL INHABITANTS OF THE SKIN
IN SHEEP AND GOATS
CAUSE OF SKIN DISEASE TESTS USED
SPECIES BACTERIA FUNGI
Parasites Acetate tape
Skin scraping Goat Staphylococcus aureus Aspergillus
Fecal flotation Coagulase-negative Mucor
Fungi Potassium hydroxide Staphylococcus
Mineral oil mount Sheep Bacillus
Wood’s lamp Escherichia coli
Fungal culture Micrococcus
Cytology S. aureus
Bacteria Direct smear S. epidermidis
Bacterial culture Streptococcus
Viruses Viral isolation
Adapted from Scott DW: Large animal dermatology, Philadelphia,
Electron microscopy 1988, WB Saunders.
Serology
Allergy Intradermal skin tests
Miscellaneous pathology Histopathologic tests— hydroxide solution may be used to clear the sample for
biopsy sections, examination.
immunofluorescent
tests, antinuclear Microbial culture. Bacterial and fungal cultures can be
antibody tests, special used to determine the presence of pathogenic organisms.
stains Culture results may be challenging to interpret because
Adapted from Scott DW: Large animal dermatology, Philadelphia,
some cultured microbes may be part of the normal resi-
1988, WB Saunders. dent flora of the skin of sheep and goats (Table 8-4). Bac-
terial cultures may be obtained by aspirating pustules, ab-
scesses, and other nodules. If a skin biopsy is to be
surface of the skin. Bacteria observed in pustule fluid are performed, bacterial culture may be obtained from a
more diagnostic. The contents of skin pustules or ab- sample of skin tissue. The clinician cleanses the desired
scesses may be aspirated and cultured for identification. A sample area with alcohol and obtains a hair sample from
direct smear should be done and a Gram’s stain per- the periphery of an active lesion. Cultures for dermato-
formed for immediate identification of infectious bacte- mycotic agents must be set up on special media. Fungal
ria. The presence of phagocytized bacteria supports a di- cultures may require weeks in a favorable environment
agnosis of bacterial infection. Bacteria in the absence of before a positive or negative result can be reported.
neutrophils or macrophages suggests that the bacteria are
contaminants rather than causes of disease. Impression smear. Impression smears may be of some
Description of the morphology of groups of bacteria (albeit limited) value, particularly in the diagnosis of very
may be helpful. For example, Dermatophilus congolensis is exudative or very dry lesions. A moist lesion or an area
a gram-positive filamentous branching bacterial colony. from which a scab has just been removed is selected. A
Scales and crusts also can be examined under a micro- clean glass microscope slide is carefully pressed against the
scope. Direct examination is usually not rewarding, but lesion and is allowed to air dry or is fixed. The slide is then
softening the material with sodium nitrate solution may suitably stained and the cytologic evaluation is performed.
allow for visualization of ectoparasites or fungal hyphae.
These organisms often float to the top of the solution; a Biopsy. Skin biopsy is most useful to identify lesions
slide placed on top of the solution aids in identification consistent with ectoparasites and allergic and autoim-
because mites often are carried with the water adhesion mune disease. Skin biopsy is indicated when a lesion is
onto the slide. unusual, has failed to respond to treatment, is suspected
Skin scrapings can be frustrating to interpret. The to be neoplastic, or is persistently ulcerative or exudative.
scraping should be done firmly and deeply into the skin It also can be used to rule out various pathologies during
surface. The presence of blood at the site of scraping indi- differential diagnosis. Biopsy specimens should be ob-
cates that the depth is adequate to collect any infesting tained from primary lesions and ideally should include
ectoparasites. Careful microscopic examination of the the junction of normal and abnormal skin. Commercial
debris is useful to identify mites or their eggs. Potassium skin biopsy instruments (with internal diameters of 4 to 8
 Chapter 8 Diseases of the Integumentary System • 203

mm) provide the best quality samples for pathologists.

VIRAL DISEASES
Areas with minimal skin tension should be chosen. A
needle and scalpel blade can be used to harvest a skin
Contagious Ecthyma
sample, or the entire lesion may be submitted if surgical Contagious ecthyma (contagious viral pustular dermati-
excision is performed. Full-thickness skin biopsy is rec- tis, orf, sore mouth, contagious pustular dermatitis, cuta-
ommended to allow examination of all layers of the epi- neous pustular dermatitis, scabby mouth) affects sheep
dermis and dermis. Sedation or tranquilization of the and goats and is caused by an epitheliotrophic Para-
patient may be required. The clinician may clip the hair poxvirus (140 kilobase [kb] deoxyribonucleic acid
surrounding the area of skin biopsy; however, hair emerg- [DNA]).1-7 Lesions occur most severely on the mouth
ing from the skin sample is desirable to enhance the and face but also occur on the feet, teats, and genitalia.
pathologist’s evaluation. Therefore only minimal clipping The poxvirus is present worldwide and can remain infec-
should be performed, and a razor blade should not be tive in scabs in the environment for months or years.
used. A small amount of lidocaine hydrochloride 2% is Transmission occurs either by direct contact or indirectly
deposited in the subcutaneous tissue deep within the from environmental contaminants. The poxvirus gains
specimen. This should be done carefully and immediately entry through abrasions; morbidity is highest among
before biopsy because the side effects of lidocaine include animals subjected to coarse feeds and pasture plants that
vascular dilatation and edema, both of which may confuse cause injury to the oral mucosa. The virus remains in the
histologic evaluation. Many pathologists prefer that skin local tissues and is shed with the scab. Infection of the
specimens be preserved attached to a wooden plank such respiratory and gastrointestinal systems is rare.2 The in-
as a piece of a tongue depressor. Fixatives for skin samples cubation period can be as short as 4 days or as long as 2
include 10% neutral buffered formalin for routine light weeks. Commingling sheep is a common risk factor and
microscopy and glutaraldehyde for electron microscopy. younger sheep, especially 3- to 6-month-old feeder
Skin biopsies may be fixed with Michel’s fixative or fresh- lambs, are most susceptible. The infection is self-limiting,
frozen without fixative if immunohistochemistry or other with most sheep developing protective immunity.
such tests are desired. In one study shrinkage was similar However, reinfection is possible. If it occurs, the course of
for formalin-fixed and fresh-frozen specimens (approxi- the disease is less severe and more rapidly cleared. Neona-
mately 20%).9 Skin biopsy specimens should be submit- tal lambs may achieve only limited protection through
ted to a veterinary pathologist experienced in the inter- passive transfer of maternal antibodies in colostrum, and
pretation of skin histology (dermatohistopathologist). maternal protection wanes near weaning age.
Because skin histology varies dramatically among species,
a pathologist experienced in evaluation of the skin of Clinical signs. Early clinical signs of contagious
sheep and goats is preferable. If preferred by the clinician ecthyma include papules, vesicles, and pustules in affected
or owner the biopsy site can be closed (using a simple in- skin. Thick, brown-to-black crusts form rapidly and are
terrupted or cruciate pattern) with either absorbable or most evident at the commissures of the mouth. Lesions
nonabsorbable material. may spread to the oral cavity, feet, eyelids, and teats.
Mastitis may develop because of compromise to the
teat defense mechanisms. Lesions typically resolve in 14
R EFERENCES
1. Scott DW: Large animal dermatology, Philadelphia, 1988, WB
to 21 days but may persist in immunocompromised pa-
tients. Nursing lambs may spread the infection to the
Saunders.
udders of susceptible ewes. Oral lesions may be severe
2. Smith MC, Sherman DM: Skin. In Smith MC, Sherman DM, enough in lambs to cause anorexia, weight loss, and dehy-
editors: Goat medicine, Baltimore, 1994, Williams & Wilkins. dration or malnutrition. Lesions involving the coronary
3. Scott DW, Smith MC, Manning TO: Caprine dermatology. Part I. band may cause lameness and udder lesions may result in
Normal skin and bacterial and fungal disorders, Comp Cont Ed Pract mastitis in affected sheep. Rarely, the respiratory and gas-
Vet 6:S190, 1984. trointestinal systems are involved. In these cases pneumo-
4. Abouheif MA, Johnson CL, Botkin MP: Heritability estimates of nia and diarrhea, respectively, may occur. Secondary bac-
wool follicle traits in sheep skin, Anim Prod 39:399, 1984. terial infection of the skin is common. Differential
5. Eythorsdottir E: Genetic variation in woolskin quality of Icelandic diagnoses include ulcerative dermatosis, sheep pox, and
lambs, Livestock Prod Sci 57:113, 1999. dermatophilosis.
6. Henderson M, Sabine JR: Secondary follicle development in Aus-
tralian cashmere goats, Small Rumin Res 4:349, 1991.
7. Dragnev Z, Nedelchev D, Vladov K: Zhivotnovudni Nauki 13:80,
Diagnosis. Observation of typical histopathologic
1976. lesions in skin biopsy specimens is supportive of a diag-
8. Steffen DJ: Congenital skin abnormalities, Vet Clin North Am 9:105, nosis of contagious ecthyma. These lesions include ep-
1993. ithelial proliferation, ballooning degeneration, and
9. Steinhagen O, Bredenhann AEJ: The effect of histological process- eosinophilic intracytoplasmic inclusions. Viral particles
ing on sheep skin samples, S Afr J Anim Sci 17:151, 1987. may be observed in vesicular fluid, skin, and crusts with
204 • Sheep and Goat Medicine
electron microscopy. Fluorescent antibody tests may be
performed on cell cultures that have been inoculated with
material from lesions.

Treatment. Treatment of individually affected animals

is not provided unless lesions are severe. In these cases
therapy is supportive and includes the administration of
oral fluids and nutrients. Application of topical astringent
agents may speed recovery.

Prevention. Control measures should be implemented

immediately, and affected sheep should be isolated.
However, these measures alone may not be effective in
controlling contagious ecthyma because of the short in-
cubation time and survivability of the agent in the envi-
Figure 8-1 Malignant contagious ecthyma. Note the proliferative
ronment. Commercial vaccines are available; they require lesions around the face. In traditional contagious ecthyma, lesions last
application to the surface of scarified epithelium in the only 2 to 4 weeks. Lesions around the mouth make grazing painful and
axilla, groin, inner thigh (not in lactating ewes), underside can result in weight loss. Lesions around the udder can result in the
of the tail, or ear. These vaccines are not recommended refusal of dams to allow nursing. Lesions may become infected with
secondary bacteria, at which time topical antibiotics may be indicated.
for use in disease-free herds because the vaccine virus
remains viable in the environment for a long period. De-
velopment of immunity occurs over a period of 3 weeks
and may persist for as long as 2 years. Contagious contact. Infection is typically complicated by pathogenic
ecthyma is highly zoonotic and may produce lesions on bacteria such as Fusobacterium necrophorum. These viral
the hands or fingers of persons handling infected sheep or and bacterial agents cause ulcers, necrosis, and scabs.
goats. Therefore hygiene is imperative during handling of Morbidity with ulcerative dermatosis is less than that
infected herds. In endemic flocks vaccinating lambs and seen in contagious ecthyma in a susceptible population,
kids at 2 to 3 days of age may help reduce the severity of seldom exceeding 20% of the flock.
a flock outbreak. In lambs this may be coordinated with
tail docking. Clinical signs. During breeding season, ulcerative der-
matosis appears clinically as vulvitis or balanoposthitis.
Epithelial abrasions that occur during breeding allow
Malignant Contagious Ecthyma transmission from one animal to the other. Infected
A persistent form of contagious ecthyma known as malig- tissues become red and swollen and develop a moist
nant contagious ecthyma has been recognized in a limited exudate. During winter or periods of high risk for feet
number of sheep within infected flocks. Proliferative and lip abrasions, ulcerations may develop on the feet and
lesions develop, especially on the distal legs and feet and mouth. Lesions do not involve the oral mucosae. Lesions
less commonly on the head. However, unlike ordinary are present for 2 to 6 weeks and are self-limiting. When
contagious ecthyma, the lesions fail to regress and may lesions are severe, scar tissue may cause phimosis or para-
continually enlarge (Figure 8-1). Secondary bacterial in- phimosis. When necrosis is severe, sepsis of the interpha-
fections, fly strike, and hemorrhage are major complica- langeal joint, urethral fistula, or sloughing of the urethral
tions. Although a poxvirus morphologically similar to the process may occur.
contagious ecthyma virus has been identified by electron
microscopy in typical lesions, the disease has a different Diagnosis. Ulcerative dermatosis is differentiated clin-
course. Affected sheep do not pass the infection to com- ically from contagious ecthyma because of the ulcerative
mingling animals. Preliminary studies of the cellular nature of the disease, rather than the proliferation typical
immune systems of affected sheep have failed to of contagious ecthyma. Histopathologic lesions observed
demonstrate any deviation from normal. in skin biopsy specimens confirm this differentiation.

Treatment. Treatment should include isolating af-

Ulcerative Dermatosis fected animals, cleansing wounds and treating them with
Ulcerative dermatosis occurs most commonly in sheep in antiseptic or antimicrobial (triple antibiotic) ointments,
the western United States. It is caused by a similar but and managing secondary infections. Control may include
antigenically distinct virus from that causing contagious removing hair from the animals’ genital areas to prevent
ecthyma.3,4 Transmission occurs by direct or indirect abrasion of genital tissues.
 Chapter 8 Diseases of the Integumentary System • 205

Sheep Pox
Sheep pox is caused by an extremely virulent poxvirus. It
R EFERENCES
1. Smith MC, Sherman DM: Skin. In Smith MC, Sherman DM,
produces marked pyrexia, anorexia, and apparent depres- editors: Goat medicine, Baltimore, 1994, Williams & Wilkins.
sion.3,7 Sheep pox is found in Eastern Europe, North 2. Haig D et al: Cytokines and their inhibitors in orf virus infection,
Africa, and Asia. Lesions rapidly transform from macules Vet Immunol Immunopath 54:261, 1996.
to papules and then to vesicles on skin with limited wool 3. Lofstedt J: Dermatologic diseases of sheep, Vet Clin North Am Large
coverage (mouth, face, eyelids, perineum, udder, prepuce). Anim Pract 5:427, 1983.
Tissue necrosis and scab formation ensues. The epithelial 4. Mullowney PC: Skin diseases of sheep, Vet Clin North Am Large
tissues of the lungs and gastrointestinal system may Anim Pract 6(1):131, 1984.
5. Mullowney PC, Baldwin EW: Skin diseases of goats, Vet Clin North
become involved, with a mortality rate as high as 50%
Am Large Anim Pract 6(1):143, 1984.
among affected sheep. 6. Scott DW, Smith MC, Manning TO: Caprine dermatology. Part
II. Viral, nutritional, environmental, and congenitohereditary disor-
Goat Pox ders, Comp Cont Ed Pract Vet 6:S473, 1984.
7. Kimberling CV: Diseases of the skin. In Kimberling CV, editor:
Goat pox virus infection causes papules, vesicles, pus- Jensen and Swift’s diseases of sheep, ed 3, Philadelphia, 1988, Lea &
tules, and scabs that can be difficult to distinguish Febiger.
from those of contagious ecthyma.1,6,8 However, these 8. Smith MC: Dermatologic diseases of goats, Vet Clin North Am
lesions usually occur on the teats, udder, scrotum, Large Anim Pract 5:449, 1983.
and thighs but are uncommon on the face. Although
not diagnosed in the United States, a virulent strain of BACTERIAL DISEASES
goat pox has been documented to cause anorexia,
pyrexia, rhinitis, and conjunctivitis in herds in Africa Dermatophilosis (Streptothricosis,
and the Middle East. Research into the nature of goat
pox virus revealed the presence of numerous precip-
Lumpy Wool Disease, Rain Scald)
itinogens, some heat stable and some enzyme resis- Dermatophilosis causes a severe suppurative inflamma-
tant.1,7 Death may ensue, with pulmonary lesions tion of the skin.1-4 Dermatophilus congolensis is the
found at necropsy. causative organism and is a gram-positive, filamentous,
aerobic bacteria. This disease is associated with skin abra-
sion and moist conditions. Therefore the ears, muzzle,
Scrapie face, and tail are common sites for disease. In geographic
A discussion of scrapie is beyond the scope of this chapter areas with long periods of rainfall and high humidity, the
(see Chapter 11).3,4 However, scrapie-infected sheep may disease also may affect the dorsum of the neck and back.
demonstrate intense pruritus and body tremors. Wool The bacteria may be spread by mechanical vectors
may be missing or distorted because of the scratching, but (shears, flies), by contaminated dipping solutions, and by
the underlying skin is normal. direct contact. Animals debilitated by malnutrition, para-
sitism, or other disease are most susceptible to clinical
infection.
Bluetongue
A discussion of bluetongue is beyond the scope of this Clinical signs. Clinical signs include the formation of
chapter (see Chapters 4 and 14).2 However, bluetongue thick crusts with a significant inflammatory response in
virus infection may cause ptyalism, lacrimation, conjunc- the skin. Crusts contain infective zoospores of the bac-
tivitis, oral ulceration, and swelling of the mouth, muzzle, terium that are released when the crust softens in moist
and ears. Hyperemia and eczema may be noted in hairless conditions. These zoospores are stable in the environ-
areas. The coronary band may be inflamed and lameness ment within crusts for at least 4 months. Sheep may carry
may occur. Lesions can be severe enough to cause slough- the infection subclinically and serve as carriers of the
ing of the hooves.1 disease. Periods of prolonged moist skin allow penetra-
tion of the bacterium into the skin and establishment of
infection. Strawberry footrot is another name for D. con-
Vesicular Stomatitis golensis infection of the distal extremities and large crust
Vesicular stomatitis may cause vesicle formation on the formation around the carpus, tarsus, and coronary bands.
commissures of the lips in goats.1 Pseudorabies can cause Pastures contaminated with D. congolensis may produce
intense pruritus in goats. Viral encephalitis and rapid widespread disease in a flock; clinical cases are most
death are typical of pseudorabies infection. Viral isolation severe in young stock (less than 1 year old). Lesions heal
and serology are recommended to differentiate the by granulation, which is observed with forced removal of
various viral diseases (see Chapter 14). crusts (hence, the strawberry appearance).
206 • Sheep and Goat Medicine
Diagnosis. Cytologic examination of the deep layer of Clinical signs. Characteristic lesions include head and
the crusts (adjacent to the granulation tissue) reveals neck edema, especially of the eyelids, that is not associ-
coccoid bacteria branching into formations similar to ated with hemorrhage or emphysema. Early in the course
“railroad tracks.” Maceration of crusts may allow identifi- of disease, rams have marked pyrexia (41° to 43° C) that
cation of motile zoospores. Diagnosis is confirmed by can progress to death within 72 hours.
culture of a skin biopsy or crusts. Secondary mycotic der-
matitis is common and confuses diagnostic efforts. Treatment. Treatment (penicillin, oxygen insufflation
of affected tissues, antitoxins) is usually futile. Prevention
Treatment. Local and systemic treatment of der- is easily attained with multivalent clostridial vaccines at
matophilosis has been recommended. Empirical antibi- least 6 weeks before the onset of the first breeding season.
otic therapy may include procaine penicillin G (dosage
range 20,000 to 70,000 units/kg body weight) or oxytet-
racycline (20 mg/kg subcutaneously [SC] or intramuscu-
Actinobacillosis
larly [IM] every 72 hours). Topical treatment may include Actinobacillus lignieresii, a non–spore-forming, gram-
administration of copper sulfate (0.2%), zinc sulfate negative rod, causes a pyogranulomatous bacterial infec-
(0.2% to 0.5%), or potassium aluminum sulfate (1%). tion of the soft tissues of the head.6 These bacteria usually
Clinicians should take precautions during treatment are inoculated into the tissues by grass awns or stemmy
because D. congolensis is capable of infecting human forage. A local granulomatous reaction occurs, but these
beings. Improving the dietary protein, energy, and bacteria also may spread to regional lymph nodes or the
mineral intake and providing shelter from rain are all bloodstream. They can produce chains of small nodules
good methods of promoting skin healing and preventing leading to the lymph nodes.
the disease.
Clinical signs. Purulent material may be observed
draining from lymph nodes. Severe enlargement of sub-
Fleece Rot maxillary or parotid lymph nodes may cause difficulty in
Excessive moisture trapped by the wool and held against breathing or eating; sheep may die from malnutrition.
the skin for a prolonged time can result in a bacterial der- Nasal exudate may be noted if the infection drains into
matitis known as fleece rot.2,5 Prolonged wetting of the the nasopharynx.
skin causes hyperkeratosis, acanthosis, and edema. Eco-
nomic losses are incurred because of discoloration of the Diagnosis. The diagnosis is made by performing cytol-
wool by exudate or chromogenic bacteria. Although it is ogy and a Gram’s stain on the exudate. The gram-
not the exclusive cause of fleece rot, Pseudomonas aerugi- negative rods are filamentous and form sulfur granules in
nosa is commonly isolated from lesions. the pus that can be seen without the aid of a microscope.

Clinical signs. Infection with P. aeruginosa may cause a Treatment. Therapy includes surgical drainage, antibi-
greenish discoloration of the wool, and infection with P. otics (procaine penicillin G, 22,000 to 66,000 units/kg
indigofera may cause a bluish discoloration. Lesions are body weight SC every 24 hours for 7 days), and iodine
most commonly found on the back and withers. The un- therapy. Sodium iodide can be administered (80 mg/kg
derlying skin is soft, macerated, and cyanotic. Sheep with body weight) intravenously (IV) and repeated once or twice
dense hair follicles and a variety of hair shaft diameters at 7-day intervals. Alternatively, organic iodides can be
are most susceptible to Pseudomonas infection. Fleece rot added to the feed (7.5 to 15 g/head/day) for 14 to 21 days.
is distinguished from dermatophilosis in that no scab is
associated with the infection.
Staphylococcal Dermatitis
Treatment. Marked improvement of lesions occurs Staphylococcus aureus can cause a bacterial infection of the
after shearing and drying of lesions. skin.2,4,7 The bacteria become established when puncture
wounds or other injuries allow entry into the skin.
Malignant Edema (Swelled Head, Bighead) Clinical signs. Affected animals have an exudative der-
Malignant edema is a rare condition most commonly af- matitis that is most severe around the eyes, ears, base of
fecting young rams.1,3,5 The disease is caused by Clostrid- the horns, and bridge of the nose. In goats, vesicles and
ium novyi, C. sordelli, and C. oedematiens and is most com- pustules may be found on the teats and udder soon after
monly seen in summer and autumn. Rams 6 months to 2 parturition.
years of age are most commonly affected. The bacterial
spores gain entry to the skin through fighting wounds Diagnosis. The diagnosis is made by culture of he-
among pubertal rams. molytic S. aureus. This disease must be differentiated
 Chapter 8 Diseases of the Integumentary System • 207

from elaeophoriasis because of the distribution of lesions

on the head.

Treatment. The application of topical antiseptics or

antimicrobial ointments may be of benefit. If clinical
signs are severe or the distribution of lesions is wide-
spread on the body, systemic antibiotic therapy should be
based on results of culture and sensitivity tests. Empirical
antibiotic therapy may include penicillin (22,000 IU/kg
once a day [SID] or twice a day [BID]), ampicillin (10 to
20 mg/kg IM or IV BID), or oxytetracycline (10 mg/kg
IV BID or 20 mg/kg SC or IM every 48 to 72 hours).
Figure 8-2 Caseous lymphadenitis abscesses in a young adult
The causative bacterium is contagious and affected sheep ewe.
should be isolated from the flock. Affected dairy goats
should be removed from the milking line or milked last.
Careful attention to hygiene is necessary to prevent a
b
staphylococcal mastitis and spread of these pathogenic
bacteria to other lactating does.

Abscesses
Abscesses of the soft tissues are not uncommon in sheep
and goats. Abscesses usually begin when wounds allow c Wattle e
entry of surface bacteria through the epidermis. There- f
fore Staphylococcus species, Corynebacterium species, Acti- g
d
nomyces species, and streptococcal bacteria are expected
on culture. Noncontagious abscesses may be treated by
lancing after infiltration of local anesthesia. The interior
capsule of the abscess is débrided and flushed with a
dilute iodine solution (1%). Systemic antimicrobial
agents are not indicated in most cases but may be admin-
Figure 8-3 Locations of the most common palpable lymph nodes
istered if numerous abscesses or deeply seeded abscesses that can become enlarged in caseous lymphadenitis. The nodes are
are present. the parotid (a), retropharyngeal (b), mandibular (c), prescapular (d),
prefemoral (e), and popliteal (f); the arrow points to the superficial
inguinal lymph node (g). This illustration also shows the most common
Caseous Lymphadenitis location for wattles. However, wattles also can be found in other areas
of the cervical region. (Adapted from Williams CSF: Routine sheep and
Caseous lymphadenitis is caused by Corynebacterium goat procedures, Vet Clin North Am Food Anim Pract 6(3):753, 1990.)
(Actinomyces) pseudotuberculosis, formerly called C. ovis. C.
pseudotuberculosis is a facultative, gram-positive, coccoid
bacillus that is an intracellular parasite of macrophages manure. Some breeds (Merino, because of their wrinkled
and monocytes.8,9 It may cause abscesses in the skin or skin) and certain management practices (e.g., the use of
subcutaneous lymph nodes that may break open to the dip tanks, improper shearing techniques, housing with
skin surface (Figure 8-2).8 Bacterial infection may spread nails or wire) predispose to this disease.9 These lesions
rapidly through a sheep flock at the time of shearing have thick, often caseated exudate. Spontaneous rupture
because of skin abrasions and contamination of shears, of the abscess causes clumping of wool or hair with
tail docking equipment, and dip tanks. Experimental exudate. In an experimental study, draining abscesses
studies have described abscess formation as early as 41 continued to contaminate the environment for as long as
days after inoculation.10 In many animals the organism 37 days after rupture.9,10
disseminates to the viscera, most commonly the mediasti-
nal lymph nodes or lungs, resulting in dyspnea and Clinical signs. Clinical signs include swelling of super-
tachypnea. Therefore some animals may present with a ficial lymph nodes (i.e., prescapular, prefemoral) (Figure
history of respiratory disease. This disease may be spread 8-3), occasionally with draining tracts. In sheep these ab-
by the respiratory route, and lung abscesses may pose a scesses initially contain pale green material that eventu-
potential source of flock contamination in high-density ally forms an “onion ring”–like structure and matures
areas such as barns and dry lots. This organism can into a calcified mass. Abscesses in goats usually remain
survive for extended periods in dark, damp areas, soil, and greenish-cream colored with a pasty texture.9 These skin
208 • Sheep and Goat Medicine
lumps may occur in chains or as solitary lesions. As ab- formalin (10% solution) attached to a 14-gauge needle.
scessation of the viscera occurs, chronic weight loss may The needle is inserted into an infected node and the
be encountered, more commonly in sheep than in goats. caseous material is aspirated. The clinician leaves the
Poor fertility, decreased milk production, decreased lamb needle in the node, detaches the syringe from the needle,
crop and weaning weights, and poor growth and wool caps it, and mixes its contents. If fluid easily runs out of
production also are encountered. The organism can the needle in sheep the etiologic agent is probably C. pyo-
spread to the central nervous system or superficial in- genes (or others) and not C. pseudotuberculosis. Abscesses
guinal lymph nodes and mammary glands, resulting in may be more commonly caused by C. pyogenes rather than
neurologic signs and mastitis, respectively.9 C. pseudotuberculosis in pre-weaning and weaning-age
lambs. If the aspirated material is very thick, after it is
Diagnosis. Diagnosis is based on serologic testing of shaken into solution the syringe is uncapped, reattached
infected animals, culture of the organism (particu- to the needle, and injected back into the node.12 Contro-
larly from the peripheral portions of the necrotic area), versy exists regarding the use of such “autovaccines” in
and necropsy with consistent pathologic findings. C. animals intended for food because of the potential for
pseudotuberculosis is a catalase-positive, urease-negative, formalin to be introduced to the food chain. However,
phospholipase-D–positive, pyrazinamide-negative or- one of the authors (Dr. Pugh) has used this procedure for
ganism.10,11 To culture the abscessed lymph node, the many years in pet goats and sheep with excellent clinical
skin over the node is clipped and surgically scrubbed. The success. Culling such animals is still the best treatment.
clinician inserts a sterile needle and aspirates the abscess.
If no fluid can be withdrawn, sterile saline is injected and Prevention. Identification of infected animals and
the node is re-aspirated. If the abscess is plated onto removal from the flock is the most effective method of
blood agar after 48 hours, the organism grows as a thin control. Housing should be maintained free of objects
colony with slight hemolysis. Organisms should stain that can cause skin injury. Needles, surgical equipment,
gram-positive, but occasionally they are variable in their and tattoo pliers should be cleansed and disinfected
staining characteristics. C. pyogenes may be a secondary after use. All animals with open draining lesions should
invader and is not uncommonly cultured. The hemolysis be culled or quarantined. Both agglutination tests and
synergistic inhibition test measures antibodies to exotox- hemolysis synergistic inhibition tests may aid in identi-
ins produced by the organism. Most infected animals fication, but they are not accurate enough for clinicians
produce antibodies to the exotoxins within a month of in- to base decisions to cull animals that have early non-
fection. A complete blood count (CBC) may reveal a clinical infections. Special care should be taken to keep
leukocytosis with a normal lymphocyte-to-neutrophil all shearing and hoof trimming equipment and dipping
ratio, anemia of chronic disease, and hypoproteinemia, al- vats clean and free of contamination from infected
though findings are usually nonspecific. Occasionally an draining wounds. Animals with poor body condition
increase in total serum protein and gamma globulin is should be culled. Although controversial, the use of
seen before the onset of symptoms. Other diseases that commercially produced or autogenous formalized vac-
cause chronic weight loss should be considered, including cines may be beneficial. Vaccination is of value and can
parasitism, ovine progressive pneumonia (OPP), caprine reduce the incidence of abscesses in a flock by more than
arthritis-encephalitis (CAE), Actinobacillus infection, tu- 70% but will probably not result in disease eradication
berculosis, and Johne’s disease.9 in a flock.9 Box 8-1 presents a generic lymphadenitis
control program.
Treatment. C. pseudotuberculosis abscesses should not
be opened within the vicinity of the flock. Affected FUNGAL DISEASES
animals should be isolated for treatment; however, an-
timicrobial treatment is usually unrewarding. When eco- Dermatophytosis (Ringworm, Lumpy
nomically feasible, the authors of this chapter prefer to
surgically remove the intact abscess, including the
Wool, Club Lamb Fungus)
capsule. Complete removal of the abscess markedly Fungi are not major pathogens in sheep.2,5,11 Fungi cul-
reduces the likelihood of contamination of the environ- tured from clinical lesions include Trichophyton verruco-
ment. This procedure is best done under general anesthe- sum, T. gypseum, T. mentagrophytes, and Microsporum canis.
sia because these abscesses are often located in areas with Dermatophytosis is transmitted by direct contact or indi-
vital neurovascular structures. If abscesses have already rect contact with contaminated equipment or environ-
ruptured, the animal should be isolated, the abscessed mental vectors. These fungi invade keratinized tissues
area flushed with an antiseptic solution (3% iodine or and hair fibers. Breaks in the hair and alopecia occur
2% chlorhexidine), and the area packed with antiseptic- because of breakdown of the hair shaft. The close shear-
saturated gauze.11 Bulgin12 has described a treatment ing and washing practices used on show lambs leave them
technique using a 60-ml syringe filled with 10 to 25 ml of susceptible. Crust formation occurs because of the accu-
 Chapter 8 Diseases of the Integumentary System • 209

BOX 8-1 Treatment. Treatment can help limit spread of the

disease to other herd members. Topical iodine com-
AG C ENERIC ASEOUS L YMPHADENITIS
pounds (2% to 5%), chlorhexidine (2%), lime sulfur (2%
to 5%), and topical antifungal medications (3% captan)
C PONTROL ROGRAM are useful for local treatment of lesions. Administration of
systemic drugs such as griseofulvin produces variable
results. Persons providing treatment should wear gloves
because these diseases have zoonotic potential.

Prevention. Dermatophytosis is spread by clippers,

blankets, and other equipment. Therefore proper cleaning
of equipment after use with antiseptic solutions helps
control the spread of this disease.

Mycetoma
Mycetomas may be formed by fungal or bacterial ele-
ments or a combination of both.4 Lesions most often
occur on the limbs and may be initiated by a wound.
These lesions cause focal swelling and have an exudate
that contains granules composed of microbial organisms
coated with host immune elements (e.g., immunoglobu-
lins, fibrin).1 These granules may be red, yellow, or
purple. Actinomadura madurae and A. pelletierii have been
found in goats with mycetoma, as has Nocardia brasilien-
sis. Although success rates are unknown, treatment
strategies include the use of antimicrobial drugs, surgical
excision, and limb amputation depending on the severity
of the disease.

Candidiasis
Adapted from Gessert ME: Proceedings of the 1998 Symposium on
Small Ruminants for the Mixed Animal Practitioner Western Veterinary Yeast or Candida dermatitis has been diagnosed in
Conference, 1998, Las Vegas, NV. goats.1,4 Candida albicans, C. tropicalis, C. pseudotropicalis,
C. stellatoidea, C. parapsilosis, C. krusei, C. parakrusei, C.
stellatoidea, C. guilliermondii, and other yeasts may be iso-
lated from lesions. If yeast dermatitis is diagnosed, a com-
mulation of fungal hyphae and epithelial debris on the promised immune system or malnutrition must be sus-
skin surface. pected. Chronic moist conditions resulting in maceration
of the skin allow the yeast to become established.
Clinical signs. Some pruritus may be seen with infec-
tion with Trichophyton species. Typical circular lesions Clinical signs. Clinical signs include alopecia, scales,
may be seen on the face, and involvement of the ears and crusts, a greasy layer to the skin, and lichenification of
neck is common. Young stock are most severely affected, the skin.
and mild pruritus may be observed when significant
scaling or crusting is present. Diagnosis. Diagnosis is made by observation of bud-
ding yeasts and pseudohyphae on skin cytology.
Diagnosis. Use of the Wood’s lamp during clinical ex-
amination may help with differential diagnosis. However,
Trichophyton species do not fluoresce. Diagnosis is con-
Others
firmed by culture of skin and hair samples on Sabouraud’s Several other fungi have been isolated from chronic der-
dextrose agar. A 20% potassium hydroxide solution can matopathy in goats. Peyronella glomerata is associated with
be used to prepare wet mounts of arthrospores on the hair hyperkeratotic lesions of the ears of goats in the United
shafts for microscopic examination. The course of disease Kingdom.1 Aspergillus species can cause clinical disease in
is 4 to 5 weeks in animals with competent immune animals with compromised immune systems. These fungi
systems. also may cause granulomatous lesions in the skin.
210 • Sheep and Goat Medicine
R EFERENCES
1. Scott DW, Smith MC, Manning TO: Caprine dermatology. Part
TABLE 8-5

I. Normal skin and bacterial and fungal disorders, Comp Cont Ed REPORTED THERAPEUTIC STRATEGIES FOR
Pract Vet 6:S190, 1984. TREATMENT OF EXTERNAL PARASITES
2. Lofstedt J: Dermatologic diseases of sheep, Vet Clin North Am
Large Anim Pract 5:427, 1983. DRUG TREATMENT PARASITE EFFICACY
3. Kimberling CV: Diseases of the skin. In Kimberling CV, editor:
Jensen and Swift’s diseases of sheep, ed 3, Philadelphia, 1988, Lea & Amitraz 250 ppm dip Mites
Febiger. Chlorpyrifos 0.05% to 0.25% Keds, lice, mites
4. Smith MC: Dermatologic diseases of goats, Vet Clin North Am spray
Large Anim Pract 5:449, 1983. Coumaphos 0.05% to 0.3% Keds, lice, mites
5. Mullowney PC: Skin diseases of sheep, Vet Clin North Am Large spray or dip
Anim Pract 6(1):131, 1984.
0.5% to 1% dust
6. Smith MC, Sherman DM: Skin. In Smith MC, Sherman DM,
Lime-sulfur 2% to 5% dip Keds, lice, mites
editors: Goat medicine, Baltimore, 1994, Williams & Wilkins.
7. Mullowney PC, Baldwin EW: Skin diseases of goats, Vet Clin
Lindane 0.03% to 0.05% Keds, lice, mites,
North Am Large Anim Pract 6(1):143, 1984. spray ticks
8. Fubini SL, Campbell SG: External lumps on sheep and goats, Vet Trichlorfon 0.2% spray or dip Keds, lice, mites
Clin North Am Large Anim Pract 5:457, 1983. Methoxychlor 0.5% spray or dip Keds, lice, mites,
9. Pugh DG: Caseous lymphadenitis in small ruminants, Proc North 5% dust ticks
Am Vet Conf 11:983, 1997.
10. Lloyd S: Caseous lymphadenitis in sheep. In Melling M,
Adler M, editors: Sheep and goat practice, ed 2, London, 1998, WB
pedalis may survive in the environment away from the
Saunders.
11. East NE: Common infectious conditions, Proceedings of the 1998
host for at least 2 weeks.
Symposium on Small Ruminants for the Mixed Animal Practitioner
Western Veterinary Conference, 1998, Las Vegas, NV. Clinical signs. The clinical signs associated with lice
12. Bulgin MS: Central nervous disorders of sheep, Proceedings of the infestation include intense pruritus, wool loss, weight
1998 Symposium on Small Ruminants for the Mixed Animal Practi- loss, and anemia, if infestation is severe. Lameness may be
tioner Western Veterinary Conference, 1998, Las Vegas, NV. observed with infestation.

Treatment. Therapy is centered on the animal because

PARASITIC DISEASES the life cycles of lice depend on the host. Keepers and vet-
Parasitic diseases are presented here with respect to their erinarians must exercise caution in treating meat- and
importance in causing lesions in the skin and hair. A milk-producing animals to avoid volatile residues. Treat-
summary of common treatments for ectoparasites is pro- ment of the environment is usually impractical. Treat-
vided in Table 8-5. ment may include dips, sprays, or dusts of coumaphos
(0.125% as spray or 0.5% as dust), malathion (0.5% as
spray or 4% as dust), or permethrin. Injections of aver-
Lice (Pediculosis)
mectin anthelmintics (ivermectin or doramectin; 0.2
Lice infestation is most common during winter months, mg/kg body weight) are useful in treating sucking lice but
presumably because temperatures, crowding, and feeding have limited efficacy against biting lice. Treatments
management practices are optimal for spread and prolif- should be repeated at 2-week intervals for at least two
eration of these pests.1-6 Infestations are more severe in treatments to ensure that lice emerging from eggs are
debilitated animals such as those suffering malnutrition killed. Oral administration of these drugs is of very
and intestinal parasitism. Lice can be divided into two limited value. If used topically, cypermethrin can pene-
forms: biting and sucking. The body louse, Damalinia trate sheep skin at a rate of approximately 11 cm per
ovis, is the biting louse of sheep, and D. caprae is the hour.7 The drug penetrates to the stratum compactum
biting louse of goats. D. crassiceps and D. limbata also have and then spreads laterally with some penetration of the
been found to infest Angora goats and can cause signifi- dermis. The effect of deltamethrin on sheep skin has been
cant damage to the fleece. Linognathus ovillus (sucking evaluated.8 This drug was found to cause irritation,
face lice) and L. pedalis (sucking foot louse) are the edema, disruption of the lipid layer, and some degenera-
sucking lice of sheep. Linognathus stenopis is the sucking tive changes in the epidermis. This reaction was deter-
louse of goats. L. ovillus infests the wool around the face, mined to be caused by the solvent mixture of the formu-
and L. pedalis infests the tissues distal to the carpus or lation. A formulation of deltamethrin was found to
tarsus. Lice may be transmitted by direct contact or by spread from the back to the lower body within 24 hours,
contact with contaminated areas of the environment. L. but peak concentrations in the wool did not occur for 4
 Chapter 8 Diseases of the Integumentary System • 211

to 5 days with a xylene-based formulation and 11 days days old. In sheep these mites infest heavily wooled areas
with a water-based formulation.9 A concentration of and cause papules, crusting, and matting of wool. These
deltamethrin in the skin sufficient to kill lice was present mites may be observed on the skin surface with a magni-
for approximately 12 days, but remained high in the tips fying lens. Local administration of louse medications is
of wool fibers. However, insecticide in the fleece was in- curative.
sufficient to kill lice after 14 days, suggesting that inacti-
vation occurred in vivo. Topical drugs should be carefully
evaluated before they are applied to small ruminants.
Sarcoptic Mange
S. scabiei is rare in sheep and goats and is not known to be
present in the United States.1-6,10 Scabies is a reportable
Melophagus ovinus (Sheep Ked) disease in the United States and is zoonotic. This mite
The sheep ked spends its entire 6-week life cycle on the prefers to infest the skin around the eyes and ears and
host; therefore transmission is by direct contact with in- causes intense pruritus. The mites are round in head and
fested animals. These blood-sucking insects cause skin ir- body and have long, nonjointed stalks for the first pair of
ritation and pruritus, stain the wool, and may cause dis- legs. These mites burrow through the epidermis, and the
comfort. Although they may occur year-round, most of female lays eggs in these tunnels. The life cycle of Sar-
their damage occurs during the winter. coptes ranges from 10 to 17 days. The mites are most com-
monly transmitted by direct contact but can survive in the
Treatment. Treatment is similar to that for lice and environment for variable periods. Excoriations, alopecia,
should be repeated at 14- to 21-day intervals. and crusting occur on the face and non-wooled areas but
do not spread to the bodies of the affected sheep. Chronic
infection causes hyperpigmentation and lichenification of
Mange Mites the skin, and affected sheep and goats suffer weight loss
Mange occurs rarely in sheep but more commonly in and ill thrift because of the discomfort. In goats, sarcoptic
goats. 1-6,10 Mange mites known to infest sheep include mange may affect the entire body, causing alopecia, crust-
Psoroptes communis var ovis, Sarcoptes scabiei ovis, Psor- ing, pruritus, and subsequent weight loss. Regional lymph
ergates ovis, Chorioptes bovis var ovis, and Demodex ovis. nodes may become enlarged because of the severity of
Mange has been essentially eradicated from sheep in the skin damage. Diagnosis requires deep skin scraping of the
United States, with the exception of demodectic mange. periphery of active lesions, but mites are difficult to find
In goats, clinically important forms of mange include sar- and diagnosis is often based on clinical signs and response
coptic mange, demodectic mange (D. caprae), psoroptic to therapy. Numerous scrapings may be required to find
mange (P. cuniculi), and chorioptic mange. these mites. An alternative to direct examination is to mix
skin scrapings and crusts with sodium nitrate solution, a
Treatment. Treatment for mange is most easily per- technique similar to fecal floatation. Treatment consists
formed after shearing. Various products have been used of ivermectin anthelmintic administration and dips such
with variable success, including coumaphos (0.3% dip), as 1% lime sulfur. Dips may be required weekly for 4 to 12
toxaphene (0.5% dip), lime sulfur (2% dip), and phosmet weeks before the condition resolves completely. Sponta-
(0.15% to 0.25% dip) (see Table 8-5). neous resolution of sarcoptic mange can occur in goats.

Psoroptic Mange (Psoroptes cuniculi, Psorergates ovis (Sheep Itch Mite)

Common Sheep Scab) The smallest of the sheep mange mites, Psorergates ovis,
Psoroptic mange is a reportable disease in the United has a rounded body with indentations between the at-
States.1-5,10 These mites have elongated heads, are oval in tachments of the legs.1-6,10 This mite has a 4- to 5-week
shape, and their first pair of legs are jointed. These mites life cycle and lives in the epidermis. Alopecia, crusts, and
are transmitted by direct contact, are host-specific (no scales are primarily distributed along the trunk (withers
zoonoses), have a 2-week life cycle, and can live off the and sides) of the body. Infested sheep demonstrate severe
host for as long as 3 weeks. In sheep, clinical disease is pruritus, including biting at affected regions. These mites
most severe in the fall and winter. The saliva of the mite may be observed on the skin surface with a magni-
causes an intense inflammatory reaction in the skin, with fying lens.
severe pruritus resulting in self-trauma and alopecia.
These lesions are primarily distributed along the trunk.
In goats, P. cuniculi usually infests the ears and may cause
Chorioptic Mange
alopecia, pruritus localized to the ears, and head shaking. The Chorioptes mite (Chorioptes ovis, C. caprae) has an oval
Infestation of the ears may be seen in goats as young as 10 body shape; the first pair of legs are short, unsegmented,
212 • Sheep and Goat Medicine
These nodules exude a thick exudate. Cytology of this
exudate reveals the presence of large numbers of cigar-
shaped mites. These mites are readily spread among kids
and may remain unnoticed for many months. Spread
among adults is not common, therefore isolation of af-
fected animals from kids is prudent but not necessary
from adult herd members. Severe infestation suggests a
compromised immune system. Therefore clinicians and
keepers should pay close attention to the nutrition
program and general health of affected goats. Treatment
may include weekly dipping with 0.5% malathion, 0.2%
trichlorfon, or 0.5% amitraz.

Fly Strike
Fly strike has been known to effect the skin of sheep.
Screw-worm (Cochliomyia hominivorax) has been eradi-
cated from the United States but continued surveillance
for larvae of this fly is prudent. These larvae are 1 to 2 cm
long, pink, and tapered. The adult fly is blue-green, with
an orange head and three dark longitudinal stripes on the
body. Cutaneous myiasis (black blowfly, Phormia regina)
occurs in sheep in the United States and is most common
among breeds that have excessive skin folds such as
Merino sheep. In Australia the sheep blowfly, Lucilia
cuprina, is the major ectoparasite of sheep, causing severe
Figure 8-4 Chorioptic mange in a ewe that was associated with damage from myiasis and death from secondary infec-
pruritus. Chorioptic mange mites cause wrinkling of the skin and
pustules in the interdigital spaces, legs, scrotum, and brisket. tions.11-13 However, a variety of fly larvae can infest
wounds that have necrotic tissue present. Skin lesions
cause staining of wool and alopecia.

and have suckers attached to the ends.1-6,10 Chorioptes is

host-specific (no zoonoses), has a 2- to 3-week life cycle,
Elaeophorosis (Sorehead)
and can only live off the host for a few days. These mites Elaeophora schneideri is a filarial nematode that can cause
and their associated lesions are limited to the scrotum and dermatopathy. The filaria cause thrombosis of capillary
distal rear limbs of sheep and the lower limbs, abdomen, beds and terminal arteries. Tissue ischemia resulting
and hindquarters of goats (Figure 8-4). Lesions include from vascular injury causes severe lesions that appear
alopecia, erythema, excoriation, crusts, and pruritus. In- similar to those of photosensitization and ulcerative der-
fested sheep may be restless, stomp, and chew at their feet matitis (Figure 8-5). Horse flies (Hybomitra, Tabanus)
because of discomfort. Scrotal infestation may cause der- are intermediate hosts that transmit infective larvae
matitis and temporary infertility in rams. These mites from one host to another. Infective larvae migrate and
may be observed on the skin surface with a magnifying develop to young adults in the leptomeningeal arteries.
lens. Lime sulfur dips are usually curative. If thrombosis occurs at this level, circling, opisthotonos,
convulsions, and other neurologic signs or sudden death
may occur. Alternatively, the young adults may migrate
Demodectic Mange
to the common carotid and maxillary arteries and
Demodectic mange (D. ovis, D. caprae) affects the face, develop into mature adults. These adults produce micro-
limbs, and back.1-6,10 D. ovis mites infest hair follicles, filaria that embolize the capillary beds of the face and
causing severe folliculitis often complicated by secondary may cause ischemia or an allergic reaction. Lesions pri-
pyoderma (evidenced by the presence of pustules or marily occur on the face but may develop on other areas
abscesses). Diagnosis requires deep skin scraping and of the body. They are focal and consistent with vascular
should include follicles bordering active lesions. D. compromise and may require months or years to heal
caprae infestation may be the most common mange of completely. Elaeophorosis should be included in the dif-
goats. Disease is characterized by 2- to 12-mm diameter ferential diagnosis of any unilateral lesions of the head.
nodules in the skin along the neck, shoulders, and trunk. Skin biopsy may reveal the microfilaria either by histo-
 Chapter 8 Diseases of the Integumentary System • 213

keeper or clinician notes as excoriations or nonhealing

ulcers.

R EFERENCES
1. Smith MC, Sherman DM: Skin. In Smith MC, Sherman DM,
editors: Goat medicine, Baltimore, 1994, Williams & Wilkins.
2. Lofstedt J: Dermatologic diseases of sheep, Vet Clin North Am
Large Anim Pract 5:427, 1983.
3. Mullowney PC: Skin diseases of sheep, Vet Clin North Am Large
Anim Pract 6(1):131, 1984.
4. Mullowney PC, Baldwin EW: Skin diseases of goats, Vet Clin
North Am Large Anim Pract 6(1):143, 1984.
5. Smith MC: Dermatologic diseases of goats, Vet Clin North Am
Large Anim Pract 5:449, 1983.
6. Manning TO, Scott DW, Smith MC: Caprine dermatology. Part
III. Parasitic, allergic, hormonal, and neoplastic disorders, Comp
Cont Ed Pract Vet 7:S437, 1985.
7. Jenkinson DM, Hutchinson G, McQueen DJL: Route of passage
of cypermethrin across the surface of sheep skin, Res Vet Sci
41:237, 1986.
8. Britt AG et al: Effects of pour-on insecticidal formulation on
sheep skin, Aust Vet J 61:329, 1984.
9. Johnson PW et al: Kinetic disposition of xylene-based or aqueous
formulations of deltamethrin applied to the dorsal midline of
sheep and their effect on lice, Int J Parasitol 25:471, 1995.
Figure 8-5 Suppurative dermatosis with lesion distribution typical 10. Fadok VA: Parasitic skin diseases of large animals, Vet Clin North
of elaeophoriasis. Filarial showers result in thrombosis of the capillary Am Large Anim Pract 6(1):3, 1984.
beds of the face. (Courtesy Dr. Mike Pope, Paris, Kentucky.) 11. Colditz IG, Eisemann CH: The effect of immune and inflamma-
tory mediators on growth of Lucilia cuprina larvae in vitro, Int J
Parasitol 24:401, 1994.
12. Sandeman RM et al: Hypersensitivity responses and repeated in-
logic examination or by tissue maceration and harvest of fections with Lucilia cuprina, the sheep blowfly, Int J Parsitol
larvae. Avermectin drugs (ivermectin 200 g/kg SC) 22:1175, 1992.
can kill the microfilaria, but repeated doses may be re- 13. Young AR, Meeusen EN, Bowles VM: Characterization of ES
products involved in wound initiation by Lucilia cuprina larvae, Int
quired. Adult nematodes can be killed by the adminis-
J Parasitol 26:245, 1996.
tration of piperazine salts (50 mg/kg by mouth [PO]) or
ivermectin.
AUTOIMMUNE DISEASES
Onchocerca Species Infestation
Onchocerca species can parasitize sheep and goats. Adult
Pemphigus Foliaceus
Onchocerca species can live in the connective tissues of Pemphigus foliaceus is a rarely diagnosed autoimmune
sheep and goats, where they induce nodules. Adults skin disease of goats characterized by widespread crusty,
produce microfilariae that migrate into the dermis of the pruritic lesions.1 It has been classified as a type II hyper-
ventral abdomen and thorax. Alopecia, erythema, and sensitivity reaction. Lesions are often first noted over the
thickening of the skin develop because of the host’s face or limbs but may be found on the abdomen, per-
response to dying larvae. ineum, and scrotum as well (Figure 8-6). The proposed
Other nematodes diagnosed in cases of focal dermati- mechanism is the development of autoantibodies directed
tis include Pelodera strongyloides, Strongyloides papillosus, against the skin, specifically the glycocalyx of kera-
and Parelaphostrongylus tenuis. These nematodes have tinocytes. Loss of intercellular cohesiveness results in
been associated with dermatitis, but their clinical signifi- blister formation and acantholysis.
cance is minimal. Strongyloidiasis is seen on dependent
regions of the body; the localized dermatitis is caused by Diagnosis. A diagnosis of pemphigus foliaceus may be
an immune reaction to migrating larvae. P. tenuis infesta- made from skin biopsy specimens obtained from charac-
tion of the central nervous system may cause focal regions teristic skin lesions. Numerous biopsies should be taken
of hyperesthesia. This may lead to self-trauma that the from suspect goats to improve the accuracy of the diagno-
214 • Sheep and Goat Medicine
Copper Deficiency
Copper deficiency or molybdenosis decreases wool quality
and color. Wool quality suffers because of decreased crimp
and a limp and steely texture. Dark wool loses color inten-
sity until it is gray-white in color. This disease can result
from absolute copper deficiency (pasture grass with less
than 3 ppm dry matter copper) or excessive molybdenum
(pasture grass with more than 10 ppm dry matter molyb-
denum), sulfur, or iron in the diet. Diagnosis can be made
by assessing copper concentrations in the blood or liver.
Copper deficiency is diagnosed if the blood copper con-
centration is less than 0.7 mg/dl or the liver concentration
is less than 80 mg/kg dry weight (see Chapter 2).

Iodine Deficiency
Figure 8-6 Pemphigus foliaceus in a pygmy goat. This
autoimmune disease results in vesicles, pustules, and crusts over the Iodine deficiency (goiter) of newborn lambs manifests as
body. Immunofluorescence of biopsied skin is a good diagnostic tool. alopecia, thick scaly skin, weakness, and enlarged thyroid
glands.2 Neonatal death, poor reproductive performance,
and abortion may be seen in the flock or herd. Familial
sis. The presence of acantholytic keratinocytes within goiter occurs in Merino sheep, Dutch goats, and Nubian
vesicles is a diagnostic feature of pemphigus. Because and Angora goats, among others. Iodine deficiency causes
acantholysis can be seen in other dermatologic condi- kids to be born hairless or with fine hair. The kids may be
tions, biopsies should be evaluated by a veterinary pathol- weak or stillborn and have goiters. Goiter also may be
ogist with expertise in dermatopathies. caused by congenital defects or ingestion of goitrogens in
the diet. Dietary iodine deficiency is most common in
Treatment. Treatment of pemphigus is aimed at di- geographic regions with sandy soil and heavy rainfall. In-
minishing the body’s immune response. Prednisolone (1 gestion of large amounts of calcium, cyanogenic glyco-
mg/kg every 24 hours for 7 days) in conjunction with au- sides, and cruciferous plants also may induce iodine defi-
rothioglucose (1 mg/kg IM every 24 hours for 7 days) has ciency. Diagnosis of iodine deficiency can be made by
been reported effective in controlling symptoms, followed identifying protein-bound iodine in serum (normal serum
by 1 mg/kg of prednisolone every 48 hours. protein-bound iodine for adult ewes is 2.4 to 4 g/dl
serum). In herds known to be at risk for iodine deficiency,
potassium iodide (250 mg) may be administered at 60 and
NUTRITIONAL DISEASES again at 30 days before lambing (see Chapters 2 and 7).
Nutritional deficiencies and excesses are beyond the scope Providing a good-quality iodine-containing trace mineral
of this chapter and are discussed in other chapters (see supplement and removing pregnant animals from pas-
Chapter 2). However, changes specific to the skin or hair tures containing goitrogenous plants decreases the
are briefly discussed in the following paragraphs. occurrence of goiter.

Fescue Toxicity Zinc Deficiency

Fescue toxicosis is caused by ingestion of tall fescue grass Zinc deficiency is associated with parakeratosis and may
(Festuca arundinacea) contaminated with an endophyte cause reduced growth rate, wrinkled skin, swollen hocks,
(Acremonium [Neotyphodium] coenophialum). During and salivation in sheep. Parakeratosis is most pronounced
winter months the toxins may cause a peripheral vasocon- on the face, feet, and scrotum of affected animals. Rams
striction leading to a gangrenous necrosis of the distal fed a zinc-deficient diet develop abnormal testicles and
limbs and tail. Of the 35 to 40 million pasture acres in the experience impaired spermatogenesis. In goats the most
United States, approximately 80% is infected. About 8 prominent clinical signs include rough hair coat; hair loss
million acres of fescue grass are not infected with the en- on the head, limbs, and scrotum; overgrowth of the dental
dophytic fungus and therefore do not contain the ergova- pad; small testicles; and fissures of the feet. The predomi-
line toxin. Sheep and goats appear to be less sensitive to nant histologic lesions are hyperkeratosis and parakerato-
the toxin than cows. Feeding noninfested fescue and di- sis.3 Increased calcium and phosphorus intake decreases
luting fescue by planting other species of grasses both zinc absorption. Some goats may have a genetic predispo-
help reduce the incidence of this condition. sition to depressed zinc absorption. This is magnified in
 Chapter 8 Diseases of the Integumentary System • 215

the face of high calcium (and other mineral) intake.4

Diets rich in legumes (high calcium) or “homemade”
high-phosphorus grain supplements (corn-soybean, corn-
oats-barley) with no added minerals all predispose to zinc
deficiency. A biopsy of the affected area indicating parak-
eratosis coupled with properly collected serum zinc con-
centrations of less than 0.8 ppm is diagnostic.3 Blood
drawn for zinc analysis should be collected in a special
tube that does not have a butyl rubber stopper. Animals
benefit from supplementation of a good-quality trace
mineral salt offered free choice. Adding zinc to the feed or
administering zinc sulfate (1 g/day PO) is usually effec-
tive.3 If calcium makes up 1.5% of the diet, the zinc
sulfate may not be effective and chelated zinc should be
administered or added to a premixed salt supplement. Re-
sponse to zinc supplementation should be rapid (within Figure 8-7 Phenothiazine photosensitization in a goat.
Photosensitization is associated with edema, erythema, and pruritus.
14 days) (see Chapter 2). Removing legumes and cereal Lesions occur on unpigmented regions (e.g., back, ears, face). The
grains from the diet and feeding grass hay and commer- primary form of the disease results from ingestion of a photodynamic
cially prepared concentrate feeds (with added zinc) is chemical (in this case phenothiazine).
usually preventative.

caused by the ingestion of plants containing pyrrolizidine

Vitamin A Deficiency
alkaloids or carbon tetrachloride, Pithomyces chartarum–
Vitamin A deficiency may cause hair loss and night infected grasses, or blue-green algae (Anacystis cyanea).
blindness, overgrown hooves, and corneal ulceration in
adult goats.2 Deficiency is rare if animals have access to Clinical signs and diagnosis. Clinical signs of photo-
green forage. If dry, brown forage is fed, inclusion of sensitization include head shaking, restlessness, ery-
vitamin A in a supplement (mineral mixture) or use of a thema, and edema of eyelids, muzzle, ears, and tail. Skin
commercial injectable product helps prevent deficiency lesions characteristically affect exposed, nonpigmented
disease. regions of the skin. Yellow serum may seep through the
skin within 2 days and pruritus causes self-trauma. The
transudate accumulates as a crust and superficial skin
Photosensitization
sloughing occurs. Secondary bacterial infection is
Photosensitization is segregated into primary and sec- common. Necropsy reveals subcutaneous edema and
ondary causes based on the pathophysiology of disease sloughing tissue. In cases of secondary photosensitiza-
(Table 8-6). Photosensitization refers to conditions under tion, liver disease may be obvious.
which photodynamic chemicals accumulate in the skin
and become stimulated by sunlight on exposed and un- Treatment. Treatment for photosensitization is symp-
pigmented areas of the skin.2,5-7 These substances tomatic and includes the provision of shade, control of
damage the capillary beds and result in skin necrosis and secondary infections, treatment of primary disease if liver
sloughing. Primary photosensitization refers to ingested damage is present, removal of animals from high-risk
photodynamic substances that do not require alteration in forage, allowance of grazing at night only, maintenance of
the body to cause disease (Figure 8-7) (see Table 8-6). hydration and access to electrolytes, and administration
Primary photosensitization may occur after ingestion of of nonsteroidal antiinflammatory drugs (NSAIDs) and
St. John’s wort, which contains hypericin; aphids contain- antibiotics in severe cases. Photosensitization can be pre-
ing an unknown photodynamic agent; or lush forage with vented by good pasture management and provision of ad-
accumulated phylloerythrin. This condition is most equate shade.
common in late summer and early autumn during periods
of rapid pasture growth. Ingestion of alfalfa and other
plants, including clover, lucerne, vetch, and oats, has been
MYCOTOXINS
associated with photosensitization. The mechanism of
pathology is not well understood. Secondary photosensi-
Pithomycotoxicosis
tization occurs when liver damage results in the accumu- Pithomycotoxicosis (facial eczema) occurs in sheep and
lation of photodynamic substances such as phylloerythrin cattle of all ages in Australia, New Zealand, and South
in the bloodstream (Table 8-6). Liver damage may be Africa. Pithomyces chartarum is a fungus that produces the
216 • Sheep and Goat Medicine
TABLE 8-6

CAUSES OF PHOTOSENSITIZATION IN SHEEP AND GOATS

SOURCE TOXIN SPECIES AFFECTED

PRIMARY PHOTOSENSITIZATION
Plants
St. John’s wort Hypericin Any ruminant
Buckwheat Fagopyrin, photofagopyrin Any ruminant
Bishop’s weed Furocoumarins Any ruminant
Dutchman’s breeches Furocoumarins Any ruminant
Wild carrot Furocoumarins Any ruminant
Perennial ryegrass Perloline Any ruminant
Burr trefoil Aphids Any ruminant
Toxins
Phenothiazine Phenothiazine alkaloids Any ruminant
Thiazides Any ruminant
Methylene blue Any ruminant
Sulfonamides Any ruminant
Tetracyclines Any ruminant

HEPATOGENOUS PHOTOSENSITIZATION
Plants
Rape, kale Any ruminant
Kleingrass Sheep
Caltrops Saponins Sheep
Lantana Triterpene Any ruminant
Ragworts, heliotrope Pyrrolizidine alkaloids Any ruminant
Mycotoxins
Pithomyces chartarum (pasture grass, especially ryegrass) Sporidesmin Sheep, cattle
Anacystis (blue-green algae) Alkaloid Any ruminant
Periconia (Bermuda grass) Any ruminant
Phomopsis leptostromiformis (lupin) Acid-phenolic compounds Any ruminant
Chemicals
Copper Any ruminant
Phosphorus Any ruminant
Carbon tetrachloride Any ruminant
Phenanthridium Any ruminant
Bacterial hepatitis
Viral hepatitis
Parasitic hepatitis
Hepatic neoplasia
Adapted from Scott DW: Large animal dermatology, Philadelphia, 1988, WB Saunders.

mycotoxin sporidesmin; it is most often found in rye- the feet, and lethargy. Edema of the eyelids and ears may
grass. Sporidesmin is a hepatotoxin that causes he- be noted. Exudate accumulates on the skin, which then
patogenous photosensitization and phylloerythrin accu- begins to slough. Sheep may suffer secondary infections
mulation in the bloodstream. Morbidity is highest in and die in 2 weeks to 2 months.
summer and fall, especially when rains follow a period of
drought. Treatment. Feeding zinc sulfate (0.5 to 2 g/head/day)
is protective for sheep grazing infected pastures. Apply-
Clinical signs. Clinical signs of pithomycotoxicosis ing thiabendazole (1 kg per acre) to the pasture has been
include conjunctivitis, keratitis, restlessness, stomping of reported to control the fungus.
 Chapter 8 Diseases of the Integumentary System • 217

Stachybotryotoxicosis celerate this process because hydration of the skin

Stachybotryotoxicosis (poisoning by fungi of the genus weakens its resistance elasticity.
Stachybotrys) has been reported in sheep. This fungal my-
cotoxin causes cutaneous necrosis, ulceration, petechiae,
and ulceronecrotic areas, most pronounced in the muco-
Foreign Bodies
cutaneous junctions. The toxin is a macrocyclic tricho- Foreign bodies can become lodged in the skin by injury or
thecene that also causes bone marrow suppression, neu- surgery. In a study of skin reaction to suture materials in
tropenia, and thrombocytopenia. Borno white goats, researchers found that a prolonged in-
flammatory phase was associated with nylon and silk but
ENVIRONMENTAL not cotton or stainless steel suture material.8 Stainless
steel and nylon sutures produced a moderate amount of
PATHOLOGIES granulation tissue reaction, cotton suture produced a
marked granulation response, and silk produced the
Intertrigo smallest amount of granulation. Wounds sutured with
Intertrigo occurs in areas of skin-to-skin contact; exces- cotton or stainless steel healed faster than those sutured
sive motion results in moist dermatitis and inflammation with nylon or silk.
because of friction. This most commonly occurs in rumi-
nants between the udder and the inner aspect of the
thigh. Treatment includes cleansing the region and ap-
Subcutaneous Emphysema
plying an astringent ointment with the goal of drying the Penetrating wounds or full-thickness lacerations that act
lesion. The disease is self-limiting in most animals, but as one-way valves can result in subcutaneous emphysema.
pain may cause apparent lameness; moreover, the area In these cases air is allowed to enter but not freely exit
may have a foul odor and secondary infection may in- from the subcutaneous tissues (bellows effect). Subcuta-
crease the risk of mastitis. neous emphysema also occurs in sheep and goats with
pneumonia, especially after parturition. The weakened
lung parenchyma may rupture into the mediastinum if
Callus excessive intrathoracic pressure is applied against a closed
A callus is formed on areas of the skin that receive glottis (as occurs during parturition). The air dissects
chronic mild to moderate abrasion from objects in the en- along tissue planes and exits through the thoracic inlet to
vironment. The most common location in sheep and the subcutaneous spaces.
goats is the dorsal aspect of the carpi and the sternum.
Other locations include the cranial aspect of the stifle and Clinical signs. Subcutaneous emphysema typically is
the caudal aspect of the elbow. These lesions are normal noted along the neck, dorsal to the shoulder; it may
unless they have associated exudate, swelling, or pain. dissect along the back. The condition also may occur with
clostridial infections. Often affected animals are found
dead and subcutaneous emphysema is discovered during
Hematoma necropsy. However, emphysema may be noted on physical
Blunt trauma can result in the formation of a hematoma. examination early in the infectious process. Clostridial
Hematomas may develop in exposed highly vascular disease should be considered in the differential diagnosis
tissues such as the ears or on the main body. Causes of if the animal exhibits severe systemic disease in the
trauma include injury from horned breeding males, fight- presence of subcutaneous emphysema.
ing injury, attack by dogs or other predators, equipment-
related injury, and entanglement with fences or other
objects. Spontaneous bleeding under the skin is rare but
Burns
may occur if ingestion of toxins causes coagulopathy. Skin burns are most commonly found on animals that
have been trapped in building fires. Pour-on products
containing alcohol are flammable but usually do not
Cutaneous Ulceration ignite the hair coat and do not continue to burn after the
Pressure sores (or cutaneous ulcerations) form when bony fluid volume is consumed. Burns may be classified by
prominences are in prolonged contact with hard surfaces. severity and extent of the body surface area involved. Se-
They most commonly occur when sheep or goats rest in quelae of burn injuries include secondary infection, espe-
lateral recumbency because of musculoskeletal or neuro- cially with Pseudomonas, and hypoproteinemia from
logic disease. Pressure sores form because of prolonged protein exudation from the wounds. Severe or extensive
ischemia and cellular injury (pressure necrosis). They can burns are more likely to result in fatal infection or protein
therefore be prevented or controlled by frequent move- losses. Smoke inhalation and thermal damage to the
ment of the animal. Contact with moist surfaces can ac- lungs also can cause death. The clinician should perform
218 • Sheep and Goat Medicine
a thorough evaluation of the thorax after the initial injury monly involved. Death from low body core temperature
and follow up later because the onset of clinical disease ensues if treatment is not initiated before vital organs are
may be delayed. Burns in sheep and goats are likely to compromised. Frostbite may occur at a variety of temper-
occur as a result of inappropriate heat lamp placement in atures depending on environmental conditions (sunlight,
maternity pens. Lambs and kids stand under the lamps moisture, wind). The crucial temperature threshold for
for warmth and may burn the dorsum as a result. Pour-on milk-fed neonates has been suggested to be 13° C (55°
products or irritants such as creosote and strong iodine F).7 Injury is caused by vasoconstriction, subsequent arte-
can cause chemical burns on areas of skin contact. rial thrombosis, and ischemic necrosis. After sloughing,
damaged ears tend to be rounded with alopecic tips.3 If
Clinical signs. Depending on its severity a burn may the surface of the skin is wet, ice crystals can form, accel-
produce only superficial scabbing or it may result in erating the process. Frostbite injuries occur in four
serum exudation and suppuration with deeper skin layer phases.10,11 Phase one (pre-freeze) is characterized by ar-
involvement. Because wool is fire-retardant, the most teriolar constriction, venous dilatation, congestion, and
severe burns on sheep exposed to barn or grass fires are serum transudation. Phase two (freeze-thaw) begins with
likely to be found around the head and limbs, whereas extracellular ice crystal formation. Phase three (vascular
goats are likely to have severe burns over their entire stasis) is denoted by more severe and persistent venous
bodies. dilatation and arterial spasm, which causes arteriovenous
shunting and tissue hypoxia. Phase four (ischemia) is
Treatment. Evaluation of the patient’s overall condi- denoted by nervous tissue damage caused by prolonged
tion is essential in a fire because smoke inhalation and local hypoxia.
thermal damage to the respiratory tract may cause death.
Treatment is aimed at preventing or controlling second- Treatment. The therapy for frostbite may result in
ary infection. Pain management and administration of reperfusion injury. Nevertheless, it should be instituted
plasma (if needed to address hypoproteinemia caused by immediately and continued for at least the first few days
excessive serum exudation from the wounds) are common after injury. Warming in water of 104° to 106° F is recom-
therapeutic elements. mended, as is the use of antibiotics and antiinflammatory
drugs as needed to control tissue damage. Necrotic tissue
should be débrided as needed to facilitate healing and
Sunburn limit secondary bacterial infection.
Sunburn in animals, as in human beings, is caused by skin
damage from ultraviolet light. Sunburn is different from Prevention. An easily accessible shelter should be pro-
photosensitization.3,4 It is more commonly seen in white- vided. For each degree drop in ambient temperature
faced sheep (especially on the face and ears), particularly below 0° C, the keeper should offer a 0.5% to 1% increase
those that have been recently shorn, and light-colored in feed. Feeding ewes and does in barns keeps them and
goats (especially on the udders, ears, and nose).3 Pro- their lambs and kids out of the cold weather and in a
longed sun exposure is associated with tumors (e.g., squa- warmer condition.
mous cell carcinoma).

Clinical signs. Clinical signs of sunburn include ery-

Wool Slip and Wool Break
thema, swelling, crusting of skin, head shaking, and pru- Goats naturally shed their coats in spring. Sheep,
ritus. If the udder is affected, animals will resent milking however, continuously grow wool and should not shed it.
or being nursed.9 Shorn sheep being housed for winter can, however, expe-
rience complete loss of wool (wool slip).3,9 The affected
Treatment. Treatment includes the application of pig- skin is smooth, free of ectoparasites, and shows no signs
mented teat dips and the application of sunburn lotion on of disease. No treatment is required and the wool does
the udder (for dairy goats), the provision of adequate grow back.3,9 Wool slip has been associated in some
shelter, and gradual light exposure for light-pigmented sheep with copper deficiency (low serum copper and cold
animals. In cases of secondary bacterial infection the stress).9 Therefore possible deficiencies in dietary copper
use of topical or systemic antimicrobial agents is should be investigated.
warranted.3,4 Stressors such as parasitism and systemic disease can
cause sheep to undergo a cessation in wool growth and
can weaken the fiber (wool break). Wool can be lost
Frostbite within days of a systemic stress (anagen defluxion) or
Prolonged exposure to extremely cold temperatures may within 2 to 3 months after the stress (telogen defluxion).
result in frostbite. Young stock are most prone to frostbite In both cases the wool does grow back over time. The
injury, and the extremities (ears, tail, feet) are most com- practical application of this information is in educating
 Chapter 8 Diseases of the Integumentary System • 219

the owners of pet sheep that survive a systemic illness— epidermal junction in the absence of epidermolysis. The
the clinician should warn the neophyte owner of the po- hooves may slough and ulcers of the gingiva, hard palate,
tential for fiber loss. tongue, and mouth form rapidly.14

CONGENITAL PATHOLOGIES Hairy Shaker Disease of Lambs

Several forms of congenital skin disorders are of clinical Border disease, or hairy shaker disease, is a congenital
interest. Because of good identification and culling prac- condition caused by a pestivirus that may be transmitted
tices, most are fairly rare.12,13 vertically from the ewe to the fetus in utero. Newborn
lambs have domed heads, short limbs, and thick trunks.
Viral infection of the fetus before day 80 of gestation may
Hepatogenous Photosensitization interfere with the development of primary hair follicles
Southdown lambs have an autosomal recessive trait that and result in the formation of “kempy” fibers and long
can result in hepatogenous photosensitization.13 The halo fibers in the fleece. Affected lambs appear abnor-
defect causes congenital hyperbilirubinemia and subse- mally hairy and are called hairy shaker lambs because
quent photosensitization. Corriedale lambs have an tonic-clonic contractions of their skeletal muscles cause
assumed inherited condition, similar to Dubin-Johnson them to shake. Diagnosis is confirmed by virus isolation
syndrome in human beings, characterized by a failure to or a necropsy finding of hypomyelinogenesis in the
transfer phylloerythrin and conjugated bilirubin. central nervous system (see Chapters 6 and 13).

Epitheliogenesis Imperfecta NEOPLASIA

Epitheliogenesis imperfecta has been diagnosed in nu- Neoplasia is occasionally diagnosed in sheep and goats.
merous breeds of sheep. It is an autosomal recessive Some breed predilections have been described for various
genetic defect in cattle. Epithelial defects in the oral tumors (Table 8-7).
cavity (including the tongue and hard palate) are noted at
birth. Hoof horn can easily be separated from the PAPILLOMAS (WARTS,
underlying laminae.
FIBROPAPILLOMATOSIS)
Collagen Tissue Dysplasia Warts in sheep are caused by species-specific papo-
vaviruses. These DNA viruses cause papillomas on the
(Ehlers-Danlos Syndrome) face and legs that vary in size but may be as large as 4 cm
Collagen tissue dysplasia, or Ehlers-Danlos syndrome, in diameter and 2 cm in height. These lesions are vascular
appears to be a hereditary skin disease of Norwegian and bleed when disrupted. Secondary bacterial infection
sheep. Skin wounds develop rapidly after birth because of may occur with repeated trauma to the lesion. A cellular
collagen defects.13 Affected lambs die soon after birth immune response eventually clears the lesions, which may
because of secondary infection. This genetic defect results require months to regress. Failure of lesions to regress or
in the failure of collagen bundles to form in a functional excessive numbers of lesions suggests that the immune
configuration.

Hypotrichosis Congenita
TABLE 8-7
Hypotrichosis congenita is a viable hypotrichosis—that
is, the disease is not immediately fatal to affected BREED PREDILECTIONS FOR SKIN TUMORS
neonates. It is hereditary in polled Dorset sheep. Affected
lambs have sparse hair fibers, most pronounced on the BREED TUMOR
face and limbs.
Saanen goats Udder papillomatosis
Angora goats Squamous cell carcinoma
Epidermolysis Bullosa Melanoma
Merino sheep Squamous cell carcinoma
Epidermolysis bullosa is a recessive heritable defect of
Follicular cysts
Weisses Alenschaf sheep and has been diagnosed in
Suffolk sheep Melanoma
Suffolk and South Dorset Down breeds of sheep as
Nubian goats Wattle cysts
well.13,14 Affected animals are born without type VII col-
lagen and develop wounds rapidly after epidermal abra- Adapted from Scott DW: Large animal dermatology, Philadelphia,
sion.13 Skin biopsy reveals separation of the dermal- 1988, WB Saunders.
220 • Sheep and Goat Medicine
system is not competent. A viral cause has not been con-
firmed in goats. Papillomas on the udder of Saanen goats
have been documented; they tend to persist without un-
dergoing the regression typical of viral papillomas.

SQUAMOUS CELL CARCINOMAS

Squamous cell carcinomas are most commonly diagnosed
in Merino sheep and are usually seen in sheep older than
4 years. The peak incidence (12%) was observed in 12-
year-old sheep. Tumors occur on the face, ears, and vulva
but most commonly involve the ears. As the tumor grows,
the surface may become ulcerated because of tissue necro-
sis or self-trauma. Diagnosis is made by histopathologic
examination of tissue specimens. Characteristic lesions
exhibit acanthosis, pseudoepitheliomatous hyperplasia,
and hyperkeratosis. Inflammation associated with ulcera-
tion or secondary bacterial infection is not uncommon.
Ultraviolet radiation has been implicated in squamous
cell carcinoma; photosensitive sheep are at greatest risk.
Lesions in the ear, such as from ear tags, are more prone
to mutate into squamous cell carcinoma. Treatment is by
surgical excision with wide margins, but early culling is
common.

MELANOMA
Melanoma has an unknown incidence in sheep and goats.
One survey of the skins of 37,026 sheep and 23,429 goats
found only two melanomas, both occurring on goats.15
Another survey indicated an incidence of 0.03% cuta-
neous melanoma in goats.12 Figure 8-8 Hemangioma on the frontal surface of the rear leg of a
ewe. Note the proliferative nature of the lesion. Such lesions can be
surgically excised.
HEMANGIOMA
Hemangioma has been diagnosed in a sheep by one of
the authors (Dr. Rings). The lesion affected the distal rear
R EFERENCES
1. Scott DW: Large animal dermatology, Philadelphia, 1988, WB
limb of a ewe (Figure 8-8). Diagnosis was confirmed by
Saunders.
histology after surgical excision.
2. Scott DW, Smith MC, Manning TO: Caprine dermatology. Part
II. Viral, nutritional, environmental, and congenitohereditary
DRUG RESIDUE ISSUES disorders, Comp Cont Ed Pract Vet 6:S473, 1984.
3. Smith MC: Small ruminant dermatology, Proceedings of the 1998
Preservation of a wholesome product, free of contami- Symposium on Small Ruminants for the Mixed Animal Practitioner
nants, is paramount to the sheep and goat industry.16 Western Veterinary Conference, 1998, Las Vegas, NV.
Nearly all treatments for skin diseases are performed in 4. Linklater KA, Smith MC: Color atlas of diseases and disorders of the
an extra-label manner because relatively few drugs are ap- sheep and goat, Aylesbury, UK, 1993, Wolfe Publishing.
proved for use in sheep and goats. Veterinarians must 5. Smith MC, Sherman DM: Skin. In Smith MC, Sherman DM,
work diligently with industry personnel to ensure quality. editors: Goat medicine, Baltimore, 1994, Williams & Wilkins.
6. Kimberling CV: Diseases of the skin. In Kimberling CV, editor:
In the United States keepers and clinicians should respect
Jensen and Swift’s diseases of sheep, ed 3, Philadelphia, 1988, Lee &
the treatment guidelines described in the Animal
Febiger.
Medical Drug Use and Clarification Act (AMDUCA) to 7. Smith MC: Dermatologic diseases of goats, Vet Clin North Am
avoid residue contamination of meat and milk. Sheep and Large Anim Pract 5:449, 1983.
goats differ from cattle in both size of drug dosages and 8. Mohammed A, Rabo JS, Ibrahim AA: Reaction to skin suture ma-
drug elimination times. Therefore whenever possible, terials in Borno white goats, Small Rumin Res 16:191, 1995.
drug withdrawal times should be established from 9. Mitchell GBB: Non-parasitic skin diseases in sheep. In Boden E,
research performed specifically on sheep and goats. editor: Sheep and goat practice, London, 1991, Bailliere Tindall.
 Chapter 8 Diseases of the Integumentary System • 221

10. Gonzalez-Jimenez E, Blaxter KL: The metabolism and thermal a

regulation of calves in the first month of life, Br J Nutr 16:199,
1962.
11. Pelton JA et al: Frostbite in calves, Comp Cont Ed Pract Vet
22:S136, 2000.
12. Venkatesan RA et al: Survey of the incidence of various surface
defects in goat and sheep skins in Madras, Leather Sci 24:255,
1977.
13. Basrur PK, Yadav BR: Genetic diseases of sheep and goats, Vet
Clin North Am Food Anim Pract 6:779, 1990. b
14. Steffen DJ: Congenital skin abnormalities, Vet Clin North Am
9:105, 1993.
15. Venkatesan RA, Nandy SC, Santappa M: A note on the incidence
of melanoma on goat skin, Ind J Anim Sci 49:154, 1979.
16. Bretzlaff K: Special problems of hair goats, Vet Clin North Am Food Figure 8-9 A view of the kid from the top of its head. The area for
Anim Pract 6:721, 1990. applying the cauterizing unit for descenting (a) and dehorning (b) is
shown. The clinician should take care to avoid causing excessive
thermal damage to the underlying bone and nervous tissue. (Adapted
from Williams CSF: Routine sheep and goat procedures, Vet Clin North
REMOVAL OF WATTLES, SCENT Am Food Anim Pract 6(3):753, 1990.)

GLANDS, AND HORNS, AND

horning iron (for cattle or goats) or an electric cautery
OTHER SKIN PROCEDURES unit may be used. Regardless of the method, clipping all
hair around the area aids the process. If an electric de-
Wattles
horning iron is used for this purpose, Williams2 has rec-
Wattles are skin appendages that are found in the cervi- ommended allowing it to heat and then applying it to a
cal regions of some goats (see Figure 8-3). Although pine board. If the iron makes a slightly depressed black
they are usually encountered in the mid-neck, they also ring on the board, the proper temperature has been
may be found on the face or ears.1 They are composed of achieved.2 The dehorner should be applied in a rocking
connective tissue, nerves, blood vessels, smooth muscles, manner over the horn buds (Figure 8-9). The area should
and a cartilaginous core.1 Cysts may be found in the be burned until a copper color is attained. If the hot iron
bases of some wattles.1 These cysts may be hereditary is correctly applied the horn “cap” should be easily
and either bilateral or unilateral. If swollen, the cysts will removed. Williams2 recommends burning the horn until
be filled with a clear fluid. Wattles may become injured the central core is removed. Common mistakes with this
(e.g., caught in feeders or fences), detract from the ap- method are heat-induced meningitis and underheating of
pearance of show animals, make clipping and grooming the germinal epithelium of the horn, resulting in the re-
difficult, and may be chewed or nursed by other kids or growth of abnormal horn tissue.1,2 If the germinal horn
adults.1,2 For these reasons, some owners wish to have tissue is not completely destroyed, the scar that regrows
them removed. When animals are young (2 to 4 days), can be removed later. The calvarium of a kid is thin and
wattles can be removed at castration or dehorning. Slight the cornual sinus is small compared with those of calves.
tension can be placed on the wattle before its base is cut Heat-induced malacia of the underlying cerebrum can
with scissors.1,2 If excessive bleeding occurs, pressure result in depression, blindness, abscess formation, and
should be applied. The skin should heal without further death.
therapy. Meat-induced meningitis and malacia is rarely re-
versible. Still, in such cases immediate treatment with
glucocorticosteroids (dexamethasone sodium phosphate
Disbudding
1 to 2 mg/kg IV), mannitol (0.25 to 1 mg/kg IV over 5
Some management styles prefer that goats (and occasion- minutes), and possibly NSAIDs are indicated.
ally rams) have their horn buds removed during the first 2 An alternative to cauterization of the horn buds is sur-
weeks of life.2 However, many meat, fiber, and pet goat gical removal. This can best be accomplished in 2- to 4-
owners prefer to keep horned animals. Disbudding is day-old kids using a similar method as described for heat
more common among dairy goat producers to reduce removal. Instead of using a dehorning iron or electric
fighting-related injuries. Kids can be held or placed in a cautery, the clinician makes a circumferential incision
dehorning box. They can be sedated (xylazine 0.05 to 0.2 through the anesthetized skin and removes the horn bud
mg/kg), have a ring of tissue around the horn anes- and germinal tissue. To control hemorrhage the area can
thetized (2% lidocaine SC), or be placed under general be cauterized or firm digital pressure can be applied.
anesthesia. A dehorning box encloses all of the body Caustic paste also is used to remove the horns of
except the head. The heat from a commercial electric de- young kids. Clipping the hair around the horn buds aids
222 • Sheep and Goat Medicine
in the application of the paste. If caustic paste is used, be instituted. The bandage should be changed and the
lanolin or petroleum jelly should be applied around the area examined every 2 to 4 days or as needed. An alter-
area, particularly around the eyes. The clinician should native is to use a small Barnes dehorner to cut or nip off
take care to prevent the caustic ointment from injuring the horn tissue. The cut should be made carefully to
the kids’ eyes or other soft tissues. This method should be avoid injuring the thin skull. The area can then be cau-
relegated to animals kept indoors (out of the rain), kids terized to control bleeding and destroy all remaining ger-
not nursing their dams, and those not able to rub the minal epithelium.
caustic ointment onto other kids. An alternative method is to cut the horn off at the tip,
mid-horn, or as close to level with the skull as possible,
depending on the desire of the owner and the animal’s
Dehorning use. This should be done on a sedated or an anesthetized
Kids older than 2 to 3 weeks of age, those whose previous goat. The horn can be cut with obstetric wire or a de-
dehorning has resulted in the growth of an abnormal horning saw. The animal should be monitored for
horn tissue (scur), and adult goats are all candidates for sinusitis, and the horn will continue to grow.
dehorning. The animal can be sedated or placed under
general anesthesia; alternatively, a ring of skin around the
horn or the cornual branches of the lacrimal and supra-
Descenting
trochlear nerves can be anesthetized (see Figure 16-7). Because of the smell associated with bucks, some owners
In adults and particularly in males with large horns, request the removal of these animals’ sebaceous glands.
general anesthesia is recommended. However, sedation Removal of these glands may improve the smell, but odor
(xylazine 0.05 to 0.2 mg/kg) and local anesthesia of the will probably not be completely prevented. In young buck
cornual branches of the lacrimal and infratrochlear kids the area behind the horns (see Figure 8-9) can be
nerves may be employed. The owner should be fore- cauterized during dehorning. In the adult the glands are
warned that this procedure is usually a “bloody mess.” located in thickened, folded skin caudad-medial to the
The wounds can take a long time to heal, result in sec- horn base. The gland opening is a hairless area at the base
ondary sinusitis, leave holes that never completely heal, of a skin fold.2 Washing the head helps the clinician visu-
or possibly result in brain abscesses. The skin around the alize the scent glands. The buck should be anesthetized
horns should be clipped and surgically prepared. The cli- or heavily sedated, the hair clipped, and the area surgi-
nician makes a circular incision through the skin 2 mm cally prepared. The clinician then makes an incision
outside of the horn-skin junction.3 The strip of skin through the skin 1.5 to 2 cm around the gland opening.
between the two horns should be left to improve and The incision should be deepened to the periosteum, the
shorten healing time. An obstetric wire is then “laid into” area dissected, and the gland identified and removed.2
the incision. A helper-technician holds the head to The clinician should attempt to close the skin defect.
prevent excessive motion, and the surgeon stands in front However, this is most difficult in older males because of
of the animal. The cut should be made in a rostral-ventral the skin hypertrophy in this area. If the skin is not easily
direction. Hemorrhage can be controlled by cautery or sutured, an antibiotic ointment can be applied and the
pressure. If the animal has a small horn base, the sur- area allowed to granulate.
rounding skin can be undermined and stretched over the
opening created by the horn removal.1 Pulling the skin
over the surgical site allows for a more speedy recovery
but is rarely possible in adult males. An antibiotic oint-
R EFERENCES
1. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lee
ment (triple antibiotic) can be applied and a gauze pad or
& Febiger.
other absorbable material can be placed over each horn. 2. Williams CSF: Routine sheep and goat procedures, Vet Clin North
The pads can be held in place by tape wrapped around Am Food Anim Pract 6:737, 1990.
the head or by a stocking with eye holes.1 Animals can 3. Hooper RN: General surgical techniques for small ruminants: Part
be given antibiotics (penicillin 20,000 IU/kg BID), I, Proceedings of the 1998 Symposium on Small Ruminants for the
NSAIDs, tetanus prophylaxis (tetanus antitoxin 150 to Mixed Animal Practitioner Western Veterinary Conference, 1998, Las
300 IU), or tetanus toxoid. Fly control measures should Vegas, NV.
 Chapter 9

DMusculoskeletal
iseases of the
System
LAURA K. REILLY, A.N. BAIRD, AND D.G. PUGH

EXAMINATION ANATOMY
Sheep and goats are naturally herd animals that prefer Sheep and goats, like cattle, are members of the Bovidae
living and staying in a group. Therefore any examination family. They join several other even-toed animals in the
of these animals on the farm should include initial ob- order Artiodactyla. Animals in this order share three
servation of the entire group if possible. Flock observa- skeletal characteristics: the talus has distal and proximal
tion is probably less important in the evaluation of trau- trochleae; the calcaneus and fibula articulate with each
matic musculoskeletal conditions than when animals are other; and the limb axis divides the fused third and fourth
affected by infectious diseases, parasitism, nutritional metacarpal-metatarsal bones and the associated digits.1
disorders, and improper management. When the herd Sheep have short, blunt spinous processes of the cervical
has a higher than expected incidence of fractures or vertebra, whereas those of goats are longer, pointed, and
injury, the practitioner should look for potential hazards have sharp edges. Small ruminants have 7 cervical verte-
around feeders and other objects. Veterinarians should brae, 13 thoracic vertebrae, 6 or 7 lumbar vertebrae, 4
look closely for animals that lay down or walk on their sacral vertebrae, and 16 to 18 caudal vertebrae. The pres-
knees when their herdmates are moving around. ence of seven cervical vertebrae is a reliable trait in iden-
Animals also should be observed for difficulty in rising, tification. However, variations are not unusual, such as 12
swollen or enlarged joints, lameness, and abnormal or 14 thoracic vertebrae or 5 lumbar vertebrae. Occasion-
stance. ally, an unusual transitional vertebra that is difficult to
When examining an individual animal, the clinician classify is found between the thoracic and lumbar verte-
should perform careful, meticulous palpation and close brae.1 The authors describe a few of the musculoskeletal
examination. Some animals may have obvious fractures differences between sheep and goats within this chapter,
and wounds. Those with more subtle problems require as well as some of the variations from cattle. However, a
thorough examination. The clinician should first thorough description of small ruminant anatomy is
examine the feet for overgrown hooves, abscesses, inter- beyond the scope of this text.
digital lesions, exudate, and any foul smell. The coro-
nary band should be examined for swelling, hyperemia,
and proliferative lesions. All limb joints should be eval-
uated for swelling associated with trauma, septic arthri-
R EFERENCE
1. Getty R, Sisson S: Sisson and Grossman’s the anatomy of domestic
tis, and infectious disease. The clinician should flex and animals, ed 5, Philadelphia, 1975, WB Saunders.
extend the animal’s joints through the entire range of
motion to detect pain or laxity. In cases of hindlimb
lameness, the clinician also should evaluate the patella
GENERAL HOOF CARE
for laxity, movement, and pain. Any asymmetry associ- Most lameness in small ruminants is associated with
ated with swelling or muscle atrophy should be noted. pathology of the foot. Surveys have found that the inci-
Sciatic or peroneal nerve injury can occur after intra- dence of foot disorders varies from approximately 10% to
muscular injections and may produce lameness and 19%.1,2 Overgrown hooves are one of the most common
muscle atrophy. foot disorders. Many foot disorders can be attributed to
• 223 •
224 • Sheep and Goat Medicine
environmental, nutritional, and anatomic factors, but termine the amount of toe horn to be removed. After
some can be prevented by proper trimming and manage- trimming, the hoof wall and the coronary band should be
ment. With increased nutritional intake, and particularly almost parallel. Trimming of the lateral wall corrects
with enhanced protein intake, hooves tend to grow more many hoof problems. After trimming the toe and lateral
rapidly. wall, the clinician or keeper should cut the inner wall
The hooves of small ruminants have fewer problems in shorter than the outer wall. The rubbery heel should be
a dry environment. The incidence of hoof disorders is cut if it is excessively long or overgrown. The outer hoof
higher in seasons of more precipitation and when housing wall should be slightly longer than any other hoof struc-
is allowed to become humid, wet, or muddy. Fewer prob- ture because it is a weight-bearing surface (Figure 9-2). If
lems are seen when the animals can move about on hard, the hoof is improperly trimmed, the sheep or goat may
dry surfaces. Most sheep and goats require hoof trimming walk on the toe or side of the foot or on the heel with the
because of lack of adequate exercise on a hard, dry surface toe pointing up. A common cause of foot problems is an
to wear down hoof material naturally; because of chronic inward-turning outer wall that produces areas that accu-
laminitis; or because of fast hoof growth resulting from mulate debris and become infected. The inner wall may
intensive feeding practices designed to increase produc- occasionally overgrow toward the interdigital cleft and
tion. Some herds may require foot trimming every 6 predispose the animal to interdigital disease. The foot will
weeks to 2 months to minimize the incidence of foot dis- be better balanced if the operator removes the toe curl by
orders. Hooves can usually be trimmed adequately with trimming the solar surface of the hoof and keeping it
shears, although a hoof knife also may be useful.1 level rather than dubbing or shortening the toe. In sheep
During trimming some goats will stand, others need and goat flocks kept on soft pastures or paddocks, placing
to be “set up” on their rumps, and others will stand in a feeders on rough surfaces helps decrease the amount of
stanchion. Some individuals prefer to trim the feet of trimming needed. Building or stacking rough material
sheep with them restrained in a tilt chute. The authors of (cement or concrete blocks) for goats to play on also may
this chapter prefer to trim the feet of sheep with them help minimize the need for frequent trimming.
sitting on their rumps; foot trimming in goats is easier if Feeding affects hoof condition and growth. Animals
the animals stand and the operator stands to the side. If being overfed energy and protein and living on soft
an animal is allowed to stand, it should be tied. This ground may be more prone to some abnormalities. As a
allows the animal to be secured between the operator and general rule a well-balanced feeding program with a free
a wall during foot trimming.1 Regardless of the method, choice mineral salt supplement consisting of calcium,
complete restraint is crucial to proper hoof care. phosphorus, and trace minerals is all that is required.
The clinician or keeper should shape the foot to match However, some feeding programs may enhance hoof
the angle of the coronary band while trimming the toe growth and health and are useful in special circumstances.
wall and sole (Figure 9-1). Dirt that has become packed
into the toe should be cleaned out so the operator can de-

Figure 9-1 The bottom of the sheep or goat’s foot. The toe (a) Figure 9-2 This hoof requires trimming. After cleaning the toe, the
should be cleaned out, and the outer hoof wall (b) should be cut to practitioner trims the toe and lateral walls. The inner wall is then
remove all overgrowths, bring the wall down to the sole, and make the trimmed, and the procedure is repeated on the other toe.
outer wall parallel with the coronary band. The inner hoof wall (c) is
then cut, with more inside wall than outside wall being removed. The
heel (d) should not be cut unless it is badly overgrown.
 Chapter 9 Diseases of the Musculoskeletal System • 225

In other ruminants (cattle), diets that change normal systems in the body. Copper deficiency in the body may
rumen function by increasing the fermentation rate nega- be primary (inadequate copper in the diet) or conditioned
tively affect the hoof health.3 The ingestion of high- by other dietary factors (excessive dietary molybdenum,
energy feeds coupled with inadequate fiber intake can sulfur, or iron). The dietary copper-to-molybdenum ratio
result in suboptimal hoof health. In rations in which con- should be maintained between 41 and 61 to maintain
centrates and roughage are fed separately, the concen- adequate copper availability.
trated portion of the diet should be divided into two or Excessive nitrogen fertilization and liming of soils may
more equal feedings each day. This not only promotes depress copper and selenium uptake by plants. Heavily
overall health but also may help reduce the microflora fertilized forage and roughage harvested after a drought
changes that alter normal rumen fermentation and pre- may be sources of nitrates, which are reduced to nitrites
dispose animals to founder. Forage should always make by anaerobic microbial metabolism in the rumen. Ni-
up more than 30% to 50% of the dry matter content of trites can have a direct effect on hoof growth, resulting
the ration. Lush, young forage rarely provides enough in abnormal horn tissue in cattle and possibly other
effective fiber to optimize rumen fermentation. The ruminants.3
feeding of buffers, particularly in high-concentrate diets, The key to maintaining healthy hoof tissue with
may help the rumen resist digestive upsets and thereby respect to nutrition lies in minimizing rumen acidosis
prevent subsequent hoof disease. Abnormal rapid hoof and fortifying the diet with certain nutrients (e.g., biotin,
growth can occur when abnormal rumen fermentation is calcium, zinc).
induced by the ingestion of lush, well-fertilized pastures.3
Hoof health also can be affected by certain vitamins
and minerals. The addition of 20 mg of biotin improves
DISEASES OF THE FOOT
short-term healing of hoof and claw lesions and decreases
hoof disease in cattle.3 Furthermore, diets that acidify the
Infectious Footrot
rumen decrease the microbial synthesis of biotin. One of Infectious footrot is a severe, contagious disease of sheep,
the authors (Dr. Pugh) prefers to include biotin (3 to 4 and to a lesser extent goats, that leads to significant eco-
mg/day) in sheep and goat rations for animals with a nomic losses as a result of weight loss, low fleece weight,
history of hoof disease. Other vitamins that play major labor and treatment costs, and premature culling. Many
roles in hoof health include vitamins A and E and the factors contribute to the disease, but the primary agent is
vitamin A precursor beta-carotene. Adequate dietary the anaerobic bacterium Dichelobacter nodosus (Bacteroides
vitamin A and beta-carotene are needed for normal nodosus). Previous infection by Fusobacterium necrophorum
cell replication, epithelial repair, and immune function. contributes to the development of footrot. Corynebac-
Vitamin E maintains cellular integrity and normal terium (Actinomyces) pyogenes infection may increase the
immune function. Diets should be fortified with both of susceptibility of the hoof to the other two bacteria. Many
these nutrients if hoof problems occur and in cases in strains of D. nodosus have been identified, and they can
which production practices predispose to hoof disease generally be classified as benign or virulent. Virulent
(see Chapter 2). strains have a greater keratolytic ability, which is associ-
Calcium is the largest mineral component of hooves ated with the production of a heat-stable protease.1,2,7-9
and is required for normal hoof growth. Dietary calcium Footrot occurs worldwide wherever periods of warmth
concentrations should range between 0.6% and 0.8% of and prolonged wetness occur. In many regions the spring
the diet, with the calcium-to-phosphorus ratio being and fall are the times when transmission is most likely. If
maintained between 11 and 21. Of the trace minerals conditions are favorable, a significant portion of the flock
that appear to affect hoof growth, zinc, copper, and, to a can be affected. All ages are susceptible, but the severity
lesser extent, molybdenum and manganese, are most of disease generally increases with age. Merino sheep are
crucial.3 Zinc is required for normal immunity, horn most susceptible to disease, and some breeds (Gulf Coast
tissue production, vitamin A metabolism, epithelial native) are more resistant. Some individuals do not
repair, and hoof hardness. Studies in range, dairy, and become infected or have less severe signs, and a genetic
feedlot cattle have all shown improved hoof health and basis for resistance is suspected.8,9 Excessive hoof growth
decreased lameness when zinc is added to the diet, partic- and, anecdotally, hoof color (white) may predispose to the
ularly in a chelated form (zinc methionine).3 The use of condition.4
such minerals also may be of value in improving overall The source of D. nodosus is the feet of infected animals,
hoof health. In sheep the administration of oral zinc which transfer the organism to the soil where it contacts
sulfate (0.5 g daily) to prevent footrot has shown mixed the feet of other sheep.8 The organism can survive only a
results.4-6 In cases of high legume intake (high calcium), few days to a few weeks in the environment but can persist
zinc in the chelated form (zinc methionine) may be ben- for years in carrier sheep and goats. New infections usually
eficial. Copper is needed for keratin synthesis and normal are preceded by the introduction of new animals or expo-
immune function and as a cofactor for many enzyme sure to ground that has recently been occupied by an in-
226 • Sheep and Goat Medicine
fected flock. Management practices that allow the concen- other differential diagnoses include foot abscess, lam-
tration of animals in small areas, irrigated pastures, long initis, bluetongue, and foot and mouth disease.
grass (which may abrade the interdigital skin), and wet or
rainy conditions all predispose to infection.4,8 Treatment. The mainstay of therapy is proper hoof
trimming. Trimming can increase short-term lameness,
Pathogenesis. Wet conditions leading to maceration of but appropriate trimming also can produce very high cure
tissue encourage infection with F. necrophorum (and occa- rates without other forms of therapy.4 Applying antibac-
sionally A. pyogenes) which is thought to be necessary for in- terial agents to the foot after trimming it further im-
fection by D. nodosus to occur.4 F. necrophorum produces a proves cure rates. Topical treatments include antibiotics
mild clinical syndrome known as interdigital dermatitis in (tetracycline) and antiseptics (copper sulfate, zinc sulfate,
sheep that usually resolves when the ground becomes drier.8 cetrimide, or 4% to 5% formalin). If only a few animals
Interdigital dermatitis may produce severe lameness in goats. are affected, these agents may be applied with a spray ap-
When sheep or goats with interdigital dermatitis are plicator or brush; bandaging ensures contact of the med-
exposed to a benign strain of D. nodosus, the soft horn ication with affected tissue.8
becomes under-run but no further pathology occurs. This The use of foot baths is a more practical method to
condition is known as benign (or nonprogressive) footrot. If treat numerous animals. Typically, affected animals
sheep come into contact with a virulent strain of D. nodosus, should be separated from unaffected animals. Both
a much more severe disease known as virulent footrot results. groups of animals are passed through a foot bath and then
kept in a dry place for a few hours before being placed on
Clinical signs. Footrot usually affects both claws in separate clean pastures. If this procedure is repeated
more than one foot. Benign footrot is characterized by in- several times, the majority of the animals will be cured,
flammation and necrosis of the interdigital tissue. The and the rest should be culled. A prolonged soaking time
soft horn is pale, pitted, and may be separated from the (1 hour) may be more effective than brief passes through
skin, but this separation does not involve the hard horn. foot baths, even when they are performed every 10
With benign footrot, often only one or a few animals in a days.12 Copper sulfate (5%), zinc sulfate (10%), and for-
flock are affected. Virulent footrot, in contrast, is marked malin (5%) have been used in foot baths and seem to have
by severe lameness in numerous animals in the flock, with similar efficacy. Zinc sulfate is preferred because it is less
under-running of the hard horn beginning near the heel hazardous and causes less discomfort than formalin, does
on the axial surface. In severe cases the entire horn may not stain the wool, and has a reduced risk of toxicity com-
separate from the underlying tissue. Affected areas pared with copper sulfate. An anionic surfactant, sodium
produce a malodorous exudate. Animals may carry the af- lauryl sulfate, appears to enhance penetration of the zinc
fected leg, graze on their knees, or remain recumbent. sulfate solution.8,12 Dry foot baths (85% powdered lime-
Some animals develop fever, anorexia, and weight loss. stone, 15% zinc sulfate) also may be beneficial. The clini-
Secondary bacterial infection and flystrike may compli- cian should remember that sheep are capable of jumping
cate footrot infection. long distances and goats can walk on the thin edge of a
Footrot in goats is generally less severe than in sheep, small plank. Therefore foot baths should have solid sides
although significant lameness may develop. Interdigital and be at least 21⁄2 to 3 m long. Regardless of the type of
dermatitis is a more prominent sign, and under-running foot bath used, trimming the feet before the therapy
of the horn is a less prominent sign compared with sheep greatly enhances its effectiveness.
infected with the same virulent strain of D. nodosus.7,10 Several systemic antibiotics have been shown to be ef-
fective in the treatment of footrot. Penicillin (20,000 to
Diagnosis. The diagnosis of virulent footrot is usually 30,000 IU/kg intramuscularly [IM] twice a day [BID]),
based on the clinical presentation of interdigital dermati- long-acting oxytetracycline (20 mg/kg subcutaneously
tis and lameness in numerous flock members (virulent [SC] every 72 hours), erythromycin (3 to 5 mg/kg IM
footrot). A Gram’s stain of the interdigital exudate may BID), lincomycin, spectinomycin, and florfenicol (20
show the large, curved, gram-negative, barbell-shaped mg/kg IM every 48 hours) have been used successfully,
rods characteristic of D. nodosus; however, they may not especially when conditions are dry. These treatments are
always be isolated because of their special growth require- not approved in all countries.13,14
ments.11 Several tests may be performed to differentiate Vaccination has been shown to shorten the course of
between benign and virulent strains.8 Serologic tests are disease in flocks. However, a significant number of injec-
of limited utility but may aid in identifying carrier tion reactions are reported.8 The decision to vaccinate
animals. Antibody levels are only elevated for a short time during an outbreak must be carefully considered.
and are not always accurate. Vaccination may confound
the interpretation of the antibody tests. Footrot is the Prevention. Eradication of virulent footrot is possible
most common cause of lameness in sheep. However, but often difficult, especially in areas that are wet most of
 Chapter 9 Diseases of the Musculoskeletal System • 227

BOX 9-1
Clinical signs. Clinical signs of laminitis include lame-
ness and warm feet. Animals move with a stiff gait and
F OOTROT P REVENTION P ROGRAM*
prefer recumbency. In chronic cases, foot deformity,
marked by “turning up” of the toes, occurs. Laminitis is
often accompanied by signs of primary gastrointestinal
• Trim feet, separate infected animals, and disinfect illness such as bloat, diarrhea, and toxemia. Differential
trimming equipment between animals. diagnoses include footrot, caprine arthritis-encephalitis
• Move all animals through a 15% zinc sulfate foot (CAE), and nutritional conditions that produce lame-
bath. Where possible, have them stand in the foot ness, stiff gait, and recumbency.
bath for 30 minutes. Foot baths should be repeated
two to 4 times at weekly intervals. Treatment and prevention. The mainstay of treatment
• Put both affected and nonaffected sheep in a is nonsteroidal antiinflammatory drugs (NSAIDs) such
previously unused (clean) pasture or paddock. as phenylbutazone (10 mg/kg by mouth [PO] once a day
• Cull all severely affected animals and those not [SID]), flunixin meglumine (1 mg/kg SID), and aspirin
responding to treatment. (100 mg/kg PO BID), as well as treatment of the primary
• Vaccinate 8 to 12 weeks before the season when disorder. If the inciting cause can be corrected, many
large numbers of footrot cases are anticipated animals recover.16 The risk of laminitis can be reduced by
(disease tends to occur at the same time each year). slowly increasing the amount of grain being fed. Prevent-
• Selectively breed for animals that appear less ing accidental exposure to large amounts of concentrate,
susceptible. ensuring adequate forage intake, and adding rumen
buffers to the diet all help decrease the incidence of
*Some or all of these procedures can be employed. The main laminitis.
ingredient in any protocol for footrot prevention is vigilance.

the year.8 Box 9-1 describes a footrot prevention

Hairy Heel Wart
program. Treating affected animals, culling chronic cases, Cases of unusually severe footrot in sheep in the United
and isolating new animals are the mainstays of an eradi- Kingdom have been described in the past few years. Af-
cation program. New animals should be segregated fected animals usually have only one digit involved but
through a wet season before they are placed with a the severe undermining of the hoof wall causes pain that
footrot-free flock. Obviously, any animal showing signs of leaves the animal unable to bear weight. Examination
footrot during quarantine should be culled. with dark field microscopy of swabs taken from these
In flocks with endemic footrot, vaccination may be animals revealed the presence of spirochetes. The spiro-
useful in reducing the number and severity of footrot chetes isolated were enzymatically and biochemically
cases, but aggressive hoof trimming, foot bathing, and similar to those found in dermal dermatitis (hairy heel
culling should be continued for the best control. Several warts) cases in cattle.17 This condition may become
types of vaccines are available. Two doses given at least 6 severe enough that amputation is the treatment of choice.
weeks apart, followed by boosters a few weeks before the However, topical therapy with tetracycline should be at-
wet season may improve effectiveness.4 The protection is tempted before resorting to amputation. Tetracycline can
not complete and only lasts for a short time (4 to 12 be placed in a foot bath, injected, or painted onto the
weeks). Knowledge of seasonal infection patterns and lesion.
vaccination before the predicted increase in clinical cases
improves vaccination effectiveness.4 Some animals
develop fairly severe local reactions to the vaccine that
Interdigital Fibromas
may reduce production and be undesirable in show or sale Interdigital fibromas occasionally occur in small rumi-
animals. Genetic selection for resistance to footrot should nants but are much more common in cattle. This hyper-
be a primary adjunct to disease control. plasia of the interdigital skin may not cause lameness
until the lesion is quite large or infected. Some reports
speculate that predisposing factors include obesity,
Laminitis
footrot, and abnormal hoof conformation.13 Complete
Laminitis (inflammation of the dermal and epidermal surgical excision under general anesthesia or sedation and
laminae) is fairly common in sheep and goats. The local anesthesia is the treatment of choice, although
history often includes consumption of a highly concen- cryotherapy, cautery, and topical caustic agents also have
trated or lush forage diet. Laminitis also may be associ- been employed. After surgery the foot is bandaged.
ated with systemic illness such as pneumonia, mastitis, Healing may be enhanced by securing the toes with
and metritis; it can occur after parturition.15 wire to prevent spreading and movement of the interdig-
228 • Sheep and Goat Medicine
ital skin. Recurrence of interdigital fibromas is not one form of myotonia congenita in human beings and has
uncommon. 13 therefore been used as a research model for the human
disease. The condition is related to a block of the normal
R EFERENCES
1. Cottom DS, Pinsent PJ: Lameness in the goat, Goat Vet Soc J
conductance of chloride in the membrane of muscle
fibers.2 The primary abnormality is a delay of relaxation
of contracted muscle that is most likely caused by re-
9(1):14, 1988. peated firing of action potentials. Histochemical and ul-
2. Chakrabarti A: Incidence of foot disorders in goats in Tripura, trastructural abnormalities are present in goats with myo-
Indian Vet J 74:342, 1997.
tonia congenita.1,2
3. Greenough PR, Schugel LM, Johnson AB: Illustrated handbook on
cattle lameness, Eden Prairie, MN, 1996, ZinPro.
4. Morgan K: Footrot. In Boden E, editor: Sheep and goat practice, Hereditary Chondrodysplasia
London, 1991, Bailliere Tindale. (Spider Lamb Syndrome)
5. Cross RF, Parker CF: Oral administration of zinc sulfate for
control of ovine footrot, J Am Vet Med Assoc 178(7):704, 1981. Spider lamb syndrome is an inherited musculoskeletal
6. Cross RF, Parker CF: Zinc sulfate foot bath for control of ovine condition seen primarily in the Suffolk and Hampshire
foot rot, J Am Vet Med Assoc 178(7):706, 1981. breeds.3 Clinical signs may be present at birth or affected
7. Egerton JR: Footrot of cattle, goats, and deer. In Egerton JR, Yong lambs may appear normal at birth, only to have the
WK, Riffkin GG, editors: Footrot and foot abscess of ruminants, severe skeletal abnormalities develop by 6 weeks of age.4
Boca Raton, FL, 1989, CRC Press. This latter group may have longer legs with angular de-
8. Stewart DJ: Footrot in sheep. In Egerton JR, Yong WK, Riffkin
viations, shallower bodies, and narrower chests than
GG, editors: Footrot and foot abscess of ruminants, Boca Raton, FL,
normal lambs,4 and these animals display the expected
1989, CRC Press.
9. Kimberling CV, Ellis RP: Advances in the control of foot rot in
radiographic abnormalities associated with this condition
sheep, Vet Clin North Am Food Anim Pract 6:671, 1990. at birth. Skeletal abnormalities exhibited by affected
10. Ghimire SC, Egerton JR, Dhyngyel OP: Transmission of virulent lambs vary in severity and type. Chondrodysplasia is
footrot between sheep and goats, Aust Vet J 77:450, 1999. evident in the skull, sternum, appendicular skeleton, and
11. Rings DM: Ovine contagious foot rot. In Howard JL, Smith RA, vertebrae.
editors: Current veterinary therapy 4, food animal practice, Philadel- Radiographically, the dorsal silhouette of the skull may
phia, 1999, WB Saunders. be rounded, the occipital condyles may be elongated (oc-
12. Bulgin MS et al: Comparison of treatment methods for the control casionally with cartilage erosion), and thickening of the
of contagious ovine foot rot, J Am Vet Med Assoc 189:194, 1986. occipital bone between the condyles and the poll may be
13. Radostits OM et al: Veterinary medicine, ed 9, Philadelphia, 2000,
evident. The sternebrae may be of abnormal size and
WB Saunders.
shape. The sternum is often misaligned, dorsally devi-
14. Vandyke S et al: Treatment of ovine foot rot: use of florfenicol
versus oxytetracycline for treatment of ovine foot rot, Sheep and
ated, and not fused across the midline. The scapula and
Goat Res J 15:54, 1999. olecranon usually have more cartilage and less bone dis-
15. Guss SB: Management and diseases of dairy goats, Scottsdale, AZ, tally than normal. Animals with spider lamb syndrome
1977, Dairy Goat Journal Publishing. have several islands of ossification near the anconeal
16. Bulgin MS: Diagnosis of lameness in sheep, Compend Contin Educ process that can be seen on flexed lateral radiographs of
Pract Vet 8:F122, 1986. the elbow. The distal physis of the radius is flared, and
17. Naylor RD, Martin PK, Jones JR: Isolation of a spirochete from a angular limb deformities are common. Generally the
case of severe virulent ovine footrot, Vet Rec 25:690, 1998. forelimbs are more severely affected than the hindlimbs.
Erosion of articular cartilage is common if the lamb sur-
vives for a few months. The vertebrae commonly have ab-
CONGENITAL CONDITIONS normal and excessive cartilage. Vertebral body abnormal-
ities may contribute to scoliosis or, less commonly,
Myotonia Congenita kyphosis.4 Histologically, the typical osseous lesion is
Myotonia congenita is a heritable condition of goats in manifested as uneven growth cartilage.
which the animal experiences tetanic muscle contraction Spider lamb syndrome is inherited as an autosomal re-
when startled. Occasionally the contraction is severe cessive trait with complete penetrance but variable ex-
enough that the goat collapses to the ground. This phe- pression. The pathologic changes are found by the end of
nomenon has led to affected animals being referred to as the second trimester of gestation.4 The carriers of the re-
fainting goats. This condition is caused by an autosomal cessive gene have a normal phenotype that makes elimi-
dominant trait.1 Some speculate that the variability in nation of the condition difficult. The locus that causes
clinical signs and intensity of muscle contractions may be spider lamb syndrome has been localized to ovine chro-
related to the animal being homozygous rather than het- mosome 6, and deoxyribonucleic acid (DNA) tests may
erozygous for the trait.1 The condition closely resembles soon allow identification of carrier animals.5
 Chapter 9 Diseases of the Musculoskeletal System • 229

Arthrogryposis verely affected animals the patella remains luxated and is

Arthrogryposis and hydranencephaly are congenital con- difficult to reduce into its normal position. This manipu-
ditions that must be differentiated from spider lamb syn- lation is more easily accomplished with the stifle held in
drome. The two conditions cause severe deformities in extension.
sheep. Arthrogryposis and hydranencephaly may result Standard radiographic views with the addition of a
from infection with Akabane virus, Cache Valley virus, skyline image demonstrate the position of the patella, the
bluetongue virus, and possibly other organisms that affect depth of the trochlear groove, and other osseous abnor-
the developing fetus. Affected animals have severely malities that may be present. The skyline view, which
flexed forelimbs and overextended hindlimbs. A spiral allows the best assessment of the trochlear groove, is
deviation of the spine also is present. Neurologic condi- taken with the stifle flexed and the x-ray beam directed
tions that may be seen with arthrogryposis and hydranen- proximally to distally perpendicular to the tibia. However,
cephaly include cerebellar hypoplasia, hydrocephalus, mi- the ease of luxation on palpation of the patella is much
cromelia, and hydrocephaly. more important diagnostically than is the location of the
patella on a single craniocaudal radiograph. The affected
patella is often in a normal position for a given radi-
Polydactyly ograph if it is not purposely luxated by the examiner
By definition, polydactyly is a congenital anomaly in before the radiograph is taken.
which extra digits are present. It is seldom seen in sheep Surgery is usually indicated for young animals with
and goats. The condition is certainly heritable in cattle congenital patella luxation. Most young animals respond
and probably heritable in pigs, where cleft palate may well to imbrication of the fibrous joint capsule and over-
concurrently be seen. Polydactyly is suggested to be heri- lying fascia on the side opposite the direction of patella
table in horses. One report of polydactyly in goats de- luxation. However, the veterinarian must fully evaluate
scribes an affected female that was sired by a male with the limb before surgery and assess the joint at surgery.
polydactyly.6 Polydactyly usually has only cosmetic con- Some severe cases may require trochleoplasty or tibial
sequences for affected animals. However, polydactyly may crest osteotomy and relocation. The reader should refer to
cause serious gait abnormalities in some animals. The small animal surgery texts for detailed descriptions of the
practitioner must thoroughly examine animals with gait more complex stifle surgeries.7
abnormalities to determine whether the lameness is Affected animals should be thoroughly examined for
because of some other anomaly or clinically significant other congenital abnormalities. Specifically, severely af-
lesion. Radiographs are necessary to assess the anomaly fected newborns may not be able to stand and suckle.
fully and determine any treatment to be rendered. Therefore failure of passive transfer and associated illness
may become more significant to the health of these
Treatment. Treatment involves surgical removal of the animals than even the primary patella luxation. Small ru-
extra digits and primary closure of the skin incision. minants may compensate for mild cases of patella luxa-
Removal of some of the digits can be done by sharp exci- tion (especially if the condition is unilateral) and go undi-
sion; however, orthopedic instrumentation is sometimes agnosed until they are seen by veterinarians as adults with
required to disrupt osseous attachment. Appropriate lameness caused by luxation or degenerative joint disease
postoperative care should be given after surgical excision. caused by intermittent luxation. Adult animals also may
exhibit acute lameness as a result of traumatic patella lux-
ation. Surgical treatment of these adults tends to be
Patella Luxation more involved in that orthopedic implants such as screws
Animals with congenital patella luxation are usually and wires may be required to secure the patella. The prog-
brought to veterinarians shortly after birth because they nosis for a return to soundness is not good compared
tend to crouch on the rear legs when attempting to stand. with the prognosis for treated neonates with congenital
The patella luxation functionally disrupts the quadriceps luxations.8,9
apparatus, rendering the animal unable to hold the stifle
in extension. The primary differential diagnosis that must
be ruled out with this presentation is femoral nerve
Spastic Paresis
injury, which also causes failure of the quadriceps appara- Spastic paresis has been described in pygmy goats.10 Af-
tus because of lack of strength in the quadriceps muscle, fected goats suffer constant contraction of the gastrocne-
producing the same abnormal stance. Femoral nerve mius muscles in the hind legs. The contraction produces
injury is more commonly seen in calves after dystocia extension of the tibiotarsal joint and arching of the back.
than it is in small ruminants. A diagnosis of patella luxa- Clinical signs are not significantly different than those
tion is easily made by palpating the patella; a luxated described in several breeds of cattle.11-13 The condition is
patella easily dislocates either medially or laterally. In se- suspected to be inherited, but the exact mode of trans-
230 • Sheep and Goat Medicine
mission is unknown. No lesions have been noted in the piratory difficulties and subcutaneous emphysema. Sub-
spinal cord, tibial or peroneal nerves, or gastrocnemius cutaneous emphysema also can result from the under-
muscle. The clinical signs appear to be caused by a defect mining skin wounds alone, making diagnosis of tracheal
in the myotactic reflex that results in an overstimulation perforation difficult in some cases and adding to the dif-
or relative lack of inhibition of the efferent motor ficulty of detecting a tracheal wound. Perforation of the
neurons.10 esophagus is common. Esophageal injury may lead to
abscess formation and tissue necrosis as a result of con-
R EFERENCES
1. Bryant SH, Lipicky RJ, Herzog WH: Variability of myotonia signs
tamination of surrounding tissues by esophageal con-
tents. Abscess formation may physically impinge on the
airway and make swallowing difficult. Neurologic
in myotonic goats, Am J Vet Res 29(12):2371, 1968. damage from the primary injury or damage caused by
2. McKerrell RE: Myotonia in man and animals: confusing compar- abscess formation may inhibit normal function of the soft
isons, Equine Vet J 19:266, 1987. palate.
3. Rook JS et al: Diagnosis of hereditary chondrodysplasia (spider
Tetanus antitoxin should be administered to these
lamb syndrome) in sheep, J Am Vet Med Assoc 193(6):713, 1988.
4. Oberbauer AM et al: Developmental progression of the spider
animals, as well as broad-spectrum antibiotics (florfenicol
lamb syndrome, Small Rumin Res 18:179, 1995. 20 mg/kg every 48 hours) to combat wound infection and
5. Cockett NE et al: Localization of the locus causing spider lamb sepsis. Antibiotics with good efficacy against anaerobic
syndrome to the distal end of ovine chromosome 6, Mammal bacteria (penicillin 20,000 IU/kg BID) should be consid-
Genome 10:35, 1999. ered in cases in which massive trauma has resulted in
6. Al-Ani FK, Hailat NQ, Fathalla MA: Polydactyly in Shami breed some tissue devitalization. All skin wounds must be thor-
goats in Jordan, Small Rumin Res 26:177, 1997. oughly cleaned of organic debris and foreign material.
7. Hulse DA, Shires PK: Textbook of small animal surgery, Philadel- Establishing drainage in undermined skin wounds also is
phia, 1985, WB Saunders. important. Some of these wounds lend themselves to
8. Baron RJ: Laterally luxating patella in a goat, J Am Vet Med Assoc débridement and delayed primary closure, whereas others
191(11):1471, 1987.
are best managed by allowing second intention healing.
9. Gahlot TK et al: Correction of patella luxation in goats, Mod Vet
Pract, p 418, May 1983.
The veterinarian must be conscious of injury to muscle
10. Baker J et al: Spastic paresis in pygmy goats, J Vet Int Med 3(2):113, and joints deep beneath these skin wounds. Supportive
1989. care in the form of fluids and NSAIDs (flunixin meglu-
11. Leipold HW et al: Spastic paresis in beef shorthorn cattle, J Am Vet mine 1 to 2 mg/kg intravenously [IV]) is important in
Med Assoc 151(5):598, 1967. treating any myopathy.
12. Thomason KJ, Beeman KB: Spastic paresis in Gelbvieh calves: an
examination of two cases, Vet Med 82(5):548, 1987.
13. Harper PAW: Spastic paresis in Brahman crossbred cattle, Aust Vet Fractures
J 70(12):456, 1993. The hallmark of long bone fracture in small ruminants is
acute non–weight-bearing lameness. A thorough physical
examination must be performed to rule out other causes
TRAUMATIC CONDITIONS of severe lameness, including septic arthritis, joint luxa-
tion, and severe footrot. The clinician should readily
Predator Attack detect instability and crepitance on palpation of the frac-
Sheep and goats are of the stature and disposition to ture site. The exception is an incomplete or greenstick
make them susceptible to predators. Small ruminants fracture that manifests itself as a less severe acute lame-
seldom survive attacks by wild carnivores. However, vet- ness that improves with time. The clinician should not
erinarians are sometimes called to treat survivors of overlook the possibility that an incomplete fracture may
attacks by domestic animals or interrupted attacks by suffer a catastrophic breakdown and become unstable
wild animals. These survivors often ultimately die rather than heal. Because of economic constraints, radi-
because of either lethal injury to internal organs or physi- ographic examination may be impractical. However,
cal exhaustion from the chase and the attack. A veterinar- whenever possible, radiographic evaluations before and
ian treating animals that survive the initial trauma may after repair enhance the success of the procedure.
face a significant challenge. Although skin wounds are The most commonly treated fractures occur in the
quite obvious after the animal is thoroughly examined metacarpal and metatarsal bones.1 These fractures are
and clipped, injuries to deeper structures and serious my- usually treated successfully with a cast. Fractures of the
opathy are more difficult to assess. distal half of the metacarpal and metatarsal bones often
Attacking predators tend to “go for the jugular,” which respond well to lower limb casts that incorporate the foot
leads to a concentration of wounds in the head and neck and extend proximally to a point just distal to the carpus
area. The associated injury to the great vessels is usually and tarsus. Proximal or comminuted metacarpal and
obvious and often fatal. Tracheal puncture can cause res- metatarsal fractures may require full-limb casting with or
 Chapter 9 Diseases of the Musculoskeletal System • 231

without transfixation pins to stabilize the fracture prop- form a plan for treating unusual orthopedic injuries in
erly and prevent collapse. small ruminants by considering principles of small animal
Many fractures of the carpus or tarsus also respond to orthopedics and cost-benefit decision-making processes
treatment with a full-limb cast.2 However, these injuries of food animal medicine.
are often associated with contamination of the joint, and Mandible fractures may occur in small ruminants that
the incidence of septic arthritis is high. Septic arthritis re- have been kicked by a large animal such as a horse or cow
quires more intensive antibiotic therapy, as well as local and those that have caught the rostral mandible in a fence
treatment through a window in the cast. One complica- or some other object. A kick injury may result in any
tion with using treatment windows in casts is the number of fracture configurations; the veterinarian must
“window edema” that sometimes develops. The cast refer to information on small animal fundamentals to de-
window should be cut out as one piece. Edema can be termine whether plates, wires, or pins are the most appro-
avoided by securing this piece in the window with tape priate surgical stabilizers. Occasionally external fixators
between treatments. The management of carpal tarsal can be used to treat mandibular fractures (Figure 9-3).
fractures with concomitant septic arthritis is difficult. Rostral fractures may involve mostly teeth and soft tissues
Ankylosis of the joint often results even if successful frac- but very little bone. They often cause loss of teeth but
ture healing occurs.2 minimal instability. Therefore the veterinarian may wish
Radial fractures must be evaluated individually to de- to débride the area, institute antibiotic therapy, and
termine the best mode of treatment. Fractures of the modify the animal’s diet. If the mandibular fracture
distal radius may respond to a full-limb cast. Proximal occurs between the incisors and the cheek teeth, it may be
radius fractures may heal better with the use of an exter- stabilized by securing wires from the rostral mandible to
nal fixator, a transfixation cast, or possibly a modified the cheek teeth.5,6 Animals with these types of fractures
Thomas splint. Splints may be very applicable for require nutritional support, either orally or parenterally
neonates, and need only stay in place for 2 to 4 weeks in (see Chapter 2). Many of these animals can be fed a
most instances.3 Some radial fractures may require inter- moistened pelleted diet.
nal fixation with plates and screws. However, internal fix- Occasionally digit or leg amputation is required to
ation is seldom required and often not economically fea- treat septic conditions, fractures, or luxations (Figure
sible in small ruminants. If a splint is used for radial 9-4). Amputation can be done with the animal under
fractures, it should extend to the elbow and preferably general anesthesia or with the animal sedated and under
above it.3 local anesthesia (see Chapter 16). For digit amputation a
Treatment decisions for tibia fractures are very similar tourniquet should be applied proximal to the fetlock after
to those for radius fractures. Distal fractures heal well the surgical site is prepared in an aseptic manner. A cir-
with full-limb casting.4 The tibia is an area where one of cumferential skin incision is made just proximal to the
the authors (Dr. Baird) often chooses to employ an exter- coronary band. Many texts recommend two incisions per-
nal fixator or in larger goats a transfixation full-limb cast.
Fractures of the humerus and femur occur less fre-
quently in small ruminants.1 Humeral fractures often
heal with stall rest alone. However, the distal limb fre-
quently suffers carpal contracture, rendering the animal
unsound regardless of fracture healing. Femoral fractures
may heal if the limb is taped in a modified Ehmer sling
(made of tape placed in figure eights around the limb)
that is taped to the abdomen.3 This method is less costly
but is still an effective method in young or light-weight
animals.3 Fractures of the humerus and femur usually
require internal fixation with plates and screws or in-
tramedullary pins. The mode of internal fixation depends
on the complexity of the fracture and the experience of
the veterinarian. Financial considerations may dictate the
use of intramedullary pins rather than plates and screws if
possible.
Fractures in other areas such as the scapula and pelvis
can be treated much as they are in the dog. Small rumi-
nants are usually good orthopedic patients because of
Figure 9-3 This intraoperative photograph shows the repair of a
their relatively small size and ability to maneuver well on mandibular fracture with an external fixator. The pin ends are within
three limbs. Often pelvic or scapula fractures heal if the the pieces of 2-inch plastic tubing, which will be filled with hoof
animal is confined for 3 to 6 weeks.3 The veterinarian can acrylic to function as connecting rods.
232 • Sheep and Goat Medicine

Figure 9-4 A dorsoplantar radiographic view of the phalanges of Figure 9-5 Intraoperative photograph of digit amputation showing
a sheep with lameness caused by a chronic wound of the medial digit. the flaps of the inverted T incision being retracted with towel clamps
Note the pronounced soft tissue swelling with minimal osseous and the Gigli wire being crossed as the amputation is performed.
changes.

pendicular to the circumferential incision (one dorsal and should be considered. If all or part of a leg is to be ampu-
another palmar or plantar) to create a skin flap that is el- tated, as much of the limb as possible should be left in
evated to allow amputation with Gigli wire. The authors place. Similar techniques as those used in other small
prefer to make one incision over the abaxial aspect of the animals can be applied to limb removal in sheep and goats.
affected digit perpendicular to the coronary band to
create an inverted T incision. The two flaps of the in- Cast. The previous description of fractures discussed
verted T can be undermined to allow the passage and casting as a primary treatment option for fixation of frac-
crossing of the Gigli wire (Figure 9-5). The amputation tures. The clinician should prepare the limb for cast ap-
should be completed on an angle at the distal aspect of plication by removing any organic debris to ensure the leg
the proximal phalanx, with the clinician removing all of is clean. Cotton or gauze sponges should be placed in the
the articular cartilage and synovial membrane of the interdigital space to prevent pinching of the interdigital
proximal interphalangeal joint while leaving the interdig- skin within the cast by the hooves. Orthopedic felt or
ital ligaments intact to provide stability to the fetlock. gauze sponges should be placed over the dewclaws to
The corners of the flaps of the inverted T can be trimmed provide padding; however, holes should be cut to allow
to minimize dead space when the surgical site is closed. the dewclaws to protrude. Without this precaution, pres-
The site can be closed completely if the amputation is sure from the cast over the dewclaws can cause skin ulcer-
performed as a treatment for fracture or luxation. ations and may even result in dewclaw sloughing. The cli-
However, if infection is present in the form of septic nician then applies a double layer of stockinette to the
arthritis or osteomyelitis, the clinician should consider limb and places a strip of orthopedic felt around the limb
the advantages of drainage facilitated by partial closure. where the most proximal part of the cast will end. The
With either closure, a bandage should be placed on the authors prefer to put this proximal felt between two layers
foot to aid in hemostasis before the tourniquet is of stockinette so the felt is encased in the stockinette
removed. The bandage should be changed as needed until when it is rolled down over the felt during application of
the incision site has healed. The use of broad-spectrum the cast. However, others place the felt beneath the stock-
antibiotics (oxytetracycline 10 mg/kg IV or IM BID, or inette. Other padding materials may be used according to
20 mg/kg SC every 48 hours) and antiinflammatory drugs preference, but the clinician should remember that the
 Chapter 9 Diseases of the Musculoskeletal System • 233

relatively small size of many sheep and goats demands BOX 9-2
that the cast not be overly heavy or bulky. The authors
believe no padding beyond the previously mentioned in-
terdigital cotton, orthopedic felt, and stockinette is neces-
Z F IPP ORMULA*
sary to prevent skin ulceration under a properly applied
cast. If the wool of heavily wooled animals is not clipped, Zinc oxide—4 parts
it may act as excellent padding.3 The one exception in Iodoform—4 parts
which more padding is useful is for very young animals, Mineral oil—4 parts
which are likely to experience significant growth while in
the cast and tend to be more prone to cast sores than *Zipp formula can be applied under a cast and may have an
adults. antibacterial effect for as long as 2 weeks. If zinc oxide ointment is
used, no mineral oil is required, and the ointment can be made of
Fiberglass casting material has replaced plaster in most equal parts zinc oxide and iodoform (30 ml of each).
practices because of its increased strength, lighter weight,
and faster drying time. The foot should be included in the
cast. The clinician should be careful to apply the cast
without wrinkles (which may cause cast sores) and in a figuration. The transfixation pins are placed through stab
timely manner so that all layers bond together as one incisions using aseptic technique. Intraoperative radi-
rather than laminate in several layers. The cast is not as ographs are helpful in the placement of the transfixation
strong if it dries in laminated layers. The solar surface of pins. However, this technique is usually successful even
the cast should be protected from wear in some manner. when pin placement is directed by palpation alone. An-
Methods of protecting this part of the cast include tape timicrobial ointment (“Zipp” ointment or neomycin-
alone, a section of tire inner tube and tape, and a walking polymyxin B-bacitracin) can be applied to the skin at the
pad made of hoof acrylic. The particular method chosen pin sites and covered with gauze sponges. The limb is
is less important than achieving the desired result of pre- then prepared as previously described for cast application.
venting exposure of the hoof through a worn cast. The formula for an ointment that can be applied under a
Any animal in a cast must be monitored closely to cast and has an antibacterial effect for as long as 2 weeks
detect complications as soon as possible. The clinician is given in Box 9-2. The clinician should cut holes into
should consider complications under the cast as the cause the stockinette to accommodate the pins and cut the pins
of any abnormal clinical signs such as fever, inappetence, so that they protrude about 1 to 1.5 cm beyond the antic-
increased lameness in the cast limb, and swelling proxi- ipated thickness of the cast. The cast material should be
mal to the cast. The cast should be palpated daily to de- applied so that the bone pin ends perforate the cast mate-
termine its fit and check for any areas of increased heat rial or the material placed around the pin. When the cast
that may indicate the formation of cast sores. However, material has set or become hardened, the pin ends should
some areas of the cast (e.g., over wounds and bony protu- be covered to prevent injury to the contralateral limb.
berances) are normally warmer than other areas of the Hoof acrylic or cotton and tape can be used to cover the
cast. Therefore, it is more important to recognize changes pin ends (Figures 9-6 and 9-7). As the fracture heals,
in relative warmth in the same area of the cast from day to bone resorption occurs around the pins, causing them to
day than differences in temperature between different loosen. Neither special instrumentation nor general anes-
areas of the cast. A fiberglass cast applied over stockinette thesia is required for pin removal (Figure 9-8).
is porous, and exudate from a wound or cast sore will
penetrate the cast. If the environment makes fly control External fixation. External fixators are preferable to
difficult, flies may be observed concentrating over these simple casts or transfixation casts in some fractures of the
localized areas of the cast before exudate can be seen pen- radius and tibia. Either traditional fixators or modified
etrating the cast. This part of the cast also may have an fixators using cast material to support the transcortical
increased relative temperature before the exudate pene- pins work well in small ruminants. Traditional external
trates it. fixation techniques described for small animals can be
Transfixation casts add stability in cases in which cast used for sheep and goats.8 A modified fixator designed to
immobilization alone is not adequate.1 Transfixation pins treat calf tibia fractures is less technically demanding to
help immobilize proximal fractures in ways that casting apply than a traditional external fixator9 but allows more
alone does not. In some cases comminuted distal fractures flexibility in pin placement. The authors have found this
collapse unless transfixation pins transfer the weight away technique to be most useful in tibia fractures but also of
from the distal limb to the transfixation pins.7 Applica- value for treatment of other fractures. The procedure is
tion of a transfixation cast often requires general anesthe- performed on a surgically prepared animal, under general
sia, although casting of hindlimbs can be done with seda- anesthesia (see Chapter 16) and according to aseptic
tion and spinal anesthesia. Pin diameter and placement technique. At least two pins must be placed proximal and
depend on animal size, bone diameter, and fracture con- two pins distal to the fracture site. The pins can be placed
234 • Sheep and Goat Medicine

Figure 9-6 A transfixation cast used to treat an open fracture in a Figure 9-8 Craniocaudal radiograph of the goat in Figure 9-6 at
175-pound goat. In this case the transfixation cast was chosen to give the time of cast removal 6 weeks after the initial injury.
added stability to enhance healing of the open fracture. Note the hoof
acrylic covering the pin ends. This cast also had a window on the
medial side of the limb for wound management, which is not shown.
through stab incisions from lateral to medial (type II
pins) through the skin on each side. One major advantage
of this technique is that a single type I pin can be placed
from the dorsal aspect. The type I pin passes through one
skin surface and both cortices of the bone, but not
through the caudal soft tissues and skin. A second type I
pin is not required because the cast material itself con-
nects and stabilizes the pins. This is a major advantage in
fractures (either proximal or distal) in which the fragment
size does not allow placement of two type II pins. The
pins should be incorporated into a cast of the same length
described previously for the transfixation cast and the
limb treated with topical ointment. This technique incor-
porates more padding than that used with a standard cast.
Cotton or some other padding should be wrapped around
the entire length of the tibia. No stockinette or orthope-
dic felt is required. Fiberglass cast material should then be
placed over the length of the tibia to incorporate the pins,
as is done with the transfixation cast. After the cast
hardens completely, the caudal quarter to third of the cast
can be removed and the padding cut away from the
caudal part of the limb. This modification allows unen-
cumbered movement of the gastrocnemius. Occasionally
the dorsal distal portion of the cast also must be trimmed
Figure 9-7 Lateral radiograph of the goat in Figure 9-6 at the time to allow flexion of the hock. Some patients initially
of transfixation cast application. require a splint or bandage over the fetlock to ensure the
 Chapter 9 Diseases of the Musculoskeletal System • 235

Figure 9-9 Craniocaudal radiograph of a modified external fixator

in a 3-month-old lamb with a tibia fracture.

animal bears weight on the solar surface of the foot. Most

patients become fully ambulatory in 48 to 72 hours.
Treatment of young animals should be tailored to prevent
a compensatory tarsal varus of the contralateral limb
(Figure 9-9). This procedure is technically less difficult Figure 9-10 Application of a Schroeder-Thomas splint on the
because the practitioner is allowed more variation in pin front limb of a goat. Note the wire in the hoof wall being used to
placement than if traditional connecting bars are used. secure the foot to the distal aspect of the splint. The splint is finished
The pin ends should be covered as they are in transfixa- with adhesive tape to secure the entire limb within the splint.
tion casting.9

Splints. Splints can be useful in treating some muscu- carpus is allowed to remain flexed for a prolonged period
loskeletal conditions in small ruminants. However, the in a non–weight-bearing animal. With this technique a
veterinarian should be selective in using them. Many padded bandage is placed on the limb and the splint is
practitioners are more comfortable using casts and exter- conformed to the bandage and secured with adhesive
nal fixators than applying and monitoring splints. The tape.
majority of small ruminants referred to one of the authors Another type of splint occasionally used in small rumi-
(Dr. Baird) for malunion or delayed-union healing of nants is the traction splint, commonly referred to as the
fractures had been treated with splints before referral. For Schroeder-Thomas splint (Figure 9-10). This splint is
this reason alone, practitioners should consider using usually made of aluminum rods and consists of a ring that
other techniques that achieve more stable fracture fixa- fits in the axillary or inguinal region of the animal with
tion. However, splints can be useful in selected cases if the bars on the dorsal and palmar or plantar aspect of the
practitioner is skilled at splint management. In emer- limb joined distally. The shape of the splint varies, as does
gency situations a splint can be made of cut polyvinyl the way particular parts of the limb are secured to the
chloride (PVC) pipe or other such material.6 splint depending on the specific reason the splint is
A spoon splint, either commercially manufactured or applied. Traction is applied by securing the foot to the
fashioned from cast material, is probably best used to distal splint with adhesive tape or by placing wires
support greenstick fractures of the distal limb. When through the hoof wall. A soft bandage should be placed
used in this way it helps prevent catastrophic breakdown on the limb, after which the limb is secured strategically
of the fracture. However, a more important role may be in to the splint. Usually tape is placed over the entire limb
preventing the limb contracture that can occur if the and distal splint10 (see Figure 9-10).
236 • Sheep and Goat Medicine
INFECTIOUS AND TRAUMATIC severe (non–weight-bearing) and animals may remain re-
cumbent. Affected animals are often febrile and anorexic.
CONDITIONS Other signs of systemic disease such as omphalitis,
meningitis, and uveitis may be evident.
Septic Arthritis
Bacterial infections of the joints (septic arthritis) occur Diagnosis. A sterile aspirate of synovial fluid should be
most commonly in neonates. However, older sheep and obtained and the fluid submitted for culture and cytology.
goats sporadically suffer from joint infection as a result of The character of the synovial fluid varies according to the
a penetrating injury or spread from adjacent infected etiology and stage of disease. Synovial fluid from infected
tissues, as in the case of footrot. In neonates, septic arthri- joints may be thin and watery (lacking normal viscosity)
tis is most often a sequela to septicemia and often a con- or thick and cloudy with purulent material. Infected sy-
sequence of failure of passive transfer. The bacteria iso- novial fluid often has characteristic pleocytosis and neu-
lated from lambs include Streptococcus, Escherichia coli, A. trophilia (more than 30,000 to 100,000 white blood
pyogenes, Erysipelothrix insidiosa (rhusiopathiae), Pas- cells/ml and more than 75% neutrophils), as well as an in-
teurella haemolytica, Corynebacterium pseudotuberculosis, creased total protein. Not all aspirates from septic joints
and Fusobacterium necrophorum. Staphylococcus aureus yield bacteria, but some do. Culture results may improve
arthritis is associated with tick pyemia, a disease seen in with the use of enhancement media or synovial mem-
lambs 2 to 6 weeks old in areas infested with Ixodes brane biopsy, particularly if the animal has been treated
ricinus. Streptococcus dysgalactiae has been reported as a with antimicrobial agents. Radiography may be used to
cause of arthritis in dairy goats and was the most determine the severity of degenerative changes, although
common pathogen isolated from arthritic lambs in bony changes may not be visible for several days after the
England and Wales. Other isolates included E. coli, onset of disease. Radiography may be more important to
coagulase-positive Staphylococcus, E. rhusiopathiae, and A. monitor the progression of septic arthritis during therapy.
pyogenes.12 Coexisting omphalitis was found in 16% of Ultrasonography also may be useful in evaluating existing
arthritic lambs. soft tissue pathology.
Erysipelothrix polyarthritis is a nonsuppurative condi-
tion usually seen in 2- to 6-month-old lambs, but it also Treatment. The administration of antimicrobial agents
can cause neonatal disease. Outbreaks may affect as many and joint lavage are the mainstays of treatment of septic
as 40% of the lambs in a flock. Hallmarks of this infection arthritis. Antimicrobials, which may be administered sys-
are fever and lameness, with minimal swelling of joints. temically or intraarticularly, should be chosen based on an
This nonsuppurative polyarthritis will progress to chronic assessment of specific pathogens (gram-positive bacteria
arthritis if not treated appropriately.11 are more likely) and culture results when available.13
Lavage of the joint with sterile polyionic solution aids in
Pathogenesis. Septicemia often contributes to hema- removal of inflammatory products. Light sedation of the
togenous seeding of joints with bacteria that localize in animal is usually indicated. The skin over the joint should
the synovial membrane. The resulting synovitis causes be clipped and surgically prepared, and the clinician
the affected animal to exhibit joint pain, heat, swelling, should adhere strictly to aseptic technique. The clinician
and synovial effusion. Progression of the septic arthritis inserts a needle (16- or 14-gauge) attached to a sterile
and associated synovitis causes damage to articular carti- syringe into the affected joint at the most obviously dis-
lage and subchondral bone. As bacteria proliferate, an tended area and aspirates fluid (for culture and cytology).
influx of inflammatory cells produce hydrolytic enzymes The joint is then distended with an isotonic solution
that destroy bacteria and normal cartilage, resulting in (e.g., saline, lactated Ringer’s). A second needle is placed
cartilage erosion. In the chronic stages of infection in the joint on the opposite side of the joint. Between 0.5
animals develop thickening of the synovial tissue, fibrosis to 1 L of fluid should be flushed through the joint. The
of the joint capsule, and signs of degenerative joint joint should be distended several times during the lavage
disease. by occluding the egress needle. The joint should be
flushed daily for 2 to 3 days; the need for subsequent
Clinical signs. The hallmarks of septic arthritis are flushings should be based on the presence of pain or
lameness and warm swelling of the joints. The joints most swelling and cytologic evaluation of joint fluid. Removing
commonly involved are the carpus, tarsus, and stifle. Any inflammatory mediators by lavage can improve clinical
joint may be infected, including the hip, shoulder, or signs, although such improvement is often temporary.
elbow; infection here may be more difficult to diagnose Some cases have accumulated fibrin within the joint and
than in the more commonly affected joints. Several joints over the articular cartilage that requires drainage and
may be affected, and the practitioner should always débridement by arthrotomy. Lavage of these joints may
perform a thorough examination when one septic joint is yield clear fluid after treatment, but any improvement is
discovered to rule out polyarthritis. Lameness may be short-lived. Just after lavage, nonirritating antibiotics
 Chapter 9 Diseases of the Musculoskeletal System • 237

should be instilled into the joint. In general products for joints and edema of surrounding tissue. The articular car-
IV use are adequate for intraarticular use. tilage is minimally affected.15,20
Regional limb perfusion with antibiotics is an adjunc-
tive procedure that may be beneficial in some cases.13 Diagnosis. Joint fluid may contain fibrin but is not pu-
This technique entails instilling small volumes of antimi- rulent. Elementary inclusion bodies may be seen on
crobial agents in targeted locations to achieve high con- Giemsa-stained smears of synovial fluid (see Chapters 5,
centrations in infected areas. Regional perfusion can be 6, and 11). Isolation of Chlamydia requires special media
accomplished with intramedullary administration of an- and is not routinely performed. The use of DNA-based
timicrobial agents but is more easily and commonly per- tests should aid and improve the understanding of the
formed by IV injection distal to a tourniquet. Sheep and epidemiology of different chlamydial infections.
goats generally should be sedated before this procedure. Differential diagnoses for chlamydial polyarthritis
The skin over the peripheral vein is aseptically prepared. include white muscle disease and nutritional osteodystro-
The clinician inserts a needle (20- or 21-gauge) into the phy. These diseases lack fever and synovial effusion,
vein in a proximal direction and infuses the antibiotic of however, and laboratory testing should help differentiate
choice (ceftiofur sodium 1 mg/kg or potassium or sodium these conditions.
penicillin 20,000 IU/kg). For repeated administration in
chronic conditions, a catheter (22-gauge) can be placed in Treatment and prevention. Oxytetracycline (20
the vein and the leg wrapped to help maintain catheter mg/kg SC or IM every 48 to 72 hours), erythromycin (3
patency.14 The prognosis for septic arthritis is guarded to 5 mg/kg IM three times a day [TID] or BID), and
and chronic lameness is a sequela in many cases. tylosin (20 mg/kg IM BID) may be useful.17 Treatment
early in the course of disease speeds recovery.15,20 During
Prevention. Ensuring adequate passive transfer in an outbreak, lame and febrile lambs should be isolated
neonates helps prevent septicemia and septic arthritis re- from healthy lambs to minimize the spread of infection.
sulting from hematogenous spread of bacteria to joints. A vaccine is available for chlamydial abortion, but re-
Maintaining a clean environment for lambing and kid- searchers have not determined whether it provides pro-
ding and providing appropriate umbilical care also help tection against C. pecorum arthritis (see Chapter 6).
prevent neonatal septicemia.
Mycoplasmal Polyarthritis
Chlamydial Polyarthritis Mycoplasmal arthritis is a highly fatal disease of goats
Chlamydial polyarthritis is a common contagious disease marked by polyarthritis, septicemia, and mastitis. This
of feedlot lambs in the United States. The disease is sus- disease is usually caused by Mycoplasma mycoides sub-
pected to occur in goats as well.15 The causative agent species mycoides (Mmm), although other mycoplasmas
was formerly considered to be a strain (immunotype 2) of (M. agalactiae, M. capricolum, M. putrefaciens) cause
Chlamydia psittaci but has been recently classified as similar syndromes.21 Disease in goats is caused by the
Chlamydophila pecorum.16,17 Economic losses associated large-colony (LC) or caprine biotype of Mmm. This
with chlamydial arthritis result from weight loss and is distinct from the small-colony (SC) or bovine bio-
treatment costs. Disease occurs in 1- to 8-month-old type that causes contagious bovine pleuropneumonia
lambs, with 3- to 5-month-old lambs most commonly af- (CBPP), a disease eradicated from the United States in
fected.18 In feedlots outbreaks often occur a few weeks 1892. Sheep may be experimentally infected, and natural
after lambs are introduced.18 Morbidity can be as high as infection in sheep is suspected to occur.22
80%, with less than 1% mortality.17 Mycoplasmal arthritis occurs as an epizootic condition
in many countries throughout the world. In the United
Pathogenesis. C. pecorum is present in nasal and ocular States, most outbreaks are in large goat dairies. Morbidity
secretions, feces, and urine of infected animals.18 As many and mortality rates as high as 90% have been reported in
as half the lambs on some farms shed C. pecorum in feces kids.23 M. putrefaciens was responsible for the loss of 700
without signs of clinical disease.16 goats in one California dairy.24
Mmm is usually introduced to a farm by an asympto-
Clinical signs. Affected lambs have fever (up to 108° matic shedder. The bacteria are shed in the colostrum and
F) and are reluctant to move, often appearing “tucked up” milk of infected does, and ingestion is thought to be the
or becoming recumbent. Lameness is apparent in one or primary source of infection of kids.22-24 In one outbreak
more limbs, and affected joints are typically enlarged.15,18 about half of the does shed Mmm in milk. Some animals
Chlamydial conjunctivitis may occur concurrently.18-20 were intermittent asymptomatic shedders, but most ulti-
The course of the disease is about 10 to 14 days without mately developed clinical mastitis.25 Horizontal trans-
treatment. Most lambs recover, but some remain lame.15 mission was documented among kids housed together
Significant necropsy findings include fibrinous exudate in and is likely to occur among adults, especially in the
238 • Sheep and Goat Medicine
milking parlor.26 Illness often follows stresses such as cas- teurized goat milk. Disease in adults can be controlled by
tration, dehorning, concurrent disease, bad weather, and identifying carriers by milk culture and either culling car-
overcrowding.24,25,27 riers or isolating infected animals and milking them after
uninfected animals. Cultures of individual does and the
Pathogenesis. Infection leads to mycoplasmosis and bulk tank should be performed periodically to identify
involvement of numerous body systems, with fibrinous newly infected animals or intermittent shedders, and
polyarthritis, pneumonia, peritonitis, mastitis, conjunc- colostrum should be cultured at the time of freshening.
tivitis, and pericarditis being among the more common No vaccine is currently commercially available (see
presentations. If animals recover, the organism may be Chapter 5).
shed in ocular and nasal secretions and in milk.28

Clinical signs. Kids 3 to 8 weeks old are most suscepti-

Osteomyelitis
ble, but animals of any age may be affected. Clinical signs Bone infections usually result from hematogenous spread
include fever, warm swellings of numerous joints, masti- of organisms or from direct inoculation associated with
tis, lameness, conjunctivitis, weight loss, and pneumonia. trauma to soft tissues covering the bone. The soft tissue
Three syndromes have been described in kids. A peracute damage may be from either an acute injury (trauma or
form results in death in 12 to 24 hours with fever being surgical incision) or decubital ulcers in a recumbent
the only sign. A second group of kids showed signs of animal. Occasionally the ulcers develop during normal
brain disease (opisthotonos) and died in 24 to 72 hours. recumbency when animals are housed on hard, rough sur-
The third syndrome was characterized by fever, warm faces and are not sequelae of debilitation. The infectious
swollen joints, lameness, recumbency, and pneumonia. agents include Corynebacterium, A. pyogenes, Rhodococcus
Many in this group died within a few days, but some lame equi, and E. coli.
kids recovered over a few weeks.23 Adult females may
develop acute or peracute mastitis, the latter causing Clinical signs. Lameness, pain on palpation, and focal
death in 1 to 3 days. Does that recover may have udder fi- swelling are common clinical signs of osteomyelitis.
brosis and may shed Mmm intermittently. Arthritis is a Severe lameness may result in recumbency. Infection of
less common finding in adults compared with kids. Mas- vertebrae may produce signs of spinal cord dysfunction.17
titis and severe lameness without fever were observed in
an M. putrefaciens outbreak.24 Diagnosis. Radiographic changes usually cannot be
seen before the infection has persisted for 10 to 14 days.
Diagnosis. Laboratory work usually shows leukocyto- When radiographic changes are present they consist of a
sis, neutrophilia, and hyperfibrinogenemia. Peracute cases combination of lysis and proliferation. Avascular frag-
may exhibit neutropenia with a left shift. Synovial fluid ments of dead bone and sequestra also may be seen. If the
has an elevated cell count with neutrophilia and fibrin osteomyelitis is related to a surgical infection, the incision
clots. Mycoplasma can be cultured using special media. usually dehisces and the surrounding skin shows signs of
The LC type of Mmm is considered less fastidious than inflammation or even vascular compromise. The site may
other mycoplasmas.23 be aspirated for culture. Laboratory tests may reveal
Postmortem findings include suppurative polyarthri- leukocytosis, leukopenia, or hyperfibrinogenemia.
tis, osteomyelitis, fibrinous pleuritis, pneumonia, peri- Trauma without bone infection must be considered as
tonitis, meningoencephalitis, and pericarditis.23,25,27 The a differential diagnosis for this condition. These cases
joints most commonly affected are the carpus, stifle, exhibit soft tissue inflammation but no osseous radi-
tarsus, hip, and elbow. Joint fluid is purulent and contains ographic changes. The radiographic changes of lysis and
fibrin, and the joint capsules are thickened, with erosions proliferation also may resemble the changes seen in re-
of articular cartilage. Mmm can be cultured from synovial sponse to neoplasia. Osteomyelitis may predispose the
fluid and from many internal sites.25 animal to pathologic fracture if bone lysis becomes severe
enough. The distinction must be made between a patho-
Treatment. Antibiotic treatment does not eliminate logic fracture related to neoplasia and a fracture that is in-
infection in most cases. Some animals appear to improve fected or becoming a proliferative nonunion.
only to relapse later. Tylosin is the antibiotic most com-
monly recommended (10 to 50 mg/kg TID), but its effi- Treatment and prevention. The prognosis is guarded.
cacy is uncertain.28 The use of newer antibiotics (florfeni- Antimicrobial therapy alone is rarely successful because
col) for mycoplasmal disease in goats has not been of its poor penetration of infected bone. Surgical débride-
examined, but may be of value. ment of infected tissue is an important component of
therapy. Antibiotics, particularly those used based on
Prevention. Effective preventive measures for kids culture and sensitivity patterns, should be continued for
include the feeding of heat-treated colostrum and pas- several weeks after surgical débridement. Regional perfu-
 Chapter 9 Diseases of the Musculoskeletal System • 239

sion of antibiotics may be useful in treating osteomyelitis. system. Proposed mechanisms for persistence include
Amputation is the only possible way to rid the animal of latent infection by a DNA provirus, viral replication that
infection in some cases. The possibility of control of in- waits for monocytes to differentiate into macrophages in
fection varies with the cause of the infection. Environ- tissue, low levels of neutralizing antibodies, and viral
mental control is probably the most important mecha- mutation of env genes. The virus localizes in the
nism to prevent trauma to the animal. Adherence to macrophages of the synovium, lung, central nervous
aseptic technique when performing any surgery on or system, and mammary gland. Initially the virus prolifer-
near osseous structures decreases surgical infection. ates rapidly and induces a vigorous immune response
that limits but does not eliminate the virus. Virus-
infected macrophages may be more prone to activation
Caprine Arthritis-Encephalitis and thereby induce proliferation of lymphocytes and
CAE is a chronic multisystemic disease of goats caused macrophages. Lymphocyte proliferation is a hallmark
by a nononcogenic retrovirus. Infection with caprine pathologic lesion seen in CAEV infection. The impor-
arthritis-encephalitis virus (CAEV) is widespread and tant target tissues of CAEV include the joints,
chronic polyarthritis is the most common clinical mani- mammary glands, lungs, and brain. At these target sites
festation.29 CAEV infection in sheep has been in- CAEV induces chronic inflammation by invoking the
duced experimentally but not reported in nature.30 host’s immune responses. The virus is capable of making
Other lentiviruses that are closely related to CAEV antigenic variants of itself to help it evade the host
include maedi-visna and ovine progressive pneumonia immune response. CAEV can often be isolated from
virus (OPPV). the synovial fluid and milk of infected animals.29,34
The seroprevalence of CAEV in goats in the United Disease results from inflammation elicited by the reac-
States, Canada, and Europe ranges from 38% to tion of the immune system to the virus. Infected macro-
81%.29,31,32 Seroprevalence in England, Australia, and phages express viral proteins near major histocompati-
developing countries is usually less than 10%.33 Clinical bility complex (MHC) antigens, which are recognized
arthritis is estimated to occur in less than 25% of seropos- by T lymphocytes and stimulate cytokine production.
itive animals but it may be more prevalent in some Goats usually seroconvert in 2 to 8 weeks but can have a
herds.29,32 The prevalence of other clinical syndromes is long clinical latency (years).
not known. Infection occurs by transmission of fluids that
contain infected macrophages from an infected animal Clinical signs. CAEV can cause chronic disease in
to an uninfected animal. The most efficient manner of several body systems; however, most infected animals
transmission is from dam to kid by ingesting colostrum or remain asymptomatic. Four clinical syndromes have been
milk from infected does.34 The presence of antiviral anti- described for CAEV-infected goats: arthritis, leukoen-
bodies in colostrum is not protective. Feeding nonpas- cephalomyelitis, interstitial pneumonia, and mastitis.
teurized milk increases the risk of infection.31,32 Hori- Chronic progressive arthritis is seen in goats older
zontal transmission of CAEV has been documented.34,35 than 6 months and is usually characterized by swelling of
When uninfected goats are housed with infected goats one or both carpal joints. Arthritis of the hock, stifle, hip,
for long periods a significant number seroconvert.34 Un- and atlantooccipital joints occurs but is not usually de-
infected does readily seroconvert when milked with in- tected clinically. In the initial stages, joint swelling may
fected does, presumably as a result of transfer of the virus wax and wane, and lameness is minimal. Some animals
during the milking process.34 Venereal transmission is experience a sudden onset of lameness. The time course is
possible, especially if one of the animals is clinically in- variable, with some animals deteriorating over a few years
fected.36 Transmission from doe to kid before or during and others remaining stable for several years.29 As the
parturition has been documented.35 No evidence sup- disease progresses, animals become lame or recumbent
ports transmission by an insect vector. Iatrogenic trans- and debilitated. Effusion of the atlantooccipital and
mission (by dehorning equipment or needles) also is supraspinous bursae may be detected. Radiographs of
possible. joints show soft tissue swelling initially, and calcification
of periarticular structures occurs in more advanced cases.
Pathogenesis. CAEV is a single-stranded ribonucleic The synovial fluid has a decreased protein concentration
acid (RNA) virus in the Lentivirus family that replicates and an increased cell count comprised of 90% mononu-
by forming a reverse transcriptase–dependent deoxyri- clear cells, primarily lymphocytes.29 Postmortem exami-
bonucleic acid (DNA) intermediate that may become nation usually reveals pathology in numerous joints in ad-
integrated into the host genome. CAEV infects mono- dition to the carpus. The joint capsule is thickened, often
cytes and macrophages and induces a persistent (life- with periarticular mineralization, but articular cartilage is
long) infection despite host antibody production. “Re- usually intact. Histopathology shows chronic proliferative
stricted replication” allows the virus to remain latent in synovitis with infiltration by lymphocytes, macrophages,
the host’s monocytes and undetected by the immune and plasma cells.
240 • Sheep and Goat Medicine
Diagnosis. No abnormalities are typically seen on temperature the virus is inactivated but the immunoglob-
hematology or blood chemistry except for mild anemia in ulins remain intact.36 Kids then are kept isolated and
some cases.29 Routine diagnosis is based on serologic raised on pasteurized (74° C [165° F] for 15 seconds) goat
testing, although sensitivity and specificity are not well or cow milk or milk replacer. At least every 6 months,
defined and tests are not standardized. The agar gel im- keepers should test kids for CAEV and cull animals that
munodiffusion (AGID) test is the most widely used test test positive. Kids fed pasteurized milk are less likely to
because of its low cost and rapid results. It has good seroconvert than kids fed unpasteurized milk. However,
specificity and fair sensitivity. Laboratories perform the cases presumed to result from horizontal transmission
test with either CAEV or OPPV. The enzyme-linked may continue to occur.31,32 Contact transmission of
immunospecific assay (ELISA) test may detect infection CAEV infection has been demonstrated in goats of all
earlier than the AGID.36 Polymerase chain reaction ages, although the exact nature of the contract required
(PCR) assays can detect viral proteins in blood, milk, and for transmission is unknown. Transmission during breed-
tissue and may prove useful in diagnosing early infec- ing or gestation (transplacental) is unlikely. In a dairy
tion.37 Virus isolation takes 3 to 4 weeks and sensitivity herd, CAEV-infected does should be milked last. New
is poor. additions should be quarantined and tested within 60
A positive antibody test signifies infection, although days of arrival. Under normal husbandry practices, trans-
animals may remain asymptomatic for years. The time to fer of CAEV from goats to sheep is unlikely.
seroconversion varies and may not occur for months after Chemical disinfection of equipment between use with
infection. Therefore false negatives may occur early in the seropositive and seronegative animals should include the
disease process. Intermittent negative AGID tests have use of phenolic and quaternary ammonium compounds.
been reported in seropositive animals.38 Complete eradication of CAEV infection in a herd may
be impossible without the culling of seropositive goats.
Treatment. No specific treatment exists or is likely to Nevertheless, iatrogenic transmission by needles or in-
be developed. Affected animals are a source of infection struments can be avoided through the use of aseptic tech-
to others and their symptoms worsen over time. Most nique. Segregation of seropositive and seronegative does
symptomatic animals are ultimately culled or euthanized by a solid wall or 2 m alley is advisable.36
because of lameness, recumbency, weight loss, or poor
production. Supportive care for affected goats consists of
nutritional management and the provision of high-
Ovine Progressive Pneumonia
quality, easily digestible, readily accessible feed. Goats Ovine progressive pneumonia (OPP) is a chronic disease
with the arthritic form of the disease require frequent of sheep caused by a nononcogenic retrovirus. Predilec-
proper foot trimming, administration of NSAIDs tion sites for this virus include the lung, udder, and, less
(phenylbutazone or aspirin 100 mg/kg PO BID), good commonly, joints. OPPV is similar to maedi-visna virus
pasture management, and soft and thick bedding to (MVV), and together the two are referred to as ovine
prevent trauma to the limbs. Treatment as described for lentivirus (OvLV).40 OPPV also is closely related to
degenerative joint disease may be of benefit. CAEV, and arthritis caused by OPPV in sheep closely re-
sembles that caused by CAEV in goats. Cross-infection
Prevention. Attempts to induce immunity to CAEV with CAEV in sheep and OPPV in goats has been
with formalin-inactivated virus in adjuvants have not been induced experimentally but not reported in nature.30
successful. In fact, vaccinated goats develop more severe Lentiviruses induce persistent infections (life-long) and
disease than unvaccinated controls when challenged.39 replicate by integrating DNA into the host genome (see
A program of periodic testing and culling of all posi- Chapter 5).
tive animals should eradicate the virus from a herd. This
method is not often chosen because of the large number Clinical signs. The majority of sheep infected with
of animals likely to be culled from herds with high infec- OPPV are asymptomatic. Clinically apparent illness,
tion rates. which usually occurs years after infection, may involve
The following management protocol should signifi- one or more body systems. The lungs and udder are the
cantly reduce the prevalence of CAEV in a herd by elim- sites most commonly affected, but chronic arthritis also
inating the transmission of CAEV in colostrum and occurs in association with OPPV infection.41-43 In some
milk. Kids should be removed from the dam at birth to sheep lameness is the chief clinical sign, although other
prevent nursing. They should be removed immediately body systems (typically lung or udder) may be concur-
because licking of the kid by the doe may allow transmis- rently affected.41,42
sion of CAEV, presumably via saliva.36 Kids should be Because of OPP’s long incubation period, clinical
isolated from older animals and given colostrum that has signs are observed in adults. Slowly progressive joint
been heat treated at 56° C (133° F) for 1 hour. At this swelling, lameness, and weight loss despite good appetite
 Chapter 9 Diseases of the Musculoskeletal System • 241

are the typical musculoskeletal manifestations of OPPV Clinical signs. Common clinical signs in human
infection. The carpi are the joints most commonly af- beings and dogs include arthritis, skin rash, neuritis,
fected; the tarsi are affected less frequently.40,42,43 Exam- meningitis, and cardiac disease. Arthritis, abortion, poor
ination of the affected joints reveals firm soft tissue milk production, and laminitis have been linked with B.
swelling.41,42 Radiography may reveal mineralization of burgdorferi infection in cattle.45 Few cases of Lyme
soft tissue and osseous proliferation of adjacent bones.41 disease have been reported in sheep or goats. However,
Sheep usually die within 1 year of developing clinical borreliosis has been suggested as a cause of arthritis in
signs.43 Postmortem examination reveals severe degener- lambs even when B. burgdorferi could not be isolated.46 A
ative changes of the joints, with fibrosis of the joint seroprevalence study using sheep from nine farms in
capsule, proliferation of synovial membranes, and erosion Scotland revealed that 40% of 1-year-old ewes were
of the articular cartilage. Histology reveals nonsuppura- seropositive although no clinical disease was reported.
tive lymphoid infiltration.43 OPPV can frequently be iso- The tick Ixodes ricinus was present on these farms.47 Ex-
lated from the synovial fluid of affected joints.42 The joint perimental infection of lambs produced no signs of
pathology is very similar to that reported in goats with disease.48
CAEV infection.42 Differential diagnoses include
mycoplasmosis, chlamydial arthritis, and laminitis. Diagnosis. Ideally diagnosis depends on the identifica-
tion of B. burgdorferi by culture, PCR, or other tech-
Diagnosis. Serologic tests are useful in diagnosing niques, but the organism is difficult to culture and other
OPPV infection. The AGID test is the most widely used techniques are not widely available. Serology is often used
serologic test for OPPV because it is quick, inexpensive, to confirm a diagnosis, but the high seropositive rate in
very specific, and fairly sensitive. Other common sero- the absence of clinical disease is a confounding factor.
logic tests include ELISA, complement fixation (CF), Frequently in endemic regions a clinical diagnosis is
serum neutralization, immunoblot, and immunoprecipi- made based on clinical signs, elimination of other causes
tation. A diagnosis of OPP infection also may be made by of lameness, and response to treatment.
virus isolation or identification of viral nucleic acid, but
these methods are costly and rarely useful in clinical case Treatment. An optimal treatment for Lyme disease in
management. ruminants has not been determined. A typical treatment
Because OPPV infection is lifelong, the presence of regimen is a prolonged (2- to 4-week) course of oxytetra-
antibodies confirms infection, except in the instance of cycline, ceftiofur, or penicillin. Prevention of the disease
passive transfer of antibodies to a neonate from a positive currently relies on eliminating the tick with insecticides.
dam. (Even in this instance, the lamb is likely to become A vaccine has been developed for use in dogs, but none is
infected by ingesting colostrum or milk from the infected available for large animals.
ewe).44 The majority of infected animals are asympto-
matic, so the clinician should rule out other differential
diagnoses before concluding that clinical signs are caused
Clostridial Myonecrosis (Blackleg)
by OPP. Obviously, a negative test helps rule out infec- Clostridial myonecrosis is a highly fatal infection of
tion. Reasons for false negative results include early infec- muscle caused by the anaerobic spore-forming bacterium
tion (seroconversion may not take place for months after Clostridium chauvoei. Other clostridial species (chiefly C.
infection) and seroreversion, which is seen rarely in ad- septicum and C. novyi) have been isolated from cattle with
vanced stages of the disease. blackleg, either alone or with C. chauvoei. The disease is
most common in cattle, but sheep also may be affected.
Treatment. No specific treatment is available for Goats appear less susceptible than sheep.49
OPPV. Palliative treatment with antiinflammatory drugs Clostridial myonecrosis is not contagious, but often
could be considered in certain cases; however, affected occurs in outbreaks in sheep because the predisposing
animals are a source of infection to others (see Chapters 5 conditions affect many animals simultaneously. Infection
and 14). is usually associated with wounds from castration, de-
horning, tail docking, shearing, dystocia, or injections.50
Animals of any age, including fetal lambs, may be af-
Lyme Disease fected.51 The mortality rate is close to 100%. C. chauvoei
Lyme disease is a multisystemic infection caused by a is ubiquitous and persistent in the soil and is frequently
spirochete, Borrelia burgdorferi. Ixodes species ticks trans- identified in the gastrointestinal tract.
mit the organism from rodents such as the white-footed
mouse (Peromyscus leucopus), the primary reservoir species Pathogenesis. In cattle most cases of blackleg arise
in the eastern United States, to larger mammals, includ- when endogenous clostridial spores that have lodged in
ing deer, human beings, cattle, horses, and sheep. tissues after absorption through the gastrointestinal tract
242 • Sheep and Goat Medicine
begin to proliferate and produce toxins. These cases Carcasses should be buried deeply or burned to reduce
do not usually have an associated break in the skin, al- contamination of soil.51
though the animal may have a history of blunt trauma
that might create a hypoxic environment conducive to
clostridial growth in the muscle. In contrast, clostridial
Sarcocystosis
myositis in sheep most often develops after contamina- Sarcocystis species parasites are coccidia that cycle
tion of a wound by spores from the environment. The between a carnivorous host and a herbivorous intermedi-
vegetative organisms liberate exotoxins that induce ate host. In ruminants, infection is often subclinical, but
severe necrotizing myositis followed by systemic toxemia abortion, failure to thrive, and neuromuscular disease
and death. Clostridial cardiac myositis has been reported have been reported.52 The development of clinical disease
in lambs.50 depends on the species of Sarcocystis as well as the dose
ingested. S. tenella is considered the most pathogenic
Clinical signs. Clostridial myonecrosis progresses very species for sheep, and S. capracanis is most pathogenic in
rapidly and animals are often found moribund or dead. goats.52 The sarcocysts from some species (S. gigantea, S.
Systemic signs observed early in the disease include fever, medusiformis) are large enough to be seen macroscopically
anorexia, and depression. Local signs depend on the site and result in carcass condemnation.
of infection. If a wound is infected, severe swelling and a The prevalence of infection in sheep and goats is high,
malodorous discharge are often evident.51 Blackleg is but clinical disease is uncommon. A postmortem survey
almost always fatal. of range goats in Texas revealed microscopic Sarcocystis
species in 60% of the animals, with the tongue being the
Diagnosis. Diagnosis is made based on culture of a most commonly affected site.53 The presence of working
clostridial pathogen from wounds or necrotic muscle as dogs that are fed raw meat is associated with sarcocystosis
well as necropsy findings. Samples for anaerobic culture in a herd. Administration of monensin may predispose to
should be taken quickly because the normal proliferation the development of clinical disease.54
of clostridial organisms in tissue after death can confound
results. A Gram’s stain of material from diseased muscle Pathogenesis. The definitive host, a carnivore,
may show large gram-positive rods. On gross examina- becomes infected by eating tissue from an intermediate
tion, affected muscle is darker than normal and has a host that contains sarcocysts. The parasite develops into a
rancid smell. Lesions tend to be deeper and have less as- sporocyst that is passed in the feces of the definitive host.
sociated gas than lesions typically found in cattle.51 The intermediate herbivore host is infected by consum-
When external wounds are involved, edema is evident. ing contaminated feed or water. After ingestion, sporo-
Histology shows myonecrosis, edema, and neutrophilic zoites penetrate the mucosa of the small intestine and
inflammation; clostridial organisms can usually be visual- lodge in the endothelial cells of the blood vessels.
ized. Identification of C. chauvoei is aided by fluorescent Damage to the vasculature results in hemorrhage and
antibody tests because culture of this organism may be anemia. The parasites ultimately enter muscle and nerve
difficult. Differential diagnoses include lightning strike cells, where they develop into sarcocysts.
and peracute infections such as anthrax and other
clostridial diseases. Clinical signs. Common clinical signs in sheep include
muscular weakness, ataxia, and flaccid paralysis. Poor
Treatment. The rapid death of most patients precludes growth and anemia also have been reported. Lambs are
treatment. However, if animals are detected by their early most susceptible. Sarcocystis infection also has been asso-
signs, high doses of penicillin (44,000 IU/kg IV every 4 ciated with esophageal dysfunction in sheep.52 Experi-
to 6 hours) are indicated until the animal’s condition sta- mental infection of two sheep with coyote-origin Sarco-
bilizes. Surgical incision of the skin and fascia over the af- cystis produced fever, anorexia, and anemia; one sheep
fected area is thought to be beneficial. Supportive exhibited abnormal behavior. Myositis was found in
measures include IV fluids and NSAIDs. many sites.53,55
Goats experimentally infected with S. capracanis
Prevention. Vaccination against C. chauvoei, C. novyi, showed a range of clinical signs. Goats receiving the
and C. septicum is recommended to reduce losses at smallest dose remained clinically normal, but goats re-
lambing and shearing time. Ewes should receive two ceiving higher doses developed fever, depression, and
doses, the second being administered 1 month before weakness, and many died acutely in the first weeks after
lambing. Annual boosters before lambing are necessary to infection. Microscopically, stages of the parasite were de-
protect ewes and neonatal lambs. Some of the literature tected in the endothelial cells of arteries in many organs.
also recommends vaccinating older lambs before shear- Myocardial necrosis was observed in many goats. Multi-
ing. The efficacy of vaccination programs is unknown. focal necrosis, gliosis, and vasculitis of the central nervous
 Chapter 9 Diseases of the Musculoskeletal System • 243

system was noted, and sarcocysts were found in the brain overriding the balancing repair processes normally
and spinal cord.55 present. This lack of balance in the joint leads to inflam-
mation that produces heat, swelling, and pain. Degenera-
Diagnosis. Laboratory findings reported in cattle tive joint disease in small ruminants is most often a
include a regenerative anemia, and elevations of the sequela to infectious arthritis. However, trauma such as
muscle enzymes creatine phosphokinase (CPK), aspar- direct injury to a joint also can result in degenerative joint
tate aminotransferase (AST), and lactate dehydrogenase disease. Pet goats and sheep (particularly geriatric
(LDH). Similar results are expected in sheep and goats. animals) tend to develop degenerative joint disease, and
Demonstration of a rise in titer after acute illness aids in the condition can be exacerbated by CAE infection.56
diagnosis. Histology of skeletal or cardiac muscle reveals Other joints may be affected as well because of abnormal
the presence of sarcocysts. Differential diagnoses include stresses resulting from aberrant gait or weight-bearing
the numerous other causes of fever, anemia, and poor patterns used by the animal to compensate for the injured
growth. joint. Unfortunately, small ruminants function well with
mild lameness and therefore degenerative disease is often
Treatment and prevention. No approved treatment quite advanced before an affected animal is brought to
exists for sarcocystosis. The use of amprolium (100 the attention of a veterinarian (Figures 9-11 through 9-
mg/kg/day) or salinomycin has been reported.53 Carni- 13). If a clinician can examine an animal early in the
vores should be kept away from sheep and goats and ex- process of degenerative joint disease, he or she may be
posure to uncooked meat or carcasses should be mini- able to address the etiology directly or at least change
mized to help control this disease. However, removing management procedures in order to slow the progression
carnivorous guard dogs may increase losses to predators. of the disease. Some affected animals refuse to walk or
No vaccine is currently available. have a stiff gait; many often have overgrown feet.

Treatment. Several dietary supplements and chon-

Degenerative Joint Disease droprotective agents are available to veterinary practition-
Degenerative joint disease is a complex physiologic ers today. No scientific studies support the efficacy of
process that can destroy articular cartilage and cripple these agents in small ruminants, but anecdotal reports
animals. Lameness is the most common clinical sign seen suggest some may be beneficial.56 Injections of a polysul-
in animals with degenerative joint disease. This lameness
results from normal destructive processes in the joint

Figure 9-11 This photograph shows an animal with advanced Figure 9-12 Ventrodorsal radiograph of the animal in Figure 9-11
degenerative joint disease. She had a history of an injury to the hip 3 showing extensive bone loss of the left femoral head, which most
years before this photograph was taken. By the time of presentation to likely resulted from the reported injury to the hip.
the veterinary hospital this animal needed assistance to stand and
would cross her hind legs as shown here.
244 • Sheep and Goat Medicine
low. Most deaths are seen in young animals as a result of
myocardial necrosis.57,58
FMD is readily spread by direct contact with affected
animals; aerosolization of the virus is another important
source of infection. Ruptured vesicles, respiratory secre-
tions, saliva, milk, urine, and semen are sources of the
virus. FMD also may be spread to new premises by
human beings, animal products, fomites, and even wind
currents.59 Most animals stop shedding the virus within a
few days of vesicle rupture, but cases of long-term (weeks
to years) carriers have been reported.57,58 The virus may
persist in the environment for months, and it is not de-
stroyed by common disinfectants. Wild hoof stock are
susceptible to FMD and in some cases may act as reser-
voirs for the virus.

Pathogenesis. The FMD virus, an aphthovirus (family

Picornaviridae), consists of seven serotypes (O, A, C, Asia
1, SAT 1, 2, and 3) and more than 60 subtypes that vary
in virulence and species-specificity.17 FMD virus gains
access to the animal through the mucosal epithelium,
Figure 9-13 A lateral radiographic view of the right stifle of the viremia ensues, and the virus localizes to epithelial sites
goat in Figure 9-11. Note the osteophyte formation. The degenerative throughout the body. Lesions are most evident in the oral
joint disease observed here is probably the result of abnormal stress mucosa and feet. Necrotizing myocarditis has been re-
in compensating for the chronic coxofemoral lesion.
ported to affect primarily young animals. Immunity con-
ferred by infection is fairly short-lived (a few years), and
cross-protection against other strains is poor.17

fated glycosaminoglycan (Adequan) (125 mg/week for 4 Clinical signs. In cattle infection with FMD virus pro-
weeks) have been suggested. Issues of expense and man- duces fever, vesicles, erosions, and ulcers of the oral
agement regarding long-term treatment of individual mucosa, teats, coronary band, and interdigital area. The
animals must be addressed by the owner before institut- lesions seem to be very painful, and the resulting clinical
ing therapy with chondroprotective agents. Administra- signs include anorexia, depression, salivation, agalactia,
tion of NSAIDs (phenylbutazone 10 mg/kg PO SID, and lameness. Weight loss, mastitis, and secondary bacte-
aspirin 100 mg/kg BID), provision of proper care, main- rial infections are common sequelae.17 Most animals
tenance of good body condition scores (2 to 3) in animals, recover within 2 to 3 weeks. Sheep and goats usually
and avoidance of obesity are all valuable parts of the ther- show milder clinical signs than cattle; however, severe
apeutic plan.56 outbreaks have been reported in sheep. Oral lesions are
usually mild and transient, and foot lesions and lameness
are the predominant symptoms noted.57,58 If the oral
Foot and Mouth Disease lesions are not detected, FMD may resemble infectious
Foot and mouth disease (FMD) is a highly contagious footrot.
viral disease of ruminants and swine characterized by Lesions detected on postmortem examination include
fever and vesicles of the mouth, feet, and teats. Cattle and vesicles, erosions, and ulcers of the mouth and feet. The
pigs are most severely affected, but sheep and goats are udder, pharynx, trachea, esophagus, forestomachs, and in-
susceptible. FMD often produces a mild clinical syn- testines also may be affected. The myocardia of neonates
drome in sheep and goats and therefore these species may often have pale streaks caused by necrosis, an appearance
be inapparent sources of the virus during outbreaks.57,58 known as tiger heart.17
FMD has significant economic impact resulting from loss
of production and limitations on movement of animals Diagnosis. Rapid confirmation of FMD is essential
from affected areas. FMD is endemic in Asia, Africa, because of the far-reaching consequences of this disease.
South America, and parts of Europe. North America, The clinical signs of FMD resemble those of other vesic-
Central America, and Australia are currently free of ular diseases such as bluetongue, vesicular stomatitis
FMD.59 FMD usually occurs as an outbreak that spreads (which rarely causes disease in small ruminants), and
rapidly. All hoof stock except for horses are susceptible. poxvirus infection. If FMD is suspected, a state veterinar-
Morbidity is high (close to 100%), although mortality is ian should be contacted immediately.
 Chapter 9 Diseases of the Musculoskeletal System • 245

Treatment. FMD has no specific treatment. Antiin- 18. Bulgin MS: Diagnosis of lameness in sheep, Compend Contin Ed
flammatory agents and topical dressings may be used to Pract Vet 8:F122, 1986.
alleviate discomfort. 19. Stephenson EH, Storz J, Hopkins JB: Properties and frequency of
isolation of Chlamydia from eyes of lambs with conjunctivitis and
polyarthritis, Am J Vet Res 35:177, 1974.
Control. FMD-free regions maintain their status by
20. Cutlip RC, Smith PC, Page LA: Chlamydial polyarthritis of
restricting the entry of live animals and animal products lambs: a review, J Am Vet Med Assoc 161:1213, 1972.
from endemic areas. Outbreaks in nonendemic areas are 21. DaMassa AJ, Wakenell PS, Brooks DL: Mycoplasmas of goats and
generally controlled by quarantine and eradication of af- sheep, J Vet Diagn Invest 4:101, 1992.
fected animals and those with which they have had 22. Rosendal S: Experimental infection of goats, sheep, and calves
contact. In endemic regions vaccination is employed to with the large colony type of Mycoplasma mycoides subsp. mycoides,
control FMD. Ideally the vaccine should contain local Vet Path 18:71, 1981.
strains of virus. The immunity provided by killed vaccine 23. DaMassa AJ, Brooks DL, Adler HE: Caprine mycoplasmosis:
is short-lived (6 to 8 months) and is protective against widespread infection in goats with Mycoplasma mycoides subsp my-
only a few strains of virus. Cattle are usually the focus of a coides (large colony type), Am J Vet Res 44:322, 1983.
24. DaMassa AJ et al: Caprine mycoplasmosis: an outbreak of mastitis
vaccination program, but vaccination of sheep and goats
and arthritis requiring the destruction of 700 goats, Vet Rec
in endemic regions is recommended.57,58
120:409, 1987.
25. East NE et al: Milkborne outbreak of Mycoplasma mycoides sub-

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1. Kaneps AJ: Orthopedic conditions of small ruminants, Vet Clin
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26. DaMassa AJ, Brooks DL, Holmberg CA: Induction of mycoplas-
North Am Adv Rumin Orthop 12(1):211, 1996. mosis in goat kids by oral inoculation with Mycoplasma mycoides
2. Nyack B, Padmore CL, White M: External fixation of carpal and subsp mycoides, Am J Vet Res 47:2084, 1986.
metacarpal fractures in a goat, Bovine Pract 3(3):23, 1982. 27. Rosendal S: Mycoplasma mycoides subspecies mycoides as a cause of
3. Smith MC: Practice tips for small ruminant veterinarians, Proceed- polyarthritis in goats, J Am Vet Med Assoc 175:378, 1979.
ings of the 1998 Symposium on Small Ruminants for the Mixed Animal 28. East NE: Mycoplasma mycoides polyarthritis in goats. In Smith BP,
Practitioner Western Veterinary Conference, 1998, Las Vegas, NV. editor: Large animal medicine, ed 2, St Louis, 1996, Mosby.
4. Mbiuki SM, Byagagaire SD: Full limb casting: a treatment for 29. Crawford TB, Adams DS: Caprine arthritis-encephalitis: clinical
tibial fractures in calves and goats, Vet Med 79(2):243, 1984. features and presence of antibody in selected goat populations, J
5. Monin T: Tension band repair of equine mandibular fractures, J Eq Am Vet Med Assoc 178:713, 1981.
Med Surg 1(10):325, 1977. 30. Banks KL et al: Experimental infection of sheep by caprine
6. DeBowes RM: Equine fracture repair, Philadelphia, 1996, WB arthritis-encephalitis virus and goats by progressive pneumonia
Saunders. virus, Am J Vet Res 44:2307, 1983.
7. Nunamaker DM et al: A new skeletal fixation device that allows 31. Rowe JD et al: Risk factors associated with the incidence of sero-
immediate full weight bearing application in the horse, Vet Surg conversion to caprine arthritis-encephalitis virus in goats on Cali-
15(5):345, 1986. fornia dairies, Am J Vet Res 53: 2396, 1992.
8. Egger EL, Greenwood KM: Textbook of small animal surgery, 32. East NE et al: Serologic prevalence of caprine arthritis-
Philadelphia, 1985, WB Saunders. encephalitis virus in California goat dairies, J Am Vet Med Assoc
9. St-Jean G, Clem MF, DeBowes RM: Transfixation pinning and 190:182, 1987.
casting of tibial fractures in calves: five cases (1985-1989), J Am Vet 33. Adams DS et al: Global survey of serological evidence of caprine
Med Assoc 198:139, 1991. arthritis-encephalitis virus infection, Vet Rec 115:493, 1984.
10. Arnoczky SP, Blass CE, McCoy L: External coaptation and band- 34. Adams DS et al: Transmission and control of caprine arthritis-
aging. In Slatter DH, editor: Textbook of small animal surgery, encephalitis virus, Am J Vet Res 44:1670, 1983.
Philadelphia, 1985, WB Saunders. 35. East NE et al: Modes of transmission of caprine arthritis-
11. Lamont MH: Arthritis. In Martin WS, editor: Diseases of sheep, encephalitis virus infection, Small Rumin Res 10:251, 1993.
Oxford, UK, 1983, Blackwell Scientific. 36. Rowe JD, East NE: Risk factors for transmission and methods for
12. Watkins GH, Sharp MW: Bacteria isolated from arthritis and control of caprine arthritis-encephalitis virus infection, Vet Clin
omphalitic lesions in lambs in England and Wales, Vet J 156:235, North Am Food Anim Pract 13:35, 1997.
1998. 37. Smith MC, Cutlip R: Effects of infection with caprine arthritis-
13. Trent AM, Plumb D: Treatment of infectious arthritis and os- encephalitis virus on milk production in goats, J Am Vet Med Assoc
teomyelitis, Vet Clin North Am Food Anim Pract 7:747, 1991. 193:63, 1988.
14. Navarre CB et al: Ceftiofur distribution in plasma and joint fluid 38. Hanson J, Hydbring E, Olsson K: A long term study of goats nat-
following regional limb injection in cattle, J Vet Pharmacol Ther urally infected with caprine arthritis-encephalitis virus, Acta Vet
22:13, 1999. Scand 37:31, 1996.
15. Adams DS: Infectious causes of lameness proximal to the foot, Vet 39. McGuire TC et al: Acute arthritis in caprine arthritis-encephalitis
Clin North Am Food Anim Pract 5:499, 1983. virus challenge exposure of vaccinated or persistently infected
16. Everett KDE: Chlamydia and chlamydiates: more than meets the goats, Am J Vet Res 47:537, 1986.
eye, Vet Microbiol 75:109, 2000. 40. de la Concha-Bermejillo A: Maedi-visna and ovine progressive
17. Radostits OM et al: Veterinary medicine, ed 9, Philadelphia, 2000, pneumonia, Vet Clin North Am Food Anim Pract 13:13, 1997.
WB Saunders.
246 • Sheep and Goat Medicine
41. Oliver RE et al: Ovine progressive pneumonia: pathologic and vi- NMD occurs in selenium-deficient areas throughout
rologic studies on the naturally occurring disease, Am J Vet Res the world. It is a significant disease in North America, the
42:1554, 1981. United Kingdom, Europe, Australia, and New Zealand.
42. Cutlip RC et al: Arthritis associated with ovine progressive pneu-
In the United States the northeast, southeast, and north-
monia, Am J Vet Res 46:65, 1985.
west regions are deficient in selenium; the central region
43. Cutlip RC et al: Ovine progressive pneumonia (maedi-visna) in
sheep, Vet Microbiol 17:237, 1988.
has sufficient selenium in its soil.2 Even within a region
44. Knowles DP: Laboratory diagnostic tests for retrovirus infections the selenium content of soil and forage may vary depend-
of small ruminants, Vet Clin North Am Food Anim Pract 13:1, 1997. ing on pH, season, and type of plants grown. For
45. Parker JL, White KK: Lyme borreliosis in cattle and horses: a example, alkaline soils encourage selenium uptake by
review of the literature, Cornell Vet 82:253, 1992. plants, whereas plants grown in areas of high rainfall and
46. Fridriksdottir V, Overnes G, Stuen S: Suspected Lyme borreliosis acidic soils are usually low or marginal in selenium
in sheep, Vet Rec 130:323, 1992. content.3 In most instances the selenium content of
47. Mitchell GBB, Smith IW: Lyme disease in Scotland: results of a pasture is lowest in the spring. Nitrogen and to a certain
serological study in sheep, Vet Rec 133:66, 1993. degree phosphorus fertilization and irrigation may de-
48. Stuen S. Fridriksdottir V: Experimental inoculation of sheep with
crease selenium uptake by plants. Faster-growing plants
Borrelia burgdorferi, Vet Rec 129:315, 1991.
have a lower selenium content; this condition is exacer-
49. Guss SB: Management and diseases of dairy goats, Scottsdale, AZ,
1977, Dairy Goat Journal Publishing.
bated when plants are grown on soils already marginal in
50. Radostits OM et al: Veterinary medicine, ed 9, Philadelphia, 2000, selenium. Hay grown in drier areas tends to have a higher
WB Saunders. selenium concentration. Hay analysis is crucial in deter-
51. Glastonbury JR et al: Clostridial myocarditis in lambs, Aust Vet J mining dietary selenium intake.
65:208, 1988. Selenium is absorbed, as are other minerals, in the
52. Dubey JP, Livingston CW: Sarcocystis capracanis and Toxoplasma small intestine. Therefore high concentrations of other
gondii infections in range goats from Texas, Am J Vet Res 47:523, minerals (e.g., calcium, sulfur, copper) may decrease its
1986. absorption. Also, certain feed contaminants (e.g., nitrate,
53. Jeffrey M, Low JC, Uggla A: A myopathy of sheep associated with unsaturated fats, sulfates) may further suppress selenium
Sarcocystis infection and monensin administration, Vet Rec 124:422,
uptake and availability.4 Forage with less than 0.1 ppm of
1989.
selenium on a dry matter basis is deficient.
54. Dubey JP, Fayer R, Seesee FM: Sarcocystis in feces of coyotes from
Montana: prevalence and experimental transmission to sheep and
Vitamin E helps prevent peroxidation of cell mem-
cattle, J Am Vet Med Assoc 173:1167, 1978. brane lipids, aiding in the maintenance of membrane in-
55. Dubey JP et al: Sarcocystosis in goats: clinical signs and pathologic tegrity. It also is somewhat protective against selenium
and hematologic findings, J Am Vet Med Assoc 178:683, 1981. deficiency. Of the forms of vitamin E, the d-isomer of
56. Smith ME: Exotic disease of small ruminants. Geriatric medicine alpha-tocopherol has the greatest biologic activity. It also
for small ruminants, Proceedings of the 1998 Symposium on Small is absorbed in the upper small intestine.5 Because bile
Ruminants for the Mixed Animal Practitioner Western Veterinary acids are needed for proper absorption, derangements in
Conference, 1998, Las Vegas, NV. small intestine function can decrease the absorption of
57. Sharma SK: Foot and mouth disease in sheep and goats, Vet Res J vitamin E, even if dietary concentrations are adequate.
4:1, 1981.
Vitamin E–deficient sheep and goats probably absorb
58. Barnett PV, Cox SJ: The role of small ruminants in the epidemiol-
50% to 75% of dietary tocopherol, whereas animals re-
ogy and transmission of foot and mouth disease, Vet J 158:6, 1999.
59. Scott GR: Foot-and-mouth disease. In Sewell MMH, Brocklesby
ceiving adequate vitamin E absorb only 20% to 30%.
DW, editors: Handbook on animal diseases in the tropics, ed 4, Vitamin E activity is good in green pasture and good hay.
Philadelphia, 1990, Bailliere Tindall. Legumes often have less available vitamin E than grass.3
Vitamin E can be destroyed by oxidative destruction, par-
ticularly if large amounts of unsaturated fats and certain
METABOLIC AND minerals (e.g., copper, iron) are added to the same supple-
ment or mineral mixture. Long-term storage of feedstuffs
NUTRITIONAL CONDITIONS decreases vitamin E activity by as much as 50% per
month.3
Nutritional Muscular Dystrophy Deficiencies occur when animals are fed poor-quality
Nutritional muscular dystrophy (NMD), also known as hay or straw and lack access to pasture. Diets high in
white muscle disease, is a disease of all large animals caused polyunsaturated fatty acids contribute to the develop-
by a deficiency of selenium and/or vitamin E. The disease ment of NMD by increasing the requirement for vitamin
affects skeletal and cardiac muscle and is most common E. Vitamin E requirements also are increased if vitamin
in young, rapidly growing animals. Selenium and vitamin C and/or carotenoids are deficient or if dietary nitrate
E deficiencies also produce syndromes of ill thrift and re- intake is increased. However, adequate vitamin C and
productive losses (see Chapter 2).1 beta-carotene in the diet help lower vitamin E require-
 Chapter 9 Diseases of the Musculoskeletal System • 247

ments. Adequate dietary selenium is almost completely common, sometimes accompanied by a heart murmur.
protective against vitamin E deficiency.6 Animals are often alert and their struggles to arise may be
Limited vitamin E transport occurs across the pla- interpreted as seizures. A history of collapse after exercise
centa, but colostrum has a large quantity of vitamin E. is typical (see Chapter 15). Differential diagnoses include
Therefore lambs and kids deprived of colostrum need toxicities, fulminant infectious diseases, pneumonia, and
supplemental vitamin E. neurologic disease such as polioencephalomalacia or
NMD occurs most commonly in kids and lambs tetanus.
whose mothers were fed a selenium-deficient diet. Most Animals with skeletal muscle degeneration have a dif-
cases occur in animals less than 6 months old, and NMD ferent appearance. These animals have a stiff gait and
has been reported in neonates. Kids are believed to be tremble while standing. Many prefer to remain in sternal
more susceptible than lambs, possibly because they have a recumbency. The muscles may feel firm. Signs described
higher requirement for selenium. Further, sudden muscu- in this form of the disease include hunched appearance,
lar activity in deficient animals unaccustomed to exercise stiff gait, and overall poor production.3 Lambs and kids
often triggers episodes of NMD.1 continue to weaken and eventually become unable to
Hydrogen peroxide and other free radicals are toxic nurse.7 Many young have aspiration pneumonia resulting
byproducts of cell metabolism that have the ability to from dysfunction of the glottis. Some adult animals con-
cause oxidative damage to biologic membranes. Selenium tinue to eat, but others are dysphagic because of involve-
is a cofactor in several enzyme systems in the body, but ment of the tongue. Skeletal and cardiac muscle disease
much of the pathology associated with selenium defi- may occur concurrently. Careful assessment of flock
ciency is caused by an impairment of the enzyme glu- history and a through physical examination are required
tathione peroxidase (GPx). GPx protects cell membranes to determine the underlying cause of the pneumonia.
against destruction by these endogenous peroxides by Other diseases that may appear similar include enzootic
converting them to relatively benign hydroxy fatty acids. ataxia, polyarthritis, and nutritional osteodystrophy.
The lipid-soluble vitamin E molecule acts as a free radical Vitamin E–associated NMD is most commonly encoun-
scavenger within the cell membrane. High concentra- tered in lambs and yearling ewe lambs.3
tions of dietary fat can overwhelm the vitamin E protec-
tion system.6 Selenium and vitamin E act as antioxidants Diagnosis. Elevated creatine kinase (CK) is a good in-
by separate mechanisms; diets that are deficient in sele- dicator of subclinical NMD.3 Marked elevations in CK
nium or vitamin E permit oxidative damage, which leads (10 to 50 ) can occur in NMD. CK has a short half-life
to muscle degeneration. The deficiency of these two nu- (2 to 4 hours), so elevations indicate recent or ongoing
trients result in a buildup of free radicals and increases in muscle damage. CK levels return to normal as the animal
subsequent damage. Muscles with high metabolic activity recovers. AST also is elevated with muscle injury;
are most susceptible (e.g., heart, diaphragm). This syn- however, it is not specific to muscle disease—hepatic
drome and other selenium-responsive diseases are most disease also may cause elevations in AST. AST has a
commonly encountered in young growing lambs, particu- longer half-life than CK, and concentrations are elevated
larly those 2 to 4 months of age.3,7 Selenium deficiency for several days after an episode of NMD. Elevations in
also may impair the body’s immune system. In cattle and CK and AST are not specific for NMD, and these
possibly in sheep and goats, deficient selenium intake can enzymes may be elevated in any recumbent animal.
result in reduced neutrophilic response, a higher inci- However, CK and AST generally occur in much higher
dence of mastitis and metritis, and poor overall body con- serum concentrations in the presence of primary muscle
dition. Because of their compromised immune systems, disease such as NMD.
many of these lambs are more susceptible to other conta- Selenium deficiency can be confirmed by measuring
gious diseases. Sheep consuming selenium-deficient diets selenium levels in whole blood or tissues. In cases of flock
produce low wool yields and may have an increased inci- problems, 10% of the flock or 7 to 10 ewes and/or
dence of periodontal disease. Adults consuming a defi- lambs should have blood collected for selenium analysis.3
cient diet may have these signs, whereas growing lambs Erythrocyte GPx concentrations are highly correlated
and kids exhibit NMD. with selenium concentration, and activity of this enzyme
is a useful diagnostic test. However, GPx samples must be
Clinical signs. Two syndromes of NMD are classically handled with care, and many diagnostic laboratories do
described: an acute to peracute cardiac form and the more not offer the test. Testing for serum selenium levels may
common subacute skeletal muscle form. Animals with in- be of value for flock assays if the diet has been maintained
volvement of cardiac muscle show acute signs that for weeks to months. It is of questionable value in assess-
include recumbency, respiratory distress, and death. Res- ing individuals, particularly those that have experienced
piratory signs include tachypnea and frothy nasal dis- any dietary changes. Obviously, most sick animals have
charge resulting from pulmonary edema. Tachycardia is undergone a diet change, and many have anorexia. Evalu-
248 • Sheep and Goat Medicine
ating whole blood selenium is the easiest and most reli- 0.7 mg/head/day or 90 ppm in the mineral mixture for
able test. Selenium concentrations in whole blood reflect free choice feeding.3 Although the use of free choice
the selenium concentration of the diet over the life of a mineral supplementation is an excellent mode of sele-
red blood cell.8 More than 95% of blood selenium is nium supplementation, ensuring a complete diet or pro-
located inside the red blood cell and was placed there viding a dietary supplement of 0.2 ppm selenium ensures
when the cell was manufactured. Vitamin E status can be more consistent mineral intake.7 Fresh legumes and
assessed by measuring serum tocopherol. Some special- grasses are good sources of vitamin E.9 Silage, oil seeds,
ized laboratories offer a vitamin E assay. This chapter cereal grains, and dry hays tend to be poor sources of
does not provide guidelines for adequate or deficient con- vitamin E.5 Therefore, diets high in grain content should
centrations because of the variance in techniques and be supplemented with vitamin E.
assays among laboratories. Instead, the clinician should Alternatively, selenium and vitamin E can be incorpo-
inquire about normal values from the laboratory where rated in mineral mixes that are fed free choice to pregnant
samples are assayed. and lactating ewes. If feedstuffs contain oxidizing agents
At necropsy, affected muscles are friable and contain (e.g., copper, iron), fats, or a high content of disulfide
pale streaks that correspond with regions of degeneration bonds (onions), vitamin E potency may be reduced, with
and mineralization. The distribution is bilaterally sym- resultant deficiency.3 Whenever these dietary factors are
metric. Similar changes are seen in the myocardium if encountered, supplemental vitamin E is indicated. Diets
animals have cardiac involvement. Histology of muscle high in corn also may be associated with vitamin E defi-
shows hyaline degeneration, necrosis, and mineralization. ciency because a lowered rumen pH reduces vitamin E
Chronic infections (caused by depressed immune func- activity. This condition can be clinically significant in the
tion) and aspiration pneumonia (resulting from compro- young growing lamb or kid.
mised glottis-closing ability) also may be encountered.1-3 If it is not practical to supplement the diet, monthly
injections of a commercial vitamin E–selenium selenite
Treatment. One injection of a vitamin E and/or sele- compound may be useful, although they may need to be
nium preparation should result in improvement within a repeated more often in lambs.1 Injecting the dam 30 days
few days. The treatment can be repeated in 24 hours. Fol- before birth can help prevent NMD.3,7 Injecting lambs
lowing the label doses of some commercial products will with selenium–vitamin E preparations at tail docking (1
provide adequate selenium but very little vitamin E, and mg selenium) and again at weaning (2 mg selenium) may
supplementation may be required. If other animals show be protective on some farms. In addition to injected sup-
clinical signs, they also should be treated. The clinician plements, another source of vitamin E should be provided
should avoid exposing the animals to stress or exertion because the amount in commercially available injectable
during treatment. Most animals respond to treatment; compounds are too low to prevent disease in deficient
however, those with cardiac involvement have a poor animals. Access to pasture or quality forage should
recovery rate. provide adequate levels of vitamin E.
Other options for selenium supplementation are prac-
Prevention. NMD can be prevented by supplementing ticed in some regions. A slow-release formulation of se-
the diet of susceptible animals with selenium and vitamin lenite can be given by SC injection. A dose of 1 mg/kg
E. Supplementation of pregnant animals helps reduce selenium given to ewes 3 weeks before lambing protects
disease in newborns because selenium is transferred lambs for as long as 12 weeks after birth. An intraruminal
across the placenta and also is present in colostrum and selenium pellet also is available for sheep. Top-dressing
milk. Clinicians and keepers should pay careful attention of pasture with sodium selenite at a dose of 10 g
to the proper dosage of selenium to prevent toxicosis in selenium/hectare is practiced in some countries. This
the animals and should adhere to withdrawal periods to method is safe and prevents NMD for at least 12
limit concentrations in tissues at slaughter. Pasture, hay, months.1 For bottle-fed lambs, the keeper should ensure
and any grain supplements should be assayed to deter- an intake of adequate vitamin E in the milk replacer.
mine the amount of selenium to be added to a supple-
mental pellet, grain, or mineral mixture.
Selenium and vitamin E supplementation can take
Rickets and Osteomalacia
many forms. The dietary concentration of selenium Rickets is a disease of young animals caused by a failure of
should be more than 0.1 to 0.3 mg/kg.1,7 Feed supple- proper cartilage mineralization. Vitamin D deficiency is
mentation is commonly recommended. In some circum- the most common cause, but rickets may occur as a result
stances, higher levels of selenium are necessary to prevent of deficiencies in phosphorus and calcium as well. In older
NMD in lambs. Dietary supplementation appears to be animals the same deficiencies result in abnormal mineral-
the least expensive, most efficient method of ensuring ization of osteoid, a condition known as osteomalacia.
selenium adequacy. Current regulations in the United Rickets occurs mostly in rapidly growing animals that
States limit selenium supplementation for sheep to have low vitamin D levels because of limited sun expo-
 Chapter 9 Diseases of the Musculoskeletal System • 249

sure. Animals housed indoors, those fed green (uncured) ered animals frequently maintain a short stature with
forage, and those living at high latitudes in winter are limb deformities.
most prone. Animals that consume a diet low in calcium
or phosphorus occasionally develop rickets. Ingestion of Prevention. Rickets and osteomalacia can be managed
some poisonous plants, particularly those containing ox- by providing access to sunlight and properly cured forage.
alates (which bind calcium in the intestine); chronic lead Dietary calcium and phosphorus levels should be ad-
or flouride aluminum toxicity; and chronic parasitism can justed if they are low, and a calcium-to-phosphorus ratio
all produce or add to the pathogenesis of rickets.6 of 11 to 21 should be maintained. Any potentially toxic
substances or plants should be removed from the diet.
Pathogenesis. The primary problem is failure of min-
eralization of cartilage and osteoid, which leads to per-
sistence of cartilage and irregular osteoid deposition.4 Ir-
Osteodystrophia Fibrosa
regular osteochondral junctions and widened physes Osteodystrophia fibrosa is a metabolic disease of goats
result. The metaphyses at the costochondral junctions are and sheep in which bone mineral is resorbed as a result of
noticeably affected. In the long bones the persistent soft prolonged hypersecretion of parathyroid hormone
tissue in the physis is deformed by weight bearing. In the (PTH). High phosphorus or low calcium levels in the
diaphysis, osteoid is not properly mineralized.10 Long- diet frequently contribute to osteodystrophia fibrosa.
haired or woolly animals raised in latitudes closer to the Clinically, this disease is similar to rickets.
earth’s poles, those raised indoors, and those fed milk Osteodystrophia fibrosa is most commonly seen in
replacers with inadequate vitamin D concentrations may animals consuming a high-phosphorus diet. Diets with a
be particularly deficient in vitamin D and predisposed high proportion of bran or other cereal grains are often
to NMD. associated with this disease. Cereal grains have an inap-
propriate calcium-to-phosphorus ratio, and much of the
Clinical signs. Affected animals are usually less than 1 phosphorus in cereal grains is in the form of phytic
year old and have a stiff gait, shifting legs, lameness, and acid. High phytic acid content can further depress
recumbency. Joints and bones of the distal aspects of the calcium absorption from the intestine. The dietary
limbs may be enlarged, and enlargements of the ribs at calcium–to–phosphorus ratio should be maintained at
the costochondral junctions (rachitic rosary) are fre- 11 to 21. Many cereal grains or byproduct feeds (bran)
quently seen. Limbs are frequently deformed and may be have a ratio of 16 or greater.
bowed. Teeth may be mottled and their eruption delayed.
Animals may be thin as a result of failure to graze ade- Pathogenesis. Primary hyperparathyroidism caused by
quate forage.8 Differential diagnoses include NMD and hyperplasia or neoplasia of the parathyroid gland is ex-
infectious arthritis. tremely rare. Most cases of hyperparathyroidism are se-
quelae of nutritional or metabolic conditions that
Diagnosis. Blood chemistry shows elevations in alka- produce hypocalcemia. Diets with low levels of calcium,
line phosphatase greater than those seen in normally high levels of phosphorus, or deficient amounts of
growing animals. Blood levels of calcium and phosphorus vitamin D may result in hyperparathyroidism; frequently
may be low. Serum vitamin D is low but usually within more than one factor is present. PTH stimulates vitamin
normal ranges. Radiographic changes include widened D production, which in turn induces resorption of bone
growth plates, bowing of long bones, and thinned cor- in the animal to maintain calcium homeostasis. Renal
tices.10 In adults with osteomalacia, radiographic exami- failure also may result in hyperparathyroidism, but this
nation reveals porous bone. manifestation is uncommon in sheep and goats. All the
Postmortem examination reveals thickening of growth bones of the body are affected, but the bones of the face
plates and epiphyseal enlargement of long bones. Rib and mandible are most obviously abnormal.
fractures are often apparent. Histopathology of samples
from the costochondral junction in live animals also may Clinical signs. Bilateral enlargement of the mandible
be useful.10 Normal bone contains an ash–to–organic is typically the most obvious sign. The mandible feels soft
matter ratio of 32, whereas the ratio in rachitic bone is and the animal may not be able to open its mouth prop-
12 to 13. erly. Lameness and stiffness are often observed as a result
Careful investigation of feed content; access to sun- of pathologic fractures. Animals are often thin because of
light; and vitamin D, calcium, and phosphorus levels aid decreased food intake.
in determining the underlying cause of rickets.
Diagnosis. Radiographs show enlargement of the
Treatment. Vitamin D3 injections (10,000 to 30,000 mandible, decreased bone density, and rotation of the
IU/kg) may be beneficial if dietary supplementation of cheek teeth with the occlusal surfaces pointed lingually.
calcium and phosphorus occurs concurrently.10,11 Recov- Fractures of other bones may be apparent.12 Laboratory
250 • Sheep and Goat Medicine
results may show low calcium or high phosphorus levels, that have been fed diets high in grain to produce
but these tests often fall within the normal range. Alka- rapid weight gain develop lameness or joint swelling.
line phosphatase is sometimes elevated.13 Postmortem Radiographs of affected animals reveal osteochondrosis
examination shows the mandible to be quite soft and lesions as seen in other domestic animals.
malleable. Histology of the mandible shows a lack of
mineralization of bone and replacement of bone by an ex-
tensive fibrous matrix.
Caseous lymphadenitis (CL) commonly causes man-
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tion and radiographs should aid in distinguishing be- ians and state veterinary diagnostic laboratories for selenium defi-
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tween CL and osteodystrophia fibrosa.
3. Maas J, Parish SM, Hodgson DR: Nutritional myodegeneration.
In Smith BP, editor: Large animal internal medicine, St Louis,
Treatment. Animals may recover if placed on a diet 1996, Mosby.
with a calcium-to-phosphorus ratio of 11 or 21. The 4. Jubb KVF, Kennedy PC, Palmer N: Pathology of domestic animals,
enlarged mandible may not improve.13 Formulation of a ed 3, Orlando, FLA, 1985, Academic Press.
ration that ensures a calcium-to-phosphorus ratio of 11 5. Bulgin MS: Diagnosing nutritional difficulties, Proceedings of the
or greater should prevent nutritional hyperparathy- 1998 Symposium on Small Ruminants for the Mixed Animal Practi-
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6. Smart ME, Cymbaulk: Trace minerals. In Naylor JM, Ralston SL,
editors: Large animal clinical nutrition, St Louis, 1991, Mosby.
Epiphysitis 7. Naylor JM: Vitamins. In Naylor JM, Ralston SL, editors: Large
animal clinical nutrition, St Louis, 1991, Mosby.
Epiphysitis is a condition of rapidly growing animals in
8. Ogilvie TH: Musculoskeletal disorders. In Ogilvie TH, editor:
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Large animal internal medicine, Baltimore, 1998, Williams &
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about 1% of yearling dairy does.14 Large animal clinical nutrition, St Louis, 1991, Mosby.
10. Maas J: Rickets in ruminants. In Smith BP, editor: Large animal
Clinical signs. Clinical signs reported in a pregnant internal medicine, St Louis, 1996, Mosby.
yearling Nubian doe included insidious onset of lameness 11. Bonniwell MA et al: Rickets associated with vitamin D deficiency
progressing to recumbency. Enlargement of the carpi, in young sheep, Vet Rec 122:386, 1988.
tarsi, and fetlock joints were observed, as was angular 12. Andrews AH, Ingram PL, Longstaffe JA: Osteodystrophia fibrosa
in young goats, Vet Rec 112:404, 1983.
limb deformity. Radiographs revealed delayed matura-
13. Hesters NL, Yates DJ, Hunt E: Nutritional secondary hyper-
tion of cartilage and overgrowth of new bone. The
parathyroidism. In Smith BP, editor: Large animal internal medi-
animal’s gait improved shortly after parturition, but a cine, ed 2, St Louis, 1996, Mosby.
degree of limb deformity resulting from premature 14. Guss SB: Management and diseases of dairy goats, Scottsdale, AZ,
closure of a portion of the physes remained. The cause 1977, Dairy Goat Journal Publishing.
was attributed to trauma to the physes as a result of ad- 15. Bulgin MS: Diagnosis of lameness in sheep, Compend Contin Ed
vanced pregnancy.15 After noting epiphysitis in animals, Pract Vet 8:F122,1986.
the keeper should examine the diet to assess the adequacy 16. Hintz HF: Physitis (epiphysitis). In Smith BP, editor: Large
of copper and maintain a proper calcium-to-phosphorus animal internal medicine, ed 2, St Louis 1996, Mosby.
ratio of 41 to 61. Adequate calcium, phosphorus, 17. Anderson KL, Adams WM: Epiphysitis and recumbency in a
protein, and energy should all be maintained. Proper foot yearling prepartum goat, J Am Vet Med Assoc 183:226, 1983.
trimming, the provision of pain relief (NSAIDs), and the
removal of animals from hard surfaces may all be of
benefit.16,17
TOXIC CONDITIONS
Selenium Toxicity
Osteochondrosis Selenium toxicity may result from grazing pastures with a
Osteochondrosis is a disease of abnormal endochondral high selenium content or from exogenous administration
ossification. It is common in pigs and chickens and occurs of selenium by injection or feed supplementation. Acute
in most domestic animals, but it is rarely reported in poisoning may result in death, but chronic overdose leads
small ruminants. However, osteochondrosis should not to hoof malformation and lameness. The toxic dose for
be omitted from a differential diagnosis list when animals sheep has been reported to be 2.2 mg/kg orally as a single
 Chapter 9 Diseases of the Musculoskeletal System • 251

dose or chronic ingestion of 0.25 mg/kg body weight.1 Treatment. No specific treatment is effective. If
Sheep are considered more susceptible to selenium toxi- possible the source of excess selenium should be removed.
cosis than cattle. Little information is available about the
natural occurrence of selenium toxicosis in goats, but the Prevention. Selenium supplementation should be
administration of high doses of selenium can result in carefully monitored to ensure safe dosage. In regions
death.2 with seleniferous soils, supplemental forage can be pro-
Soils in specific regions of North America, Ireland, vided to reduce consumption of selenium-containing
Australia, and South Africa have a high selenium content plants and increase dietary protein. Rich sources of
because of the composition of the underlying rock.1 Soils sulfur-containing amino acids (soybean meal) in the diet
in areas of low annual rainfall often have an alkaline pH are partially protective. Alternate grazing of areas with
and are more likely to have high selenium levels. Plants plants that do not accumulate toxic concentrations of se-
extract selenium from the soil, and certain plants are con- lenium is another option. The addition of 0.01% arsanilic
centrators of selenium. These plants are not highly palat- acid or 20 ppm copper to the ration also may be preven-
able, but animals that graze in these areas may develop tive, but these substances are potentially toxic.
signs of toxicity if more palatable forage is lacking. Docu-
mented cases of naturally occurring selenium toxicity are
uncommon.3
Ergot Toxicosis
Selenium poisoning also occurs when incorrect doses Ergot toxicity results from ingestion of alkaloid com-
of selenium are administered to flocks in an attempt to pounds produced by the fungus Claviceps purpurea. This
prevent NMD. fungus infects cereals and grasses, most commonly rye,
Organic selenium compounds (i.e., those found in wheat, and oats. The seeds of the plants turn dark as
plants) are considered more toxic than inorganic com- they are filled with the fungal sclerotia, and this grossly
pounds such as selenite and selenium dioxide. This re- visible structure is referred to as an ergot. C. purpurea
ported difference does not always correlate with clinical is the fungal species most frequently linked with ergo-
disease.1 tism, but Acremonium coenophialum may cause a similar
syndrome.1
Pathogenesis. Selenium concentrates in the kidney, The pathology occurs in animals grazing ergot-
liver, and keratinized tissue and has a dystrophic effect on infested pasture or eating grain or hay made from such
skeletal muscle. Toxic concentrations of selenium may plants. It is fairly common in cattle, but reports in sheep
displace sulfur in some of the amino acids (methionine, and goats are rare. In one report of goats and sheep co-
cystine), preventing them from forming disulfide bonds grazing a fescue pasture, only goat kids were affected.4
and thereby weakening keratin formation. Hoof material The condition usually occurs after a warm wet season,
has high concentrations of methionine and cystine. The conditions that favor growth of the fungus.
mechanism of toxicity has not been determined, but sele-
nium also may interfere with the function of certain Pathogenesis. Ergots contain alkaloid compounds and
enzymes. A high-protein diet is protective against sele- other pharmacologically active compounds known as er-
nium toxicosis in sheep.1 gotoxins. The effects of this group of toxins, which in-
cludes ergotamine, ergotoxine, and ergometrine, include
Clinical signs. Acute poisoning results in dyspnea, constriction of arterioles and endothelial damage leading
tachycardia, fever, depression, and death. Signs of chronic to gangrene of the extremities.
toxicity include poor hair coat, alopecia, ill thrift, abnor-
mal appetite, respiratory failure, and lameness. Hoof Clinical signs. Clinical signs of ergotism include
lesions are apparent in all feet and include edema of the swelling, coolness, and hair loss, followed by drying and
coronary bands and deformity or separation of hooves. discoloration of the skin of the distal limbs, tail, and ears.
Neonates may have hoof abnormalities apparent at birth. A distinct demarcation between normal and gangrenous
skin is observed, and affected tissue may slough. Lame-
Diagnosis. Diagnosis is based on identifying toxic ness is evident, and animals may remain recumbent. Clin-
levels of selenium in the animal. Selenium levels in ical signs reported in goats include lameness, most often
blood, urine, and hair are all elevated. Anemia and low in the hindlimbs, with separation of the hoof in the most
hemoglobin levels are characteristic of chronic selenium severe cases.5 Ulceration of the oral, ruminal, and intes-
poisoning. Necropsy findings in chronic selenium poi- tinal mucosa has been reported in sheep.1
soning show myopathy of skeletal and cardiac muscle
and hoof and hair coat abnormalities as described previ- Diagnosis. Feed samples should be analyzed for ergot
ously. Lesions in many other organs also have been or similar compounds. Differential diagnoses include
described. thrombosis secondary to sepsis and trauma.
252 • Sheep and Goat Medicine
Treatment. No specific treatment exists for ergot toxic- storage of fluorine in bone. Urinary fluorine is often ele-
ity. Animals should be removed from the source of toxin. vated (16 to 68 mg/kg is normal for cattle). Serum alka-
line phosphatase levels are usually elevated.1,6
Prevention. Feed should contain less than 0.1% in- Radiographic abnormalities include increased bone
fected seedheads.1 Pastures with severe ergot infestations density, enlarged bones, narrowing of the marrow cavity,
should not be used for grazing or hay. and spontaneous fractures that heal poorly.
Postmortem examination reveals chalky, brittle bones
with diaphyseal exostoses. Histology shows abnormal cal-
Fluorosis (Fluorine Poisoning) cification of bone. Hypoplasia of enamel is observed in
Chronic fluorine poisoning (fluorosis) occurs after the in- animals with dental disease. Degenerative changes of
gestion of toxic amounts of fluorine compounds by feed many tissues, including bone marrow, are observed. The
or water. The severity of disease depends on the fluorine fluorine content of bones can be measured to confirm the
compound ingested. Sodium fluoride is more toxic than diagnosis. The mandible and metacarpal and metatarsal
rock phosphate; calcium fluoride or sodium fluorosilicate bones are considered the most reliable sources of bone for
are much less toxic. Sheep and goats are reported to be fluorine assay.1
less susceptible than cattle.5
Fluorine occurs naturally in rocks, usually in associa- Treatment. Keepers should remove animals from the
tion with phosphate. Soils derived from these rocks and source of fluorine. Cases of acute toxicity can be treated
water that percolates through these rock formations may with aluminum salts (to neutralize hydrofluoric acid in
contain high levels of fluorine. Other sources of fluorine the stomach) and IV calcium salts to control tetany.
include industrial contamination (as far as 14 km down- Dental and bone lesions do not usually improve. Animals
wind), deep water wells, volcanic ash, and phosphatic should be fed good-quality hay. The addition of calcium
supplements given to combat hypophosphatemia.1 carbonate or aluminum sulfate to the diet at 1% of the dry
matter intake may be beneficial in decreasing bone
Pathogenesis. The mechanism of fluorine toxicity has flouride content.
not been determined. Excess fluorine is deposited in
bones and teeth. Bony lesions may develop at any time in Prevention. Phosphate feed supplements for cattle
the animal, but dental lesions occur only if fluorine levels should not contain more than 0.2% to 0.3% fluorine. A
are high during the formation of the teeth. Urinary excre- phosphorus-to-fluoride ratio greater than 1001 should
tion of fluorine, accompanied by calcium and phospho- be maintained. Rock phosphate can be a source of fluo-
rus, leads to mobilization of calcium and phosphorus and rine, and deep water wells should be assayed for fluorine
results in osteomalacia and osteoporosis. Many other levels before use. Careful management of grassland and
sites, including the bone marrow, undergo degenerative water in high-fluorine areas may reduce losses caused by
changes.1 fluorine toxicosis.8 Some guidelines recommend feeding
aluminum salts to bind fluorine and reduce accumulation
Clinical signs. Acute fluorine toxicity is marked by in tissue, but these compounds are unpalatable.1
gastrointestinal signs, tetany, and death. Chronic inges-
tion leads to decreased feed consumption and unthrifti-
ness. Dental lesions, which consist of surface pitting and
Plant Toxicity
increased wear caused by improper enamel formation, are Australian sheep eating lupine stubble infested with the
the first to appear, although they may not be noticed. fungus Phomopsis (Diaporthe toxica) developed a myopa-
With time, rapid wear and tooth breakage occurs, leading thy of skeletal muscle marked by stiff gait and recum-
to impaired mastication.6,7 bency.9 Ingestion of Cassia roemeriana (twin-leaf senna) is
Signs of osteofluorosis include ill thrift, stiffness, and believed to cause a similar syndrome in cattle and sheep
lameness that is most prominent in the hindlimbs. Patho- in Texas, New Mexico, and Mexico.10
logic fractures, often of the third phalanx (P3), may occur
in several animals in the group. The affected bones are
painful to palpation and may be enlarged.1
R EFERENCES
1. Radostits OM et al: Veterinary medicine, ed 9, Philadelphia, 2000,
Differential diagnoses include other causes of lame-
WB Saunders.
ness on a herd or flock basis, including hypophos-
2. Ahmed KE et al: Experimental selenium poisoning in Nubian
phatemia, vitamin D deficiency, selenium toxicity, and se- goats, Vet Hum Toxicol 32:249, 1990.
lenium deficiency. 3. Edmondson AJ, Norman BB, Suther D: Survey of state veterinar-
ians and state veterinary diagnostic laboratories for selenium defi-
Diagnosis. Serum fluorine levels are often elevated in ciency and toxicosis in animals, J Am Vet Med Assoc 202:865,1993.
toxicosis (the normal level for cattle is 0.2 mg/dl), but 4. Hibbs CM, Wolf N: Ergot toxicosis in young goats, Mod Vet Pract
normal levels do not rule out toxicity because of the 63:126, 1982.
 Chapter 9 Diseases of the Musculoskeletal System • 253

5. Choubisa SL. Some observations on endemic fluorosis in domestic leading to flystrike or infestation of the wool with
animals in southern Rajasthan (India), Vet Res Comm 23:457, 1999. maggots. Furthermore, long tails in females appear to
6. Botha CJ et al: Two outbreaks of fluorosis in cattle and sheep, J S depress normal reproductive performance. For these and
Afr Vet Assoc 64:165, 1993.
other reasons, tails are usually removed. If the lamb is less
7. Schultheiss WA, Van Niekerk JC: Suspected chronic fluorosis in a
than 24 hours old, the stress associated with tail removal
sheep flock, J S Afr Vet Assoc 65:84, 1994.
8. Wang JD, Hong JP, Li JX: Studies on alleviation of industrial flu-
may decrease absorption of colostral antibodies and result
orosis in Baotou goats, Fluoride 28:131, 1995. in the diseases associated with failure or partial failure of
9. Allen JG et al. A lupinosis-associated myopathy in sheep and the passive transfer. Therefore lambs should be 2 to 3 days to
effectiveness of treatments to prevent it, Aust Vet J 69:75, 1992. 2 weeks old at docking. One of the authors (Dr. Pugh)
10. Rowe LD et al. Experimentally induced Cassia roemeriana poison- prefers to dock tails at 3 days on alert, healthy animals
ing in cattle and goats, Am J Vet Res 48:992, 1987. that are being cared for by their dams. The docking can
take place after the lambs and their dams are moved to a
single family unit (jug) or holding area. Placing the new
NEOPLASIA lamb and dam together helps prevent the ewe from wan-
Neoplasia of the musculoskeletal system is extremely rare dering off or abandoning the lamb after the procedure.
in sheep and goats. A study of 673 ovine neoplasms sub- Anesthesia is seldom required, with the obvious excep-
mitted to a veterinary laboratory in South Africa revealed tion of adult or pet animals (on owner’s request). If anes-
that 21 of them were of connective tissue origin. Types of thesia is required, either a sedative or a caudal epidural
tumors included chondroma, chondrosarcoma, fibroma, and ring block will suffice.1 Some studies suggest that a
fibrosarcoma, osteoma, rhabdomyosarcoma, leiomyoma, tail ring block of a local anesthetic can reduce the stress
and fibrolipoma.1 associated with tail removal.3 Still, Hooper1 has sug-
Osteosarcoma and pathologic fracture developed in a gested, and the authors of this chapter agree, that the
9-year-old Toggenburg goat 4 years after a comminuted neonatal lamb responds as much, or possibly more, to the
humeral fracture had been repaired with an in- injection of a local anesthetic as to the surgical removal of
tramedullary pin. The animal also was reported to have the tail without anesthesia.
pulmonary nodules, but these were not examined histo- The tail should be left long enough to cover the anus
logically.2 Mandibular osteoma was diagnosed in a 10- and may be extended to the dorsal aspect of the vulva on
year-old Toggenburg cross, and osteochondrosarcoma of females.2 The woolless distal attachment of the paired
the rib and sternum of a goat also has been described.2,3 caudal skinfolds on the ventral tail surface provide a good
A diagnosis of neoplasia is based ultimately on landmark for the site of tail removal. Many owners of
histopathology. Bony enlargement, lameness, and radi- show or club lambs prefer to remove the tail as close to
ographic evidence of lysis or proliferation may suggest a the body as possible. However, docking too close to the
diagnosis of neoplasia, especially in an older animal. Suc- sacrum may result in an increased incidence of rectal and
cessful treatment of connective tissue tumors has not possibly vaginal prolapse.1 The tail can be crushed, cut,
been reported. cauterized, or removed with a combination of these
methods.2 Equipment used for tail removal includes an

R EFERENCES
1. Bastianello SS: A survey on neoplasia in domestic species over
emasculator, an emasculatome, a hot chisel, a knife, or
elastrator bands. Tails should be cleaned of dirt and feces.
The lamb should be manually restrained as the clinician
a 40-year period from 1935 to 1974 in the republic of South determines the exact spot of tail removal; the tail should
Africa. II. Tumours occurring in sheep, Onderstepoort J Vet Res not be excessively stretched. Leaving some skin proximal
49:205, 1982. to the point of removal provides redundant skin to cover
2. Steinberg H, George C: Fracture-associated osteogenic sarcoma the spinal stump.1 Use of a cautery unit (e.g., hot chisel,
and a mandibular osteoma in two goats, J Comp Path 100:453, 1989.
suture heated wedge, electric wedge, electric cautery)
3. Cotchin E: Tumors of farm animals, Vet Rec 40:816, 1960.
minimizes hemorrhage. If hemorrhage does occur, the
ventral blood vessels can be clamped and sutured if
needed. If cautery units are used and the wool is burned,
TAIL DOCKING some ewes may reject the lambs.1 Removing wool over
Tail removal or “docking” is usually performed during the the docking site before the procedure and gently washing
first 2 weeks of life.1,2 Some lambs sold in niche markets or cleansing the tail after removal can minimize ewe re-
do not have their tails docked, and in some breeds (e.g., jection. Ewe rejection caused by cautery docking is rare,
Karakul) the tail should be left long because the fat at the and this method of docking is very acceptable. Cautery
base of the tail is considered a prized commodity. Still, in equipment should be used cautiously because of the pos-
most environments in which lambs are kept, long tails sibility of burning the vulva, anus, or perineal skin. Re-
can become soiled with loose stool or diarrhea (as a result gardless of the method, in the absence of complications
of high-grain diets, lush pasture, or internal parasites), the tail stump will heal within 2 weeks. Tetanus toxoid or
254 • Sheep and Goat Medicine
antitoxin should be routinely administered on farms between the vertebrae, removes the tail, and closes the
where tetanus is a problem; it also can be provided for all skin. If excessive hemorrhage occurs, the vessels can be
docked animals. cauterized or sutured with absorbable material. Animals
If an elastrator or rubber band is used, the tail sloughs can be placed on a broad-spectrum antibiotic and given
because of ischemic necrosis. This procedure is controver- tetanus prophylaxis.
sial, and elastrator band use should always be accompa-
nied by tetanus prophylaxis.
The tail of an adult sheep can be removed as it would
R EFERENCES
1. Hooper RN: General surgery techniques—Part I, Proceedings of the
be in other animals. The animal can be placed under
1998 Symposium on Small Ruminants for the Mixed Animal Practi-
general anesthesia or sedated, restrained, and given an
tioner Western Veterinary Conference, 1998, Las Vegas, NV.
epidural or ring block with local anesthetic. The surgical 2. Johnson JH et al: The musculoskeletal system. In Oehme FW, Prier
area is clipped and aseptically prepared, and the site for JE, editors: Textbook of large animal surgery, Baltimore, 1976,
tail excision is determined. The clinician then makes a Williams & Wilkins.
wedge-shaped skin incision distal to the intervertebral 3. Kent JE, Molong V, Graham MJ: Comparison of methods for the
space where the tail is to be removed. This leaves enough reduction of acute pain produced by rubber ring castrating or tail
skin to suture over the stump.1 The clinician cuts the tail docking of week-old lambs, Vet J 155:39, 1998.
 Chapter 10

Diseases of the Urinary System

ELLEN B. BELKNAP AND D.G. PUGH

EVALUATION OF THE simultaneously (using the other hand) retracting the

sheath caudally (Figure 10-1). An assistant should grasp
URINARY TRACT the free portion of the penis with a piece of gauze. The
urethral process can then be examined (and amputated if
History necessary) and the urethra catheterized. This procedure is
Obtaining a thorough history is crucial in diagnosing more easily performed on rams than on bucks. Penile ex-
urinary tract disorders. In some instances a good history tension may be impossible in prepuberal males and those
is as important as (if not more important than) the clini- castrated before puberty. In the female the vulvar hair and
cal examination. Knowledge of an affected animal’s diet, perineal area should be examined for evidence of hema-
use, onset and progression of disease, previous treatments, turia, pyuria, urine scalding, and crystalluria.
and responses to treatment is vital in making an accurate If the bladder is distended it can usually be palpated in
diagnosis. In addition, age at castration, time since partu- the caudal abdomen. If it is not palpable, the bladder can
rition, and history of dystocia also may be relevant. The be evaluated with real-time ultrasound. If the bladder has
owner’s interpretation of the clinical signs may be mis- ruptured, bilateral symmetric ventral distention of the
leading and could suggest abnormalities of the gastroin- abdomen may be observed and a fluid wave may be
testinal or reproductive tract. A selected list of plants as- appreciated with ballottement.
sociated with nephrotoxicity in sheep and goats is shown
in Table 10-1.
DIAGNOSTICS
Physical Examination Ultrasound
A general physical examination should be performed The urinary tract can be examined using real-time
before the urinary system is evaluated. Close observation ultrasonographic equipment with either a 3.5- or 5-MHz
for signs of depression, hydration status, and systemic ab- transducer. Either a sector, curvilinear, or linear array
normalities is important. The clinician may wish to transducer can be used rectally or transabdominally to vi-
observe the animal as it urinates to detect stranguria, pol- sualize both kidneys (Figures 10-2 and 10-3) by scanning
lakiuria, dysuria, and abnormal urine color. Palpation and in the right paralumbar fossa; the bladder can be evalu-
observation of the external urogenital structures should ated by scanning in the right inguinal area or transrec-
be performed routinely and followed by a digital rectal tally.1 In overconditioned or obese animals, visualization
examination. Urethral rupture is relatively easy to deter- of the kidneys or urinary bladder may be difficult.
mine in male sheep and goats. Most urethral ruptures
occur at the distal sigmoid flexure, resulting in ventral
fluid accumulation and edema. The preputial hairs should
Excretory Program
be examined for sand, calculi, and blood. Exteriorization A contrast radiographic evaluation of the bladder and
of the penis can be accomplished by sitting the animal on urethra may be conducted after bladder or urethral
the dorsum of its rump, grasping the penis through the surgery. Radiographic contrast material can be infused
sheath at the sigmoid flexure, and moving cranially while into the bladder through the catheter and the integrity of
• 255 •
256 • Sheep and Goat Medicine

A
M

Figure 10-1 Exteriorization of a ram’s penis. Note the urethral

process.

A M

Figure 10-3 A, Ultrasound of a normal caprine right kidney in the

dorsal plane using a variable-bandwidth, curvilinear, 5- to 8-MHz
transducer. C, Cortex; M, medullary region. B, Split-screen ultrasound
comparing the right and left sagittal planes of a caprine kidney.
(Courtesy Dr. Margaret Blaik, Auburn, Alabama.)

over the last rib on the right side. Using a real-time ul-
C trasound machine the clinician visualizes the kidney and
advances a 14-gauge biopsy needle through anesthetized
skin nicked with a #15 blade. Mild hematuria and sub-
B M
capsular hematoma may result from this procedure. The
resultant specimen is placed in 10% formalin and pre-
pared for routine hematoxylin and eosin (H & E) stain-
ing. For immunofluorescent testing, samples should be
placed in Michel’s medium. If amyloidosis is suspected,
special stains (Congo red) may be applied to subsequent
sections.
Figure 10-2 Ultrasound of a normal ovine kidney in the
midsagittal plane using a variable-bandwidth, curvilinear, 5- to 8-MHz
transducer. A, Right kidney. B, Left kidney. C, Cortex; M, medullary Urinalysis
region. (Courtesy Dr. Margaret Blaik, Auburn, Alabama.)
Along with serum creatinine assays, urinalysis is one of the
most important diagnostic tests. Urine may be obtained
the urethra can be evaluated (Figure 10-4). Lidocaine from sheep by occluding the nostrils. Clinicians can easily
(1 ml of 2% lidocaine/10 ml of contrast media) can be catheterize female goats using a rigid Foley or metal
added to the contrast media to prevent urethral spasms. urinary catheter (bitch catheter); they should avoid the
suburethral diverticulum while passing the catheter
toward the bladder. Obtaining urine from male goats is
Renal Biopsy difficult, although they urinate frequently during the
To perform a renal biopsy in a sheep or goat, the clini- breeding season. Clinicians should make containers readily
cian or an assistant clips and aseptically prepares the area accessible when bucks lie down in case they urinate when
 Chapter 10 Diseases of the Urinary System • 257

Figure 10-4 Contrast excretory urethrogram of a male pygmy Figure 10-5 Photomicrograph of unstained urine sediment. Note
goat. Note the filling defects in the urethra proximal to the sigmoid the struvite crystals. (10 magnification.) (Courtesy Dr. Elizabeth
flexure. Welles, Auburn, Alabama.)

TABLE 10-1

PLANTS ASSOCIATED WITH NEPHROTOXICITY*

PLANT COMMENT

Vitamin D–containing plants (Cestrum, Contain vitamin D; cause soft tissue mineralization, glomerular fibrosis,
Solanum) and interstitial fibrosis (common in cattle)
Oxalate-containing plants See Box 10-1
Amaranthus retroflexus (pigweed) An oxalate and nitrate accumulator; causes perineal edema and nephrosis
Quercus species (oak) Acorns and oak buds are most toxic; cause abdominal pain, extreme thirst,
edema, elevated blood urea nitrogen, depressing edema, rough hair coat,
and increases in serum creatinine and potassium; lesions include gastritis
and nephritis, as well as hyaline and granular casts in the proximal
controlled tubules; toxicity can be prevented by adding calcium hydroxide
to the diet
*Fluid and supportive therapy are the treatments of choice for plant-associated nephrotoxicity. Before the onset of signs, administering oral charcoal
and initiating emesis also may be of value.

they rise. Because of the presence of a urethral recess, than 7.4) but may be acidotic as a result of paradoxic
catheterization of males is most often unsuccessful.3 aciduria. This condition occurs in ruminants with
Urinalysis can help localize disease, determine causes hypochloremic, hypokalemic metabolic alkalosis as the
of discolored urine, identify inflammatory disease, and kidney tries to reduce the bicarbonate load but cannot, re-
determine the kidneys’ ability to concentrate urine. When sulting in the excretion of hydrogen ions into the
present, urinary casts suggest tubular disease. A specific urine.2,4,5
gravity greater than 1.025 and an alkaline pH make cast Urine protein concentration may be falsely elevated
identification difficult. Urine should be analyzed because of hemorrhage, inflammation, or colostral pro-
promptly for sediment because casts, crystals, and other teins in neonates less than 40 hours old. In the absence of
cellular elements degenerate or change configuration hematuria or pigmenturia, marked proteinuria indicates
with time (Figure 10-5). Specific gravity can be measured glomerular disease. However, when dipsticks are used for
with a hand-held refractometer. Specific gravity values evaluation, alkaline urine produces a falsely elevated
between 1.007 and 1.012 (Table 10-2) indicate isos- protein value and a positive blood reaction can be caused
thenuria. These values should be interpreted with consid- by hematuria, hemoglobinuria, myoglobinuria, or con-
eration of the animal’s hydration status, degree of tamination from fecal or reproductive blood. Glucosuria
azotemia, and previous drug therapy. A specific gravity occurs when the renal threshold (100 mg/dl of glucose in
less than 1.007 or urine osmolality less than plasma values peripheral blood) is exceeded. It can be caused by stress,
indicates renal medullary washout, polydipsia, or diabetes xylazine or glucose administration, enterotoxemia, or
insipidus. However, diabetes insipidus is an extremely renal disease and also is seen in moribund animals. Ele-
rare disease in sheep and goats (see Chapter 7). The urine vated levels of urinary gamma-glutamyl transferase
pH of both sheep and goats is generally alkaline (greater (GGT) indicate proximal tubular dysfunction.
258 • Sheep and Goat Medicine
TABLE 10-2

URINALYSIS FOR SHEEP AND GOATS

TEST NORMAL RESULTS

Color Pale yellow

pH 7.2 to 8.0
Glucose Negative
Specific gravity 1.015 to 1.045
Ketones Negative
Protein Negative to trace
Bilirubin Negative
Figure 10-6 A dissected urogenital tract of a buck. The arrow
Turbidity Clear points to the urethral diverticulum.
Red blood cells Less than 5 (high power field)
White blood cells Less than 5 (high power field)
Crystals Rare cemia is commonly identified as a sequela of reduced
Casts Occasional hyaline intake, gastrointestinal stasis, and hyperphosphatemia.
Sperm Variable
Epithelial cells Occasional
Gamma-glutamyl White Blood Cell Count
transferase Less than 40 U/L Leukocytosis, neutrophilia, and hyperfibrinogenemia are
commonly reported in acute renal, bladder, and urethral
infections. If the problem is chronic, globulin levels may
be elevated, and if the inflammation is still active, hyper-
fibrinogenemia also may be present. Anemia caused by
Fractional excretion (FE) of electrolytes may be useful chronic inflammation may be observed in long-standing
to detect early renal dysfunction. To perform this test, the disease. Anemia of chronic inflammatory disease is non-
clinician should collect concurrent serum and urine regenerative and is characterized by low serum iron and a
samples. The percent FE is calculated by the urine normal total iron-binding capacity.
electrolyte/urine creatinine concentration divided by the
serum electrolyte/serum creatinine concentration, then
multiplied by 100%. In sheep the normal FE of sodium
Anatomic Considerations
is less than 1%; an FE of sodium greater than 1% indi- Amputating the urethral process makes urethral catheter-
cates primary tubular disease or sodium toxicity.2 ization easier. When attempting catheterization, the
Samples should be collected before fluid therapy is authors prefer to use polyethylene tubing. In many in-
instituted. stances a catheter can be passed in a retrograde fashion to
the point of the urethral diverticulum (recess) at the
ischial arch (Figure 10-6).3 Complete catheterization re-
Biochemistry Profile quires either an ischial urethrostomy or a cystotomy.
Serum biochemistry profiles may be the easiest tests to During cystotomy, normograde catheterization of the
perform to diagnose renal failure. Creatinine levels are urethra may be attempted and is often successful.
the most reliable indicators of renal disease, although ele-
vations also may result from prerenal and postrenal
causes. Serum urea nitrogen levels may be altered because
of the ruminant’s ability to recycle nitrogen, so the
R EFERENCES
1. Braun U, Schefer U, Gerber D: Ultrasonography of the urinary tract
authors of this chapter place more emphasis on serum of female sheep, Am J Vet Res 53:1734, 1992.
creatinine levels. Hypochloremia is a consistent finding in 2. Garry F et al: Renal excretion of creatinine, electrolytes, protein, and
renal failure. Depressed serum chloride concentrations enzymes in healthy sheep, Am J Vet Res 51:414, 1990.
3. Garett PD: Urethral recess in male goats, sheep, cattle, and swine, J
may be caused by urinary loss and sequestration resulting
Am Vet Med Assoc 191:689, 1987.
from abomasal stasis. Hyponatremia also may be ob- 4. Lunn DP, McGuirk SM, Smith DF: Renal net acid and electrolyte
served, whereas hyperkalemia is not consistently observed excretion in an experimental model of hypochloremic metabolic al-
in postrenal obstruction cases. Magnesium is primarily kalosis in sheep, Am J Vet Res (11):1723, 1990.
excreted by the kidneys and may be elevated in renal 5. Michell AR, Moss P: Responses to reduced water intake, including
disease. Phosphorous, which depends on the kidney as dehydration natriuresis, in sheep excreting sodium predominantly in
well as saliva for excretion, may be elevated. Hypocal- urine or in feces, Exp Phys 80:265, 1995.
 Chapter 10 Diseases of the Urinary System • 259

UPPER URINARY TRACT cause glucosuria, bicarbonaturia, natriuresis, proteinuria,

and enzymuria. The taking of concurrent samples of
PROBLEMS urine and serum allow for the calculation of the FE rates
of a particular solute, as shown here for sodium:
Acute Renal Failure
FENa 1 %2  1UNa>SNa  UCr>SCr2  100
Pathogenesis. Acute renal failure (ARF) is caused by a
deterioration of renal function over a period of hours to where UNa is the urine sodium level, SNa is the serum
days. This rapid onset can result from prerenal, postrenal, sodium level, UCr is the urine creatinine level, and SCr is
or intrinsic renal causes. Most intrinsic renal insults are the serum creatinine level. Although it is affected by diet,
ischemic or toxic in nature and can be caused by systemic the FENa can be used to assess proximal tubular damage,
disease, injury, and various therapeutic manipulations. with elevations greater than 1% considered abnormal in
Clinical situations that enhance the risk of ARF include sheep.1 Urine GGT levels greater than 40 U/L are con-
dehydration, electrolyte abnormalities, systemic hypoten- sidered above normal.2 Damage to the distal nephron
sion, hypoalbuminemia, vasculitis, fever, sepsis, prolonged often results in loss of potassium and hydrogen ions into
surgery or anesthesia, and the use of potentially nephro- the urine. Most nephrotoxins cause a decrease in the
toxic drugs. The kidney is especially susceptible to toxic glomerular filtration rate (GFR) and tubular damage. If
injury for several reasons. First, the kidneys acquire 20% the GFR is not affected and uremia does not result,
of the cardiac output and thereby receive a relatively high tubular toxicity may not be detected.
proportion of blood-borne toxicants. The large glomeru- With acute tubular necrosis, anuria or oliguria are
lar capillary surface area provides a large contact area for usually present; polyuria can occur in subacute or chronic
toxicant interaction with epithelial cells. In the proximal cases. Identification of urine output and specific gravity is
tubule and thick ascending Henle’s loop, high metabolic crucial to treatment of these cases. Because many of the
rates and transport functions make epithelial cells espe- clinical signs are nonspecific, determining a diagnosis
cially sensitive to intoxicants that disrupt their energy can sometimes be difficult. Most animals have a
sources or membrane functions. Tubular epithelial cells hypochloremic metabolic alkalosis and experience pro-
also may actively resorb toxicants, which can accumulate teinuria, hematuria, and granular casts in the urine early
to dangerous intracellular levels. The countercurrent in the disease. An increased FE of electrolytes or urinary
mechanism and tubular concentrating function result in enzymes precedes these abnormalities.
increased levels of toxic substances in the distal portions
of the nephron.
Metal Toxicity
Treatment. Treatment of ARF should be aimed at cor- Goats are notorious for ingesting household items and
recting electrolyte and acid-base imbalances and promot- zinc-containing objects such as pennies or sheet metal
ing diuresis. Furosemide (1 mg/kg intravenously [IV] screws, both of which are potential sources of toxicity.
every 2 to 3 hours) and dimethyl sulfoxide (DMSO, Zinc is leached in the acid environment of the abomasum
1 g/kg IV as a 20% solution) may be given initially. If the and may result in toxicity. Goat kids may become intoxi-
animal remains anuric or oliguric, a dopamine drip (3 to 7 cated by ingesting zinc sulfate–containing foot bath ma-
mg/kg/min IV) should be instituted. Close monitoring of terial, but this is rare. Serum, urine, or liver zinc concen-
hydration and plasma protein levels is important to trations may be diagnostic, and the clinician should
prevent edema. After the animal is no longer oliguric, the collect samples from them in tubes designed for trace
clinician should maintain the animal on IV fluids until mineral analysis. Other metals that may cause acute
the serum creatinine level has returned to the normal tubular necrosis in ruminants include lead, mercury,
range and the animal has begun to eat and drink again. cadmium, and arsenic.
Supportive care, maintenance of normal rumen flora, and
nutritional support should be considered in these cases. Clinical signs. Clinical signs include anorexia, dehy-
Attitude is sometimes improved by having another sheep dration, diarrhea, weakness, jaundice, and death; he-
or goat nearby or moving the patient outside every day. molytic anemia and ARF may occur 2 to 3 weeks after in-
gestion. Arsenic also is known to cause gastrointestinal
signs, including colic and hemorrhagic diarrhea. With
Acute Tubular Necrosis mercury toxicosis, ulcerations of the mouth, esophagus,
Damage to the renal tubules may result in renal dysfunc- and gastrointestinal tract may lead to diarrhea.
tion. Ingestion or parenteral administration of toxins,
renal hypoxia resulting from hypovolemia, and nephritis
caused by endotoxemia or bacteremia may all damage the
Antibiotic Toxicity
renal tubules. Proximal tubular toxins result in loss of Antibiotics known to induce acute tubular necrosis
solute in the more distal parts of the nephron. This can include aminoglycosides, tetracyclines, and sulfonamides.
260 • Sheep and Goat Medicine
Of these, tetracyclines and sulfonamides are frequently higher concentrations of oxalate than other parts of the
used in sheep and goats to treat many diseases. Their plant.9 The amount of oxalate required to cause toxicity is
toxic effects on the kidney are enhanced by dehydration. variable because mature animals that are gradually intro-
Renal failure as a consequence of antibiotic overdose has duced to oxalate can experience a proliferation of oxalate-
been reported in cattle, but not in sheep and goats.3,4 degrading rumenal microflora. Less than 1% of the body
Nephrotoxicity results in part from inhibitory effects on weight in soluble oxalate is toxic to a fasted sheep.10
the oxidative enzymes of tubule cells.5 In addition, tetra- Abrupt introduction to pastures with an abundance of
cycline inhibits the concentrating ability of the kidney,6 oxalate-containing plants is risky. This risk is magnified
and when given in a propylene glycol carrier results in in animals who are thin and hungry. Sheep do not ap-
systemic hypotension and decreased pulmonary and renal pear to adapt to the ingestion of plants in the Brassica
arterial blood flow.7 Continued use of an antibiotic is family.
contraindicated if adverse renal effects are noted. Con-
current use of nonsteroidal antiinflammatory drugs Clinical signs. Signs of oxalate toxicity include
(NSAIDs) may predispose to renal tubular toxicity or lethargy, anorexia, recumbency, and death.10,11 Pul-
cause problems by themselves. monary edema, muscle fasciculations, tetany, and seizures
also may be observed. Oxalate has a strong affinity for
calcium and produces insoluble calcium oxalate calculi in
Plant (Oxalate) Toxicity the urinary tract.12 Hypocalcemia and azotemia are char-
Pathogenesis. Ingestion of many plants may result in acteristic, and hyperphosphatemia and hypermagnesemia
nephrotoxicity in sheep and goats. One of the most also may be observed.11,13 A more chronic form of
common problems is the continued ingestion of small oxalate toxicity causes calcium oxalate deposition in renal
amounts of oxalate. Oxalate is normally metabolized by tubules and vessels, renal fibrosis, renal insufficiency, and
the rumen, and oxalate tolerance increases with exposure. urolithiasis.
This helps to explain the observed decreased susceptibil-
ity over time of animals grazing pasture rich in oxalate- Diagnosis. A history of access to toxic plants, the ob-
containing plants. Grazing pasture is most dangerous servation of increased renal cortical echogenicity on ul-
when a rapid growth of lush plants occurs in a warm fall trasound, renal biopsy, and necropsy of dead animals
after a dry summer.8 Plants containing high concentra- may aid in establishing the cause of acute tubular necro-
tions of oxalate are listed in Box 10-1. The leaves contain sis.14 Birefringent crystals may be observed in the renal
cortex, papillary ducts, urine, and possibly in the rumen
during histopathologic examination of tissues.15 Ru-
menitis is a major lesion of oxalate toxicosis identified at
BOX 10-1 necropsy.

P LANTS C ONTAINING A H O IGH XALATE CONTENT Treatment. Therapy should be aimed at promoting di-
uresis and eliminating the toxin source. IV fluids, calcium
COMMON NAME GENUS AND SPECIES gluconate, oral magnesium hydroxide, and activated char-
coal (1 to 2 g/kg by mouth [PO]) may all be beneficial.
Halogeton Halogeton glomeratus Oral calcium chloride or dicalcium phosphate can precip-
Lamb’s quarter or fat hen Chenopodium album itate oxalate within the rumen and prevent its further ab-
Pokeweed Phytolacca americana sorption.10 After ingestion but before the onset of clinical
Russian thistle Salsola kali signs, survivability may be increased by administering
Purslane Portulaca oleracea large volumes of water and calcium salts orally.12,15
Bassia Bassia hyssopifolia
Pigweed Amaranthus retroflexus Prevention. Prevention requires avoidance of forage
Soursob Oxalis cernua and O. that contains large quantities of soluble oxalate. If
pes-caprae such forage cannot be avoided, gradual acclimation is
Greasewood Sarcobatus indicated.16
vermiculatus
Dock and orchard sorrel Rumex acetosella and
R. acetosa Ethylene Glycol Toxicity
Cultivated rhubarb Rheum rhaponticum Pathogenesis. Adult ruminants may be more resistant
Sugar beet leaves Beta vulgaris than monogastric animals or neonatal ruminants to the
Fungi Aspergillus niger and effects of ethylene glycol because of their ability to
A. niger degrade oxalate, a metabolite of ethylene glycol, by rumen
microorganisms.16,17 Although they are relatively un-
 Chapter 10 Diseases of the Urinary System • 261

common in sheep and goats because of their ability to Clinical signs. Clinical signs may appear 3 days after
metabolize oxalic acid, cases of ethylene glycol toxicity ingestion of the oak source. Initially the animal may be
still occur, especially in pet or club lambs.17 Sheep and listless, anorectic, and weak. Polyuria, ventral edema, per-
goats seem to like the sweet taste of ethylene glycol and ineal and vulvar edema, abdominal pain, and constipation
will drink it preferentially over water. As in other species, followed by the excretion of mucus-covered feces and
toxicity in sheep and goats is usually associated with the hematochezia may be observed. As uremia progresses the
ingestion of antifreeze that contains ethylene glycol. For scleral vessels become engorged, and a smell of ammonia
ruminants the median lethal dose (LD50) of pure ethyl- may become apparent on the animal’s breath. Azotemia,
ene glycol is 5 to 10 ml/kg.18 hyponatremia, hyperkalemia, hypochloremia, hyperphos-
phatemia, hypocalcemia, metabolic acidosis, and an ele-
Clinical signs. Clinical signs of ethylene glycol toxico- vated anion gap are found initially.22 Affected animals
sis include hypersalivation, bruxism, hindlimb ataxia, nys- also may exhibit anuria, isosthenuria, proteinuria, and
tagmus, seizures, and death. A sweet odor may be de- glucosuria. Death is generally attributable to renal failure,
tected on the animal’s breath. A diagnosis may be based although ulcerations of the mouth, esophagus, and gas-
on a history of ingestion, analysis of rumen contents for trointestinal tract may be evident.
ethylene glycol, or glycolic acid levels in urine, serum, or
ocular fluid.17 Metabolic acidosis, azotemia, and hyperos- Diagnosis. The most characteristic lesions at necropsy
molality are likely findings. Birefringent crystals arranged include edema and hemorrhagic enteritis. The kidneys
in sheaves or rosettes typical of oxalate crystals may be may be normal or enlarged with hemorrhages on the
observed in the renal tubules on histopathologic exami- surface in acute cases or roughened, pitted, and pale in
nation.17 Unlike in monogastric animals that absorb eth- more chronic cases.14,22 Hydrothorax, hydroperitoneum,
ylene glycol within 48 hours, the rumens of sheep and perineal edema, and hemorrhage may accompany these
goats may act as reservoirs for continued absorption. lesions. Histopathologic lesions include multifocal, prox-
imal convoluted tubular necrosis with proteinaceous casts
Treatment. Therapy may include activated charcoal and dilated tubules. Glomerular degeneration and fluid in
(0.11 kg PO). Aggressive fluid therapy, including Bowman’s capsule also are seen.14,20
20% ethanol at 50 ml/hour is reported to prevent con-
version of ethylene glycol to glycolic acid, a metabolic Treatment. Treatment is aimed at correcting elec-
intermediate.19 trolyte abnormalities and base deficits and promoting di-
uresis. If the animal survives the acute stage and begins
to eat, recovery may occur, although 5 to 10 weeks may
Oak (Acorn) Toxicity elapse before renal function returns to normal.22
Pathogenesis. Sheep are much more susceptible to the
effects of oak (Quercus species) leaf, bud, twig, or acorn Prevention. Prevention is more successful than treat-
toxicity than goats because goats reportedly have greater ment and includes good pasture management, the provi-
concentrations of tannase enzymes in their ruminal sion of supplemental alfalfa hay, or administration of a
mucosae.8 However, acorns are palatable and readily con- 10% to 20% calcium hydroxide (slake lime) and grain
sumed by goats.20 Gallotannic acid is thought to be the concentrate mixture. A mixture of 491 kg (1080 lb) of
toxic component in young oak leaves or acorns; it is hy- cottonseed or soybean meal, 272.7 kg (600 lb) of dehy-
drolyzed in the rumen to produce gallic acid, pyrogallol, drated alfalfa, 54.5 kg (120 lb) of vegetable oil, and 90.0
tannic acid, and other compounds.20 Tannins bind to the kg (200 lb) of hydrated lime, fed at a rate of 0.1 to 0.2
proteins of epithelial cells, resulting in ulcerations, and kg/head/day (0.25 to 0.5 lb/head/day) may protect
hydrolyzed tannins bind to plasma proteins and endothe- against acorn toxicity.
lial proteins, resulting in fluid loss from the intravascular
fluid compartment and hemorrhage.20 Toxicity is ob-
served more commonly in the spring and the fall when
INFECTIOUS DISEASES
other feed sources are limited and acorns are abundant.
The concentration of toxic compounds is higher in im-
Enterotoxemia
mature, green acorns than in mature, ripe acorns.21 Oak Enterotoxemia caused by epsilon toxin–producing
forage must comprise a large portion of the diet for clini- Clostridium perfringens type D (pulpy kidney disease) is
cal signs to be present. Concurrent protein deficiency may an important syndrome in the sheep and goat industries.
contribute to disease predisposition and development. Grain-fed lambs on a high-concentrate diet are most sus-
Poorly fed, heavily parasitized animals are therefore most ceptible, but adult sheep and goats also may be af-
susceptible. The organs and tissues most commonly af- fected.8,23 Goats are more commonly affected with the
fected are the mouth, esophagus, gastrointestinal tract, hemorrhagic enterocolitis form of enterotoxemia.24 The
and kidneys. epsilon toxin is produced when the animal’s diet provides
262 • Sheep and Goat Medicine
adequate substrate for proliferation of the type D organ- Diagnosis. Leptospirosis can be diagnosed by serology
ism in the intestine. The epsilon toxin increases vascular (microscopic agglutination test or enzyme-linked im-
permeability, leading to edema in the pulmonary system munospecific assay [ELISA]), the polymerase chain
and kidneys and explaining the name pulpy kidney reaction (PCR) test, dark-field microscopy, immunofluo-
disease.25 rescent antibody tests, culture, and phase-contrast mi-
croscopy of urine or urine sediment samples.30 The
Clinical signs. Lambs are generally found dead within kidneys are usually dark and swollen. Renal lesions
12 hours and ewes within 24 hours of the onset of during the chronic phase include enlarged kidneys, pale
disease. The body conditions of the dead animals are foci in the renal cortices, and a diffuse, chronic interstitial
usually good, glucosuria is a consistent finding, and nephritis on histopathologic examination. Kidney lesions
within a few hours of death the kidneys become soft and result from damage caused by hemolysis, lipase, and
pulpy. Other lesions include excess pericardial fluid, urease.31
pulmonary edema, and hemorrhage on serosal surfaces.
Treatment. Dihydrostreptomycin (12.5 mg/kg every
Prevention. Vaccination with the bacterin-toxoid is 12 hours intramuscularly [IM]) and oxytetracycline (10
imperative in preventing disease in lambs; antitoxin (200 to 15 mg/kg every 12 hours IM) are potentially nephro-
units/kg IV) may be given during an outbreak. The toxic antibiotics, and controversy exists regarding their ef-
vaccine is not as effective in goats as it is in lambs.25 Oral ficacy in the treatment of other species (cattle).32,33 No
sulfa and tetracycline drugs can reduce the proliferation reports have been published concerning their use in sheep
of bacteria in the intestine and are occasionally placed in and goats with leptospirosis.
diets for this purpose (see Chapter 14).
Prevention. The most effective means of preventing
leptospirosis is vaccination, but limiting contact with
Leptospirosis carrier cattle, wild animals, and rodent populations and
Leptospirosis can have a variety of clinical manifestations blocking access to standing water can help prevent trans-
depending on the serovar of Leptospira interrogans, the mission. Multivalent vaccines should be used for animals
immune status of the animal, and various virulence older than 3 months of age and should be administered
factors. L. pomona, L. icterohemorrhagica, and L. hardjo two to four times annually, depending on the prevalence
more commonly infect sheep,10,26 whereas L. pomona, L. of leptospirosis in the area.
icterohemorrhagica, and L. grippotyphosa are more com-
monly identified in goats.27 The organism is very in-
fectious, a quality that is enhanced by its ability to
Adenovirus
penetrate intact mucous membranes. Only a few organ- Adenovirus particles have been identified in the en-
isms are required to infect an animal, but as many as dothelia of renal interstitial blood vessels in a lamb.34
105 organisms/ml of urine can be shed within the first They were observed during routine histopathologic ex-
few weeks of infection. amination of several 8-month-old Merino lambs. Exper-
imental infection with some strains of ovine adenovirus
Pathogenesis. The most important mode of transmis- in lambs resulted in degeneration of epithelial cells in
sion is by contaminated urine,28 and therefore the likeli- the proximal convoluted tubules.35 Prevention requires
hood of infection increases after periods of heavy rainfall, good management practices; no adenovirus vaccines are
especially in poorly drained environments. Reservoir available.
hosts persist as infection sources within a species, but ac-
cidental infection can occur in non–host-adapted species.
Nonadapted serovar infections can cause severe he-
CHRONIC RENAL DISEASE
molytic disease, interstitial nephritis, and tubular nephro-
sis. After the organism gains entrance to the body, a
Mesangiocapillary Glomerulonephritis
period of septicemia and leptospiremia results, followed Mesangiocapillary glomerulonephritis occurs primarily in
by dissemination to most tissues. Finnish Landrace lambs less than 4 months of age, al-
though reports exist of it in cross-bred lambs sired by
Clinical signs. Clinical signs of leptospirosis may Finnish Landrace rams.36,37 Immunofluorescent studies
include fever, anorexia, depression, anemia, hemoglobin- demonstrate subendothelial deposits of immunoglobulin
uria, and icterus. Sudden death also may occur in sheep.29 M (IgM), immunoglobulin G (IgG), immunoglobulin A
Outbreaks of abortion and stillbirth may be seen in the (IgA), and third component of complement (C3) and
flock concurrently with the urogenital form of the neutrophil infiltrates in the glomerular capillary walls.
disease. Affected lambs are born with a C3 deficiency involving a
 Chapter 10 Diseases of the Urinary System • 263

complex mode of inheritance that does not necessarily Treatment. No successful treatment is available for
imply that all lambs in a litter from a carrier ewe mated to glomerulonephritis in goats and sheep. Glucocortico-
a known transmitting sire will be affected.38 steroids may help reduce the inflammation produced by
the disease, but the prognosis is poor.
Clinical signs. Clinical signs of glomerular disease
become apparent within weeks after birth. Initially the
lambs become isolated from the flock and appear
Pyelonephritis
anorexic. Some develop signs of central nervous system Pathogenesis. Pyelonephritis in sheep and goats has
disturbance, then progress to display signs of abdominal been reported to be caused by Escherichia coli43
pain. Transabdominal ultrasonographic evaluation often and Corynebacterium renale.44-46 The pili of C. renale are im-
reveals enlarged kidneys that may be painful on palpa- portant in attaching to the animal’s tissues and establishing
tion. The lambs are azotemic, with hypocalcemia, hyper- infection.47 Chlamydia psittaci also can cause pyelonephritis.
phosphatemia, hypoalbuminemia, and albuminuria.36,37
Clinical signs and diagnosis. Weight loss, anorexia,
Diagnosis. The diagnosis is based on observed expan- dysuria, and anuria are occasionally observed. The history
sion of the mesangial region of the glomeruli with cellu- may reveal recent parturition. Urinalysis can aid in diagno-
lar infiltrates; the peripheral capillary walls are swollen, sis and may reveal proteinuria, hematuria, and pyuria.
refractile, and infiltrated with neutrophils.39 Grossly, the Renal enlargement, echogenic material within the renal
kidneys appear greatly enlarged with red or yellow spots pelvis, and dilation of the renal calyces are ultrasono-
in the cortex. Concurrent neuronal lesions have been re- graphic findings supportive of a diagnosis of pyelonephri-
ported.37 To control this condition, the sire and ewe that tis. At necropsy the kidneys may appear swollen with
gave birth to the affected lambs should be culled. thickened capsules. Purulent material is found in the renal
pelvis and ureters, and some animals may have chronic
cystitis. The condition may be unilateral or bilateral, and
Glomerulonephritis hydronephrosis or hydroureter may accompany the lesion.
Pathogenesis. Glomerulonephritis of sheep tends to be
nonprogressive and asymptomatic, with no glomerular Treatment. Where possible, therapy should be based
lesions identified in lambs younger than 3 months of on bacterial culture and antibiotic sensitivity. When urine
age.40 Immune-mediated mechanisms cause deposition bacterial culture is unavailable, therapy should include the
of antigen, immunoglobulins, and complement along the administration of procaine penicillin G (22,000 IU/kg
basement membranes of the glomerular capillaries. The every 12 hours IM or subcutaneously [SC]) for at least
complexes become trapped at the basement membranes 1 week. Favorable results also may be obtained by admin-
of the glomerular capillaries, where they form suben- istering ceftiofur sodium (2.2 mg/kg SC every 24 hours)
dothelial or subepithelial electron-dense deposits. Mem- for at least 1 week. Urinalysis should be repeated to
branous glomerulonephritis is the most common form in confirm the absence of pyuria before antibiotics are dis-
sheep and results when the subepithelial deposits stimu- continued. Good sanitation practices at parturition may
late overgrowth of the capillary basement membranes, help decrease the incidence of this condition.
which thicken and form projections to enclose packets of
the complexes. The disease is usually sporadic and associ-
ated with some chronic inflammatory or infectious
Amyloidosis
process, usually chronic lung or liver abscesses.38 Pathogenesis. Amyloidosis is a chronic wasting disease
of animals caused by the tissue deposition of fibrils
Clinical signs and diagnosis. Affected animals appear formed by the polymerization of protein subunits
unthrifty and may have ascites or hydrothorax, but the arranged in a specific beta-pleated sheet biochemical con-
disease is not rapidly progressive.41 Goats may acquire a formation.48 Reactive systemic amyloidosis may occur as
spontaneous membranous glomerulonephritis but seldom a sequela to chronic inflammatory or neoplastic disease,
display clinical signs.27,41 Definitive diagnosis is achieved although in some instances no predisposing cause is iden-
by renal biopsy. The kidneys are pale and contracted. On tified.48 It most commonly occurs in sheep and goats
histopathologic examination most or all of the glomeruli used for research or production of antisera and in chronic
are shrunken and fibrosed, the capillaries are occluded, cases of caseous lymphadenitis.49,50
the tubules are atrophic, and the interstitium is thickened
and fibrous. In addition, glomerulonephritis has been de- Clinical signs and diagnosis. The signs of amyloidosis
scribed in ewes with concurrent pregnancy toxemia.42 depend on the organs involved; the most commonly af-
Clinical signs are typical of pregnancy toxemia, with con- fected organs are the kidneys, and the condition can lead
current azotemia, proteinuria, and ketonuria. to renal failure and death. A nephrotic-like syndrome
264 • Sheep and Goat Medicine
occurs and produces chronic weight loss, ventral edema, logic examination reveals distended cortical tubules con-
ascites, pleural and pericardial edema, hypoproteinemia, taining casts of serous protein-like or fibrin-like material
and proteinuria. Diarrhea may accompany these findings and lined with undifferentiated, low cuboidal cells. Al-
as a sequela of the hypoproteinemia or because of infiltra- though nephrosis was the predominant finding in one
tion of the intestine with amyloid. Affected animals are survey of 48 lambs, the authors were unable to explain the
generally anorexic. Diagnosis is confirmed by renal biopsy etiology of the condition.52 Any treatment attempted
or at necropsy. Histologic evaluation of Congo red– should be aimed at rehydration and correction of acid-
stained renal tissue reveals amyloid deposition in the base abnormalities. Management practices do not appear
glomeruli and medulla. to play a role in the progression of this disease.52
A Toxoplasma-like organism was reported to cause
Treatment. The treatment for amyloidosis is limited renal disease in a 4-year-old goat. Before death the goat
and therefore an accurate diagnosis is important. In pet showed signs of depression, weight loss, and tenesmus.54
animals the administration of DMSO may prevent the The kidneys were enlarged and hemorrhagic, with corti-
formation of some of the affecting proteins and promote cal white streaks. Cortical tubular necrosis with vasculitis
the solubility of myeloid fibrils. If the disease is associated was observed, as were large numbers of parasites, individ-
with chronic infection, appropriate antibiotics can be ad- ually or in clumps, in the affected areas. These organisms
ministered. However, the prognosis is poor. were identified as T. gondii by electron microscopy. Proto-
zoa also were observed within the bile duct, and portal fi-
brosis, hepatic necrosis, and vasculitis were reported. Pre-
Interstitial Nephritis vention of transmission of the organism to sheep and
Adenovirus has been isolated from the kidney tissue of goats is best accomplished by reducing contamination of
lambs with acute interstitial nephritis, hepatocellular feed by feline feces.
necrosis, and enteritis.34 The precise role of adenovirus in A protozoal parasite, Nosema (Encephalitozoon) cunic-
disease in lambs is not known, but it usually accompanies uli, was reported to produce numerous white spots in the
another disease. Often interstitial nephritis is diagnosed renal cortex of a goat that showed no clinical signs of
at necropsy rather than as a cause of clinical disease. In disease before death.55 Focal tubular atrophy and replace-
countries in which sheep pox is endemic, renal lesions ment with fibrous connective tissue and mononuclear
caused by direct viral damage may be observed in addi- cells were observed, and schizont-like structures were vi-
tion to skin and pulmonary lesions.38 Focal dense inter- sualized in the medullary tubular epithelium and free in
stitial infiltrates of lymphoid cells have been reported in the lumen of the tubules. This latter finding is most sig-
renal lesions of lambs persistently infected with border nificant because of its zoonotic potential to cause
disease virus. meningoencephalitis in human beings.

Parasites Abscesses
A nephrosis thought to be associated with Nematodirus Corynebacterium pseudotuberculosis infection and subse-
battus infestation of grazing lambs in the spring and early quent abscess formation throughout the body can cause
summer has been reported, primarily in the United severe economic losses in flocks and herds. Rarely, ab-
Kingdom; it has no particular breed, sex, management, or scesses may form on or in the kidneys of infected animals
feeding predisposition.51 Other reports have identified in a flock or herd. Other organisms that can cause renal ab-
nephrosis in lambs that were too young to suffer from scesses and embolic nephritis include Staphylococcus, Sal-
clinical nematodiriasis.48,52 The exact mechanism for the monella, Chlamydia, and Streptococcus species.38 Embolic
nephrosis is unknown, although histologic and biochem- nephritis and abscesses are generally discovered at
ical abnormalities suggest an acute nephrotoxic renal necropsy. The kidneys may be enlarged and uniform foci
failure.38 Most affected lambs are less than 1 month old may be noted on the cortex and in the parenchyma when
and only 1% to 2% of a flock may be affected. The lambs the kidney is opened on its longitudinal plane. The clini-
develop a progressive illness characterized by dullness, cian should document these lesions and look for other
anorexia, weakness, and staggering proceeding to recum- focal areas of infection or lesions indicative of a septic
bency and coma. Diarrhea and/or dehydration occurred process. Treatment varies depending on the underlying
in approximately half of the lambs surveyed in one problem. Other animals in the flock should be observed
study.52 Abnormalities include azotemia, hyperglobuline- for signs of sepsis, swollen joints, and other signs of illness.
mia, hypoalbuminemia, metabolic acidosis, proteinuria,
and hyperphosphatemia. N-acetyl-b-glucosaminidase is
elevated in urine, indicating proximal tubular damage.53
Caprine Cloisonné Lesions
Most affected lambs die within a few days. Enlarged, A condition reported in castrated male white Angora
pale, soft kidneys are observed at necropsy. Histopatho- goats causes pigmented thickening of the proximal con-
 Chapter 10 Diseases of the Urinary System • 265

voluted tubular basement membrane and is termed cloi- molytic crisis are 5 to 20 mg/ml, with liver and kidney
sonné kidney.56 All of the affected goats are from a specific levels exceeding 500 mg/g dry weight and 80 to 100 mg/g
area of Texas; herds and flocks in that area report an inci- dry weight, respectively. In sheep, dietary copper concen-
dence of about 2% for this subclinical condition.57,58 The trations higher than 25 mg/kg may lead to chronic toxi-
proposed etiology is repeated intravascular hemolytic cosis, but intake as low as 8 mg/kg may be harmful if
episodes.56 Because the condition is usually subclinical no molybdenum is low (0.5 mg/kg).61 Blue-black kidneys
treatment has been described. All goats in this area are observed at necropsy along with splenomegaly and an
appear susceptible, but no preventive measures have been orange-yellow liver. When cut longitudinally, the renal
reported. cortex may not be demarcated well from the medulla.64

Treatment and prevention. Ammonium tetra-

Copper Toxicity
thiomolybdate (1.7 mg/kg IV or 3.4 mg/kg SC) removes
Sheep are much more susceptible to copper toxicity than copper from the lysosomes and cytosol of copper-loaded
goats,59,60 and young lambs and kids are more vulnerable hepatic cells. The chelating agent D-penicillamine (50
than adults.61 Potential sources of excess copper include mg/kg daily for 7 days) also may be effective. Fluid
swine, equine, or cattle rations; trace mineral supple- therapy is important to maintain diuresis and avoid renal
ments; liquid from foot baths containing copper sulfate damage. The daily addition of ammonium molybdate to
(CuSO4); pastures fertilized with CuSO4 or swine or the feed at 50 to 500 mg/animal may help prevent he-
chicken manure; and feed with an improper copper-to- molytic crises if chronic copper toxicity is suspected.63
molybdenum ratio. Calf milk replacers may be a source of Maintaining the copper content of the diet at 7 to 11
excess copper for bottle-fed lambs and kids.62 Depending ppm and achieving a copper-to-molybdenum ratio of 61
on the dosage and duration of exposure to copper, the are effective preventive methods (see Chapters 2 and 4).
toxic effects can be acute or chronic. When the dietary
copper-to-molybdenum ratio exceeds 101, copper accu-
mulates in the liver and binds to the metalloprotein ceru-
loplasmin. After the liver is saturated, stress can precipi-
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2. Garry F, Chew DJ, Hoffsis GF: Enzymuria as an index of renal
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damage in sheep with induced aminoglycoside nephrotoxicosis,
togenous, and phytogenous copper poisoning are the Am J Vet Res 51:428, 1990.
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copper toxicity occurs when animals graze pastures with a multisystem disease, Mt Sinai J Med 43:129, 1976.
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New York, 1982, Plenum Press.
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7. Gross DR, Kitzman JV, Adams HR: Cardiovascular effects of in-
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steady level during the accumulation phase, but just cline in propylene glycol in calves, Am J Vet Res 40:783, 1979.
before a hemolytic crisis the levels double. Stressors such 8. Radostits OM et al: Veterinary medicine, Philadelphia, 2000, WB
as shearing, handling, and parturition may precipitate a Saunders.
hemolytic crisis. During such a crisis the liver releases 9. Adair HS, III, Adams WH: Ascorbic acid as suspected cause of
massive amounts of copper, which induces oxidation of oxalate nephrotoxicosis in a goat, J Am Vet Med Assoc 197:1626,
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compromise, rupture of the red blood cell, and release of 10. Kimberling CV, Arnold KS: Diseases of the urinary system of
“free” hemoglobin into the circulation. sheep and goats, Vet Clin North Am Food Anim Pract 5(3):637,
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11. Andreasen CB: Clinical chemistry manifestations of toxicologic
Clinical signs and diagnosis. During a hemolytic
and nutritional problems in large animals, Proceedings of the 12th
crisis, anemia, methemoglobinemia, hemoglobinuria,
American College of Veterinary Medicine Forum, 1994, San Fran-
muddy mucous membranes, dehydration, and weakness cisco.
may be observed. The sheep are depressed, anorectic, and 12. James LF, Johnson AE: Prevention of fatal Halogeton glomeratus
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or kidney copper levels may be used to diagnose the changes in acute Halogeton glomeratus poisoning in sheep, Can J
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14. Burrows GE, Tyrl RJ: Plants causing sudden death in livestock, Vet 38. Angus KW: Nephropathy in young lambs, Vet Rec 126:525, 1990.
Clin North Am Food Anim Pract 5(2):263, 1989. 39. Angus KW et al: Mesangiocapillary glomerulonephritis in lambs.
15. Panciera RJ et al: Acute oxalate poisoning attributable to ingestion II. Pathological findings and electron microscopy of the renal
of curly dock (Rumex crispus) in sheep, J Am Vet Med Assoc lesions, J Comp Path 84:319, 1974.
196:1981, 1990. 40. Lerner RA, Dixon FJ: Spontaneous glomerulonephritis in sheep,
16. Crowell WA et al: Ethylene glycol toxicosis in cattle, Cornell Vet Lab Invest 15:1279, 1966.
69:272, 1979. 41. Lerner RA, Dixon FJ, Lee S: Spontaneous glomerulonephritis in
17. Boermans HJ, Ruegg PL, Leach M: Ethylene glycol toxicosis in a sheep. II. Studies on natural history, occurrence in other species,
pygmy goat, J Am Vet Med Assoc 193:694, 1988. and pathogenesis, Am J Path 53:501, 1968.
18. Hovda LR: Toxicologic problems of small ruminants, Proceedings 42. Ferris TF et al: Toxemia of pregnancy in sheep: a clinical, physio-
of the Twelfth American College of Veterinary Medicine Forum, 1994, logical, and pathological study, J Clin Invest 48:1643, 1969.
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animal internal medicine, St Louis, 1996, Mosby. 45. Higgins RJ, Weaver CR: Corynebacterium renale pyelonephritis
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from different species of oak trees in conjunction with acorn poi- 46. Gajendragad MR, Kumar AA, Biswas JC: Unilateral pyonephrosis
soning in cattle, Vet Human Toxicol 29(4):305, 1987. in a pashmina goat, Ind Vet J 60:494, 1983.
22. Spier SJ et al: Oak toxicosis in cattle in northern California: clini- 47. Honda E, Yanagawa R: Attachment of Corynebacterium renale to
cal and pathologic findings, J Am Vet Med Assoc 191:958, 1987. tissue culture cells by the pili, Am J Vet Res 36:1663, 1975.
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terotoxemia in adult ewes, Can Vet J 34:58, 1993. amyloidosis, J Vet Intern Med 3:31, 1989.
24. Blackwell TE et al: Differences in signs and lesions in sheep and 49. Rings DM, Garry FB, Rings DM: Amyloidosis associated
goats with enterotoxemia induced by intraduodenal infusion of with paratuberculosis in a sheep, Comp Cont Ed Pract Vet 10:381,
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25. Michelsen PGE: Diseases caused by toxins of Clostridium perfrin- 50. Farnsworth GA, Miller S: An unusual morphologic form of
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26. Gerritsen MJ et al: Sheep as maintenance host for Leptospira inter- 130:475, 1974.
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1994. erratum appears in Vet Rec 124(3):62, 1989], Vet Rec 124:9, 1989.
27. Smith MC, Sherman DM: Urinary system. In Smith MC, 53. Angus KW, Hodgson JC: Recognition and management of
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Febiger. 54. Hartley WJ, Seaman JT: Suspected Toxoplasma infection in an
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sheep [letter], Aust Vet J 56:348, 1980. 56. Grossman IW, Altman NH: Caprine cloisonné renal lesion. Ultra-
30. Heath SB: Leptospirosis in cattle: a new look at an old disease, structure of the thickened proximal convoluted tubular basement
Proceedings of the Tenth American College of Veterinary Medicine membrane, Arch Path 88:609, 1969.
Forum, 1992, San Diego, CA. 57. Thompson SW, Bogdon TR, Yost DH: Some histochemical
31. Bolin CA, Zuerner RL, Trueba G: Comparison of three tech- studies of “cloisonné kidney” in the male Angora goat, Am J Vet Res
niques to detect Leptospira interrogans serovar hardjo type hardjo- 22:757, 1960.
bovis in bovine urine, Am J Vet Res 50:1001, 1989. 58. Altman NH, Grossman IW, Jernigan NB: Caprine cloisonné
32. Thiermann AB: Leptospirosis: current developments and trends, J renal lesion. Clinicopathological observations, Cornell Vet 60:83,
Am Vet Med Assoc 184:722, 1984. 1970.
33. Gerritsen MJ et al: Effective treatment with dihydrostreptomycin 59. Adam SEI, Wasfi IA, Magzoub M: Chronic copper toxicity in
of naturally infected cows shedding Leptospira interrogans serovar Nubian goats, J Comp Path 87:623, 1977.
hardjo subtype hardjo-bovis, Am J Vet Res 55:339, 1994. 60. Auza NJ et al: Diagnosis and treatment of copper toxicosis in ru-
34. Finnie JW, Swift JG: Adenovirus infection in ovine kidney and minants, J Am Vet Med Assoc 214:1624, 1999.
liver, Aust Vet J 68:184, 1991. 61. Lofstedt J: Comparative aspects of copper metabolism in rumi-
35. Belak S et al: Isolation of a pathogenic strain of ovine adenovirus nants and horses, Proceedings of the Seventh American College of Vet-
type 5 and a comparison of its pathogenicity with that of another erinary Internal Medicine Forum, 1989, San Diego, CA.
strain of the same serotype, J Comp Path 90:169, 1980. 62. Humphries WR, Morrice PC, Mitchell AN: Copper poisoning in
36. Angus KW et al: Mesangiocapillary glomerulonephritis in lambs. Angora goats, Vet Rec 121:231, 1987.
I. Clinical and biochemical findings in a Finnish Landrace flock, J 63. Bostwick JL: Copper toxicosis in sheep, J Am Vet Med Assoc
Comp Path 84:309, 1974. 180:386, 1982.
37. Frelier PF et al: Spontaneous mesangiocapillary glomerulonephri- 64. Gopinath C, Hall GA, Howell JM: The effect of chronic copper
tis in Finn cross lambs from Alberta, Can J Comp Med 48:215, poisoning on the kidneys of sheep, Res Vet Sci 16:57, 1974.
1984.
 Chapter 10 Diseases of the Urinary System • 267

LOWER URINARY TRACT A complete dietary history is crucial. It should include

hay, grain, pasture, and toxic plant ingestion; trace
PROBLEMS mineral availability; water sources; and any supplemented
feeding. In addition, information about previous health,
Urolithiasis current medications, age at castration, and duration of the
Urolithiasis is a common and frustrating problem for problem is important in determining the cause and pre-
both owners and veterinarians of male sheep and goats. It scribing proper therapy. Initial observations by the owner
is less commonly seen in females and is most common in may include anorexia and depression, with later reports of
feedlot lambs and pet goats.1 The composition of urinary urine dribbling, abdominal pain, and stranguria and
calculi (uroliths) varies according to geographic location, tenesmus in some animals.
but they are commonly composed of calcium salts and Risk factors for urolithiasis include dietary imbalances,
phosphatic complexes (e.g., calcium apatite, calcium hy- limited availability of water, abnormal urinary pH, age of
drogen phosphate dihydrate, calcium carbonate, magne- the animal at time of castration, and possibly genetic pre-
sium ammonium phosphate).2,3 disposition. High-grain, low-roughage diets decrease the
formation of saliva and increase the amount of phospho-
Pathogenesis. Phosphatic calculi are formed in re- rus excreted in the urine. As a general rule the calcium-
sponse to high-concentrate, low-roughage, low calcium- to-phosphorus ratio should be maintained between 11
to-phosphorus ratio, high-magnesium diets and alkaline and 21. Cereal grains have an abnormal calcium-to-
urine.4 Lambs fed a diet high in phosphorus and magne- phosphorus ratio of 14 to 16. High-grain diets over-
sium have a high incidence of calculi on postmortem ex- whelm the salivary excretion mechanism and cause exces-
amination. High-grain diets result in the excretion of sive urinary excretion of phosphorus. High-calcium diets
large amounts of phosphorus in the urine as a result of an are effective at reducing the absorption of phosphorus
overwhelmed salivary excretion mechanism. Certain from the gastrointestinal tract. Legumes (e.g., alfalfa,
breeds of sheep (Texel) are predisposed to increased clover, kudzu) have much more calcium than phosphorus.
urinary excretion of phosphorus.5 Increased levels of magnesium in diets with normal
Silicate calculi also are occasionally diagnosed.1,5 They calcium and phosphorus concentrations can cause an in-
occur more often in sheep fed plants grown in sandy soil creased incidence of urolithiasis in feedlot lambs.10
or water containing high levels of silica, conditions that Acidic urine (pH less than 7.0) predisposes to the forma-
are common in western North America.6 Diets high in tion of silicate calculi. Alkaline urine (pH greater than
silica with high calcium-to-phosphorus ratios that are 7.0) favors the formation of phosphate, carbonate, and
supplemented with sodium bicarbonate may predispose struvite calculi. Oxalate calculi may form in either acidic
to the formation of silica calculi.7 or alkaline urine. Some oxalate-containing plants are
Oxalate calculi are caused by the ingestion of excessive listed in Box 10-1. Forage-based diets commonly contain
quantities of oxalate-containing plants. Oxalates bind excessive amounts of potassium, which can result in an
calcium in the rumen, but bacteria in a healthy rumen alkaline urinary pH. Genetic factors may play a role;
may (over time and with continued exposure) adapt excretion of salts by the kidney and the production of
enzyme systems that more effectively degrade oxalates. crystal-inhibiting compounds appear to differ among
All uroliths are composed of salts and minerals in a animals.
crystal lattice surrounding an organic matrix (nidus) of
proteinaceous material. Nidus formation occurs when Clinical signs and diagnosis. Dysuria and stranguria
urine mucoproteins coalesce and precipitate with crystals with dribbling of urine and vocalization (especially in
in supersaturated urine.8 Urinary mucoprotein produc- goats) are the two most common signs. Forceful contrac-
tion is increased by estrogenic compounds, inadequate tion of the abdominal musculature (“heaving”) may be
levels of vitamin A, and high-concentrate diets.8 Uroliths observed. Hematuria, prolonged urination, flagging of
can be formed in either the upper or lower urinary tract; the tail, apparent abdominal pain (e.g., stretching out,
by obstructing urine flow, they cause the clinical signs of kicking at the abdomen, looking at the side), and bruxism
stranguria, dysuria, hematuria, uremia, and possibly are additional clinical signs. Exteriorization of the penis
death. and examination of the urethral process is the most im-
Because of the length and diameter of the urethra, portant step in the evaluation of these cases. In severe
urolithiasis is more commonly identified in males. Early cases the urethra can be ruptured along the penile shaft,
castration can decrease the urethral diameter and there- resulting in fistula formation. The urethral process or ap-
fore increase the incidence of obstruction. The most pendage may be necrotic from lodged calculi. Scalding of
common sites of obstruction are the urethral process the perineal region or rear legs may be observed, possibly
and distal sigmoid flexure, although the trigone of with concurrent prolapse of the prepuce or rectum.
the bladder, ureter, and renal pelvis also may become Careful examination of the preputial hairs or vulvar
obstructed.9 region may reveal attached crystals. The signs exhibited
268 • Sheep and Goat Medicine
in cases of urolithiasis may vary depending on the dura- IV) can be provided to reduce urethral irritation and
tion and severity of the obstruction. swelling; this is a relatively successful nonsurgical man-
Abdominal palpation reveals a distended bladder. agement method. In some instances, these medical treat-
Transrectal or transabdominal real-time ultrasonography ment techniques combined with dietary changes may be
can be used to visualize the enlarged urinary bladder in useful. However, because urolithiasis often causes sludge-
some cases.11 Echogenic material in the kidney, ureters, like calculi to form in the bladder, the problem tends to
bladder, or urethra cannot always be visualized. The recur in the majority of cases.
normal size of the bladder is 5 cm and 8 cm or larger in
diameter in pygmy goats and other goat and sheep Surgical treatment. Several surgical techniques can be
breeds, respectively.10 Digital rectal palpation may reveal used to manage these cases, including urethrostomy, ure-
increased urethral pulsation. However, the clinician throstomy, and cystotomy. The following paragraphs de-
should exercise caution when interpreting this sign scribe surgical techniques for perineal urethrostomy, tube
because some intact males contract the crura of the penis cystotomy, and bladder marsupialization.
normally on digital palpation of the anus.9 Renal calculi Perineal urethrostomies have been performed in many
and occlusion of the ureter may lead to hydronephrosis, sheep and goats, but surgical failure, poor long-term sur-
which can be visualized with ultrasonography. vival rates (because of strictures), and decreased reproduc-
Radiographs can demonstrate the presence of calcium tive function limit this method to a salvage only proce-
oxalate or calcium carbonate calculi, whereas struvite, dure.12,16,17 The animal can be heavily sedated, given
apatite, and silicate crystals may not be visible radi- epidural anesthesia, or placed under general anesthesia.
ographically. Rupture of the bladder (discussed later in The perineal area is scrubbed and aseptically prepared.
this chapter) is likely if ascites can be appreciated. In the The clinician then makes a midline skin incision between
case of urethral obstruction or rupture, pulsations, the scrotum and anus and identifies the retractor penis
swelling, and pain may be appreciable on palpation. muscles and the penis. The penis should be exteriorized
Blood collected for a complete blood count and bio- and rotated to expose the dorsal blood supply, which can
chemistry profile may reveal stress leukograms, azotemia, then be double ligated before the penis is incised near the
and hyperkalemia depending on severity. Urine for uri- ligatures.14,17-19 As much of the penis as possible should
nalysis may be difficult to obtain, but testing can reveal be freed of surrounding tissue in order to place the
hematuria, crystalluria (see Figure 10-5), and proteinuria. urethra in close proximity to the skin. The urethra is
incised and the urethral mucosa and tunica albuginea are
Medical treatment. Amputation of the urethral pulled up and sutured to the skin under as little tension as
process at its base near the glans penis is a commonly per- possible. The urethra is then sutured with a simple inter-
formed procedure to treat urolithiasis. Urine flow is re- rupted pattern and a monofilament, nonabsorbable mate-
stored in as many as 66% of cases.12 If this procedure fails rial.14 The skin incision should be closed with two layers
to allow normal urination, catheterization of the urethra of nonabsorbable monofilament suture placed in the skin
and retrograde flushing may dislodge some calculi. Stones using a simple interrupted pattern. A Foley catheter can
can form and adhere to any portion of the urinary tract. be passed through the urethral opening into the urinary
The male is sedated (with acepromazine 0.03 to 0.1 bladder and kept there for 3 to 4 days.14 Animals should
mg/kg IV) and positioned on his rump. The clinician ex- be placed on an antibiotic (procaine penicillin G 22,000
teriorizes the penis by simultaneously pulling the sheath IU/kg twice a day [BID]) before surgery and for 3 to 5
and prepuce caudally, straightening the sigmoid flexure, days after surgery. The clinician or keeper can remove the
and forcing the penis cranially. The urethra can then be sutures in 10 to 14 days. Animals that have undergone
catheterized for retrograde urethral lavage. A lidocaine- urethrostomy can no longer be used for breeding. If stric-
saline flush solution (1 part 2% lidocaine to 3 parts saline) tures develop after surgery, they can be treated with a pre-
may be beneficial. This initial flush can be followed with pubic urethrostomy or bladder marsupialization.6,10 The
administration of a weak acetic acid solution (1 part prognosis for long-term survival after urethrostomy is
vinegar to 1 to 4 parts sterile water) to help dissolve ure- guarded to poor because of stricture formation.
thral and bladder stones. When flushing the urethra the Cystotomy and tube cystotomy are the authors’ pre-
clinician should take care not to become overly aggressive ferred methods of surgical correction. They allow for the
because excessive inflammation or rupture of the urethra longest survival and return to normal breeding function.
may occur. Acepromazine maleate (0.03 to 0.1 mg/kg IV) Unfortunately, the cost of cystotomy may relegate its use
has been used with some success to reduce urethral to pets or breeding animals. The animal is anesthetized
smooth muscle spasms and relax the retractor penis and placed in dorsal recumbency, the skin is clipped and
muscle.13-15 If the urethra is not completely occluded and surgically prepared, and a right paramedian incision is
urine can be seen dribbling from the prepuce, ammonium made. The incision should be 2.0 to 3.0 cm off midline
chloride (300 mg/kg PO) can be administered to dissolve extending cranially approximately 6 cm from the teats.
stones and NSAIDs (flunixin meglumine 1 to 2 mg/kg The clinician then opens the abdomen and visualizes the
 Chapter 10 Diseases of the Urinary System • 269

urinary bladder. Placement of stay sutures at either end of bladder with minimal tension to the body wall in multiple
the cystotomy site allows for greater stabilization of the sites. Alternatively, the omentum may be “pleated”
bladder.18,19 The clinician then performs the cystotomy, around the purse-string site, after which the catheter
empties the bladder, and lavages the bladder to remove all is sutured to the skin and the paramedian incision is
calculi. Light massage of the bladder during lavage may closed. If a Foley catheter is to be used, the clinician
help remove any calculi attached to or imbedded in the should check for proper bulb air or saline retention before
bladder wall. Mild normograde urethral flushing with an inserting it. The authors of this chapter prefer to fill the
isotonic solution can be attempted. Some practitioners Foley’s bulb with saline. A one-way valve can be made
report greater success combining normograde and retro- from the finger of a latex glove and placed over the end
grade flushing.19 Intraoperative flushing of the urethra of the catheter to create a crude Heimlich valve (Figure
with a vinegar/distilled water solution (1:1 to 1:4) can 10-8). This helps decrease the incidence of ascending
help dissolve the stones.14 The authors do not make more infection.16,18,19
than three or four attempts to relieve obstructions in Regardless of the procedure (cystotomy or tube cys-
order to minimize urethral damage. totomy) employed, the celiotomy sites should be closed in
After the urethra is clear and the bladder is cleaned of three layers with an appropriately sized absorbable suture.
all visible stones, the cystotomy and abdominal incision The authors prefer to close the abdominal fascia with a
are closed. However, if the urethra cannot be cleared, a simple continuous pattern and the skin with a Ford inter-
tube cystotomy should be performed. The bladder inci- locking suture or a horizontal mattress pattern. The skin
sion is closed using an inverting pattern with absorbable should be closed with appropriately sized nonabsorbable
suture. Occasionally, a two-layer closure is necessary. suture; the stitches can be removed in 10 to 14 days.
Placement of a Foley (16 to 24 French) or mushroom Many goats attempt to pull or chew the tubes, so belly
catheter into the bladder and exiting through the ventral bandages, Elizabethan collars, and close observation
abdomen (Figure 10-7) allows for continual drainage of should be employed to help maintain catheter placement
urine. By routing urine flow through the catheter, the cli- (see Figure 10-8). Ammonium chloride (2 to 4 g daily
nician permits the urethra to rest, allows inflammation to
subside, and promotes healing.16 The clinician makes a
small skin incision lateral to the paramedian incision and
inserts the catheter subcutaneously, where it enters first
the abdomen and then the bladder. To position the Foley
catheter, a purse-string suture is placed in the bladder
wall. A small stab incision is made in the middle of the
purse-string, and the balloon end of the Foley catheter is
threaded into the bladder, after which the purse-string
suture is tightened. After inflating the Foley catheter or
placing the mushroom catheter, the clinician tacks the

Figure 10-7 Illustration of a tube cystotomy. Note the location of Figure 10-8 A, An Elizabethan collar is used to prevent the male
the incision and the placement of the catheter into the bladder. The from chewing or pulling on the catheter; a belly band (B) helps
catheter is secured to the body wall at several sites. Inset shows maintain the catheter. When using belly bands, the clinician or keeper
Heimlich valve. should examine the animal’s underlying skin daily. Applying antibiotic
ointment (triple antibiotic) at the catheter exit site may help minimize
infection. Note the modified Heimlich valve at the end of the Foley
catheter in B.
270 • Sheep and Goat Medicine
PO) is generally given to maintain urine pH between 6
and 6.5. Because of its bitter taste, ammonium chloride
should be mixed with syrup and given with a syringe.
Animals should be closely monitored for signs of depres-
sion, anorexia, and abdominal pain. If a belly band is used
to support the Foley catheter, the bandage should be
changed at least every other day and the underlying skin
examined daily. Clamping of the catheter should be insti-
tuted on the fourth day after surgery to allow for normal
urination. This should be done in a dry stall and with
an increasing duration until full-stream urination is
achieved.16 Normal urination should occur for 1 to 2 days
before the catheter is deflated and removed. The Foley
catheter should not be removed before day 7 after surgery.
By waiting more than 7 days to remove the catheter,
the clinician reduces the chances of urine leaking
from the bladder.16 The bladder defect is allowed to heal
spontaneously. Normograde contrast cystourethrography
through the tube cystotomy catheter can help the clini-
cian evaluate the extent and healing of urethral lesions.20
Bladder marsupialization also has been described18, 21 Figure 10-9 An 8- to 12-cm celiotomy incision (a) is placed 2 to 4
cm lateral to the prepuce (b). The smaller incision site for marsupializa-
as an alternative to urethroscopy and lithotripsy tech- tion (c) should be chosen to minimize bladder tension and urine
niques.10 It may be used as a primary surgical procedure scalding.
for urolithiasis or as a salvage technique in cases in which
perineal urethrostomy has been previously performed but
had scarred to the point of urethral closure. The laparot- and for as long as 14 days postoperatively (procaine peni-
omy portion of the marsupialization technique is similar cillin 20,000 to 30,000 IU/kg IM BID, ceftiofur 2.2
to that used in tube cystotomy or cystotomy. The animal mg/kg IM once a day [SID] to BID).21 Virginia re-
is anesthetized and placed in dorsal recumbency, the site searchers described excellent long-term survival. Of the
is surgically prepared, and an 8- to 12-cm paramedian in- cases of marsupialization they studied, 7 of 19 goats had
cision made in the caudoventral abdomen parallel and 2 undergone urethrostomy before referral for marsupializa-
to 4 cm lateral to the prepuce (Figure 10-9). The clinician tion. Short-term complications of marsupialization
carefully exteriorizes the bladder apex, decompresses the include bladder prolapse and cystitis; over time fibrotic
bladder, places stay sutures 4 to 5 cm apart, and makes a stomal closure of the marsupialization site may occur.21
cystotomy incision between them. A second abdominal No instances of fatal cystitis or upper urinary tract infec-
incision is made on the opposite side of the prepuce. The tion were reported. This technique is a good alternative
site for the second abdominal incision is chosen to mini- procedure, particularly for non-breeding animals and
mize urine scalding of the surrounding skin. The bladder those whose perineal urethrostomy sites have strictured
apex should be pulled or lifted into the second abdominal to the point of preventing urine flow.
incision by the stay sutures. Undue tension on the bladder Regardless of the surgical technique, fluid therapy
should be minimized as it is pulled into this incision (0.9% saline) is warranted for animals that are at least
site.18,21 The clinician then sutures all four corners of the moderately dehydrated or uremic. Potassium and calcium
bladder to the abdominal wall and sutures the bladder’s may be supplemented as indicated. Postoperative diuresis
seromuscular layer in a circumferential fashion to the ab- is crucial. Antiinflammatory drugs and broad-spectrum
dominal fascia using a horizontal mattress pattern and antibiotics should be given as needed. Despite alleviation
absorbable suture. The bladder margins are sutured in a of the urinary obstruction, possible sequelae include erec-
circumferential fashion to the skin with absorbable tile failure resulting from vascular occlusion of the corpus
suture. A simple interrupted, horizontal mattress, or cavernosum penis.22 If one animal in a flock or herd is
other pattern may be used. The original abdominal inci- treated for urolithiasis, preventative measures should be
sion is closed in three layers as described for tube cystot- put in place to reduce the incidence in the rest of the
omy.18,21 Urine is voided from the bladder through the group.
marsupialized site. Therefore after suturing the incision
should be large enough to allow urine flow but not large Prevention. Access to fresh, clean water encourages
enough to allow bladder eversion or prolapse. Animals consumption, decreases the supersaturation of minerals in
should be placed on antibiotics, preferably preoperatively the urine, and decreases the incidence of urolith forma-
 Chapter 10 Diseases of the Urinary System • 271

tion. In the winter, warming the water may increase con- phosphorus and ammonium chloride to the diet may help
sumption.5 Sodium chloride added at the rate of 3% to decrease the incidence in the flock or herd. Oddly, attain-
5% of the dietary dry matter intake increases water con- ing a calcium-to-phosphorus ratio of 0.71 to 11 and
sumption, and the chloride ions may reduce supersatura- acidifying the urine may be the best methods of preventing
tion of calculus-forming salts.23,24 Chloride has the silicate calculi. Silicates are associated with the feeding of
ability to prevent phosphates from binding to the muco- oats, oat straw, and some native grasses. When silicate
protein matrix that forms part of the struvite molecule. stones are discovered, the consumption of these feedstuffs
The addition of salt can help prevent phosphate-, magne- should be reduced or avoided. The plants listed in Box
sium-, and silicate-based calculi. An anionic diet in- 10-1 are all associated with oxalate calculi and therefore
creases the urinary excretion of hydrogen ions, decreases their ingestion should be avoided or minimized.
urinary pH, increases urinary excretion of calcium, and The intake of excessive protein, which is common in
decreases the precipitation of struvite. Conversely, diets feedlot lambs, can result in an increased urinary output of
and feedstuffs rich in cations (e.g., alfalfa, molasses) the mucoprotein that is the “backbone” of most uroliths.
should be avoided. Grass hays should be considered the Therefore dietary protein should be fed to meet but not
primary forage source for males because grass has a better greatly exceed requirements for maintenance or growth.
cation-to-anion balance than legumes for struvite pre- Diets high in estrogenic compounds and some growth-
vention. To avoid precipitation of magnesium and promoting implants can increase secondary sex gland size
calcium phosphate, urine pH should be maintained at or and increase the output of urinary mucoprotein; their
below 6.8.25 consumption should be avoided. Many legumes (e.g.,
Balancing levels of calcium, phosphorus, and magne- white clover) have estrogenic compounds, inappropriate
sium in the diet is important to prevent urolithiasis. If the calcium-to-phosphorus ratios, and a larger than necessary
magnesium content of the diet is greater than 0.6%, stru- protein content, contributing to some forms of stones.
vite uroliths may be encountered even if a normal Although legumes in hay and forage may improve growth
calcium-to-phosphorus ratio exists. Adding calcium to and productivity, they should be used and fed to males
the diet may help reduce intestinal uptake of phosphorus with caution.
and magnesium. Therefore analyzing the diet and adding Whenever acidifying products are fed, urine pH
calcium carbonate or calcium chloride to the diet to attain should be monitored. For pet or valuable breeding males,
a 21 calcium-to-phosphorus ratio are excellent tech- the owner can be instructed to collect urine once or twice
niques to reduce the incidence of urolithiasis. The addi- weekly and measure urine pH (pH paper is acceptable for
tion of ammonium chloride to the diet decreases the inci- this purpose). Urine pH should be maintained at or
dence of silica uroliths.1 The potential for the formation slightly under 6.8. Ammonium chloride (200 to 300
of phosphatic calculi increases when pelleted rations are mg/kg/day or 2% of the total diet) appears effective in
fed because lowered saliva production limits phosphate maintaining proper pH, but it is extremely unpalatable.
excretion by the gastrointestinal tract and increases the The ammonium chloride can be added to the feed, mixed
excretion of phosphorus by the urinary tract.13 Pelleted with honey, and sprayed onto forage to ensure adequate
rations also are associated with increased mucoprotein ex- intake. However, if animals consume too much of it, am-
cretion in the urine. Cereal grains (e.g., corn, oats, milo) monium chloride can produce a metabolic acidosis. Signs
are all high in phosphorus and relatively low in calcium; of toxicity include inappetence, depression, and diarrhea.
their consumption should be minimized. If cereal grains Vitamin C (3 to 4 mg/kg/day) also can help maintain pH
are fed, calcium should be added to the diet to maintain balance, but administering the vitamin often enough for
the proper calcium-to-phosphorus ratio (21). it to be of practical value may be difficult.14
The addition of chlortetracycline or tetracycline to If left untreated, urolithiasis will progress to rupture of
complete diets, mineral mixtures, or feed supplements the urethra or bladder. The primary sign of urethral
also can be helpful in some cases. Including beta-carotene rupture is a large, fluctuant, ventral swelling at the level of
or vitamin A in the diet can help prevent urolithiasis. the distal sigmoid flexure14 caused by urine diffusing into
Diets containing 30% green forage probably are sufficient the subcutaneous tissue of the perineum and ventral
in beta-carotene content. abdomen. The clinician should take care to differentiate
When uroliths are discovered, submission of the stones urethral rupture from preputial or penile injury or abscess
for laboratory analysis can aid in the development of a pre- and abdominal hernia. He or she can facilitate the
ventative plan for the rest of the flock. In cases in which drainage of the fluid by making numerous stab incisions
calcium oxalate or calcium carbonate calculi are identified, (0.5 to 1.0 cm in length) into the fluctuant area, taking
the feeding of legumes (e.g., alfalfa, clover, kudzu) should care to avoid superficial epigastric vessels. Affected
be limited or avoided. If silicate calculi are identified, the animals should be treated with procaine penicillin G
calcium-to-phosphorus ratio is greater than 21, and (22,000 IU/kg IM every 12 hours) for 5 to 7 days. The
sodium bicarbonate has been added to the diet, adding use of NSAIDs should be considered.
272 • Sheep and Goat Medicine
Ruptured Bladder URETHRAL HEMORRHAGE
Pathogenesis. Bladder rupture more commonly occurs AND OTHER URETHRAL
in males as a sequela of urolithiasis. However, improper
castration with an elastrator band can result in urethral
PROBLEMS
occlusion and cause bladder rupture. Because ruminant As a sequelae to dystocia, an obstructive uropathy can
urine contains high concentrations of potassium and low develop and result in stranguria, pollakiuria, and enlarged
concentrations of sodium and chloride, a diffusion of kidneys with a distended pelvis.6 In these cases, palpation
blood sodium and chloride into the peritoneal cavity may of the abdomen should reveal a firm mass cranial to the
be noted. After rupture of the bladder a concurrent move- pelvic brim.
ment of water from the intracellular and extracellular
fluid compartments occurs as a result of the greater in-
traabdominal osmolality. The release of aldosterone sec-
Urinary Incontinence
ondary to hyponatremia leads to reabsorption of sodium Pathogenesis. Urinary incontinence may result from a
by the gastrointestinal tract and increased potassium se- number of primary problems. If it is a sequela to a neuro-
cretion by the salivary glands. The reabsorbed sodium logic problem, the clinician should determine whether
causes competitive inhibition of potassium absorption by the primary lesion is affecting the detrusor muscle or the
the gastrointestinal epithelium and thereby increases the urethral sphincter muscles of the bladder.
fecal elimination of potassium. Therefore hyperkalemia
may have a slower onset in ruminants than in other Clinical signs. Sheep and goats with dysuria and lower
species with ruptured urethras or bladders. If the rupture motor neuron disease usually have bladders that are ex-
is preceded by signs of urinary obstruction, immediately tremely distended. Gentle transabdominal pressure usually
after rupture the animal acts normal and may even eat. results in the voiding of urine. Affected animals may
display ataxia of the rear limbs and have depressed rear
Clinical signs. Mild colic, depression, anorexia, ab- limb, tail, and perineal reflexes. Upper motor neuron lesions
dominal distention, dehydration, and production of little can result in a distended bladder that does not empty on
or no urine are common clinical signs. After the first firm palpation because of the increased tone of the urethral
signs are noted, the animal’s condition deteriorates over sphincter. Localization of the lesion and determination of
the next 2 to 5 days.26 The ventral abdomen is often dis- the underlying cause are crucial in making a prognosis and
tended and may assume a pear-shaped contour. outlining treatment options for these patients.

Diagnosis. Blood collected for serum biochemistry and Treatment. Catheterization of the female bladder with
electrolyte analysis may reveal azotemia, hyperphos- a Foley catheter is helpful in supporting does or ewes
phatemia, hyperkalemia, hyponatremia, and hypo- with urinary incontinence. For temporary relief, cysto-
chloremia, depending on the duration of the problem. A centesis of the urinary bladder may be indicated, particu-
fluid wave is appreciated with abdominal ballottement in larly in males. Ultrasound guidance is helpful in this pro-
some cases. Excessive abdominal fluid can be confirmed cedure. The use of pharmacologic agents to promote
by real-time ultrasonography. A definitive diagnosis is micturition has not been reported in sheep and goats, but
most easily achieved by demonstrating elevated peri- cholinergic agents such as bethanechol (0.04 to 0.08
toneal creatinine levels more than two times higher than mg/kg SC three times a day [TID] or 4 mg/kg PO four
serum levels (collected by paracentesis), by performing times a day [QID]) may be given to stimulate smooth
retrograde flushing of dye (methylene blue) into the muscle activity and detrusor contraction. Drugs used to
bladder and recovering it in the peritoneal fluid, and by decrease smooth muscle activity of the urethra are gener-
surgical exploration. Peritoneal potassium levels also may ally given orally; the authors of this chapter have not used
be higher than 10.0 mEq/L. them in ruminants. The prognosis depends on the
primary cause of the incontinence.
Treatment. Stabilization of the patient with IV physi-
ologic saline (0.9%) or 0.45% saline in 2.5% dextrose is
imperative as urine is drained slowly from the peritoneal
Cystitis
cavity. Surgical exploration of the abdomen by parame- Pathogenesis. Cystitis may develop as a sequela to
dian celiotomy can be performed as described previously. problems at lambing or kidding; the infection may ascend
The clinician identifies the rent or necrotic area and and become a pyelonephritis.27 C. renale is the most com-
débrides the edges before closing the site. Thorough monly reported causal organism. Other causal organisms
lavage and removal of calculi should be performed. Occa- include Proteus, E. coli, Staphylococcus, and Streptococcus.
sionally bladder tears heal spontaneously, with those in
the dorsal area of the bladder being more likely to heal Clinical signs. Pollakiuria, hematuria, restlessness, and
than those in the ventral area. pyuria are frequently associated with cystitis. The condi-
 Chapter 10 Diseases of the Urinary System • 273

tion is observed in females more commonly than in males the bladder may aid in identifying excessive bladder wall
because of the closer proximity of the female bladder to thickness and asymmetry. The disease may persist for
the external environment. months or years depending on the magnitude and dura-
tion of ingestion of bracken fern.9,19 One flock of Merino
Diagnosis. Cytologic evaluation of either a mid-stream wethers had access to bracken fern for at least 18 months,
voided or catheterized urine sample may be diagnostic for and 5% to 8% appeared to have bladder tumors.30
pyuria. Occasionally, bacteriuria occurs. External palpa-
tion or ultrasonic evaluation of the bladder can help Prevention. The condition can be limited by reducing
define the thickness of the bladder wall. A thickened wall or eliminating bracken fern in the diet.
suggests cystitis. Cystitis should be differentiated from
upper urinary tract infection, and bacterial causes should
be distinguished from neoplastic conditions that can
Leiomyoma
cause cystitis (enzootic hematuria). The primary tumor type known to invade the bladder of
sheep and goats is leiomyoma. Leiomyomas may be soli-
Treatment. Urine should be properly collected for bac- tary or multiple, and the animal may have other primary
terial culture and antibiotic sensitivity patterns because neoplasms.31 Most often, these tumors are incidental
any therapy is based on these results. In cases in which findings at necropsy.
cost considerations preclude bacterial culture, broad-
spectrum antibiotics (ceftiofur sodium 2.2 mg/kg SC
every 12 hours) should be given for at least 10 to 14 days.
Renal Neoplasms
With aggressive therapy most affected animals improve The multicentric form of lymphosarcoma caused by ovine
within 2 weeks. leukemia virus may involve the kidneys in sheep.24 A
nephroblastoma has been reported in a 3-month-old ovine
Prevention. Prevention is best accomplished by avoid- fetus that was aborted by an adult ewe.32 The report sug-
ing situations that compromise normal urine flow or may gested that infectious causes of abortion acted as a terato-
lead to ascending infection of the lower urinary tract. genic factor and altered normal renal embryogenesis. Only
6% of neoplasms occurring in sheep affect the kidneys.
NEOPLASTIC CONDITIONS
Congenital Defects
Enzootic Hematuria Hypospadias is a common congenital defect observed in
Pathogenesis. Chronic ingestion of bracken fern newborn male lambs or kids. It is caused by failure of
(Pteridium aquilinum) causes hemorrhagic cystitis ini- closure of the urethra and results in a visible opening on
tially and progresses to neoplastic involvement of epithe- the ventral aspect of the penis and prepuce.33 The kids are
lial, mesenchymal, and mixed cell populations. Enzootic usually genetically female intersexes.34,35 Concurrent di-
hematuria is generally a condition of adults that results aphragmatic hernia, brachygnathia, and atresia ani are re-
from grazing the plant or ingesting contaminated hay. ported.36 Urethral dilatation with a hypoplastic distal
The fern is concentrated in open areas of forest in well- urethral tip is described in an intersex Nubian/French
drained, fertile soils. All parts of the plant are toxic, and Alpine goat.37 These goats also may have hypospadias38
no single component has been identified to be the incit- (see Chapter 6). A congenital urethral diverticulum has
ing cause of clinical disease.28 Some reports state that been reported in male kids with a ventral swelling of the
bovine papilloma virus may work in concert with bracken prepuce caused by accumulation of urine in the urethral
fern to produce neoplastic lesions in the bladder. outpockets.39
Polycystic kidneys are frequently diagnosed in sheep
Clinical signs and diagnosis. Usually affected animals and goats at the slaughterhouse or at birth if the condi-
have a history of ingesting the fern or contaminated hay ted by an adult ewe.
and often numerous animals are involved. Initial signs re-
ported by owners include hematuria and even clots of
blood. With time, a decrease in body condition, produc-
tivity, and exercise tolerance occurs. As a result of anemia,
pale mucous membranes, tachycardia, and tachypnea are
reported. Infiltration of the bladder leads to dysuria,
pollakiuria, and possibly obstruction. Thickening of
the bladder wall results, and papillomas develop after 1
year, with invasive carcinoma occurring 2 to 6 years
later.28,29 Transabdominal ultrasonographic evaluation of
274 • Sheep and Goat Medicine
Ulcerative Posthitis (Pizzle Rot) Treatment and prevention. Treatment includes reduc-
Pathogenesis. Rams, bucks, and wethers are all suscep- ing the protein content of the diet; débriding necrotic
tible to bacterial posthitis-balanoposthitis.46 The most tissue; applying astringents, antiseptics, or antibiotics to
common bacterial infection of the prepuce is referred to skin lesions (e.g., gentian violet, iodine, triple antibiotic
as ulcerative posthitis, pizzle rot, or sheath rot. This condi- ointment); and possibly irrigating the sheath. In extreme
tion is caused by an interaction of the local bacterial flora cases in which the preputial orifice is scarred to the point
(most commonly C. renale) with excess urinary urea and that normal urine flow is partially or completely impeded,
typically occurs when animals consume high-protein the sheath should be opened surgically to allow for urine
diets. Diets rich in legumes may contain more than 18% escape. This salvage procedure entails making a 2- to 4-
protein, resulting in an alkaline urine that generally has a cm ventral incision through the ventral skin and into the
larger than normal concentration of urea. Whenever sheath as aseptically as possible. The incision allows urine
protein is fed above the maintenance requirement for a to drain from the sheath during or after urination. The
particular animal, ulcerative posthitis may occur. Excess incision and sheath can be infused with antiseptics (e.g.,
dietary protein is usually deaminated by the body, its organic iodine solution) and the animal can be placed on
carbon chains used as an energy source, and the amino broad-spectrum antibiotics (e.g., tetracycline 2 to 10
groups converted to urea. In the presence of the urease mg/kg SID to 20 mg/kg every 48 to 72 hours).
enzyme–producing C. renale, excess urea can be converted Affected animals should be sheared of their preputial
to ammonia. The ammonia may damage mucosal surfaces wool or mohair, and the sheared fiber should be burned or
and result in pizzle rot. It occurs more commonly during disposed of in a manner to prevent the spread of the
wet springs and when animals graze lush legume or causal organism. An unlimited supply of fresh, clean
legume-grass pastures. Young male feedlot lambs, club or water should always be available. In cases in which man-
show lambs and kids, wethers kept for wool or mohair agement conditions are favorable for this disease but
production (e.g., Merino sheep, Angora goats), and dietary changes are difficult to make, the feeding of urine
animals raised and maintained for blood or the produc- acidifiers (e.g., ammonium chloride) and/or antimicrobial
tion of blood products are all predisposed to this condi- agents (e.g., chlortetracycline) may be of benefit. Still, de-
tion because they are all fed high-protein diets. Pre-sale creasing the dietary protein intake is the best method of
and breeding diets for rams and bucks typically contain treatment and prevention. If such procedures are possible,
more than 12% protein and are often fed in confinement treating sheep wethers with 70 to 100 mg of testosterone
settings. However, diets as low as 12% protein have been propionate or implanting zeranol (12 mg) may help de-
associated with this condition. Castration before puberty crease the incidence of this disease.46
also can be a predisposing factor because castrated
animals have a decreased ability to extend the penis and
tend to urinate in the sheath. Confinement rearing con-
Ulcerative Dermatosis
centrates animals in smaller areas and is conducive to C. Pathogenesis. Ulcerative dermatosis is a contagious
renale survival. Pizzle rot may be detected as early as 2 disease of sheep caused by a parapoxvirus. This condition
weeks after an increased protein intake. The condition also is referred to as lip and leg ulceration and ovine vene-
has some similarities to and on occasion can be confused real disease. The lesions may be contaminated by Fusobac-
with the viral disease ulcerative dermatosis. A differential terium necrophorum or other bacteria, which may affect
diagnosis can be based on the location of lesions. With the severity of the clinical signs. The virus typically gains
ulcerative dermatosis the lesions occur on the penis, access into the skin through cuts, scrapes, shearing or
sheath, vulva, legs, lips, and eyes. The gram-negative coc- other wounds, and breeding trauma. This disease has
cobacillus Actinobacillus seminis is occasionally associated been associated with breeding unshorn sheep, which can
with posthitis in rams. This organism is rare in North cause abrasions around the vulva and penis.
America. C. renale can be transmitted by asymptomatic
ewes, does, and possibly cows and insects. However, clin- Clinical signs. Lesions associated with ulcerative der-
ical disease rarely appears without a concurrent protein matosis include circular crusty ulcers (typically 5 to 30
intake that exceeds the animals’ requirements. mm in diameter and 3 to 5 mm deep) on the skin of the
prepuce, penis, vulva, nostrils, eyes, legs, and hooves. The
Clinical signs. Ulcerative posthitis is characterized by ulcers may contain a viscous, odorless, purulent exudate.
straining during urination, swelling of the prepuce, Penile lesions typically involve the glans penis and may
necrosis and ulceration of the preputial mucosa, and oc- cause scarring of the glans and/or the formation of ure-
casionally stenosis of the preputial orifice. In severe cases thral fistulas. Penile damage can result in a loss of breed-
affected animals may show signs of abdominal dis- ing ability and possibly depressed libido. In severe cases
comfort or colic and a stiff-stilted gait. The urine of af- inflammation associated with these lesions may lead to
fected animals is usually malodorous and appears thick or both phimosis and paraphimosis. The course of the
semi-solid. disease may be from 2 to 6 weeks.
 Chapter 10 Diseases of the Urinary System • 275

Treatment. Treatment is aimed at reducing pain and 11. Morin DE, Badertscher RR: Ultrasonographic diagnosis of ob-
applying astringents or antibiotic ointments to the structive uropathy in a caprine doe, J Am Vet Med Assoc 197:378,
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12. Van Metre DC et al: Obstructive urolithiasis in ruminants:
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18(3):S317, 1996.
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hygiene, isolation of affected animals until the wounds 12:87, 1990.
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for as long as 4 weeks. During the quarantine period nants, Proceedings of the 1998 Symposium on Small Ruminants for the
the animals should be examined to ensure they are Mixed Animal Practitioner Western Veterinary Conference, 1998, Las
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16. Rakestraw PC et al: Tube cystostomy for treatment of obstructive
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17. Noordsy JL: Food animal surgery, Trenton, NJ, 1994, Veterinarian
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kidney in a Nubian goat (Capra hircus), Vet Path 33:708, 1996. 49. Grewal AS, Wells R: Vulvovaginitis of goats due to a herpes virus,
41. Gomez-Villamandos JC, Carmona JM, Castellano J: Possible Aust Vet J 63:79, 1986.
renal dysplasia in two related, juvenile goats, Small Rumin Res 50. Tarigan S, Webb RF, Kirkland D: Caprine herpes virus from bal-
13:311, 1994. anoposthitis, Aust Vet J 64:321, 1987.
 Chapter 11

DNeurologic
iseases of the
System
MARGO R. MACHEN, BRYAN M. WALDRIDGE, CHRISTOPHER CEBRA,
MARGARET CEBRA, ELLEN B. BELKNAP, LISA HELEN WILLIAMSON, AND
D.G. PUGH

NEUROLOGIC EXAMINATION neurologic signs are species-specific to sheep or goats. In

AND LOCALIZATION OF addition, certain breeds of animals within a species may
have a hereditary predisposition to develop a particular
LESIONS pathology. Young animals are more likely to have congeni-
The purpose of a neurologic examination is to determine tal, inherited, or infectious disorders, whereas older animals
the anatomic portion of the nervous system responsible for tend to develop neoplastic and degenerative diseases.4
the clinical signs an animal is demonstrating. In sheep and
goats a thorough general physical examination followed by
a specific neurologic examination similar to that used in
History
small animals allows the clinician to make an accurate di- The clinical history of an animal should be included in a
agnosis and provide a prognosis to the client. Localizing database that also records the results of a complete physi-
neurologic pathology requires the categorization of clinical cal examination. Important items such as the animal’s diet,
signs the animal is demonstrating to either the lower housing, purpose, vaccination history, and previous indi-
motor neuron (LMN) or upper motor neuron (UMN) vidual disease history (as well as herd health history)
pathways. The LMNs can be further divided into the pe- should all be part of the initial information gathered from
ripheral spinal nerves and spinal cord. Pathology of the the client. Construction of a sign-time graph allows the
LMN results in typical segmental physical abnormalities clinician to plot the severity of the clinical signs against
such as paralysis of the muscles innervated; areflexia; time and is a useful diagnostic tool.5 The course of disease
muscle atrophy and flaccidity; loss of resistance to passive begins with the owner’s initial observation of the present-
manipulation; and anesthesia, hypoesthesia, or hyperesthe- ing complaint. The clinician and owner should take care
sia of the affected area.1 UMN functions are performed by not to overlook early behavioral abnormalities that could
the cranial nerves, brainstem, cerebellum, and cortex. be interpreted as unrelated to the present problem. Acute
Pathology of the UMN or lesions in a portion of the tract disease processes can be either progressive or nonprogres-
from the brain to the spinal cord result in poor postural sive; however, chronic diseases are usually progressive.
performance, normal or hyperactive spinal reflexes, in- The history combined with an appropriate neurologic
creased tone in extensor muscles, abnormal reflexes, loss of examination can provide the clinician and owner with an
consciousness, and interruptions in sensory processing.1,2 accurate prognosis. A slow, progressive disease carries a
Clinical signs such as conscious proprioceptive deficits and poorer prognosis than one that has passed its peak of
ataxia make localizing lesions difficult.3 severity and is now improving.4 Neurologic deficits that
manifest themselves as sensory and motor deprivations
are associated with a poorer prognosis than those that
Signalment just produce motor losses. The duration that clinical
Breed distinctions within species of goats and sheep as well signs are observed also can be used as a prognostic indi-
as age and sex can be important clues in the diagnosis of cator because nervous tissue is fairly intolerant of long-
neurologic disease. Many infectious agents that can cause term insults.
• 277 •
278 • Sheep and Goat Medicine
Initial Observations related to abnormal behavior may include yawning, head
The sheep or goat should initially be observed unre- pressing, compulsive walking, circling, and gazing.4
strained so that the clinician can adequately assess loco- Behavioral disorders are hard to localize because abnor-
motive deficits, postural abnormalities, unilateral con- malities in the limbic system, which includes the hypo-
formational and musculoskeletal alterations, and the thalamus, hippocampus, amygdala, and portions of the
mental status of the animal. The clinician should give cerebral cortex, are all associated with complex behavior.6,7
the animal sufficient time to calm down if it is not in its
normal environment. Cranial nerves. Abnormalities in the function of the
twelve cranial nerves result from localized lesions of the
Mental status. During the period of initial observation brainstem or specific cranial nerves (CNs).8
the animal’s mental status can be assessed. For animals
to be alert and oriented two basic components of the OLFACTORY NERVE—CN I: The olfactory nerve (CN I)
nervous system must be functioning—the cerebral cortex consists of chemoreceptors in the nasal mucosa that
and the ascending reticular activating system.2 The retic- transmit impulses through axons that penetrate the crib-
ular activating system receives sensory information from riform plate to synapse on the olfactory bulb.1 From there
the spinal cord and cranial nerves and diffusely projects axons of the olfactory bulb travel ipsilaterally to the olfac-
this information through thalamic relays into the cerebral tory cortex, which is part of the rhinencephalon and
cortex. Therefore external stimulation from light, touch, limbic system.
sound, smell, and temperature helps to maintain con- Assessment of the sense of smell in sheep or goats is
sciousness in the brain. difficult; however, because they must have a sense of smell
An animal’s mental status can be categorized as hyper- in order to have a strong appetite, if they are eating the
excited, alert, depressed, stuporous, and comatose. Table 11-1 assumption is that CN I is intact.9 Substances such as
describes each category and lists an example of atypical alcohol, cloves, and benzol can be used to elicit a reaction
behavior. Normally an animal should appear as sensitive to from an animal, but smoke and ammonia should not be
its environment as its herd mates. If the animal has been used because they are irritants that also stimulate trigem-
removed from its habitat, it should be aware of the exam- inal nerve endings. The most likely cause of anosmia is
iner and follow the examiner’s movement with its head, bilateral nasal passage disease because both halves of the
eyes, and ears. All animals should avoid painful stimuli brain participate in the interpretation of smell. Tumors
and appear alert and wary of new situations. Other signs and polyps in the nasal passages of sheep and maxillary

TABLE 11-1

CATEGORIES AND DESCRIPTION OF DIFFERENT LEVELS OF CONSCIOUSNESS

LEVEL OF CONSCIOUSNESS DEFINITION DESCRIPTION OF BEHAVIOR

Hyperexcitability Rage, mania, frantic motor Striking with front limbs, kicking, charging,
activities excessive vocalization, violent struggling,
possibly normal behavior
Alertness Conscious, observant, responding
appropriately to stimuli
Dementia Inappropriate responses to Afraid of feed, running into walls, self-mutilation
external stimuli
Stupor Unresponsive to external stimuli; Droopy ears, holding head low, reluctant to move
responsive to painful stimuli
Depression Reduced responses to external Unwillingness to rise, lack of recognition,
stimuli and pain inappetence, head pressing, propulsive walking
Coma No response to external or Recumbent, convulsions
painful stimuli
Narcolepsy Episodic condition in which Rapid eye movement; after the episode animals
animals exhibit stupor without return to normal
motor activity
 Chapter 11 Diseases of the Neurologic System • 279

tooth root abscesses in both sheep and goats also can cerebelli, and penetrate the dura mater.1 The fibers of
cause disturbances in the sense of smell. CN III are then joined by nerve fibers from the
trochlear nerve (CN IV) and abducent nerve (CN VI),
OPTIC NERVE—CN II: The optic nerve (CN II) which work together to move the eyeball. After the CN
transmits sensory impulses from electrochemical recep- III fibers reach the eyeball, they synapse on the ciliary
tors in the retina to the optic chiasm. In sheep and goats, ganglion, and the postganglionic fibers of the ciliary
90% of optic nerve fibers cross at the chiasm to enter the nerves innervate the ciliary muscles and pupillary con-
contralateral optic tract, which transmits the impulses to strictor muscles. Dilation of the pupils is mediated
the lateral geniculate nucleus and visual cortex in the oc- through the sympathetic nervous system, which origi-
cipital lobe via the optic radiation.2 The brain is then able nates from the hypothalamus. The sympathetic nerve
to recognize the object in the visual field. fibers descend to the spinal cord in the lateral lectomer-
Several methods can be used to assess the function of tospinal pathway to synapse on the cell bodies of pre-
CN II. The first is observing the animal maneuver ganglionic neurons in segments T1 through T3. The
through an obstacle course. This is the least reliable preganglionic neurons then ascend in the vagosympa-
method, especially if the animal has other neurologic thetic trunk to the cranial cervical ganglion, which is
deficits.1 The menace response is the most reliable and located ventromedial to the tympanic bulla. The post-
easiest method to use for evaluation; it also assesses the ganglionic fibers then form a nerve plexus that follows
facial nerve CN VII, which is responsible for blinking. the internal carotid artery through the middle ear and
The examiner moves his or her hand toward the animal’s enters the skull at the base, eventually exiting through
eyes or drops an object into the animal’s visual field from the orbital fissure and innervating the ciliary body and
above, which should elicit a blink response from the iris dilator muscles of the eye.
animal. The optic nerve is responsible for the afferent As previously stated the direct and consensual pupil-
pathway and the facial nerves are responsible for the ef- lary light reflex is one of the methods used to assess CN
ferent pathway. The examiner should be careful not to III’s role in pupil function. After performing an initial as-
generate air currents that may stimulate deficits in the sessment of pupil size for symmetry and to rule out
trigeminal nerve endings.1 Another method is the direct primary ocular disease, the examiner should place the
pupillary light reflex, which also assesses the oculomotor animals in a dark area so that external light does not in-
nerve CN III, which mediates pupillary constriction. The fluence the examination. Pupils that are very small are
clinician examines the eyes for symmetry before the test considered miotic, and dilated pupils are mydriatic. Oc-
and then shines a light directly into one eye. The direct casionally the pupil size is unequal. If it is not extremely
response should be constriction of the pupil, and the op- pronounced this may be a normal finding for the animal,
posite eye also should constrict as a result of the consen- but severe asymmetry is called anisocoria.2 To determine
sual pupillary reflex. if there is any irregularity in pupil size, the clinician
Unilateral lesions in the optic tract, which includes the should place the animal in the dark and then in a bright
lateral geniculate nucleus, optic radiation, and occipital area. A sympathetic lesion will keep the affected pupil
lobe cortex, cause contralateral visual deficits and failure from dilating in the dark, and a CN III lesion will prevent
of the menace response with normal pupil light re- the pupil from constricting in the bright light. The direct
sponse.10 However, affected animals retain consensual pupillary light reflex is more powerful than the consen-
pupillary light reflexes when the opposite eye is stimu- sual reflex, so the eye that the light is being directed
lated. Lesions that occur in the retina and optic nerve toward constricts more than the opposite eye.
cause ipsilateral visual deficits and failure of both the Examining the animal’s eye position in relationship to
direct pupillary and consensual light reflexes. Depending its head at rest and during lateral movement of the head
on the severity of the lesion in the optic chiasm, the re- can help the examiner assess the motor function of CN
sulting clinical signs can include bilateral fixation of III. If the motor function of CN III is abnormal, the eye
pupils, no response to light, and loss of vision. is dilated and deviated to a fixed ventrolateral position
known as strabismus. In addition, CN III is responsible
OCULOMOTOR NERVE—CN III: The oculomotor nerve for innervation of the levator palpebrae muscle, which
(CN III) is responsible for constriction of the pupils; the when affected results in a drooping upper eyelid, known
sympathetic system is responsible for dilation. After the as ptosis. Ptosis is not commonly noted in sheep or goats
optic nerve fibers pass through the optic chiasm, they because they also have a frontalis muscle that can lift the
synapse on the pretectal nucleus, which sends its upper eyelid. Lateral motion of the head should cause the
neurons to the contralateral oculomotor nucleus; some animal’s eye to try to remain focused straight ahead and
innervate the ipsilateral nucleus of CN III too. The therefore result in the eye moving in the opposite direc-
neurons of CN III leave the ventral midbrain medial to tion of head movement. However, as the head continues
the crus cerebri, extend across the edge of the tentorium to turn, the eye begins to move quickly in the same direc-
280 • Sheep and Goat Medicine
tion because of vestibular influences. This is a normal sis of such a lesion requires the examiner to force the
oculovestibular response. animal’s head into an abnormal orientation in which the
Unilateral lesions of the oculomotor nucleus or nerve head is extended and the nose is elevated. Sheep and
produce mydriasis of the ipsilateral pupil without loss of goats should drop their eyes as the head is lifted. If one or
vision in either eye.9 The ventrolateral strabismus noted both eyes deviate from the normal position, the condition
with lesions of CN III is fixed regardless of the position is termed positional nystagmus. Most commonly the ab-
of the animal’s head. These types of clinical signs can be normal eye deviates ventrally; this is most easily appreci-
observed in animals with otitis media and otitis interna ated by observing the more prominent dorsal sclera of the
because of the relationship of the cranial cervical nerve affected eye.2
fibers to the middle ear.
TRIGEMINAL NERVE—CN V: The trigeminal nerve
TROCHLEAR NERVE—CN IV: The trochlear nerve (CN V) supplies sensory innervation to the head and
(CN IV) is responsible for the motor pathway to the motor innervation to the muscles of mastication. The
dorsal oblique muscles of the eye. The trochlear nucleus nerve is divided into three branches: the ophthalmic,
originates in a position similar to that of the oculomotor maxillary, and mandibular. The motor nucleus of the
nucleus. The axons of the nerve run dorsally then cross trigeminal nerve lies in the pons, and its axons run in the
before exiting the caudal colliculus. The fibers then run mandibular branch of CN V. The mandibular nerve in-
along the side of the midbrain before they join CN III at nervates the masseter, temporal, rostral digastric, ptery-
the cavernous sinus, where both nerves exit the orbital goid, and mylohyoid muscles.12 The cell bodies of the
fissure.11 sensory fibers are in the trigeminal ganglion, which is
Assessment of CN IV is easier to do in animals such as located in the canal housing the trigeminal nerve in the
goats and sheep because they have horizontal pupils. petrosal bone.1 The sensory fibers enter the brainstem
Damage to this nerve results in a dorsomedial strabismus. and run to the first cervical spinal cord segment as the
Bilateral dorsomedial strabismus occurs in several diffuse trigeminal nerve. A second set of sensory neurons re-
encephalopathies in sheep and goat such as polioen- ceives information from mechanoreceptors and transmits
cephalomalacia and listeriosis, but it is unclear whether nociceptive information through the maxillary branch to
this is the result of a true bilateral trochlear lesion.2 the pontine and spinal nucleus. Their axons travel to the
thalamus associated with the contralateral medial lemnis-
ABDUCENT NERVE—CN VI: The last of the three cus and to the facial nucleus.1 From the thalamus, the
nerves responsible for eye movement is the abducent axons project diffusely into the cerebral cortex and are
nerve (CN VI), which innervates the lateral rectus and closely associated with the respiratory centers in the
retractor bulbi muscles of the eye. The nerve originates in brain. Axons from the spinal and pontine nucleus also run
the rostral medulla and its axons run ventrally out of the to the facial nucleus through the ophthalmic branch,
medulla and lateral to the pyramid. It joins CN III and which allows for the completion of the palpebral and
CN IV in the cavernous sinus, where it exits the orbital corneal reflex.
fissure to innervate the eye muscles. To access all the functions of CN V, the examiner must
The methods previously described for use in assessing assess several areas of the face. Initiating the palpebral
CN III function can be used to assess the function of CN reflex by touching the cornea of the eye is part of the as-
VI. Lesions in CN VI result in an inability of the eye to sessment of the ophthalmic branch, which innervates the
be moved laterally, producing a ventromedial strabismus. eye and surrounding skin and is responsible for the main-
The abducent nerve also controls the animal’s ability to tenance of corneal epithelium. If the medial canthus of
retract its eyeball for protection. Stimulation of the the eye is touched the animal should close its eye. If the
corneal reflex by touching the eyeball should result in the cornea is touched the animal should retract the eye and
retraction of the eye and extrusion of the third eyelid. close the lids; this reflex also involves the facial nerve. A
Lesions in CN VI that do not involve CN III or CN IV deficient palpebral reflex with a normal menace response
are very rare.1 suggests a lesion in the trigeminal nerve or ganglion.9
Lesions affecting CN III, CN IV, and CN VI can only Loss of CN V innervation to the corneal epithelium can
be clinically assessed by moving the animal’s head and result in neurotropic keratitis.
observing the ocular position. Cerebellar and vestibular The maxillary branch supplies sensory innervation to
diseases also produce nystagmus, but the strabismus the maxillary portions of the face and external nasal
changes whenever the head and neck are moved. Com- mucosa. Touching the lateral canthus of the eye or stimu-
plete ophthalmoplegia occurs when all the muscles re- lating the external nares should elicit two responses if the
sponsible for eye movement are paralyzed. Lesions on the axons are intact. The first is a subconscious localized
floor of the skull affect CN III, CN IV, and CN VI as reflex from CN V to CN VII that causes the skin to
well as sympathetic innervation as they leave the cav- twitch. The second is a consciously mediated action in
ernous venous sinus and enter the orbital fissure. Diagno- which the animal moves its head away from the annoying
 Chapter 11 Diseases of the Neurologic System • 281

stimulus; this involves the contralateral thalamus and nerve (CN VIII) and CN VII, vestibular signs often are
parietal cortex. noted in affected animals; however, Horner’s syndrome
The mandibular branch of CN V supplies both does not occur. Inner ear infections can damage the facial
sensory and motor innervation to the mandibular muscles sympathetic nerves and cause vestibular signs, resulting in
of the face. Interruptions in motor innervation result in Horner’s syndrome.1
muscle atrophy of the temporal and masseter muscles and Lesions in the petrosal bone that occur between the
decreased jaw tone. Often the animal’s tongue protrudes internal acoustic meatus and stylomastoid foramen can
from the mouth, but the animal can withdraw it when result in keratoconjunctivitis sicca (dry eye) and loss of
stimulated. If bilateral involvement of the nerve has oc- taste. Loss of taste is difficult to assess in sheep or goats,
curred, the animal is unable to close its mouth and may but placing a noxious stimulus on the animal’s rostral
drool excessively, losing bicarbonate in the saliva. The tongue should result in head shaking, rapid tongue move-
nerve also supplies sensory innervation to the skin cover- ment, and salivation. A Schirmer’s tear test can be used to
ing the mandibular area, which when stimulated should assess lacrimal gland function (see Chapter 12).
produce a behavioral response similar to that evoked in Lesions in CN VII that occur distal to the stylomas-
the maxillary area. toid foramen or damage the motor fibers affect the facial
Damage to any branch of the trigeminal nerve results muscles, but not the ability of the animal to taste and
in sensory losses to the areas it innervates. Sensory losses form a tear film. In goats and sheep with compromised
to the facial skin are usually unilateral and can be attrib- motor function, alterations occur in ear, eyelid, lip,
uted to peripheral lesions of CN V. Diffuse loss of sensa- muzzle, and nares carriage. The facial nerve maintains
tion in the face is rare, although it may result from bilat- facial muscle tone. Goats and sheep that have erect ears
eral cerebral cortical disease.9 An animal with forebrain should hold them erect; those with pendulous ears should
disease should have an intact reflex component for CN V be able to move the base of the ear canal to follow exter-
but will not consciously move away from facial stimula- nal stimuli. Animals with CN VII paralysis have droopy
tion.2 If the damage occurs to the motor portion of the ears and are unable to move them in response to external
mandibular branch, marked muscle atrophy can be noted stimuli. The animals should have a palpebral and menace
2 to 3 weeks after the lesion occurs. response that results in them closing the palpebral fissure
when stimulated. Simultaneous loss of the menace re-
FACIAL NERVE—CN VII: The facial nerve (CN VII) sponse and the palpebral reflex suggests a lesion in the
innervates a number of facial muscles responsible for facial nerve of the orbicularis oculi muscle.9 The palpe-
expression and provides parasympathetic innervation bral fissure also should remain open when the animal
to the lacrimal, mandibular, and submandibular glands. is alert, and the upper eyelid should not droop. An in-
The nucleus of CN VII originates in the ventral medulla terruption in tone results in deviation of the muzzle to
oblongata. Its axons course through the lateral brain- the normal side and loss of the ability of the nares to
stem and enter the petrosal bone at the internal acous- retract and dilate during inspiration and expiration. The
tic meatus, where CN VII divides into several nerve tongue may protrude out of the affected side of the
branches. The major petrosal nerve branches off first and mouth and the animal may drool. Affected animals often
travels to the lacrimal ducts, where it is responsible for have feed packed into the cheek pouch of the affected
tear film production. The sensory geniculate ganglion re- side. If CN VII becomes irritated, it can cause facial
ceives fibers from the rostral two thirds of the tongue and muscle spasms, which can be observed in animals that
is responsible for detecting taste. These fibers follow the have tetanus.
trigeminal nerve back into the cortex. The next branch is
the chorda tympani nerve, which innervates the man- VESTIBULOCOCHLEAR NERVE—CN VIII: The vestib-
dibular and submandibular salivary glands. In addition a ulocochlear nerve (CN VIII) has two divisions, the
small branch of this nerve also innervates the stapedius cochlear division, which mediates hearing, and the
muscle in the middle ear. As the facial nerve exits the sty- vestibular division, which is responsible for providing in-
lomastoid foramen, its fibers fan out and provide motor formation about the orientation of the head in relation to
function to a number of muscles responsible for facial ex- gravity.4 The receptors of the vestibular division lie in the
pressions and closure of the palpebral fissure. inner ear and are located in the petrosal bone. The
Damage to CN VII can be localized according to the vestibulocochlear nerve has three semilunar canals that
clinical signs. Lesions in the brainstem can result in a are oriented at right angles to each other. They contain
number of discrete or diffuse clinical signs in affected the crista ampullaris receptors that relay information
animals. Listeriosis in sheep and goats can cause discrete related to the detection of motion in three directions. The
lesions throughout the brainstem, which may result in ab- utriculus is oriented horizontally and the sacculus is ori-
normal function of the facial muscles and stapedius ented vertically; both have receptors called maculae that
muscle and variable effects on taste and lacrimation.2 signal the static position of the head in relation to
Because of the close proximity of the vestibulocochlear gravity.1 When all of these receptors are stimulated by the
282 • Sheep and Goat Medicine
animal moving, signals are sent to the bipolar cell bodies gait, posture, ocular movement, and extensor tonus. Most
of the vestibular neurons in the petrosal bone. The axons animals have unilateral vestibular signs that include
of the cell bodies, along with those of the cochlear ataxia, nystagmus, and a head tilt toward the origin of the
nucleus, ascend through the petrosal bone via the internal lesion.7 Recumbent animals with vestibular lesions lie on
acoustic meatus into the brainstem and terminate in one the affected side. If they are rotated to the opposite side,
of four vestibular nuclei and the cerebellum. they spontaneously reposition themselves with the af-
After information has been delivered to the brainstem, fected side down. The limbs on the affected side are hy-
the lateral vestibular nuclei maintains postural tone by perreflexic and hypotonic. The animal may circle or
sending out ipsilateral signals through the vestibulospinal exhibit ataxia and is prone to falling frequently. If the
tract to stimulate extensor muscles and inhibit flexor animal remains standing, it assumes a wide-based stance
muscles. The lateral, medial, and rostral nuclei all send to maintain balance. The head tilt should be obvious and
axons to CN III, CN IV, and CN VI to mediate vestibu- can be accentuated if the animal’s eyes are covered to
lar eye movement. eliminate visual compensation. Paradoxic vestibular syn-
The assessment of unilateral hearing loss in large drome resulting from central vestibular damage causes
animals is difficult; it requires the use of sophisticated the animal’s head to tilt away from the side of the lesion.
equipment modified to assess brain stimulation from The direction of the nystagmus varies depending on
noises generated in each ear (brainstem auditory evoked the location of the lesion in the vestibular system.9 To
response [BAER]). Animals that have bilateral hearing assess an animal’s nystagmus, the examiner should first
losses are easier to assess because they do not respond place the animal standing with its head in a normal posi-
to loud environmental noises that do not generate tion and then move the animal’s head in all four direc-
vibrations. tions, observing their eye movement after the head has
Brainstem lesions must be differentiated from periph- stopped. Normally sheep keep the optic plane parallel to
eral lesions in the inner ear to aid in prognosis and treat- the ground when their heads are moved and goats main-
ment. Table 11-2 lists clinical signs associated with tain their eyes in the center of the palpebral fissure in all
central and peripheral vestibular lesions. Clinical signs as- head positions.9 Nystagmus is spontaneous eye move-
sociated with vestibular lesions include ataxia, staggering, ment that can occur as a fast or slow phase. The fast phase
head tilt, nystagmus, and ocular deviations. They usually returns the eye to its resting location, and the slow phase
occur in groups according to the portion of the nervous moves the eye in the direction of the lesion. Nystagmus is
tract affected. A thorough otoscopic examination should characterized by the direction in which movement occurs
be performed on all animals demonstrating vestibular in the fast phase—horizontal, vertical, or rotatory.2 Rota-
signs; radiographs of the tympanic bulla also may be war- tory and horizontal nystagmus can indicate peripheral or
ranted. The assessment of the vestibular system involves central vestibular lesions. It occurs when the animal’s
observing the animal’s head orientation as well as the head position changes. Vertical nystagmus indicates cen-

TABLE 11-2

SIGNS OF VESTIBULAR DISEASE

CONDITION PERIPHERAL NERVOUS SYSTEM CENTRAL NERVOUS SYSTEM

Mental status Normal Frequently depressed

Gait Asymmetric ataxia, may cause increased Asymmetric ataxia, paresis
extensor tone contralaterally, falling, rolling
Postural reactions Normal Abnormal
Cranial nerves May have deficits in CN V, VII, Horner’s May have deficits in CN
syndrome, head tilt VI, VII, IX, X, or XII
Nystagmus Horizontal or rotatory, not altered in direction Horizontal, rotatory, or vertical; may
with changes in head position; fast phases change direction with position of
away from the side of the lesion; positional the head
ventral strabismus
Bilateral peripheral vestibular No nystagmus or vestibular eye movements,
Disease symmetric ataxia, crouching posture with
jerky swinging movements of the head,
deafness
 Chapter 11 Diseases of the Neurologic System • 283

tral vestibular disease and is constant regardless of the measure the electroconductivity of the affected areas.
animal’s head movement or position. Damage to the accessory nerve is rare because it is well
protected from the overlying muscle; injury to the spinal
GLOSSOPHARYNGEAL NERVE AND VAGUS NERVE—CN canal or base of the skull is often accompanied by more
IX AND CN X: The glossopharyngeal nerve (CN IX) profound neurologic deficits that may mask clinical signs
carries sensory information from the rostral pharynx, of accessory nerve damage. The most common pathologic
larynx, and tongue through the solitary tract to the conditions associated with injury to the nerve include
nucleus of the medulla. The motor nerves of CN IX arise skull fractures, penetrating wounds (such as those caused
from the nucleus ambiguus in the ventrolateral medulla by goring with a horn), injection site infections, and
and innervate the pharynx and palate. The glossopharyn- contusions.
geal nerve also has a parasympathetic component that in-
nervates the parotid and zygomatic salivary glands. The HYPOGLOSSAL NERVE—CN XII: The hypoglossal
vagus nerve (CN X) provides motor innervation to nerve (CN XII) is the motor pathway to the intrinsic and
the pharynx, larynx, palate, and striated muscles of the extrinsic muscles of the tongue and geniohyoideus
esophagus by the recurrent laryngeal nerve. The parasym- muscle.4 The nucleus of the nerve lies in the caudal
pathetic branch of CN X arises from the vagal nucleus in medulla and its axons run from the ventral medulla lateral
the medulla and innervates all the abdominal and tho- to the pyramids as they exit into the hypoglossal canal
racic viscera with the exception of the pelvic viscera. and innervate the muscles of the tongue. The nerve
Damage to CN IX and CN X results in clinical signs allows the animal to protrude and retract its tongue. The
related to laryngeal and pharyngeal function. Affected tongue is innervated on each side by CN XII.
animals have difficulty swallowing. The examiner can Animals that have damage to CN XII often have a
assess the gag reflex of sheep and goats by placing a history of difficulty apprehending and masticating their
tongue depressor in the back of the mouth. Normally the food. The owners may observe the animals dropping
animals should gag, pushing the stimulating object out of feed and cuds out of their mouths while eating and ru-
the area with the caudal aspect of the tongue.2 A small minating. To assess the function of the tongue, the ex-
tube also can be gently passed into the pharynx to see aminer places a palatable substance on the animal’s lips
whether the animal will swallow and allow it to enter into and nose; it should be able to protrude its tongue and
the rumen. The examiner should exercise caution in han- lick the substance off of the area. In addition, the clini-
dling these animals if rabies is suspected. Often affected cian can gently grasp the animal’s tongue with gauze and
sheep and goats have stertorous breathing resulting from assess the strength with which its tries to retract it.
unilateral or bilateral paresis of the larynx. Animals with Often unilateral damage to CN XII causes the tongue to
pharyngeal paralysis can regurgitate food through the deviate or protrude toward the affected side. Atrophy of
nose.9 Functional examination of CN IX and CN X the lingual muscles can occur as early as 1 week after an
should include auscultation of the larynx for stertorous insult to the nerve.
airway sounds, passage of an oral gastric tube to evaluate
pharyngeal activity, and palpation of the cricoarytenoid LOCALIZATION OF
dorsalis muscle for atrophy..9 Loss of vagal innervation of
the rumen in goats and sheep results in uncoordinated NEUROLOGIC LESIONS
rumen contractions and the inability to have a primary
rumen contraction. Sensorium
The somatic afferent system is responsible for transmit-
ACCESSORY NERVE—CN XI: The accessory nerve ting signals related to pain, touch, and temperature. The
(CN XI) innervates the trapezius and parts of the bra- receptor organs, both encapsulated and nonencapsulated,
chiocephalic and sternocephalic muscles.1 The nerves are classified as mechanoreceptors, thermoreceptors, and
arise from the ventral roots of cervical vertebrae C1 to C7 nociceptors. They are stimulated by physical contact with
and the medulla, run cranially as the spinal root, and the external environment.12 Two types of responses can
emerge from the skull at the tympanooccipital fissure. occur in animals that have these receptors stimulated.
The muscles that CN XI innervates allow the forelimb of The first is a subconscious localized reflex withdrawal
the animal to be elevated and advance and stabilize the from a stimulus or skin twitching, and the second is a
neck laterally. conscious reaction that may include vocalization, aggres-
Observation of conformational abnormalities and pal- sion, or movement of the animal away from the stimulus.
pation of the trapezius, brachiocephalic, and sternoce- Strips of skin along the surface of an animal are inner-
phalic muscles for atrophy are used to assess damage to vated by one pair of spinal nerves in a distinct pattern re-
CN XI. A decrease in resistance to the movement of the ferred to as a dermatome. Each strip receives overlapping
head and neck contralateral to the side of the lesion also innervation from three different spinal roots.4 Sensory
may be noted. Electromyography (EMG) can be used to fibers from the dermatome enter the spinal cord at the
284 • Sheep and Goat Medicine
dorsal root and have one of two fates. The first involves pinching aggressively can elicit a deep pain response in
them synapsing on interneurons in the dorsal horn of the the limbs of sheep and goats. Determining the animal’s
gray matter, which then sends short axons to the alpha sensitivity to deep pain is important because of the grave
motor neurons to stimulate a reflex withdrawal. This prognosis that accompanies its loss. Fibers that carry deep
reflex pathway requires an intact LMN reflex arc to func- pain perception are less susceptible to the effects of pres-
tion. Therefore if the spinal cord is transected cranial to sure, and because their tracts cross and re-cross widely in
an area being stimulated, the animal maintains an intact the spinal cord, a complete transection of the cord is gen-
reflex reaction to stimulation. The cutaneous or pannicu- erally required to produce loss of pain sensation.2
lus response to stimulation of the skin covering the trunk Hyperesthesia indicates an increased sensitivity to
also relies on a reflex arc. The sensory fibers from the skin stimuli in an area that is palpated; it can result from spinal
enter the dorsal root of the spinal cord and then ascend to cord or nerve root lesions. Diffuse hyperesthesia also can
the C8 and T1 segments, where the motor neurons of the result from infectious agents that cause meningitis.
lateral thoracic nerve are located. Therefore a transection Although the dermatomes have not been mapped in
of the spinal cord caudal to T1 may result in a decreased sheep and goats, they have been in horses, cats, and dogs.
or absent cutaneous response in the area caudal to the These areas are relatively similar among species and can
transection. be used to help localize lesions to areas of the spinal cord.
Two types of pathways are responsible for transmitting In assessing the superficial pain responses of an animal
painful stimuli to the brain. The first transmits superficial the clinician must be able to accurately determine the
pain sensations primarily from the nociceptors but also boundaries of the loss of sensation and hyperesthesia.
can carry information from the other two types of recep-
tors. The axons of these receptors are small myelinated
and unmyelinated fibers that enter the dorsal root of the
Gait
spinal tract and ascend through a series of ipsilateral and Goats and sheep walk by first flexing the hindlimb on one
contralateral synapses. The second pathway relays infor- side and then the forelimb on the same side; the process is
mation about deep pain and involves proprioceptive fibers then repeated on the opposite side. Animals must inte-
that enter the spinal cord and ascend by ipsilateral dorsal grate a number of neural processes to be able to ambulate.
columns and the contralateral spinothalamic tract. Spinal cord reflexes are responsible for maintaining the
Conscious proprioceptive information is carried in limbs in extension, supporting the animal’s weight, and
the dorsal columns and spinomedullothalamus tract in initiating stepping motion. These functions are locally
the dorsolateral fasciculus of the spinal cord through the mediated at C6 to T1 and L4 to S2. The organization of
brainstem to the sensorimotor cortex.4 The information stepping motion is performed at the brainstem in the
is processed to determine the orientation of an appendage reticular formation. The cerebellum is responsible for
in relation to an environmental stimulus. smooth locomotion and coordination of the muscle
Compromises to the spinal cord result in loss of func- movement. The vestibular system maintains balance and
tion in the following order of severity: helps anticipate alterations in the animal’s center of
gravity so it can compensate appropriately. The cerebral
1. Proprioception
cortical functions control both voluntary and fine move-
2. Voluntary motor function
ment of learned functions.
3. Superficial pain sensation
To assess an animal’s gait the examiner should observe
4. Deep pain
it walking in a straight line as well as turning in a tight
Therefore an animal with a loss of pain sensation has a circle. Animals can be led through a maze of obstacles to
graver prognosis than an animal with a loss of conscious assess their cranial nerve integration with the ability to
proprioception and motor function. A positive response coordinate movement. Gait abnormalities include con-
to painful stimuli may result in the animal vocalizing, scious proprioceptive deficits, paresis, circling, ataxia, dys-
moving its head in the direction of the stimulus, moving metria, spasticity, stiffness, and myotonia. Musculoskele-
its entire body away from the stimulus, or kicking at the tal and other systemic abnormalities should be ruled out
offending object. However, limb withdrawal should not with a thorough physical examination before the animal
be interpreted as a behavioral response to a stimulus is diagnosed with a neurologic problem. The animal’s
because of the local reflex arcs in the spinal cord. Superfi- stride should be assessed to determine whether the length
cial pain is most easily assessed by using a needle to prick is normal, increased, or decreased.
the surface of the skin lightly or by using a pair of hemo- Conscious proprioceptive deficits can result in several
stats to pinch the skin. clinical signs, including knuckling over, stumbling, ad-
Deep pain assessment requires a more aggressive ap- duction or abduction, and interference of the limbs. The
proach to evaluate the animal’s response. To elicit a deep examiner tests the conscious proprioception of a limb
pain response, the examiner must stimulate the perios- either by placing the dorsum of the distal limb down and
teum of the bone. Placing a large pair of hemostats above seeing whether the animal rights it or by crossing one
the coronary band across the dorsal surface of P1 and limb over the other and observing the animal reposition
 Chapter 11 Diseases of the Neurologic System • 285

the limb correctly. Walking an animal up and over an ob- Dysmetria occurs when an animal overshoots or un-
stacle such as a curb while taking care to prevent visual dershoots its intended target. Hypermetria results in a
stimulus helps the examiner evaluate proprioception. The high-stepping gait when the animal is walking (goose-
proprioceptive pathway runs in the dorsolateral columns stepping), whereas hypometria results in a stiff, shortened
and projects into the cerebellum (unconscious) and cere- stride that is pronounced in the forelimbs. Both of these
bral cortex (conscious).4 Slight compression of the spinal gait abnormalities are observed with lesions in the cere-
cord often causes deficits in proprioception, as do lesions bellum or spinocerebellar pathway; they can be accompa-
in the cerebral cortex. nied by tremors and ataxia. In hypermetria the loss of
Paresis is a decrease in the ability of the animal to cerebellar input that normally dampens the flexion phase
move a limb properly. The term paresis is usually preceded of gait results in exaggerated movement.2
by the prefix mono-, para-, tetra-, or hemi-, which indi- Spasticity is unnatural increased muscle tone in a limb.
cates the number of limbs involved. Dragging a limb The resulting clinical signs are similar to those seen in
while walking or scuffing the surface of the hoof wall is dysmetria but also include a notable increase in muscle
often noted. Usually paresis is noted while the animal is tone when the limb is manipulated or palpated. Lesions
moving; however, abnormal hoof wear or growth also can in the white matter of the brainstem and spinal cord
provide clues. Paresis can result from a UMN or LMN often cause this type of gait abnormality.
lesion but is confined to the voluntary motor pathway that Stiffness is associated with a decrease in stride length
includes the cerebral cortex, brainstem, lateral column, and is commonly seen in diseases of the peripheral neuro-
spinal cord, and LMN. muscular apparatus (motor neuron cell body, nerve roots,
Circling occurs primarily in animals that have brain- peripheral nerve, neuromuscular junction, and muscle).2
stem lesions; the direction of circling is usually toward the Animals with orthopedic abnormalities may have similar
lesion. Tight circling is associated with brainstem lesions, clinical signs and maintain conscious proprioception.
and rostral midbrain lesions may cause the animal to circle Myotonia is persistent muscle contraction after the
away from the affected side. Twisting or tilting of the head initiation of a voluntary muscle movement. The alter-
also indicates involvement of the vestibular system. nating contraction and relaxation of muscle groups that
Ataxia is a lack of coordination without spasticity, are stimulated when the animal tries to initiate vol-
paresis, or involuntary movements, although each of these untary movement cause intention tremors. Affected
conditions may have ataxia associated with them.4 Af- animals often have a stiff gait and prolonged muscle
fected animals often have jerky leg movements and sway contractions in the affected area. Cerebellar lesions can
as they walk; lesions in the cerebellum, vestibular system, cause myotonia.
and spinal cord sensory pathways often first appear this In general, cerebellar lesions result in an animal being
way. Truncal ataxia results in animals swaying constantly able to walk, but without precision. Lesions in the brain-
when they are not in motion. They also may stand with stem and cervical spinal cord often prevent the animal
their limbs crossed. If the animals appear to have a loss of from walking or dramatically affect the gait. Often af-
conscious proprioception without muscle weakness, the fected animals exhibit increased spinal reflexes in the af-
lesion is usually of cerebellar origin. All of these clinical fected limbs. Several LMN lesions also can cause alter-
signs can be exaggerated by lifting the animals’ heads ations in gait. Table 11-3 describes the results of lesions
while they are walking or leading them up a slope. in several LMNs of the limbs.

TABLE 11-3

EFFECTS OF DAMAGE TO PERIPHERAL NERVES

DAMAGED NERVE EFFECT MANIFESTATION

Femoral nerve, caudal spinal Bunny hopping and a shortened Difficulty in bringing both rear or one
cord stride rear limb forward
Obturator nerve Limbs slide laterally without the Inability to abduct the limb; gait is normal
animal replacing them
Sciatic nerve Rear foot is thrown forward by Hock is overflexed
proximal trunk muscles
Radial nerve Inability to extend the carpus Shoulder lifts in an exaggerated motion to
advance the limb
Medial and ulnar nerve Carpus is overextended Same as for radial nerve
286 • Sheep and Goat Medicine
Posture and Postural Reactions the examiner can conduct many of the tests used in dogs
Posture is normally assessed at rest at the same times as and cats.
the animal’s head carriage and limb and trunk orientation Assessment of the righting response involves placing
are examined. The most common abnormality in head an animal on its side; the normal response should be for
carriage is a tilt to one side. After otitis has been ruled the animal to roll over into sternal recumbency and then
out, the most likely cause is a lesion in the vestibular rise up, rear limbs first. This action requires the integra-
system. Animals that exhibit not only a head tilt but also tion of the vestibular labyrinths and proprioceptive recep-
a rotation of the neck and thoracic area may have a lesion tors in the joints, tendons, and muscles.9 Information is
in the brainstem or cerebellum. To diagnose or rule out relayed to the thalamus and sensory cortex for processing
cervical lesions, the animal’s head should be rotated back and then transmitted to the motor cortex, brainstem,
to its normal position so the examiner can assess its reac- spinal cord, and LMN. It is then relayed to the muscula-
tion. An animal with neuromuscular damage or cervical ture. Deviations from the normal righting response can
pain may resist head movement and arch its thoracic ver- help the examiner localize lesions in the nervous system.
tebrae or display a painful response. An animal that is reluctant to rise but does so eventually
Limb posture should be assessed with the animal may have a lesion in the cerebral cortex or diencephalon.
standing, but if the animal is recumbent the orientation An animal that is unable to lift its head may be lying with
should be noted and the muscle tone of the legs should be the affected side up or have a lesion cranial to C4. If the
carefully palpated. Animals that are ataxic often assume animal is able to rise after it has been rotated to the oppo-
a wide-based stance. Lesions in the cerebellum, vestib- site side, the lesion can be localized to that side. Incom-
ular system, and spinal cord can produce this appear- plete lesions in the C5 to T2 area result in a recumbent
ance. Preferential distribution of the animal’s weight also animal that can lift its head; if the lesion is located from
should be noted because it may indicate pain or weakness T3 to L3, the animal may be able to assume a “dog-
on the non–weight-bearing limbs. Spasticity can be ob- sitting” position.
served at rest or while the animal is moving; it is usually Forcing the animal to hop primarily on one leg tests
indicative of a central nervous system motor pathway strength, proprioception, and voluntary movement.2 Ani-
lesion. Decerebrate rigidity is manifested as extreme mals with cerebellar lesions make exaggerated hopping
opisthotonos, extension of all four limbs, and loss of con- motions when forced to bear their weight on primarily
sciousness. It is caused by a loss of descending input from one limb. Lifting one of the forelimbs or hindlimbs and
supratentorial structures in the medullary centers, which pushing the animal’s weight over to the opposite limb
are normally responsible for flexion of the limbs, and is should force the animal to hop as its center of gravity
seen in severe brainstem lesions.2 This is a common pres- shifts over the weight-bearing limb. Animals that have
entation for sheep and goats afflicted with tetanus. De- cerebellar lesions may fall over or lean their weight
cerebellate rigidity is characterized by front limb exten- against the examiner.
sion and opisthotonos, but the rear limbs are flexed and Conscious proprioceptive deficits can result from le-
the animal is mentally alert. Cerebellar disease that does sions in several locations because the pathway responsible
not involve the ventral aspects of the cerebellum produces for relaying proprioceptive information to the brain runs
this posture. Decreased muscle tone and the ability of an ipsilaterally up the spinal column, but then crosses over to
examiner to manipulate the animal’s limbs passively are the contralateral side of the cortex at the level of the
associated with LMN disease. Affected animals also may caudal mesencephalon and rostral pons. Lesions in the
stand knuckled over on the dorsum. Increased muscle contralateral brain or ipsilateral spinal cord cause deficits
tone is usually the result of UMN disease. Schiff- on the same side. In addition, LMN lesions and somatic
Sherrington syndrome is associated with spinal cord lesions prevent neuromuscular movement.
lesions between T3 and L3; affected animals exhibit tho-
racic limb extension and normal tone and reflexes in their
pelvic limbs. This is a rare finding in large animals.
Spinal Reflexes
Trunk posture should be assessed after a thorough ex- Spinal reflexes are used to evaluate the integrity of
amination of the vertebral column. Deviations in the ver- LMNs. To have a clear knowledge of the way the infor-
tebral column such as scoliosis, lordosis, and kyphosis mation gained from spinal reflexes can be used, the exam-
may cause abnormal muscle tone and posture because of iner must understand the differences between UMNs and
malformation of the vertebral disk spaces. LMNs. Primarily UMNs are responsible for dampening
Postural reactions are responsible for maintaining an or inhibiting spinal reflexes. Their axons and cell bodies
animal in a normal upright orientation. They involve the remain within the central nervous system and influence
integration of the LMN and UMN pathways, and there- LMN activities. As a result, when interruptions occur in
fore localization of lesions can be difficult at times. Pos- UMN influence, animals often have hyperreflexia or hy-
tural reactions are hard to assess in large animals because pertonia. If muscle atrophy occurs as a sequela to a lesion
of size limitations; however, in assessing sheep and goats of the UMN, it generally results from improper use of the
 Chapter 11 Diseases of the Neurologic System • 287

affected muscle caused by poor nervous system control.2 Stimulating stretch receptors in muscle spindles as-
The afferent fibers that relay information to the cerebral sesses myotatic reflexes, which stem from a two-neuron
cortex ascend the spinal tract ipsilaterally, then cross at system. The reflexes are basic to the regulation of posture
the level of the caudal mesencephalon, which means that and movement.4 The muscle belly contains stretch recep-
lesions in the UMN cause contralateral neuromuscular tors composed of muscle spindle fibers that detect the
deficits. The resulting muscle atrophy takes longer to amount of tension placed on the muscle. Sudden changes
develop and is not as pronounced as in LMN disease. in the amount of tension in the muscle spindle cause it to
Before examining LMN reflexes the clinician should discharge and elicit a reflex reaction through the LMN
first understand the way the nerves relay and process in- pathway. Absence or depression of the reflex suggests a
formation locally to elicit a muscular reaction. The reflex lesion in the LMN pathway. The bilateral absence of re-
arc consists of an afferent receptor that relays information flexes indicates a segmental spinal cord lesion. Exagger-
into the gray matter of the spinal cord, which consists of a ated reflexes or increased muscle tone indicate a lesion in
varying number of interneurons that can stimulate in- the UMN pathways descending from the cortex or in the
hibitory and excitatory neurons and alpha motor neurons. cortex itself. A UMN lesion in the spinal cord is ipsilat-
Alpha motor neurons exit the spinal cord and innervate eral to the affected limb; additional clinical signs of neu-
the motor end plates of the ipsilateral and contralateral rologic abnormalities in the cranial limbs or trunk can be
muscle bundles. The information also is relayed to the used to determine the exact level of the spinal cord lesion.
cortex by the lateral spinothalamic, fasciculus cuneatus, If the lesion occurs in the cortex, the contralateral side of
and gracilis tracts. In turn, UMN influences are relayed the animal displays hyperresponsive activity diffusely.
back to the LMN by way of the rubrospinal and reticu- The patellar reflex is assessed by laying the animal on
lospinal tracts. Several different responses can be ob- its side as the examiner supports the femur with the stifle
served during testing of spinal reflexes. The first is a slightly flexed as seen in Figure 11-1. When the patellar
normal response indicating that both sensory and motor ligament is sharply tapped with a plexor, the normal re-
components are intact. The second is an exaggerated re- sponse is for the animal to extend the stifle quickly. This
sponse, which indicates an abnormality in the UMN test measures the function of the peroneal and ischiatic
pathways. The third is a depressed or absent response, nerves and spinal cord segments L6 to S2.
which indicates LMN disease in either the sensory or The cranial tibial reflex test is performed if the patel-
motor components. Animals that have LMN lesion lar reflex is abnormal or a sciatic nerve lesion is sus-
exhibit muscle atrophy, hyporeflexia, areflexia, hypotonia, pected. Supporting the rear leg behind the stifle, the ex-
atonia, and paresis. aminer strikes the belly of the tibial muscle right below
Before the examination begins the animal should be
placed in lateral recumbency. The musculature and tone
should be assessed by palpation to determine any obvious
signs of atrophy. Usually the pelvic limbs are examined
first. The examiner should identify any musculoskeletal
injuries before beginning the neurologic examination.
Passive extension and flexion of the limb can be used to
assess muscle tone. Animals with LMN disease exhibit
depressed or absent resistance to the flexion, whereas
those with UMN disease display increased tone of the
extensor muscles as the limb is manipulated. Normally
reflexes have two phases: the first is rapid movement of
the limb, which is LMN-mediated; and the second is
conscious recognition of the stimulus, which is UMN-
mediated. An interruption in the sensory tract of the
LMN system prevents or decreases both phases, and a
lesion in the UMN system may prevent conscious recog-
nition of the stimulus—the reflex may still be intact but
may be inappropriate. Animals with lesions in the LMN
motor pathway may consciously recognize the stimulus
but be unable to form a reflex reaction. This is rare
because damage to the motor pathway usually results in
damage to the sensory pathway too; however, in some in-
Figure 11-1 A patellar reflex examination can be performed on a
stances an animal recovering from an injury to the LMN goat to assess the function of the peroneal and ischiatic and spinal
system may regain sensory innervation before motor cord segments L6 to S2. This goat is lying on its side and the clinician
control is restored. is supporting the femur with the stifle slightly flexed.
288 • Sheep and Goat Medicine
the stifle. The hock should flex in response. The response nerves responsible for the reflex reaction; bilateral deficits
is very subtle in small ruminants and the examiner indicate a spinal cord lesion.
should be careful not to place too much emphasis on the The crossed extensor reflex can be observed when the
results. This test measures the function of the femoral flexor reflex is being evaluated. When one of the forelimbs
nerve, quadriceps femoris muscle, and L4 to L6 spinal or hindlimbs is being tested, the opposite limb should not
cord segments. extend if the animal is recumbent. Normally the UMN
The gastrocnemius reflex test can be performed after pathways inhibit this reaction in a recumbent animal.
the tibial reflex is assessed; it requires the examiner to When an animal is standing, the flexor reflex sensory
support the limb from behind the leg at the level of the fibers send collaterals to interneurons on the opposite side
stifle and slightly flex the hock while striking the tendon of the spinal cord, which excite the extensor motor
of the gastrocnemius muscle above the hock, which neurons.4 This prevents the animal from falling over as it
should extend in response. The tibial branch of the sciatic flexes its limbs and shifts weight to the opposite side.
nerve innervates the muscle and originates from L6 to S2. The perineal reflex is elicited by pinching the skin
To perform the extensor carpi radialis reflex test the ex- around the anus (Figure 11-2).9 The reflex is mediated by
aminer supports the animal’s elbow from behind, main- S1 to S5 and should result in a tightening of the anal
taining flexion of the elbow and carpus. The extensor carpi sphincter, clamping of the tail, and possibly aggressive
radialis muscle is then struck just distal to the elbow; the kicking of the hindlimbs. A lesion in this area can cause
carpus should extend. The muscle is innervated by the several complications, including absent anal tone and a
radial nerve, which originates from C5 to T2. relaxed anal sphincter. The animal’s tail does not raise
To perform the triceps reflex test the examiner re- when it defecates, and fecal pellets dribble out of the anus
strains the animal as in the extensor carpi radialis flexion as the colon becomes full. Often bladder atony is caused
test with the elbow in flexion. The triceps brachii muscle by an interruption in parasympathetic innervation, result-
is struck above the olecranon, which should cause the ing in a flaccid full bladder and urine dribbling. The
elbow to extend. The muscle is innervated by the radial animal’s perineal and inguinal area may show signs of
nerve, which originates from C5 to T2. urine scalding when examined.
The biceps reflex test is conducted with the animal’s
leg in flexion at the carpus and the examiner’s hand or
fingers placed over the insertion of the biceps muscle
LESION LOCALIZATION
above the elbow, maintaining the elbow in slight exten- To localize a lesion in the nervous system, the examiner
sion. The muscle belly of the biceps is lightly struck, must first determine whether the animal is displaying
which should cause flexion in the elbow and extension of UMN or LMN clinical signs. After this the examiner
the carpus. This tests the function of the musculocuta- should assess all the clinical findings to determine which
neous nerve and spinal segment C6 to C8. portions of the pathways are involved. The UMN system
Several other reflex tests that can be used to assess is composed of the cerebrum, basal nuclei, telencephalon,
LMN function do not involve myotatic reflexes. One such diencephalon, mesencephalon, metencephalon, myelen-
test involves the cutaneous or panniculus reflex; it was pre- cephalon, thalamus, hypothalamus, midbrain, cerebellum,
viously discussed in the Sensorium section of this chapter. pons, and medulla oblongata. The UMN system is re-
Another test is the flexor withdrawal reflex of a limb to
a noxious stimulus. The minimal amount of noxious
stimulus necessary to elicit a response from the sole of the
claw or an area right above the coronary band should be
used. A normal response is for the animal to flex its fore-
limb and hindlimb fully away from the stimulus. If used
on the forelimb this test assesses the motor components
of the axillary, median, musculocutaneous, ulnar, and long
thoracic nerves, as well as spinal cord segment C5 to T2.9
The sensory components are the median nerve, which in-
nervates the cranial, palmar, and medial sides; and the
ulnar nerve, which innervates the cranial lateral aspect of
the digit.9 Proximal portions of the forelimbs are inner-
vated through the axillary, musculocutaneous, ulnar, and
radial nerves. In the rear limb the motor component of
the flexion arises from the peroneal, tibial, and ischiatic
nerves, as well as spinal segments L6 to S2. The sensory
Figure 11-2 Assessing the perineal reflex in a goat by pinching
innervation to the rear limb arises from the peroneal and the skin around the anus. The animal should respond by clamping its
tibial nerves. Unilateral absence or depression of the tail and tightening the anal sphincter. This test assesses spinal cord
flexor test may indicate damage to any of the peripheral segments S1 to S5.
 Chapter 11 Diseases of the Neurologic System • 289

sponsible for initiation and maintenance of normal move- system is responsible for relaying sensory information to
ment and for maintenance of tone in the extensor muscles the UMN system, relaying motor control information
to support the body against gravity.4 The LMN system is from the UMN system, and maintaining local reflexes.
divided into segments from which two spinal nerves Tables 11-4 through 11-6 contain information that
emerge to innervate each side of the body. The LMN can aid the clinician in determining whether a lesion is of

TABLE 11-4

SUMMARY OF LOWER AND UPPER MOTOR NEURON SIGNS

PARAMETER LOWER MOTOR NEURON UPPER MOTOR NEURON

SEGMENTAL SIGNS LONG TRACT SIGNS

Motor function Paralysis—loss of muscle power, Paresis to paralysis—loss of voluntary

flaccidity movements
Reflexes Hyporeflexia to areflexia Normal to hyperreflexia (especially
myotatic reflexes)
Muscle atrophy Early and severe: neurologic; contracture Late and mild: disuse
after several weeks
Muscle tone Decreased Normal to increased
Electromyographic Abnormal potentials (fibrillation, positive No changes
changes sharp waves) after 5 to 7 days
Associated sensory signs Anesthesia of innervated area, paresthesia Decreased proprioception; decreased
or hyperesthesia of adjacent areas perception of superficial and deep pain

From Oliver JE, Jr, Lorenz MD: Handbook of veterinary neurologic diagnosis, Philadelphia, 1983, WB Saunders.

TABLE 11-5

LOWER MOTOR NEURON LESION LOCALIZATION CHART

VERTEBRAE AFFECTED MUSCLE OR CONDITION CLINICAL SIGNS

C1 to C6 C6 to C8—Biceps brachii Ipsilateral ataxia and paresis in all four limbs; hyperreflexia
(worse in the rear); hopping; cutaneous sensation loss to
innervated areas
C6 to T2 C6 to C8—Biceps brachii Both the forelimbs and hindlimbs can be weak and ataxic;
C5 to T2—Triceps brachii hyporeflexia in forelimbs; hyperreflexia in hindlimbs; myotic
C5 to T2—Extensor carpi radialis pupils; Horner’s syndrome; radial nerve paralysis
C8 to T1—Cutaneous trunci
C6 to T2—Brachial plexus
T1 to T3—Sympathetic nerve damage
C1 to C6—Flexor withdraw of forelimb
T2 to L3 T2 to L3—Schiff-Sherrington syndrome “Dog sitting;” hopping; normal forelimbs; hyperreflexia of
hindlimbs; polyuria; loss of cutaneous sensation in the area
innervated
L4 to S2 L4 to S2—Lumbosacral plexus Dog sitting; normal forelimbs; hyporeflexia in the hindlimbs;
L4 to L5—Quadriceps loss of cutaneous sensation
L6 to L7—Cranial tibial
L6 to S2—Gastrocnemius
L6 to S2—Patellar
L6 to S2—Flexor withdraw
S1 to S3 S1 to S3—Pelvic plexus Flaccid bladder; urine dribbling; no anal tone; tail will not lift
or move
290 • Sheep and Goat Medicine
TABLE 11-6

SIGNS OF LESIONS IN THE BRAIN

LESION MENTAL OCULAR CONSCIOUS GAIT POSTURE

LOCATION STATUS PROPRIOCEPTION

Cortical Depression, Normal vision Deficits Ataxia,

abnormal stumbling
behavior, knuckling over
seizures
Cerebrocortical No gait
abnormality if
in a straight
line
Frontal lobe Normal
palpebral
response
Diencephalon Normal, but Normal
hemiparesis
and tetraparesis
can occur

Thalamus
Lateral geniculate Ocular deviation
toward the
lesion
Limbic Behavioral
changes
Reticular activating Depression,
coma,
convulsions
Ventral hypothalamus Abnormal
appetite
Mesencephalon Depression, Mydriasis, Deficits Spasticity Delayed return
coma dorsomedial to normal
strabismus

Metencephalon Depression, Corneal reflexes Deficits Ataxia; Decerebrate

(pons, cerebellar coma present hemiparesis and rigidity
peduncles) tetraparesis can
occur

Myelencephalon Severe Medial strabismus, Deficits Ataxia, Deficits

(medulla oblongata, depression inability to hemiparesis ipsilateral to
lower brainstem) and coma retract the eye (ipsilateral), the lesion
tetraparesis
Cerebellum Normal Normal Truncal ataxia Intention
tremors

Rostral cerebellar Opisthotonos

(vermis, cerebellar
cortex)
 Chapter 11 Diseases of the Neurologic System • 291

POSTURAL REACTION CRANIAL NERVES SPINAL MUSCLE TONE ADDITIONAL

REFLEXES

Deficits (contralateral)

Problems with
complicated
movements

Poor response to
stimulation

Deficits (contralateral) Optic nerve Unilateral lesion

loss of vision, loss of contralateral signs
menace response,
normal pupillary light
reflex
Head tilt

Polyuria and polydipsia,

bradycardia
Deficits (contralateral) Trochlear, Spasticity, Clonus, Unilateral lesion,
oculomotor hyperreflexia hypertonia contralateral signs,
crossed extensor reflex
present
Deficits (ipsilateral or Trigeminal Hyperreflexia Hypertonia, Depressed sensorium,
contralateral) muscle atrophy of head tilt away from
the masseter, lesion, salivation
tongue may
protrude
Deficits (ipsilateral or Abducent, ambigmus, Hyperreflexia Unilateral lesion,
contralateral), poor contralateral), poor facial, vagus, ipsilateral signs
righting response if the vestibular, accessory,
lesion side is up glossopharyngeal
Normal to dysmetria Hyperreflexia Hypertonia, Uncoordinated
especially of the movements
extensor muscles
292 • Sheep and Goat Medicine
UMN or LMN origin and pinpointing the likely location the hindlimb that are responsible for weight bearing.
of the lesion. Sensation in the medial skin surfaces is preserved through
the saphenous branch of the femoral nerve. Injury to this
nerve often results from extreme rear-leg extension or in-
Peripheral Neuropathies jection sites that have become infected.
Peripheral neuropathies can be classified according to Obturator nerve paralysis occurs as a result of extreme
their cause, which may be congenital, inflammatory, adduction of the rear limb or as a lambing or kidding
metabolic, toxic, idiopathic, traumatic, degenerative, vas- injury. When the nerve is damaged, the animal is unable
cular, or neoplastic. The clinical findings in neuropathy to adduct its rear limb, and as a result the limb may slide
vary according to the dysfunction of the structures inner- laterally on slippery surfaces. Unilateral involvement of
vated by the afferent and efferent nerve fibers affected.1 the obturator nerve causes fewer gait abnormalities than
Clinical signs include muscle atrophy, hypotonia or bilateral involvement. The examiner should take radi-
atonia, hyporeflexia or areflexia, and decreases in sensory ographs of the pelvis of any animal with these clinical
innervation to the affected area. The peripheral neu- signs to rule out pelvic fracture.
ropathies may involve a single nerve (mononeuropathy) Sciatic nerve paralysis most commonly occurs as a
or several nerves (polyneuropathy). Histologically the sequel to a pelvic or lumbosacral fracture. The nerve
primary pathology that is observed is axonal degeneration arises from L6 to S2 and travels in the vertebral canal
or demyelination.1 Diagnosis of affected animals is based after the spinal cord has ended but before its fibers exit
on neurologic examination findings, age, breed, and the canal. Branches of the nerve supply the muscles re-
EMG studies. Several peripheral neuropathies have been sponsible for extending the hip and flexing the stifle. At
documented in sheep and goats and are reviewed in the the level of the hip the nerve divides into two branches—
following paragraphs. the peroneal and tibial nerves—that are responsible for
Horner’s syndrome is a combination of clinical signs innervating the majority of the motor and sensory func-
seen in animals that have lesions in the gray matter of the tions of the lower limb. Lumbosacral fractures usually
thoracic spinal cord cranial to T3. Lesions in this area cause bilateral hindlimb paresis or paralysis. After
injure the sympathetic nerve fibers that form the sympa- damage to the proximal sciatic nerve, which can be
thetic trunk.4 The clinical signs include miosis, enoph- caused by proximal acetabular and femur fractures, only
thalmos, ptosis, and increased warmth on the affected the extensor muscles of the stifle remain functional, al-
side of the face. Enophthalmos and extrusion of the third lowing the animal to bear weight but not flex the stifle.
eyelid results from paralysis of the periorbital smooth The animal will exhibit a dropped hock and the limb will
muscle that helps maintain the eye in its normal position. be knuckled over. The animal’s flexor response is greatly
Myosis is a result of the loss of sympathetic innervation inhibited. If the medial claw is pinched, the animal flexes
to the ciliary muscles that dilate the pupil. Horner’s syn- its hip but cannot flex the rest of the limb. This occurs
drome is often associated with dramatic injuries to the because the medial side of the limb still has sensory in-
brachial plexus, so in addition to the ocular abnormalities, nervation intact through the saphenous branch of the
paresis of the forelimb and loss of the cutaneous trunci femoral nerve. Many of these injuries resolve if given
reflex also may occur. Compressive lesions such as those time, but a poor prognosis is associated with the complete
resulting from caseous lymphadenitis abscesses, esopha- loss of deep pain.
geal perforations, and otitis interna or otitis media also The peroneal nerve supplies the muscles that flex the
can damage T1 to T3. hock and extend the claws and provides cutaneous
Radial nerve paralysis can result from rib or humerus sensory innervation to the dorsal aspect of the foot and
fractures or brachial plexus avulsion. The location of the cranial surface of the hock and tibia.4 Improperly admin-
injury determines the severity of clinical signs. In general istered injections often injure this nerve, resulting in
the more distal the injury on the limb, the less the knuckling over onto the dorsum of the fetlock and
animal’s gait is affected. Often affected animals extend overextension of the hock. Animals appear to be able to
their elbows but knuckle over onto the dorsum of their compensate fairly well with this type of injury, flexing the
hooves because of paralysis of the extensor muscles of hip and extending the stifle more to walk. The flexor re-
the carpus and digits. A loss of sensory innervation to sponse is depressed when the dorsum of the fetlock is
the dorsum of the leg below the elbow also may be stimulated; however, if the sole of the hoof is stimulated
evident. The animals may have scuffed or abnormally the animal flexes its leg but keeps the hock fixed.
shaped hooves as well as abrasions on the front of the
fetlocks.
Femoral nerve paralysis results in an animal dragging
or carrying its rear limb and hopping on the unaffected
R EFERENCES
1. Oliver JE, Mayhew IG: Neurologic examination and diagnostic
hindlimb. The femoral nerve arises from L4 to L6 and plan. In Oliver JE et al, editors: Veterinary neurology, Philadelphia,
supplies motor pathways to the major extensor muscles in 1987, WB Saunders.
 Chapter 11 Diseases of the Neurologic System • 293

2. Bagley R, Mayhew I: Clinical examination of the nervous system. Cerebrospinal fluid (CSF) can be easily collected from
In Radostits OM et al, editors: Veterinary clinical examination and the lumbosacral site. The animal can be manually re-
diagnosis, Philadelphia, 2000, WB Saunders. strained in sternal recumbency or mildly sedated. The
3. Tyler JW: Practical food animal neurology: the black box ap- lumbosacral space at the cranial aspect of the tuber
proach, Proceedings of the American College of Veterinary Internal sacrale should be clipped and aseptically prepared. A pal-
Medicine Eighteenth Annual Meeting, 2000, Seattle, WA.
pable divot should be felt at this space and 2% lidocaine
4. Oliver JE, Lorenz MD: Neurologic history and examination. In
Oliver JE et al, editors: Handbook of veterinary neurology, Philadel-
(0.5 ml) should be used to subcutaneously infiltrate this
phia, 1993, WB Saunders. site. A 5-cm, 20-gauge stylet-type spinal needle or dis-
5. Oliver JE: Neurologic examinations: taking the history, Vet Med posable needle is then slowly introduced at a slight
Small Anim Clin 67:433, 1972. caudal angle to enter the subarachnoid space. If bone is
6. Chrisman CL: Problems in small animal neurology, Philadelphia, encountered, the needle should be redirected either cra-
1982, Lea & Febiger. nially or caudally. A “pop” can be heard or felt as the
7. Jenkins TW: Functional mammalian neuroanatomy, ed 2, Philadel- needle passes through both the interarcuate ligament and
phia, 1978, Lea & Febiger. the subarachnoid membrane. The examiner should fre-
8. Brewer BD: Examination of the bovine nervous system, Vet Clin quently remove the stylet and check for CSF because
North Am Food Anim Pract 3(1):13, 1987. subtle changes are often difficult to appreciate and the
9. George LW: Localization and differentiation of neurologic
examiner may miss the subarachnoid space and advance
disease. In Smith BP et al, editors: Large animal internal medicine,
St Louis, 1996, Mosby.
the needle too far. Approximately 1 ml of CSF per 10 lb
10. de Lahunta A: Small animal neurology examination, Proceedings of of body weight may be safely removed. Gently and
the American College of Veterinary Internal Medicine Eighteenth slowly aspirating CSF or allowing it to flow freely from
Annual Meeting, 2000, Seattle, WA. the needle prevents excessive movement and blood con-
11. Liebman M: Cranial nerves. In Liebman M, editor: Neuroanatomy tamination. In addition, applying digital pressure over
made easy and understandable, Gaithersburg, MD, 1983, Aspen. both jugular veins causes engorgement of the ventral
12. de Lahunta A: Cranial nerve-lower motor neuron: general somatic venous plexus, resulting in increased CSF pressure and
efferent system, special visceral efferent system. In de Lahunta A, greater flow (see Appendix III).
editor: Veterinary neuroanatomy and clinical neurology, Philadelphia,
1983, WB Saunders.
NEUROLOGIC DISEASES
ANCILLARY TESTS Scrapie
A number of diagnostic tests are available to help deter- An important member of the slow infectious group of
mine the cause of a neuropathic condition and localize diseases known as transmissible spongiform encephalop-
the lesion. Most of these procedures are cost-prohibitive athies in sheep and goats is scrapie. Scrapie is an afebrile,
for small ruminant medicine and may not be widely avail- chronic, progressive, degenerative disorder of the central
able; however, their use can be considered when appropri- nervous system of sheep and occasionally goats.1,2,3 The
ate. After a lesion has been localized, plain survey films causative agent is poorly characterized, and several hy-
may be helpful to identify luxations of the vertebral potheses attempt to link the concept of genetic suscepti-
column, osteomyelitis, or fractures of the pelvis. Survey bility and an infectious agent. Three theories have been
radiographs of the skull can be used to diagnose fractures put forth regarding the nature of the infectious agent that
or assess involvement of the tympanic bulla in cases of causes scrapie:
otitis. Radiographic techniques used in medium to large
1. The agent is a filamentous virus.
dogs are applicable to sheep and goats. For UMN disease
2. The agent is a self-replicating protein (prion).
of the forebrain, brainstem, or cerebellum, several diag-
3. The agent is a very small nucleic acid with a
nostic imaging procedures can be performed. The struc-
protective protein coat encoded in the host DNA.
tural integrity of the UMN anatomy can be evaluated
through the use of computed tomography (CT) and The discovery of a glycoprotein termed PrPc on the
magnetic resonance imagery (MRI) (see Chapter 7). neuronal surface of normal sheep that also has been iden-
Myelography can be used to identify compressive or ex- tified within the neurons of scrapie-affected sheep (PrPsc)
pansive lesions in the spinal cord. Electromyography also has led to the most recently accepted hypothesis regard-
can be used to determine whether specific neurons are re- ing the infectious nature of scrapie. The PrPsc protein is a
sponsible for neuromuscular disease by measuring the rod-shaped protein that has in the past been referred to
electrical activity of the muscle after a neuron is stimu- as a scrapie-associated fibril (SAF); its identification has
lated. Electroencephalography can be used to assess the been correlated 100% with scrapie infections in sheep.3
electrical activity present in various parts of the brain. It is The PrPsc proteins are unique because they are not au-
primarily used in cases that are manifested by seizures, tolyzed and can be readily recovered in fresh-frozen or
narcolepsy, and encephalopathy. formaldehyde-fixed tissues.
294 • Sheep and Goat Medicine
Pathogenesis. Sheep and goats to a lesser degree are breeds that predispose to scrapie. Studies have confirmed
the natural hosts for scrapie. The transmission has been that eight polymorphisms result in six amino acid varia-
documented to occur both horizontally and vertically. tions at three different codon positions in the sheep
The majority of sheep with clinical signs of scrapie are genome: 136, 154, and 171.4 Two of these positions, 136
31⁄2 years of age.4 Although the offspring of infected ewes and 171, are associated with increased susceptibility to
and rams are objectively more susceptible to scrapie infec- scrapie and a decrease in survival time. Certain breeds of
tion, the exact mechanism of transmission is unknown. sheep are more inclined to have a particular genetic com-
The general belief is that most sheep are infected at birth, position at these two new positions and therefore appear
and therefore the age of clinical presentation is a reflec- to be more susceptible to scrapie.4 Not all breeds of sheep
tion of the incubation period.2 The primary mode of have the same genotype at the three different codon posi-
transmission is believed to be oral. These observations in- tions, and certain genotypes appear to be more prevalent
dicate that an infectious agent is responsible for the trans- among specific breeds.9 Scrapie occurs primarily in
mission of the disease and that transmission occurs after Suffolk, Cheviot, Southdown, and Hampshire breeds.
birth, not in utero.5,6 After the causative agent enters the Suffolk sheep that have the genetic composition of A136,
host it goes into a quiescent phase in which no virus can R154, Q171 are more susceptible to developing scrapie. All
be detected in tissues for as long as 8 months or more. breeds of sheep appear to be more susceptible to scrapie if
The replication of the infectious agent takes place in the they have a genotype encoding QQ171.4 The valine
lymphoreticular system during this time and can last for 2 breeds (particularly Cheviot, Swaledale, and Shetlands)
to 5 years. The end of the incubation period is marked by have the amino acid valine at position 136, which confers
the presence of detectable virus in the nervous system and susceptibility.1,9,10 However, these breeds also must have
by the conversion of the PrPc protein to PrPsc protein. the haplotype of valine, glutamine, and arginine (VQR)
Researchers have not yet determined how the wild form to develop clinical scrapie.
of the protein is converted to the mutant form. Experi- The amino acid variations that occur in sheep at these
ments have demonstrated that the PrPsc protein content three positions influence the incubation period. The
in neuronal cells can increase without the synthesis of strain of scrapie infecting the animal and the specific po-
new protein.4 Moreover, PrPsc may act as an infectious sition it targets influence the rate of conversion or resist-
agent and catalyze the conversion of PrPc in uninfected ance to conversion of PrPc to PrPsc.
cells. The PrPsc protein itself is believed to be toxic to
cells, and as it accumulates within the cells it causes Clinical signs. In the United States, scrapie is diag-
the neurodegenerative lesions histologically observed in nosed most commonly in Suffolk sheep. Most of the clin-
scrapie-affected sheep.1,7,8 ical signs indicate the locations that are damaged in the
Host genetic factors and the strain of the infectious central nervous system. The onset of disease is marked by
agent are important in determining susceptibility to the subtle changes in behavior such as mild apprehension,
development of natural scrapie infections. Currently staring or fixed gaze, failure to respond to herding, and
several genetic variants have been identified in sheep aggressiveness towards objects and people2 (Figure 11-3).

Figure 11-3 This Suffolk ewe was diagnosed with

scrapie. In this picture she is displaying a fixed gaze. Note
her floppy ears.
 Chapter 11 Diseases of the Neurologic System • 295

Several months later the animals often become intoler- Immunohistochemical (IHC) staining and micro-
ant to exercise and develop a clumsy, unsteady gait and scopic examination of brain tissue currently is considered
floppy ears. The fleece may develop whitish tips over the the standard for clinical diagnosis of scrapie in sheep.
lumbar region. Some affected sheep have intense pruritus This postmortem test is highly specific and sensitive. Re-
that causes them to self-mutilate by rubbing immobile cently a technique has been developed to examine IHC-
objects.2 Wool loss is most prevalent around the base of stained lymphoid tissue from the nictitating membrane as
the tail, the sides of the body, and above the elbow and an antemortem test. This test may aid in diagnosing
lateral neck (Figure 11-4). When affected sheep have animals in the quiescent phase, during which the protein
their lumbar regions rubbed, they often compulsively is replicating in the lymphoreticular system. A live assay
nibble their legs below the carpus and hock and may also is available. It involves injecting mice with suspen-
extend their heads and slap their lips together. Fine body sion brain tissue from suspected sheep to observe whether
and head tremors, wide-based stance, and severe progres- they develop clinical disease.
sive ataxia and paresis of the limbs may be present. If Attempts have been made to adapt a human assay
these animals are encouraged to run they will high- used to detect a specific protein that increases in con-
step with their forelimbs and bunny-hop with their centration in the CSF in patients that have spongiform
hindlimbs. During the ensuing 3 to 4 months the animals encephalopathies. If it is approved, this test could be per-
lose weight and become extremely difficult to handle. In formed as an antemortem diagnostic tool in sheep
the terminal stages sheep are recumbent and have hyper- demonstrating clinical neurologic signs. The sensitivity
tonic limbs. They may develop blindness, seizures, and an and specificity of the immunoassay in sheep has yet to be
inability to swallow just before death. determined.
Goats may exhibit signs similar to those seen in sheep.
They can develop the disease without direct contact with Treatment. No effective treatment is available for
sheep. The hallmarks of scrapie in both species are scrapie, and the condition is considered fatal. It also is a
intense pruritus, ataxia, and wasting. reportable disease that results in depopulation of affected
flocks.
Diagnosis. No specific lesions are characteristic of
scrapie. No detectable host humoral or cellular immune re- Prevention. Scrapie costs the United States sheep in-
sponses are evoked by the scrapie organism because it con- dustry $20 million annually in direct losses and millions
tains no antigens that are recognized by the host. Histolog- more in lost potential markets and flock productivity. A
ically the only consistent lesions are degenerative changes number of control programs have been instituted since
in the central nervous system consisting of bilaterally sym- scrapie was first recognized as a problem in 1952. To date
metric vacuolation of the neurons in the brainstem and all of these programs have fallen short of their goal of
spinal cord. Astrocyte proliferation precedes the vacuoliza- eliminating scrapie from the sheep industry because of
tion of neurons, and demyelination does not occur.11 Most the economic constraints that culling and depopulating
of these changes occur in the gray matter of the medulla, impose and the lack of a reliable antemortem diagnostic
pons, midbrain, and thalamus.3 These histopathologic test. One federal program that sheep producers can vol-
changes are not pathognomonic because other diseases can untarily participate in is called the Scrapie Flock Certifica-
cause the same types of pathologic changes. tion Program. It requires flocks to be assessed for 5 years
to determine that they do not contain any scrapie-
infected sheep. This program has four levels of clearance
and when the final level is attained, the producers are able
to export and sell sheep both within the United States
and internationally without restrictions.12 Currently the
United States is reviewing the federal Scrapie Flock Cer-
tification Program to ensure that it is consistent with ad-
vances in diagnostic techniques.
Some individual states and European countries are de-
veloping programs to classify herds according to genetic
susceptibility and flock health history. Although these
classifications are not based on the detection of scrapie-
infected animals, their purpose is to eliminate susceptible
animals within a breed to eradicate the disease.13
The zoonotic potential of scrapie to humans is unknown.
Evidence indicates that some variants of Creutzfeldt-
Figure 11-4 This 3-year-old Suffolk ewe displayed pruritus and Jakob disease are caused by ingestion of bovine products
wool loss on her mid-thorax, at the level of her elbow. contaminated with scrapie or scrapie-like organisms.
296 • Sheep and Goat Medicine
R EFERENCES
1. Hunter N: Scrapie, Mol Biotech 9:225, 1998.
kids before the ingestion of colostrum. If colostrum from
an unknown or infected source is all that is available, it
can be heated (56° C for 1 hour).1,2 Infected animals
2. Linnabary RD et al: Scrapie in sheep, Comp Cont Ed Pract Vet should be culled or quarantined from the flock. CAE can
13:511, 1991. be spread by fomites such as needles; they should be used
3. Detwiler LA: Scrapie, Rev Sci Tech Off Int Epiz 11:491, 1992. only once and then discarded. Proper sterilization of sur-
4. Machen MR: Scrapie: deciphering its pathophysiology and cause, gical equipment also is warranted (see Chapters 9, 13,
Comp Cont Ed Pract Vet, 23:S52, 2001.
and 14).
5. Woolhouse MEJ et al: Epidemiology and control of scrapie within
a sheep flock, Proc R Soc London B 265:1205, 1998.
6. Hoinville LJ: A review of the epidemiology of scrapie in sheep,
Rev Sci Tech Off Int Epiz 15:827, 1996.
7. Chaplin MJ, Aldrich AD, Stack MJ: Scrapie associated fibril de-
R EFERENCES
1. Dawson M: Caprine arthritis-encephalitis. In Boden E, editor:
tection from formaldehyde fixed brain tissue in natural cases of Sheep and goat practice, London, 1991, Bailliere Tindall.
ovine scrapie, Res Vet Sci 64:41, 1998. 2. Pringle J: Neurologic disorders. In Ogilvie TH, editor: Large animal
8. Stack MJ et al: The distribution of scrapie-associated fibrils in internal medicine, Baltimore, 1998, Williams & Wilkins.
neural and non-neural tissues of advanced clinical cases of natural
scrapie in sheep, Res Vet Sci 64:141, 1998.
9. Hunter N: PrP genetics in sheep and the implications for scrapie Rabies
and BSE, Trends Microbiol 5:331, 1997.
Rabies is a fatal disease of animals and humans. Rabies
10. Bossers A et al: Scrapie susceptibility-linked polymorphisms mod-
ulate the in vitro conversion of sheep prion protein to protease-re-
virus belongs to the genus Lyssavirus from the family
sistant forms, Proc Natl Acad Sci USA 94:4931, 1997. Rhabdoviridae. Outbreaks in domestic animals appear to
11. Dandoy-Dron F et al: Gene expression in scrapie, J Biol Chem be associated with a “spillover” from epizootic spread in
273:7691, 1998. affected wildlife populations.1,2 These wild reservoir
12. Detwiler LA: Scrapie control in the United States: a review of the hosts include the skunk (Midwest to North Central
past with emphasis on the present flock certification program, Dev United States), raccoon (Southeastern and East Coasts),
Biol Stan 80:109, 1993. coyote (South Texas), and gray fox (Southern Arizona,
13. Dawson M et al: Guidance on the use of PrP genotype as an aid to mid-Texas). Of these wild species, foxes and coyotes seem
the control of clinical scrapie, Vet Rec 142:623, 1998. to be the most susceptible to rabies, with skunks, rac-
coons, bats, and bobcats showing an intermediate suscep-
tibility. Opossums and armadillos appear fairly resistant
Caprine Arthritis-Encephalitis to infection. In areas where foxes and/or skunks are the
Caprine arthritis-encephalitis (CAE) is a retroviral infec- predominant wildlife reservoir hosts, the disease usually
tion of goats that is similar to ovine progressive pneumo- has a seasonal incidence. An increased incidence has been
nia in sheep. The disease takes several forms—neurologic, associated with the migratory patterns of the reservoir
arthritic, and mastitic (hard udder). It is primarily trans- host and changes in population densities. The suscepti-
mitted from dam to kid through colostrum. bility of the sheep or goat to rabies increases in propor-
tion to the quantity of inoculum (usually saliva from a
Clinical signs. The neurologic form of the disease bite) placed into a wound, the number of nerves in the
usually affects kids 1 to 4 months of age but is occasion- area around the wound (rabies virus migrates along
ally seen in adults. The clinical signs include a secondary nerves), the vaccination history of the bitten animal, and
ataxia and paresis progressing to tetraplegia. As the the location of the wound. The closer the wound is to the
disease progresses, kids may become blind and develop a central nervous system, the more susceptible to infection
head tilt, facial paralysis, and opisthotonos. The clinical the animal becomes. The virus spreads along the periph-
course of disease can last from 1 to 2 weeks.1,2 eral nerves from the site of the wound to the central
nervous system and then systematically, including the
Diagnosis. The antemortem diagnosis of CAE is salivary glands. The incubation period is from 2 weeks to
based on agar gel immunodiffusion (AGID) for CAE several months. Shorter incubation periods are associated
antibodies. CSF has an elevated protein content and with bites near the central nervous system (head or
mononuclear pleocytosis. Postmortem examination reveals neck).2 In the United States between 5 and 20 cases of
widespread perivascular foci and demyelination of the rabies are reported annually in sheep and goats.
white matter of the brain and spinal cord.
Clinical signs. Sheep and goats can have a variety of
Prevention. No treatment is available. To prevent this clinical signs, including depression or excitation, an-
disease, kids should not be fed colostrum from infected orexia, nystagmus, and muscle spasms. Rams may exhibit
dams. This can be aided by inducing parturition of the sexual excitement. Goats or sheep also can become ag-
dam or performing a Cesarean section and removing the gressive and attack objects and handlers.3 The course of
 Chapter 11 Diseases of the Neurologic System • 297

disease usually progresses as an ascending paralysis that previously used to vaccinate hogs with modified live
initially may appear as a proprioceptive deficit (rear-end pseudorabies virus.3
paralysis, knuckling), ataxia, and tail and penile paralysis.
Pharyngeal paralysis results in excessive salivation.1-3 The Clinical signs. Infected sheep or goats have extreme
disease progresses to recumbency, convulsions, and death pruritus in localized areas.1 They may vocalize, circle, and
over a 7- to 10-day period. self-mutilate by licking and scratching the skin (hence
the name mad itch). Additional clinical signs include
Diagnosis. Rabies should be part of the rule-out list in ataxia, paralysis, and death within 72 hours of the onset of
all neurologic cases. Whenever it is suspected because of signs.2
clinical signs, history, or animal death, regulatory author-
ities should be notified and the brain and salivary glands Diagnosis. Grossly, a meningoencephalitis is seen at
of the animal submitted for laboratory testing. In cases of necropsy.1 Histologically perivascular cuffing and focal
suspected rabies, collection of CSF should be avoided necrosis of the gray matter occurs, along with eosino-
because of the zoonotic potential of this disease. If philic intranuclear inclusion bodies of the dorsal horn and
CSF is nevertheless collected, it will have an increase in dorsal nerve rootlets.1,2 The diagnosis can be confirmed
total protein, mononuclear cells, and neutrophils. Tissues with virus isolation.
shipped to a diagnostic laboratory should be cooled but
not frozen. The disease produces a nonsuppurative en- Treatment and prevention. No treatment exists.
cephalitis. If formalin-fixed tissues are to be evaluated, no Contact with infected animals should be prevented.
more than half the brain should be fixed. A confirmed di- Barns and paddocks where infected animals are housed
agnosis can be made by fluorescent antibody (FA) tests of should be thoroughly sanitized (with quaternary ammo-
impression smears of the hippocampus, cerebellum, nium or compounds containing phenol).4
medulla, or salivary glands.

Prevention. Several killed vaccines are available and

R EFERENCES
1. Pringle J: Neurologic disorders. In Ogilvie TH, editor: Large animal
approved in the United States for use in sheep. Although
internal medicine, Baltimore, 1998, Williams & Wilkins.
they are not specifically approved for goats, they appear to
2. George LW: Pseudorabies. In Smith BP, editor: Large animal inter-
be efficacious.3 In endemic regions, vaccination should nal medicine, ed 2, St Louis, 1996, Mosby.
begin at 3 months of age and be followed by an annual 3. Van Alstine WG, Andersen TD, Reed DE: Vaccine induced
booster.2 However, vaccination may not be cost effective pseudorabies in lambs, J Am Vet Med Assoc 185:409, 1984.
in many instances.3 Post-exposure vaccination protocols 4. Brown TT: Laboratory evaluation of selected disinfectants as viruci-
appear less useful in sheep than in other species. If per- dal agents against porcine parvovirus, pseudorabies virus, transmis-
mitted, exposed animals should be quarantined for 6 sible gastroenteritis virus, Am J Vet Res 42:1033, 1981.
months and vaccinated immediately with a second, and
possibly third booster at 2, 4, and 6 weeks after exposure.
Because of the zoonotic potential of this disease, clini-
Bacterial Meningitis
cians should use extreme caution when handling sus- Suppurative meningitis or neuritis can occur as a sequela
pected animals and tissues. to surgical procedures (dehorning, tail docking), failure of
passive transfer (septicemia), pneumonia, gastroenteritis,
R EFERENCES
1. Pringle J: Neurologic disorders. In Ogilvie TH, editor: Large animal
omphalophlebitis, otitis, and mastitis.1-3 Escherichia coli,
Streptococcus, and Pasteurella haemolytica are common bac-
terial causes of meningitis in neonates. Pseudomonas
internal medicine, Baltimore, 1998, Williams & Wilkins.
2. George LW: Rabies. In Smith BP, editor: Large animal internal
aeruginosa can cause meningitis in some adult goats sec-
medicine, ed 2, St Louis, 1996, Mosby. ondary to mastitis. Mycoplasma mycoides subsp. mycoides
3. Biggs DJ: Rabies in food animals. In Howard JL, Smith RA, can cause disease in goat kids that ingest milk or
editors: Current veterinary therapy 4, food animal practice, Philadel- colostrum from infected dams.3
phia, 1999, WB Saunders.
Clinical signs. Meningitis associated with tail docking
can be a progressive ascending paralysis.1 Cases of
Pseudorabies meningitis resulting from neonatal septicemia can present
Pseudorabies is rarely documented in sheep and goats and with diarrhea, fever, stiff neck, nystagmus, convulsions,
infected swine are the most common reservoirs of infec- depression, and death.1,3 Many affected animals resist or
tion. This herpes virus infects sheep or goats through the display signs of pain on manipulation of the neck.3
respiratory tract or open wounds. After the virus has
gained entrance, it invades the central nervous system.1,2 Diagnosis. A tentative diagnosis can be based on clini-
Pseudorabies also can be transmitted to sheep by syringes cal signs and history. Analysis of the CSF shows a turbid,
298 • Sheep and Goat Medicine
possibly clotted sample with increased leucocytes and survive for years in soil, feces, and vegetation over a broad
protein. Sometimes bacteria can be identified in Gram’s- range of temperatures and pH. Although listeriosis is
stained CSF.3 Gross examination of the carcass at commonly associated with silage feeding, it also can occur
necropsy reveals congested meningeal vessels, swollen in animals on pasture. L. monocytogenes is resistant to
meninges, and petechiation.3 freezing conditions but cannot survive if the environmen-
tal pH is less than 5 (e.g., in properly packed silage).
Treatment. Treatment should be based on culture and Rotting forage, spoiled silage, silage at the end of trench
sensitivity patterns, antibiotic patterns, or Gram’s stain silos, and the bottoms of round bales of hay are all sources
findings of the CSF.3 However, in most situations labora- of infection.
tory results are not available when therapy is initiated. A Small ruminants are apparently more susceptible to
cephalosporin (ceftiofur 4 to 5 mg/kg intravenously [IV] listeriosis than cattle, and goats are reportedly more sus-
four times a day [QID]) can provide excellent antimicro- ceptible than sheep. The disease is more common in
bial therapy.2,3 Concurrently, glucocorticosteroids (dex- winter but may be seen throughout the year. Listeriosis is
amethasone 1 mg/kg IV) and/or dimethyl sulfoxide most commonly observed in animals grazing or browsing
(DMSO, 1 mg/kg in a 5% solution IV) can be adminis- in areas with boggy soils.
tered to help reduce inflammation.2,3 Diazepam should The organism is thought to invade the host through
be considered if the animal is convulsing, at a dosage of breaks in the buccal membrane and ascend the trigeminal
0.01 to 0.4 mg/kg.3 Aggressive therapy for 10 to 14 days nerve roots. This form is most common in adults fed con-
may yield satisfactory results if therapy is initiated early in taminated silage. The breaks in the mucosa associated
the course of the disease. As inflammation of the me- with shedding and replacing incisor are associated with
ninges subsides, some antibiotics (aminoglycosides) may infection of the cranial nerves.3 Therefore the condition
have difficulty reaching therapeutic concentrations in the is most common in animals older than 6 months. Stress;
meningeal space.3 This can result in relapse, localized in- the introduction of hard feeds, pellets, or browse in the
fection, or abscess formation. In cases of failure of passive diet; and concurrent damage to the oral cavity can predis-
transfer, plasma (intraperitoneal [IP] or IV) should be pose to listeriosis.4 Clinical signs may vary according
given. to the location of multifocal microabscesses throughout
the braistem. Unilateral deficits of CN V (dysphagia,
Prevention. Prevention is best achieved by ensuring pseudoptyalism, dropped jaw, facial anesthesia), CN VI
ingestion of adequate colostral antibodies; avoiding ex- (medial strabismus of the opposite eye), CN VII (lip or
cessive damage to tissues during tail docking, dehorning, ear droop, ptosis, absent menace and palpebral reflexes,
or disbudding; using sterile equipment; and employing exposure keratitis), CN VIII (head tilt, circling, nystag-
aseptic technique. mus), CN IX and CN X (pharyngeal paresis, dysphagia,
upper respiratory obstruction, stertor), and CN XII (uni-
R EFERENCES
1. Smith MC: Inflammatory neurologic diseases of small ruminants.
lateral tongue paresis, dysphagia) are most common.
Multiple nerves may be affected, but bilateral lesions are
infrequent. The organism has zoonotic potential and can
In Smith RA, editor: Current veterinary therapy 3, food animal prac-
cause abortion and sepsis in people.1-3
tice, Philadelphia, 1993, WB Saunders.
2. Divers TJ: Diseases of the nervous system. In Howard JL, Smith
RA, editors: Current veterinary therapy 4, food animal practice, Clinical signs. Sheep and goats with listeriosis exhibit
Philadelphia, 1999, WB Saunders. depression from brainstem involvement or concurrent
3. George LW: Meningitis (suppurative meningitis). In Smith BP, meningitis and encephalitis. Loss of the ability to eat and
editor: Large animal internal medicine, ed 2, St Louis, 1996, Mosby. drink, dehydration, and acid-base disturbances may con-
tribute to the degree of depression. Often animals with
early cases of listeriosis exhibit only depression and a
Listeriosis failure to eat; therefore the clinician must be able to rec-
Listeriosis is a disease caused by the bacterium Listeria ognize early neurologic deficits and have a degree of sus-
monocytogenes. The most common form of the disease in picion. Fever is an inconsistent finding and when present
ruminants is a focal encephalitis; however, septicemia, is often only seen during the first 3 or 4 days of illness. In
abortion, and visceral infection also may occur. The or- sheep the morbidity is low, but mortality is high. When
ganism survives for long periods in a wide variety of envi- first examined by the clinician, many goats are recumbent
ronmental conditions and latently in carrier animals. It is and comatose, with a head tilt.4 Corneal ulceration re-
shed in feces, milk, tears, and uterine fluid of sick as well sulting from keratoconjunctivitis is a common finding in
as apparently healthy goats. L. monocytogenes is a small, goats.
motile, aerobic and facultative anaerobic gram-positive Specific neurologic signs are usually associated with
rod. It has 16 serotypes, of which each has a variety of pathology in CN V through CN XII. The bacteria ascend
subtypes.1-3 It is widely distributed in nature and can up the trigeminal nerve, causing weakness of the muscles
 Chapter 11 Diseases of the Neurologic System • 299

of mastication (dropped jaw), inability to eat, and loss of ment is necessary to reach minimal inhibitory concen-
saliva (Figure 11-5). Facial and vestibular lesions are trations in macrophages and to cross the blood-brain
common, as are lesions of the glossopharyngeal and vagus barrier. The organism is sensitive to a variety of antibi-
nerves, which result in dysphagia. Other neurologic otics. However, because of cost and practicality, peni-
deficits resulting from CN damage include a medial stra- cillin (22,000 to 44,000 units/kg IM BID), oxytetracy-
bismus from paresis of CN VI and an inability to retract cline (5 to 10 mg/kg IV twice a day [BID]), and
the tongue from changes to CN XII. florfenicol (20 mg/kg intramuscularly [IM] every 48
hours) are the most commonly used antibiotics. Therapy
Diagnosis. No specific antemortem diagnosis for the is recommended for a minimum of 10 to 14 days; if
encephalitic form of listeriosis is available. Diagnosis further antibiotic treatment is necessary, IM or subcuta-
depends on an accurate neurologic examination and iden- neous medication can be administered. Antiinflamma-
tification of multifocal brainstem disease. Supporting ev- tory therapy is recommended as well (flunixin meglu-
idence can be obtained from analysis of CSF. The fluid mine 1.0 mg/kg). If the patient is dehydrated or has
may have an elevated protein (more than 40 mg/dl) and electrolyte and acid-base disturbances, these should be
white blood cell (WBC) count (more than 5 cells/ml); the addressed at the initiation of therapy. In cases of con-
CSF white cell differential is often 50% or more mono- junctivitis or keratitis, broad-spectrum ophthalmic an-
nuclear cells and the remainder neutrophils. However, tibiotics (tetracycline) and ophthalmic atropine may be
these findings are not consistent. Culture on blood agar indicated. Orally administered fluids can be used to
of the CSF is usually unrewarding because the organisms soften rumen contents and aid in rumen contraction.
are not present in the CSF unless meningitis has devel- Feeding an alfalfa slurry or other nutritional supplement
oped. Culture of the blood and milk in cases of sep- via oral gastric tube may be necessary.3 Patients should
ticemia may identify systemically ill animals and per- be kept by themselves in a stall with thick bedding. Re-
sistent shedders. The organism can be isolated more cumbent animals should be turned often, supported in
efficiently by employing microaerophilic techniques. On sternal recumbency, and given adequate supportive
postmortem examination, L. monocytogenes can be identi- care.1-3
fied with an FA test. This test is the most specific for all Animals that are treated before becoming recumbent
nonsurviving cases.1-4 have a fair to good prognosis if appropriate antibiotic and
supportive therapy are provided. Therapy appears to be
Treatment. L. monocytogenes is a facultative intracellu- less effective in sheep than in goats.2
lar organism, and therefore intensive antibiotic treat-
Prevention. Most inactivated (heated or formol-
treated) vaccines are of limited value. Good immunity,
however, is reported in sheep with some attenuated vac-
cines.1,5 All infected animals should be isolated, animals
that die should be disposed of quickly, and all barns and
contaminated equipment should be sanitized. Silage with
a pH higher than 5.5 or with a foul odor should be dis-
carded. In farms that have pastures with boggy, high-pH
soils; in areas where rough browse is consumed; and in
contaminated feedlots or paddocks, the continuous
feeding of chlortetracycline (6 to 12 mg/kg by mouth
[PO] daily) may be beneficial.1 L. monocytogenes can be
found in the feces of many healthy sheep. Therefore
feeders should be designed to prevent animals from defe-
cating in them, and fecal contamination of feed-handling
equipment should be avoided.

Public health concerns. L. monocytogenes causes a

variety of diseases in people, including bacterial meningi-
tis. Listeria may be shed by sick, recovering, or clinically
normal animals in milk and feces for prolonged periods.
It has been reported to survive during low-temperature
pasteurization in milk and in the milk products of goats.
Veterinarians and handlers should use caution when han-
Figure 11-5 This goat has listeriosis. Its jaw has dropped, its dling the secretions of affected animals. Unpasteurized
tongue is not functioning, and it is exhibiting excessive salivation. milk and milk products should not be consumed.
300 • Sheep and Goat Medicine
R EFERENCES
1. Finley MR: Listeriosis (circling disease, silage sickness). In Howard
JL, Smith RA, editors: Current veterinary therapy 4, food animal
practice, Philadelphia, 1999, WB Saunders.
2. Dennis SM: Listeriosis (circling disease, silage sickness). In Smith
RA, editor: Current veterinary therapy 3, food animal practice,
Philadelphia, 1993, WB Saunders.
3. Smith MC: Inflammatory neurologic disease of small ruminants. In
Smith RA, editor: Current veterinary therapy 3, food animal practice,
Philadelphia, 1993, WB Saunders.
4. Bulgin MS: Central nervous system disorders of sheep, Proceedings
of the 1998 Symposium on the Health and Disease of Small Ruminants,
1998, Las Vegas, NV.
5. Gudding R, Gronstal H, Larson HJ: Vaccination against listeriosis
in sheep, Vet Rec 117:89, 1985.

Figure 11-6 This goat has a brain abscess and is displaying a

Brain Abscesses head tilt and a wide-based stance. This condition should be
differentiated from listeriosis.
Brain abscesses result from seeding of the nervous tissue
by pyogenic bacteria from septicemia. Bacteria can spread
from localized infections (dehorning) and areas of exist-
ing disease (caseous lymphadenitis). Abscesses in the
nervous system are commonly caused by Actinomyces
R EFERENCES
1. Linkleter KA, Smith MC: Color atlas of diseases and disorders of sheep
(Corynebacterium) pseudotuberculosis, A. pyogenes, Staphylo- and goats, Aylesburg, UK, 1993, Wolfe Publishing.
coccus, or aberrant migration of nasal bots (Oestrus 2. Bulgin MS: Central nervous system disorders of sheep, Proceedings
ovis).1-3 of the 1998 Symposium on the Health and Disease of Small Ruminants,
1998, Las Vegas, NV.
Clinical signs. Clinical signs depend on the location 3. Pringle J: Neurologic disorders. In Ogilvie TH, editor: Large animal
internal medicine, Baltimore, 1998, Williams & Wilkins.
and size of the lesion. Animals may be febrile with alter-
4. Smith MC: Inflammatory neurologic disease of small ruminants. In
ations in the heart and respiratory rates. Circling, depres- Smith RA, editor: Current veterinary therapy 3, food animal practice,
sion, drooping ears, ataxia, and blindness also may be Philadelphia, 1993, WB Saunders.
noted. Abscess ruptures result in acute death.1

Diagnosis. A presumptive diagnosis can be based on Otitis Externa, Otitis Interna, and Otitis
clinical signs. Analysis of CSF shows an increase in Media
protein concentrations and the presence of inflammatory
Little is known about otitis in goats and sheep compared
cells. A complete blood count may yield normal findings
with the information available on cattle and horses. Otitis
or leukocytosis. Definitive diagnosis is made by identify-
is defined as inflammation of the auditory structures and
ing the abscess in the brain.
is divided into anatomic regions. Otitis externa involves
the external auditory meatus, otitis media the tympanic
Treatment. Affected animals have a grave prognosis.
bulla, and otitis interna the vestibulocochlear nerve, semi-
Antibiotics (penicillin 22,000 IU/kg IV or IM BID, oxy-
lunar canals, utricle, saccule and cochlea.
tetracycline 10 mg/kg IV BID), nonsteroidal antiinflam-
matory drugs (NSAIDs, flunixin meglumine 1 to 2 mg/kg
Etiology
IM or IV), and glucocorticosteroids (dexamethasone 1 to
2 mg/kg) should be used.4 BACTERIA: Bacterial infections in the ear canal and
external auditory canal have been reported as causes of
Prevention. The major differential diagnosis for brain injury or rupture of the tympanic membrane; they can
abscess is listeriosis (Figure 11-6). Clinicians should result in otitis media and otitis interna. Several case
identify the causative agent for the abscess and address reports in lambs indicate that otitis media and otitis
any managerial considerations. In the rare event of an interna may result from respiratory infections by bacterial
outbreak of affected animals, the inclusion of oral antimi- migration via the auditory tubes. All ages and both sexes
crobial agents (chlortetracycline, tetracycline, sulfameth- of sheep and goats can be affected, but young animals and
azine) in a complete feed, protein-energy supplement, or those placed under great stress during processing are
mineral mixture may help control the disease. more susceptible.
 Chapter 11 Diseases of the Neurologic System • 301

The most common bacterial isolates identified in

Otitis Externa
cases of otitis media in lambs with intact tympanic Pathogenesis. Many factors can predispose sheep and
membranes are P. haemolytica and P. multocida; their goats to otitis externa. The first is the anatomic orienta-
isolation has coincided with the animals also having tion of the ear canal itself. The vertical canal slopes medi-
pneumonia caused by the same organisms.1,2 A number ally into a horizontal orientation on the outside of the
of commensal bacterial organisms also have been iso- tympanic membrane. This prevents drainage of debris as
lated from sheep suffering from otitis media and otitis it accumulates. The skin lining the external ear canal has
interna. These include Neisseria catarrhalis; coagulase- a large number of glands; these include modified apo-
positive, hemolytic, and mixed hemolytic Staphylococcus; crine glands called the ceruminous glands.9 These glands
and hemolytic Streptococcus.2 In cases in which the tym- produce a large amount of secretions, setting up an envi-
panic membrane of the animal has ruptured, a wide ronment that is favorable for irritation and infection.
variety of bacteria may be involved. One case report Pendulous-eared breeds of goats and sheep that have hair
from Britain cited consistent isolation of Pseudomonas within the ear canal are predisposed to moisture collec-
aeruginosa from an outbreak of severe necrotic dermatitis tion within the canal. As the moisture content of the
and otitis media/otitis interna in a flock of sheep after stratum corneum increases, its protective immunologic
dipping.3 defenses are compromised.10 Furthermore, a number of
yeast and bacterial species commonly inhabit the ear
PARASITES: Parasitic infestation of the external audi- canal and can become secondary opportunistic invaders
tory meatus is common in goats and sheep. Infestation when conditions are favorable. In addition to the com-
with ticks, biting flies, and gnats can cause inflammation mensal organisms in the canal, parasites and foreign
and irritation to the external ear canal. Although the objects can initiate an inflammatory condition.
aforementioned are common etiologic agents in external
ear canal pathology, mite infestation can cause more Clinical signs. The most common presenting com-
severe economic and pathologic complications. plaint of sheep and goats with otitis externa is exces-
Psoroptic mange mites are non-burrowing parasites sive head shaking, ear twitching, and scratching of the
that feed on the superficial skin of the host, causing in- ears with the hindlimbs. Often the animals do not have
flammation at the site of infestation.4 The mites have a 2- any gross indications of parasite infestation or infected
week life cycle on the host but can live off the host for as lesions.8 The only abnormality that is consistently re-
long as 3 weeks.5 Mite infestation can occur in all ages ported is excessive accumulation of earwax at the base of
and both sexes of animals. Horizontal transmission can the ear canal that forms a cast.4,8,11 When animals
occur rapidly in a herd, and animals can be affected uni- develop gross clinical lesions they initially appear as small
laterally or bilaterally. Most affected animals go unde- sores and dry, flaky scabs in the external auditory meatus.
tected unless they show severe clinical signs. The mites Ear mite infestation in sheep or goats rarely leads to
appear to congregate around the tympanic membrane, rupture of the tympanic membrane and consequent otitis
making diagnosis difficult. A variety of psoroptic mites media or otitis interna.
affect sheep; their classifications are based on the sites oc- More chronically affected animals may display gross
cupied on the host and morphology.4 Psoroptes cuniculi distortion of the pinnae caused by excessive rubbing; this
causes ear infestations in goats and rabbits; another may cause the pinnae to appear crumpled. The epidermis
variant, P. ovis, is capable of causing sheep scab in the ears of the pinnae and external auditory meatus also is grossly
and throughout the body.4,6 thickened, and histologic examination of the tissues
In goats two different mites have been identified as reveals hyperparakeratosis, acanthosis, and infiltration of
causative agents of otitis: P. cuniculi and Raillietia man- the dermis with neutrophils, plasma cells, lymphocytes,
fredi. Dual infestations have been found in affected herds, and histiocytes.7 Numerous small abscesses resulting
and the majority of the mites infest the base of the exter- from infection by secondary opportunistic bacterial in-
nal ear canal around the tympanic membrane.7 Although vaders may be evident.
infestation with ear mites is common in goats, it rarely
produces clinical signs, with the exception of head
shaking and ear twitching.8
Otitis Media and Otitis Interna
Sarcoptes scabiei is a contagious mite that initially man- Pathogenesis. Otitis media and otitis interna can result
ifests itself around the external ear canal. It can affect from bacterial, viral, or fungal infection; parasitic infesta-
both sheep and goats but is difficult to diagnose, even tion; tumors; vascular lesions; and immune disorders.12
though it causes severe pruritus. The mite has a 10- to Otitis media occurs when the inner ear canal medial to
17-day life cycle; it burrows under the skin to deposit its the tympanic membrane becomes involved in an infec-
eggs.5 Sarcoptes mite infestations are reportable in the tious process. Otitis interna is the result of involvement of
United States. the vestibulocochlear nerve and usually is accompanied
302 • Sheep and Goat Medicine
by peripheral vestibular clinical signs such as a head tilt Diagnosis. A thorough history and physical and neu-
and ipsilateral facial nerve paralysis. Infectious agents can rologic examination is necessary for goats or sheep that
follow three routes of entry to cause inner ear pathology. display head shaking and deficits of the facial and
The first is hematogenous, in which the tympanic mem- vestibulocochlear nerves.12 The pinnae and external audi-
brane remains intact. Affected animals exhibit a systemic tory meatus should be examined and cartilage of the ear
disease process that has its nidus elsewhere. The second is palpated for pain. Otoscopic examination of the ear canal
colonization of the middle ear by bacteria in the pharynx for foreign bodies and assessment of mucosal inflamma-
through the pharyngeal ostia of the auditory tubes.1 This tion and integrity of the tympanic membrane also should
is believed to be the primary route of infection in sheep be performed.14 If mites are suspected, skin scrapings of
that have respiratory infections. The most common bac- the epidermis at the base of the ear canal may be neces-
terial isolates from otitis media and interna in sheep are P. sary to diagnose Sarcoptes scabiei. Diagnosing psoroptic
haemolytica, P. multocida, Pseudomonas aeruginosa, coagulase- mites with cytologic preparations on swabs taken from
positive hemolytic and mixed hemolytic Staphylococcus, the ear canal is difficult. The mites have been repeatedly
and hemolytic Streptococcus.1,2 In most case studies the demonstrated to congregate around the tympanic mem-
tympanic membrane appeared intact and showed no evi- brane deep in the ear canal and out of reach of most
dence of exudate in the external ear canal. These findings swabs.4,8 Flushing the ears gently with warm saline for
are similar to those seen in otitis in horses, but are unlike examination may be more diagnostic than swabbing.
the findings in cattle, in which the membrane is usually Culture and sensitivity testing of exudate from exter-
ruptured.12,13 Two defined stages of infection for otitis nal abscesses in the ear canal is unrewarding diagnosti-
media have been documented grossly and histopatholog- cally except in the following conditions14:
ically. In the acute stage a small amount of yellow-tinged
1. Bacterial infection persists in spite of appropriate
fluid can be visualized in the tympanic bulla, and the
antibiotic treatment
mucous membranes are swollen, hyperemic, and hem-
2. The animal has a history of frequent topical
orrhagic.1 Histologically the mucosae of the bulla are
antibiotic therapy, suggesting the possibility of a
edematous, thrombosed, and have a large accumulation
resistant gram-negative bacterial or fungal
of neutrophils; however, the tympanic membrane often
organism
appears intact. In more advanced chronic stages, in-
3. Otitis media or otitis interna is suspected.
spissated pus is present and can extend into the eusta-
chian tubes; the mucous membranes are thickened and Radiographic examination of the skull in sheep or
rough.2 Histologically the mucosae of the bulla and tym- goats with neurologic signs helps the examiner rule out
panic membrane appear hemorrhagic and fibrosed, and skull fractures that could account for the neurologic signs.
the architecture of the epithelial cells appears more The tympanic bullae also can be assessed for increased
cuboidal. density. In dogs, calcification of the auricular cartilage is
The third route of entry is through the external audi- an indication for surgical intervention.14 Endoscopy can
tory meatus after the tympanic membrane has ruptured. be used to examine the ear canal and tympanic membrane
This is an uncommon sequela to parasitic infestation of and remove any foreign objects.
sheep and goat ears by Psoroptes cuniculi. It is believed that Ancillary tests such as complete blood counts, chem-
the accumulation of secretions and mites places exces- istry profiles, and CSF analyses may be warranted if
sive pressure on the tympanic membrane, causing it to animals show signs of systemic illness, display neurologic
rupture.4 signs, or do not respond to treatment.

Clinical signs. Otitis media is often diagnosed as an Treatment of otitis externa. The goal of treatment for
incidental finding during postmortem examination of otitis externa is to remove ceruminous accumulation and
sheep.2,3 Antemortem clinical signs are not reported the inciting cause, clean and dry the ear, reduce inflam-
unless the infection progresses into the inner ear. This mation, and resolve any secondary infections.14 This may
also is believed to be the case in goats. Otitis interna as a be as simple a task as removing a foreign object and thor-
sequel to otitis media is the most common cause of pe- oughly cleaning the ear; however, it also may require the
ripheral vestibular disease in farm animals. The majority application of topical antiinflammatory agents and an-
of sheep and goats have ipsilateral peripheral vestibular tibiotics. External scabs can be removed with warm water
signs, including head tilt toward the lesion, droopy ears, and mild soap. Any solutions that are used to help flush
stumbling, and progressive weakness that can lead to re- and cleanse the ear canal must be selected with the
cumbency and death.3 Neurologic signs are a result of de- knowledge of whether the tympanic membrane is intact
creased drainage through the auditory tubes because of because many flushing solutions are ototoxic. Cerumi-
swelling in the mucosa and clogging exudate, which can nolytic agents contain surfactants and emulsifiers to
lead to persistent infection and damage to the facial liquefy earwax and aid in its removal. They should be
nerves.1 applied to the ear canal 5 to 15 minutes before the canal is
 Chapter 11 Diseases of the Neurologic System • 303

TABLE 11-7

BACTERICIDAL SOLUTIONS THAT CAN BE USED TO FLUSH THE EXTERNAL AUDITORY MEATUS

SOLUTION CONCENTRATION TOXICITY SUSCEPTIBLE ORGANISMS RESISTANT BACTERIA

Chlorhexidine 2%, 0.05% Ototoxic Gram-negative Pseudomonas

and gram-positive
bacteria; fungi
Povidone iodine 0.1% to 1%; smaller Ototoxic Gram-negative Gram-
concentrations are and gram-positive negative
more effective bacteria; fungi bacteria
Acetic acid 1:1, 1:2, or 1:3 Ototoxic Pseudomonas, Very few
dilution of a 5% Staphylococcus, bacteria are
stock Streptococcus, resistant at
Escherichia coli, 5% concentration
and Proteus but it is
irritating to
the mucosa

cleaned.10 Flushing solutions are then used to remove the 4. Morgan KL: Parasitic otitis in sheep associated with Psoroptes in-
ceruminolytic agents and debris. Saline is the safest solu- festation: a clinical and epidemiological study, Vet Rec 130:530,
tion to use, although a variety of bactericidal solutions 1992.
with a broad spectrum of activity also may be used (Table 5. Bates PG: Ear mites in sheep, Vet Rec 128:555, 1991.
11-7). After flushing the ear canal should be dried thor- 6. Evans AG: Psoroptic mange. In Smith BP, editor: Large animal in-
ternal medicine, St Louis, 1996, Mosby.
oughly; astringents such as aluminum acetate and boric
7. Cook RW: Ear mites (Raillietia manfredi and Psoroptes cuniculi) in
acid can be applied to enhance drying.10 If the canal is se- goats in New South Wales, Aust Vet J 57:72, 1981.
verely inflamed, the animal may benefit from topical cor- 8. Williams JF, Williams CS: Psoroptic ear mites in dairy goats, J Am
ticosteroids or systemic dexamethasone administration. Vet Med Assoc 173:1582, 1978.
In cases in which the inciting cause has been identified 9. Fraser G: The histopathology of the external auditory meatus of
as a psoroptic or sarcoptic mite, ivermectin can be used as the dog, J Comp Path 71:253, 1961.
an acaricide. In addition to treating the affected sheep or 10. Griffin CE: Otitis externa, Comp Cont Ed Pract Vet 3:741, 1981.
goats, all in-contact animals should be treated as well. 11. Littlejohn AI: Psoroptic mange in the goat, Vet Rec 82:148, 1968.
12. Blythe LL: Otitis media and interna and temporohyoid os-
Treatment of otitis media and otitis interna. If the teoarthropathy, Vet Clin North Am Equine Pract 13:21, 1997.
tympanic membrane is ruptured, the clinician must take 13. Jensen R et al: Cause and pathogenesis of middle ear infection in
young feedlot cattle, J Am Vet Med Assoc 182:967, 1983.
care to select ear-cleansing solutions that are not ototoxic.
14. Rosychuk RAW: Management of otitis externa, Vet Clin North Am
In general broad-spectrum antibiotics should be adminis- Small Anim Pract 24:912, 1994.
tered to eliminate bacterial infections. Systemic antiin-
flammatory agents may be warranted if neurologic signs
are present. If the animals are unresponsive to treatment
and adequate drainage of the canal cannot be achieved, a
Cerebrospinal Nematodiasis
lateral ear resection may be necessary to provide access to Etiology and pathogenesis. The larvae from Pare-
the horizontal ear canal. laphostrongylus tenuis (North America)1-6 and Setaria
species (India, Japan, Korea, and Russia)7,8 can aberrantly
R EFERENCES
1. Jensen R et al: Middle ear infection in feedlot lambs, J Am Vet Med
migrate into the central nervous system in many small ru-
minant species.
Assoc 181:805, 1982.
Setaria is found in the connective tissue and peritoneal
2. Macleod NSM, Wiener G, Barlow RM: Factors involved in cavities of adult cattle.8 Adult worms produce blood-borne
middle ear infection (otitis media) in lambs, Vet Rec 91:360, 1972. microfilaria that are picked up by blood-sucking insects
3. Davies IH, Done SH: Necrotic dermatitis and otitis media associ- and occasionally transmitted to sheep and goats.7 The
ated with Pseudomonas aeruginosa in sheep following dipping, Vet larvae can migrate into the spinal cord and cause disease by
Rec 132:460, 1993. destroying nervous tissue during their migration.
304 • Sheep and Goat Medicine

Figure 11-7 This Angora goat with P. tenuis infection has

rear limb ataxia. The CSF contains an increased number of
leucocytes, with more than 50% eosinophils. Other breeds of
goats can become infected with P. tenuis, but most of the
reported cases have been in Angora goats.

P. tenuis is a meningeal worm commonly found in

white-tailed deer (Odocoileus virginianus); it rarely causes
serious pathology and clinical disease in this specie.1 In
the white-tailed deer the adult P. tenuis lives in the
meninges, predominantly in the cranial regions. Adults
lay eggs in the venous sinuses, where they are carried to
the lungs. The eggs become lodged in small capillaries,
hatch, and migrate into the alveoli. The larvae are then
coughed up, swallowed, and passed into the feces.1 The
intermediate hosts are species of slugs and snails that
become infected by P. tenuis larvae when they feed on
deer feces. Sheep and goats accidentally ingest these gas-
tropod intermediate hosts while grazing and become in- Figure 11-8 This cross-section of the spinal cord shows both an
fected. The larvae is freed of the gastropod during diges- increase in inflammatory cells and the parasite. (Courtesy Dr. Christine
tion in the abomasum. The P. tenuis larvae migrate along Navarre, Auburn, AL.)
peripheral nerves toward the spinal cord. On reaching the
spinal cord of the host, the larvae migrate along the
nervous tract, causing inflammation. low-lying, wet areas, 8 goats showed clinical signs. In this
outbreak only the Angoras were affected. The diagnosis
Clinical signs. Clinical signs depend on the migration was confirmed on necropsy. Angora goats may be more
pattern of the parasite through the central nervous prone to infection because of their grazing versus brows-
system. Setaria larvae movements are apparently random, ing behavior. P. tenuis signs usually appear during the fall
whereas P. tenuis larvae migrate in a cranial direction. and winter months in North America, and then only in
Animals usually display an acute onset of signs. If lesions areas that have white-tailed deer and the gastropod inter-
occur only in the spinal cord, the affected animal remains mediate hosts.1
bright and alert, may have a good appetite, and will make
attempts to rise. Depression, ataxia, and paralysis of the Diagnosis. A definitive diagnosis is made by identify-
hindlimbs or of all four limbs may occur. Signs tend to ing the larvae on histologic examination of the spinal
be symmetric, but a vertically oriented strip of self- cord (Figure 11-8). Diagnosis depends on the entire
excoriation may be evident as a result of pathology of the spinal cord and brain being removed at necropsy, cooled
dorsal nerve roots.8 Occasionally lesions occur in the (not frozen), and quickly delivered to a suitable diagnos-
brain and the animal may be depressed, become blind, or tic laboratory. Good presumptive evidence of this disease
die; the animal also may exhibit opisthotonos, circling, is a bright and responsive animal that nevertheless has an
and a head tilt.1 All breeds appear susceptible, but anec- increased number of white blood cells, mostly eosino-
dotally Angora goats may be more likely to become in- phils, in the CSF and exhibits some degree of rear-
fected (Figure 11-7).2 In one outbreak (attended by one limb paralysis or ataxia.3 Reports suggest that 70% of
of the authors, Dr. Pugh) in which 80 Angora, Nubian, goats with P. tenuis infestations have increased eosino-
Spanish, and cross-bred goats were grazing and browsing phils in the CSF.8 Trauma, spinal cord abscess, spondy-
 Chapter 11 Diseases of the Neurologic System • 305

litis, and enzootic ataxia must be ruled out.7 Com- 2. O’Brien TD et al: Cerebrospinal parelaphostrongylosis in Min-
plete blood count results are usually normal, but serum nesota, Minn Vet 26:18, 1986.
chemistry findings usually reveal an elevation of muscle- 3. Kopcha M et al: Cerebrospinal nematodiasis in a goat herd, J Am Vet
specific enzymes (e.g., lactate dehydrogenase [LDH], Med Assoc 194:1439, 1989.
creatine phosphokinase [CPK]). Gross lesions are usually 4. Jortner BS et al: Lesions of spinal cord parelaphostrongylosis in
sheep: sequential changes following intra medullary larval migra-
undetectable; however, small hemorrhagic areas may be
tion, Vet Path 22:137, 1985.
seen in the spinal cord. Histologic lesions include de- 5. Alden C et al: Cerebrospinal nematodiasis in sheep, J Am Vet Med
myelination, axonal degeneration, and malacia. Infiltra- Assoc 166:784, 1975.
tion of eosinophils, lymphocytes, and macrophages often 6. Mayhew IG, deLahunta A, Georgi JR: Naturally occurring cere-
occurs around any larvae that may be found on histologic brospinal parelaphostrongylosis, Cornell Vet J 66:56, 1976.
sections. 7. Kimberling C: Diseases of sheep, ed 3, Philadelphia, 1988, Lee &
Febiger.
Treatment and prevention. Treatment with anthel- 8. Smith MC: Inflammatory neurologic diseases of small ruminants.
mintics (ivermectin 500 mg/kg subcutaneously [SC] once In Smith MC, editor: Current veterinary therapy 3, food animal prac-
a day [SID], followed by 200 mg/kg SC SID for 5 days tice, Philadelphia, 1993, WB Saunders.
and/or fenbendazole 15 mg/kg PO SID for 3 to 5 days), 9. Pugh DG, personal communication.
NSAIDs (flunixin meglumine 1mg/kg IV or IM as needed)
or glucocorticosteroids for nonpregnant animals, and
other antiinflammatory drugs (DMSO) has been em-
Tetanus
ployed in other species susceptible to infestation.1,8 Re- Tetanus is caused by Clostridium tetani. The organism is a
covery depends on the site of the lesion(s), the onset of common inhabitant of the herbivore intestinal tract and
treatment with respect to the occurrence of clinical signs, its spores may be present in large numbers in feces. C.
and the diligence of nursing care. Ivermectin is thought tetani spores appear to have a long extra-intestinal life
to be unable to pass the blood-brain barrier, but in areas span and may remain viable in soil for years. Infection in
where the worm has caused a localized inflammatory re- sheep and goats is most commonly through a contami-
sponse, ivermectin may cross into the inflamed area.8 nated skin break (injury, umbilicus, tail docking, castra-
However, ivermectin’s effect may be relegated to prevent- tion) but also can occur as part of postpartum metritis.
ing any larvae remaining in peripheral tissues from reach- The organism proliferates and produces toxins under
ing the spinal cord. acidic, anaerobic conditions; therefore it is most common
Prevention of infestation with Setaria is difficult, but in deep, necrotic wounds. The organism can remain
minimizing biting insects may be of value. To minimize P. dormant as a spore in tissue until a favorable environment
tenuis infestation, suppressive deworming programs have for replication develops. Therefore clinical tetanus is
been used in llamas.1 However, suppressive deworming often seen several weeks after the original injury.1,2
may be too expensive to use in sheep and goats and can
result in anthelmintic resistance of other nematode Pathogenesis. The organism produces three toxins, the
(HOTC complex) parasites (see Chapter 4). Still, the use most important of which is the plasmid-derived tetano-
of a short-term monthly suppressive deworming program spasmin. Tetanospasmin binds to gangliosides in nerves
(late fall and winter) with ivermectin (200 mg/kg SC) ap- and is carried by retrograde axoplasmic flow through the
peared to be of value in stopping an explosive outbreak (8 smooth endoplasmic reticulum to the central nervous
of 80 animals in a 1-week period).9 Susceptible animals system, where it prevents the release of the inhibitory
should be removed from low-lying or moist pastures, par- neurotransmitter glycine. The toxin can initially bind to
ticularly those adjacent to habitats where a white-tailed nervous tissue near the site of infection, in which case
deer population exists. If alternative pastures are unavail- local neurologic signs develop before the disease becomes
able, frost or freezing temperatures may alleviate some generalized (ascending tetanus). Alternatively, it can cir-
of the risk. Fencing off damp areas and instituting snail culate in the blood and bind to nervous tissue near the
and slug control measures (often done with geese) may head, in which case head and neck signs are seen before
reduce the incidence of clinical disease. Such pastures limb signs (descending tetanus). In both cases the effect
should first be grazed by less susceptible species (cattle). of the toxin on the central nervous system is to prevent
Minimizing contact with white-tailed deer and/or inter- inhibition of muscular contraction, resulting in continu-
mediate hosts is an excellent, yet difficult, method of ous tetanic contraction of muscle groups. Postural and
prevention. facial muscles are most commonly affected.
The other two toxins are tetanolysin and a non-

R EFERENCES
1. Pugh DG et al: Clinical parelaphostrongylosis in llamas, Comp Cont
spasmogenic neurotoxin. Tetanolysin is thought to en-
courage necrosis and thereby create a favorable site for
proliferation of the organism. The second neurotoxin
Ed Pract Vet 17:600, 1995. appears to cause neuromuscular blockage and activate the
306 • Sheep and Goat Medicine
sympathetic nervous system. Tetanus occurs worldwide. BID to QID) are the antibiotics of choice to kill C. tetani.
Sheep and goats are generally considered more suscepti- Tetanus antitoxin can be administered with tetanus
ble to tetanus than cattle. toxoid (at different sites) to help neutralize unbound
toxin and provide active immunity. Slings and deep, soft
Clinical signs. With ascending tetanus the clinical bedding are important to prevent decubital ulcers and
signs first noted are often stiffness or perceived lameness maintain circulation in the extremities. A rumenotomy
in one leg. Within 24 hours generalized stiffness, a stilted may be necessary in some sheep and goats that are
gait, raised tail head (“pump-handle”), saw-horse stance, anorexic and suffering from ruminal tympany. Animals
trismus (“lockjaw”), and retraction of the lips from the should be kept in a dark, quiet place with minimal stimu-
teeth (“sardonic grin”) may be noted. Stimulation can lation to reduce muscle spasms and stress. Sedation also
cause tetanic muscular spasms, particularly of postural and may be beneficial.
facial muscles and the third eyelid. The infected animal
may appear restless and have pyrexia. Severely affected Prevention. In addition to general matters of hygiene,
animals are recumbent and display rigid, uncorrectable ex- especially during surgical procedures, the administration
tension of the neck and all four limbs (Figure 11-9). Bloat of tetanus toxoid may help prevent this disease. A two-
and aspiration also are common findings. Rigid paralysis dose course in the first year of life followed by annual
of the muscles of respiration induce hypoxemia and se- boosters is recommended. Additional boosters may be
verely limit the animal’s ability to function. Clinical signs given to individual animals after injuries.2
are present for several weeks in animals that recover;
however, death is the usual outcome. R EFERENCES
1. Hagan WA, Bruner DW, Timoney JF: Hagan and Bruner’s microbi-
Diagnosis. Stress leukograms and marked increases in ology and infectious diseases of domestic animals, ed 8, Ithaca, NY,
muscle enzymes are the most typical antemortem abnor- 1988, Comstock Publishing.
malities. The clinician may determine the original route 2. George LW: Tetanus (lockjaw). In Smith BP, editor: Large animal
of entry for the organism and attempt to isolate the or- internal medicine, ed 2, St Louis, 1996, Mosby.
ganism from that area. Diagnosis is by characteristic signs
with or without isolation of the organism.
Botulism
Treatment. The clinician must keep several goals in Clostridium botulinum is the cause of botulism. The or-
mind when treating small ruminants with tetanus. They ganism proliferates and produces toxin under neutral or
include muscle relaxation; supportive care, including the alkaline, anaerobic conditions. Spoiled feedstuffs, moist
provision of good footing; fluid and nutritional support; alkaline silage, brewer’s grains, decaying vegetation, and
elimination of the infection; neutralization of unbound animal carcasses are common sites of proliferation. Feed-
toxin; and provision of active antitoxic immunity. Ex- related outbreaks are common and often are associated
tremely high doses of penicillin (20,000 to 40,000 IU IV with contamination of a feedstuff with a decaying animal
carcass. Factors that promote pica (such as hypophos-
phatemia and starvation) may promote outbreaks by en-
couraging animals to consume sources of the toxin they
would otherwise not eat. Several strains of C. botulinum
have been identified. Strain C is the most common cause
of disease in sheep. Botulism occurs worldwide.

Pathogenesis. In sheep and goats, botulism is almost

always caused by ingestion of preformed toxin, rather
than production of the toxin by viable bacteria within the
intestinal tract (toxicoinfectious botulism) or a wound.
Adult ruminants are less susceptible than neonates and
animals that lack a fermentative stomach because most
Figure 11-9 This lamb developed tetanus as a sequela of tail ingested botulism toxin is degraded by rumen microbes
docking. Any wound, particularly one in which tissue trauma and and therefore ingestion of large doses of toxin is necessary
depressed oxygen tension are evident, is susceptible to C. tetani to cause disease. Toxin that survives the rumen is ab-
infection and elaboration of the neurotoxin. The first signs occur by 3 sorbed across the intestinal wall, where it enters the circu-
weeks after an injury or surgical procedure (tail docking, dehorning, lation. It binds gangliosides at the neuromuscular junc-
castration). Death usually occurs as a result of respiratory failure. On
farms and ranches with a high incidence, tetanus antitoxin (150 to 300 tion and thereby prevents the fusion of acetylcholine
IU) and tetanus toxoid should be given at the time of any surgical vesicles with the presynaptic membrane. Flaccid paralysis
procedures. results, usually within a week of ingestion of the toxin.1-3
 Chapter 11 Diseases of the Neurologic System • 307

Clinical signs. Generalized muscle weakness is the junction, resulting in paresis.1,2 Ticks of the genus Der-
most common clinical sign. Affected animals move macentor are associated with this disease. Tick paralysis
slowly and reluctantly, often dragging their feet or occurs in North America west of the Rocky Mountains.
swaying from side to side. Once they become recumbent, A similar condition is reported in Australia and is caused
they often have difficulty rising. The head is usually held by the tick Ixodes holocyclus. However, in the Australian
low, and protrusion of the tongue may cause pseudoptyal- strain of the disease animals usually do not recover even if
ism and dysphagia. Bloat, regurgitation, rumen hypo- the tick is removed.
motility, and a distended, hypomotile bladder may occur.3
Clinical signs. A progressive paralysis and weakness
Diagnosis. No clinicopathologic abnormalities or occurs. If left untreated, it results in death by respiratory
postmortem lesions are specific to botulism. Transudates paralysis.
may be found in body cavities and tissues may be edema-
tous. Cardiac disease must be ruled out as a cause for Diagnosis. Diagnosis is based on clinical signs and
these lesions. Diagnosis is made by characteristic signs finding ticks. This condition must be differentiated from
and identification of the toxin in feed, blood, or gastroin- botulism.
testinal contents. Identification of the specific strain is
made by use of a live animal assay or an enzyme-linked Treatment and prevention. Animals can be sprayed
immunospecific assay (ELISA). with pyrethrins or given ivermectin; however, ticks
should be removed. Animals should be sheared if neces-
Treatment. Therapy consists of fluid and nutritional sary in order for the examiner to find the tick(s). Animals
support, general nursing care (including wound manage- quickly recover after the tick has been removed. Applying
ment), and supportive ventilation if warranted. Penicillin- tick or insect repellents is helpful in some high-risk
class antibiotics are effective, but intramuscular procaine areas.1,2
penicillin should be avoided if possible because it can ex-
acerbate the neuromuscular blockage. Metronidazole also
is effective, especially if wound contamination has oc-
curred, but it should not be used in ruminants that may be
R EFERENCES
1. Schofield LN, Saunders JR: An incidental case of tick paralysis in a
slaughtered for food. Polyvalent antitoxin may be effective Holstein calf exposed to Dermacentor andersoni, Can Vet J 33:190,
in the early stages of the disease and in animals at risk of 1992.
contracting botulism. A beneficial effect may be achieved 2. Fowler ME: Tick paralysis, Cal Vet 39(2):25, 1985.
by administering anticholinesterase (neostigmine methyl-
sulfate 0.01 to 0.02 mg/kg SC).
Organophosphate Toxicosis
Prevention. Proper handling and avoiding the feeding Some sheep have a familial predisposition to chronic
of contaminated feedstuffs are the best methods of pre- organophosphate toxicity,1 although all sheep and goats
vention. This includes proper fermentation of silage, are susceptible. Organophosphates inhibit cholinesterase,
rodent control, and removal of carcasses from feeds before and toxicosis caused by the compound may be cumulative.
processing. A vaccine is available in the United States
against type B botulism, but not against type C.3 Clinical signs. Acute signs include hypersalivation, de-
pression, incoordination, and death. This slow, progressive
R EFERENCES
1. Hagan WA, Bruner DW, Timoney JF: Hagan and Bruner’s microbi-
condition is characterized by dyspnea, weakness, rear-
limb ataxia, apparent loss of proprioceptive ability, and
bloat. With chronic organophosphate toxicosis, animals
ology and infectious diseases of domestic animals, ed 8, Ithaca, NY,
become recumbent and lose tail, rectal, and bladder
1988, Comstock Publishing.
2. Allison MJ, Maloy SE, Matson RR: Inactivation of Clostridium bot-
function. However, most maintain a good appetite.1,2
ulinum toxin by ruminal microbes from cattle and sheep, Appl
Environ Microbiol 32:685, 1976. Diagnosis. Red blood cell cholinesterase concentra-
3. Smith MO: Botulism. In Smith BP, editor: Large animal internal tions are depressed at the onset but soon return to
medicine, ed 2, St Louis, 1996, Mosby. normal. No gross lesions are noted on postmortem evalu-
ation. Histologic examination reveals demyelination,
swelling, and Wallerian degeneration that progresses
Tick Paralysis from the periphery to more central areas of the central
Tick paralysis is a rapidly progressive LMN paralysis that nervous system.
occurs in both sheep and goats. The tick, probably the
female, releases a toxin in its saliva that blocks or de- Treatment. No treatment is available for the chronic
creases the release of acetylcholine at the neuromuscular form of the disease. Acute cases may be treated with high
308 • Sheep and Goat Medicine
doses of atropine (0.2 to 0.4 mg/kg IV) or pralidoxime (2 is beneficial.2,3,5 A combination of thiamine (5 mg/kg
PAM, 20 mg/kg). IM SID or TID) and EDTA appears to give the best
results.7 The administration of oral magnesium sulfate

R EFERENCES
1. Williams JF, Dade AW: Posterior paralysis associated with an-
may help decrease the absorption of lead salts in sheep
and goats, as it does in other species.8 Nutritional (oral or
total parenteral nutrition) and fluid support are required.
thelmintic treatment of sheep, J Am Vet Med Assoc 169:1307, 1976. If convulsions occur, they can be controlled with di-
2. Linklater KA, Smith MC: Color atlas of diseases and disorders of the azepam (0.5 to 2 mg/kg IV).
sheep and goat, Aylesburg, UK, 1993, Wolfe Publishing.

Lead Toxicity
R EFERENCES
1. Allcroft R: Lead poisoning in cattle and sheep, Vet Rec 63:58, 1951.
Lead toxicity (plumbism) in sheep and goats is most 2. Baker JC: Lead poisoning in cattle, Vet Clin North Am Food Anim
likely to result from a single accidental ingestion of Pract 3:137, 1987.
harmful amounts of lead.1,2 Common sources of lead ex- 3. Radostits OM, Blood DC, Gay CC: Diseases caused by inorganic
and farm chemicals. In Radostits OM, Blood DC, Gay CC, editors:
posure include lead-containing paints, petroleum prod-
Veterinary medicine, ed 8, London, 1994, Bailliere Tindall.
ucts, and discarded batteries.1-4 Lead is believed to
4. Davis JW et al: Experimentally induced lead poisoning in goats:
produce neurologic disease by a direct toxic effect on the clinical observations and pathologic changes, Cornell Vet J 66:490,
vasculature of the central nervous system that causes cap- 1976.
illary edema and hemorrhage. Goats are more resistant to 5. Smith MC, Sherman DM: Nervous system. In Smith MC,
lead toxicity than other species5 and lethal doses of lead Sherman DM, editors: Goat medicine, Philadelphia, 1994, Lea &
vary widely among goats.4 Sheep were experimentally fed Febiger.
lead at 4.5 mg/kg for 27 weeks without developing any 6. Carson TL et al: Effects of low level lead ingestion in sheep, Clin
apparent clinical signs of plumbism.6 Toxicol 6:389, 1973.
7. George LW: Diseases of the nervous system. In Smith BP, editor:
Clinical signs. Clinical signs of plumbism in sheep Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
8. Pringle J: Neurologic disorders. In Ogilvie TH, editor: Large animal
include cortical blindness, dullness, anorexia, circling, and
internal medicine, Baltimore, 1998, Williams & Wilkins.
gait abnormalities.3 In contrast to other species, blindness
did not occur in goats with experimental lead toxicity.4
Clinical signs of lead toxicity in goats include anorexia,
diarrhea, weight loss, and death.4
Sodium Toxicosis and Water Deprivation
Sodium toxicosis and water deprivation (salt toxicity)
Diagnosis. Diagnosis of plumbism is based on consis- occur under the following conditions1-3:
tent clinical signs and blood lead concentrations. Back-
1. Excessive sodium ingestion with adequate water
ground blood lead concentrations vary geographically,
intake
and therefore the normal range of blood lead concentra-
2. Consumption of normal amounts of sodium with
tions differs among diagnostic laboratories.2 If exposure
limited access to water
to lead is chronic, anemia may result. CSF analysis may
3. Consumption of water with a high sodium
show an increase in protein concentration and in the
concentration
number of neutrophils and monocytes. At necropsy, af-
4. The administration of hypertonic oral electrolyte
fected goats have cerebral edema, microscopic lesions of
solutions
meningeal and perineuronal edema, neuronal degenera-
tion, and vascular congestion of medullary and cerebellar Feeding salt-limited diets, particularly during periods
white matter.4 The kidneys and livers of suspected cases of water deprivation or weather changes, may result in
should be measured for lead concentration. salt toxicity. Prolonged hypernatremia causes an increase
in CSF and brain sodium concentrations. As an addi-
Treatment. Treatment of lead toxicity involves the ad- tional response to hypernatremia, iodogenic osmoles ac-
ministration of lead chelating agents such as ethylenedi- cumulate inside neurons. Both of these protective mecha-
amine tetra-acetic acid (EDTA).5 In goats, 110 mg/kg nisms increase osmolality and retain water within the
EDTA (6.6% solution) is administered IV twice a day at CNS. Neurologic disease results from cerebral edema
12-hour intervals for 2 days. Alternatively, EDTA (70 to when the animal is rehydrated too quickly and water
75 mg/kg IV) can be administered slowly for 3 to 5 days, follows an osmotic gradient into the CNS.1,4
followed by 2 days of no treatment and then 5 more days
of therapy. The 2-day rest allows bone lead stores to Clinical signs and diagnosis. Clinical signs reported in
equalize with the soft tissues.7 Thiamine administration affected sheep include increased thirst, somnolence, hy-
as described for treatment of polioencephalomalacia also perthermia, tachycardia, tachypnea, muscle fasciculation,
 Chapter 11 Diseases of the Neurologic System • 309

rumen stasis, diarrhea or mucus-coated feces, regurgita- Treatment. Infusing a cold 2% acetic acid solution
tion, nasal discharge, convulsions, and death.3 Affected (1 mg/kg PO) into the rumen improves the blood acid-
lambs may have serum and CSF concentrations of base status and slows bacterial production of ammonia.
sodium in excess of 180 mEq/liter.3,4 Oral charcoal (0.5 kg PO) also may be helpful in decreas-
ing ammonia absorption.1
Treatment. Treatment of sodium toxicosis and water
deprivation initially involves restricting water intake to Prevention. Slow introduction of sources of non-
frequent, small quantities and reducing cerebral edema protein nitrogen is a good method of prevention (see
with corticosteroids (dexamethasone 1 to 2 mg/kg IV), Chapter 2).
mannitol (0.25 to 1 mg/kg IV), or possibly furosemide
(1 to 2 mg/kg IV). Severely affected animals may require
IV fluid replacement to gradually restore sodium and
water homeostasis.1,3
R EFERENCE
1. Divers TJ: Diseases of the nervous system. In Howard JL, Smith
RA, editors: Current veterinary therapy 4, food animal practice,
Prevention. Fresh, clean water should be made avail- Philadelphia, 1999, WB Saunders.
able. If salt-limited feeds are offered, changes in water
intake associated with weather should be anticipated.
Owners should be instructed in the proper use of oral
Polioencephalomalacia
electrolyte solutions for rehydration. Polioencephalomalacia (PEM), or cerebrocortical necro-
sis, is most commonly diagnosed in 2- to 6-month-
R EFERENCES
1. Miller PE: Neurogenic vision loss. In Howard JL, Smith RA,
old lambs and kids that are typically being fed high-
concentrate diets.1-4 However, PEM can occur in animals
of any age. Other nutritional factors associated with
editors: Current veterinary therapy 4, food animal practice, Philadel- PEM include sudden changes in diet, feeds high in mo-
phia, 1999, WB Saunders.
lasses (horse feed), moldy hay, rumen acidosis, and the
2. Kopcha M: Nutritional and metabolic diseases, Vet Clin North Am
Food Anim Pract 3:119, 1987.
dietary stress of weaning.4 In ruminant animals the
3. Divers TJ: Diseases of the nervous system. In Howard JL, Smith ruminal bacteria normally produce sufficient thiamine
RA, editors: Current veterinary therapy 4, food animal practice, (vitamin B1) to meet their requirements. Rumen acidosis
Philadelphia, 1999, WB Saunders. (most commonly caused by feeding excess concentrates)
4. Scarratt WK, Collins TJ, Sponenberg DP: Water deprivation- predisposes animals to the development of PEM in
sodium chloride intoxication in a group of feeder lambs, J Am Vet several ways: the population of thiamine-producing bac-
Med Assoc 186:977, 1985. teria decreases, bacterial thiaminase production increases,
and ruminal thiaminase activity is potentiated by acidic
conditions.2,5 Bracken fern (Pteridium aquilinum) also
Urea (Ammonia) Toxicity contains thiaminase and experimental feeding trials in
Urea (ammonia toxicity) is seen in animals fed non- sheep have produced clinical signs and necropsy lesions
protein nitrogen (e.g., urea, ammoniated feeds). It is more consistent with PEM.6 Overdosage of thiamine analogs
common in animals newly introduced to such diets (see such as amprolium has caused PEM in sheep by compet-
Chapter 2). Excess non-protein nitrogen, particularly at a itive inhibition.7 Thiamine is a necessary cofactor for
high rumen pH, is catabolized to ammonia. If adequate enzymes involved in glucose metabolism, including
carbon chains from readily fermentable feeds are lacking transketolase and pyruvate decarboxylase. The brain
(corn, oats) or if the rumen pH is high because of poor- derives energy from glucose through the pentose phos-
quality forage intake (resulting in enhanced function of phate pathway, which requires thiamine diphosphate as a
the urease enzyme), bacterial production of protein from coenzyme for transketolase. When energy production in
the released ammonia is overwhelmed, resulting in alka- the neurons is impaired as a result of thiamine deficiency,
losis and encephalopathy. cellular osmotic gradients cannot be maintained and neu-
ronal swelling results in PEM.
Clinical signs. Trembling, facial twitching, incoordi- High dietary sulfate also may cause clinical signs and
nation, blindness, recumbency, and death are all encoun- necropsy lesions consistent with PEM. Excessive dietary
tered. Animals also may become bloated, dyspneic, and sulfur intake may result from mixing errors, high-sulfur
hyperesthetic. water sources, feed intake limiters such as gypsum
(calcium sulfate), and urinary acidifiers such as ammo-
Diagnosis. The clinical signs coupled with a history of nium sulfate.8 Sulfur-induced PEM also has occurred in
an abrupt introduction to non-protein nitrogen are useful sheep allowed to graze areas that were recently sprayed
for a presumptive diagnosis. Blood and CSF ammonia with an elemental sulfur solution.9 The neurotoxic mech-
concentrations are usually elevated. anism of sulfur is not completely understood but may
310 • Sheep and Goat Medicine
result from the production of large amounts of hydrogen slight elevations may occur in protein concentration or
sulfide in the rumen. High concentrations of sulfides in- mononuclear cell count.2,4 If sulfate-induced PEM is
terfere with energy production in the brain by inhibiting suspected, the sulfate content of the ration and water
cytochrome oxidase, which participates in the electron sources should be determined. Examination of rumen
transport chain to eventually produce ATP. Dietary sulfur contents reveals an increased number of gram-positive
concentrations of 0.43% and greater have caused PEM in bacilli and decreased numbers of gram-positive cocci
sheep.10,11 organisms.15
Necropsy lesions of PEM are limited to the brain and
Clinical signs. Clinical signs of PEM include central include a softened, edematous cerebral cortex that often
blindness, dorsomedial strabismus, depression, incoordi- has a gray to yellowish discoloration. The cerebral gyri
nation, head pressing, recumbency, opisthotonos, and may appear flattened and the cerebellum may be herni-
convulsions1-9 (Figure 11-10). Diarrhea and anorexia ated through the foramen magnum in severe cases.3,4 If
may be noticed before clinical signs occur or soon after transverse sections of the cerebrum are examined with an
onset.1,4 Severely affected animals can become comatose ultraviolet light, the necrotic areas fluoresce because of
and die. PEM caused by thiamine deficiency usually only the presence of lipofuscin pigment. Histopathologic find-
affects a few individuals in the herd or flock, but sulfur ings include laminar necrosis in affected cerebral gyri,
toxicity may involve a large number of animals.10 with separation of the white and gray matter. The
neurons have an eosinophilic cytoplasm and may appear
Diagnosis. Diagnosis of PEM is most often based on degenerated and shrunken. Pericellular edema, nuclear
the animal’s clinical signs and response to therapy.1,2,4 chromatolysis, and vacuolization may occur.3,4
Blood thiamine concentration and erythrocyte transke-
tolase activity can be measured, but these tests are not Treatment. Treatment most importantly involves thi-
routinely available. Using high-pressure liquid chro- amine replacement at a dosage of 10 mg/kg. The initial
matography, normal blood thiamine concentrations have dose should be given IV; additional injections can be IM
been reported to be between 75 and 185 nmol/l and 66 or SC and should be administered every 6 hours for the
to 178 nmol/l in sheep12 and goats,13 respectively. The first day of therapy.1,4,5 Thiamine injections (10 mg/kg
most useful assay of transketolase activity determines every 6 to 12 hours IM, SC, or IV) should be continued
the thiamine diphosphate (TPP) effect, which is a for at least 2 days. The frequency of injection may be
measure of the percentage increase in transketolase ac- gradually reduced as the animal improves and regains a
tivity after the addition of excess TPP to a sample.5 In normal appetite.1,3,4 Many affected animals exhibit sig-
sheep affected with PEM, transketolase activity in- nificant improvement within 24 hours of the first thi-
creases from 96% to 158% when they are tested for the amine injection. In severe cases, cerebral edema can be
TPP effect.14 Blood thiamine concentration and trans- reduced with furosemide, mannitol (1 to 2 g/kg IV), or
ketolase activity are normal in animals with sulfur- dexamethasone (0.1 mg/kg IV, IM, or SC).1,4 Seizures
induced PEM.8 CSF analysis is usually normal, but may be controlled with diazepam (0.5 to 1.5 mg/kg IV)
as needed.1,4 Euthanasia should be recommended for
animals not responding to therapy within 3 days;
however, some animals may take as long as 1 week to fully
recover.1 Blindness is usually permanent in severely af-
fected animals because of extensive cerebrocortical necro-
sis.3,4 In contrast with animals affected by PEM of differ-
ent etiologies, animals affected with PEM because of
excess dietary sulfur usually do not respond well to thi-
amine administration.8-10

Prevention. Sudden dietary changes to more energy-

dense feeds should be avoided. The addition of thiamine
(3 to 10 mg/kg/day) to the diets of animals prone to this
condition and thiamine administration before weather
changes may be preventative.16 Other measures to reduce
the incidence of PEM include allowing free access to a
Figure 11-10 A lamb with polioencephalomalacia resulting from a good-quality trace mineral salt, paying careful attention
diet deficient in forage and rich in cereal grains. Note the characteristic
dorsomedial strabismus. Feedlot animals, club lambs and goats, and pet to animals fed a diet with calcium sulfate as a component
animals fed diets rich in energy or sulfate and low in forage are at high and to those offered water with a high sulfate content,
risk to develop this disease. and providing free access to good-quality forage.
 Chapter 11 Diseases of the Neurologic System • 311

R EFERENCES
1. Miller PE: Neurogenic vision loss. In Howard JL, Smith RA,
months of age. Adults can be affected by many forms of
copper deficiency (e.g., anemia, fever, diarrhea) (see
Chapter 2).
editors: Current veterinary therapy 4, food animal practice, Philadel-
phia, 1999, WB Saunders. Diagnosis. Antemortem diagnosis is based on clinical
2. Smith MC: Polioencephalomalacia in goats, J Am Vet Med Assoc signs, dietary deficiency of copper (4 ppm), and deficient
174:1328, 1979. serum or liver concentrations of copper (deficient con-
3. Pierson RE, Jensen R: Polioencephalomalacia in feedlot lambs, J
centration in the liver is less than 0.5 ppm; serum concen-
Am Vet Med Assoc 166:257, 1975.
4. Smith MC, Sherman DM: Nervous system. In Smith MC,
trations less than 0.6 ppm are deficient). CSF values are
Sherman DM, editors: Goat medicine, Philadelphia, 1994, Lea & unremarkable.
Febiger.
5. Rammell CG, Hill JH: A review of thiamine deficiency and its di- Treatment and prevention. Affected animals should
agnosis, especially in ruminants, N Z Vet J 34:202, 1986. be given copper either orally (copper wire, copper parti-
6. Evans WC et al: Induction of thiamine deficiency in sheep, with cles) or parenterally. However, much of the developmen-
lesions similar to those of cerebrocortical necrosis, J Comp Path tal pathology (hypomyelinogenesis, demyelination, of
85:253, 1975. lower motor neurons) appears irreversible. Increasing the
7. Loew FM, Dunlop RH: Induction of thiamine inadequacy and dietary copper to 5 to 15 ppm and maintaining a copper-
polioencephalomalacia in adult sheep with amprolium, Am J Vet to-molybdenum ratio of 61 in pregnant females is
Res 33:2195, 1972.
usually protective.
8. Jeffrey M et al: Polioencephalomalacia associated with the inges-
tion of ammonium sulfate by sheep and cattle, Vet Rec 134:343,
1994. Spinal Trauma, Abscesses, and Tumors
9. Bulgin MS, Lincoln SD, Mather G: Elemental sulfur toxicosis in a
flock of sheep, J Am Vet Med Assoc 208:1063, 1996. Trauma to the spinal cord can result from injuries caused
10. Low JC et al: Sulfur-induced polioencephalomalacia in lambs, Vet by other animals (e.g., predators, other goats or sheep,
Rec 138:327, 1996. horses), cars, and hunting accidents, among other causes.
11. Gooneratne SR, Olkowski AA, Christensen DA: Sulfur-induced Young growing animals occasionally have vertebral frac-
polioencephalomalacia in sheep: some biochemical changes, Can J tures secondary to dietary or metabolic calcium disorders.
Vet Res 53:462, 1989. These fractures occur in animals consuming diets defi-
12. Hill JH, Rammell CG, Forbes S: Blood thiamine levels in normal cient in calcium and vitamin D and/or rich in phospho-
cattle and sheep at pasture, N Z Vet J 36:49, 1988.
rus. Spinal cord tumors (e.g., lymphosarcoma) are space-
13. Rammell CG, Hill JH, Orr M: Blood thiamine levels in clinically
normal goats and goats with suspected polioencephalomalacia, N
occupying lesions that compress the spinal cord. Vertebral
Z Vet J 36:99, 1988. abscesses may be a component of caseous lymphadenitis
14. Edwin EE et al: Diagnostic aspects of cerebrocortical necrosis, Vet or may result from omphalophlebitis or septicemia.1
Rec 104:4, 1979.
15. Haven TR, Caldwell DR, Jensen R: Role of predominant rumen Clinical signs. The clinical signs depend on the loca-
bacteria in the cause of polioencephalomalacia (cerebrocortical tion of the injury and the degree of severity of damage to
necrosis) in cattle, Am J Vet Res 44:1451, 1983. the spinal cord. The signs are usually symmetric and vary
16. George LW: Diseases of the nervous system. In Smith BP, editor: from paresis and stiffness to paralysis. In some cases of
Large animal internal medicine, ed 2, St Louis, 1996, Mosby. spinal tumors or vertebral abscesses the signs may either
be progressive or appear to have an acute onset. In cases
of spinal trauma the onset is acute.
Enzootic Ataxia
Enzootic ataxia, or swayback, is a neurologic condition Diagnosis. In cases of trauma a complete physical ex-
seen in newborn and growing lambs and kids. Pregnant amination may reveal cuts, punctures, abrasions, and
ewes and does that graze pastures or are fed diets defi- hemorrhages. Palpation of the spinal cord may indicate
cient in copper can give birth to lambs with swayback. displacement of the spine in the area of the fracture. Ra-
Conditional copper deficiency (secondary to excess diographs are useful in aiding the diagnosis of demineral-
molybdenum, sulfate, iron, or other contaminants, and ization, spinal cord abscess, osteomyelitis, or fractures.2
minerals such as cadmium) also may predispose to the In these cases, serum calcium and phosphorus concentra-
condition. tions are normal, but urinary calcium clearance is de-
pressed and phosphorus clearance is increased (see Chap-
Clinical signs. Lambs affected in utero may be still- ters 2 and 10). Serum vitamin D concentrations may be
born; those that live are weak and ataxic and may die depressed. With spinal cord abscesses a complete blood
within the week. Lambs and kids that develop the condi- count may show a normal leukogram, an elevated white
tion after birth display ataxia between 2 weeks and 3 count, and/or elevations in fibrinogen concentrations. In
312 • Sheep and Goat Medicine
most instances of trauma the CSF reveals xanthochromia should in the fetus. The causative agent is usually an in
and an increase in total protein.2 Occasionally spinal cord utero infection in the fetus caused by a virus during a spe-
tumors are indicated by the presence of exfoliated cells on cific stage of gestation. A fetal cerebrovascular insult also
cytologic examination of collected CSF. One of the may result in massive necrosis and reabsorption of tissue.3
authors of this chapter (Dr. Pugh) has encountered this in The extensive loss of neural tissue results in the limbs of the
one case each of melanoma and lymphosarcoma. affected fetus being severely contracted (arthrogryposis).

Treatment. In cases caused by trauma, the use of

NSAIDs (flunixin meglumine 1 to 2 mg/kg IV or IM
Hydrocephalus
BID, phenylbutazone 5 to 10 mg/kg IV SID) and The pathophysiology behind hydrocephalus is still not
DMSO (1 mg/kg in 5% dextrose IV SID or BID) is indi- completely known. In congenital forms the obstruction
cated.2 In cases of vertebral abscesses, antibiotic therapy results from stenosis during fetal development. The sites
is indicated (penicillin 22,000 IU/kg BID) but is rarely of obstruction are most commonly the lateral apertures,
rewarding.2 mesencephalic aqueduct, lateral ventricles, interventricu-
lar foramina, and fourth ventricles.4 A genetic predisposi-
R EFERENCES
1. Smith MC: Inflammatory neurologic diseases of small ruminants.
tion for the development of hydrocephalus in Suffolk
sheep along with cerebellar hypoplasia is called Dandy-
Walker syndrome.5 Some poisonous plants such as Vera-
In Smith RA, editor: Current veterinary therapy 3, food animal prac-
tice, Philadelphia, 1993, WB Saunders.
trum californicum and Conium maculatum can cause ter-
2. Sweeney RW: Spinal cord diseases. In Howard JL, Smith RA, atogenic defects that result in hydrocephalus if they are
editors: Current veterinary therapy 4, food animal practice, Philadel- ingested in large enough quantities by ewes during preg-
phia, 1999, WB Saunders. nancy.6 Acquired hydrocephalus is rare in small rumi-
nants but can potentially result from inflammation of the
arachnoid villi. This can occur as a result of vitamin A de-
Hydrocephalus and Hydranencephaly ficiency and meningitis because these conditions interfere
Hydrocephalus results from fluid accumulating in exces- with the absorption of CSF by the arachnoid villi.
sive amounts in the ventricular system of the cranium. Trauma resulting in obstruction and neoplastic masses
Compensatory hydrocephalus results from destruction of also are potential causes of hydrocephalus. In obstructive
neural tissue and replacement of that space with CSF. hydrocephalus, pressure from accumulating CSF and
This form of hydrocephalus also is referred to as hydran- ventricular enlargement may result in disruption of the
encephaly, and is discussed separately. Obstructive hy- pellucid septum; atrophy of associated structures, includ-
drocephalus can occur as an internal accumulation of ing subcortical white matter; and optic radiations.7
CSF in the ventricular system or an external accumula-
tion of CSF in the subarachnoid space. In addition, two
classifications are used to describe the cause of hydro-
Hydranencephaly
cephalus: normotensive (in which the pressure of the CSF The pathophysiology behind hydranencephaly is not
is normal, as it is in the case of hydranencephaly) and hy- completely understood. The disease has several recog-
pertensive. Hypertensive hydrocephalus results from an nized causes, including bony malformation with hypopla-
increase in the amount of CSF because it cannot be ab- sia of tissue, degeneration associated with ischemia, and
sorbed properly as a consequence of a blockage or partial inflammation or injury that results in the destruction of
obstruction in the ventricular system. The obstruction neural tissue.1 Whatever the cause, the effects on the
can be communicating or noncommunicating, acquired neural tissue result in a loss of dorsolateral ventricular
or congenital. Most forms of hydrocephalus recognized in ependyma, thinning of the white matter, and poren-
sheep and goats are congenital. Communicating hydro- cephalic cyst formation. The space that is left from the
cephalus results from an extraventricular obstruction and absent tissue is then filled with CSF. Because CSF pres-
is associated with an inability of the arachnoid villi to sure (normotensive) in the cranium does not increase
absorb CSF. Noncommunicating hydrocephalus results during fetal development, affected animals rarely have
from an intraventricular obstruction that prevents the enlarged craniums. Many viral organisms that infect
flow of CSF from the ventricular system to the cerebel- sheep and goats during pregnancy produce in utero infec-
lomedullary cistern of the subarachnoid space.1 tions that cause degenerative changes in neuronal tissues
Hydranencephaly is the complete or almost complete during their development.
absence of the cerebral hemisphere and basal ganglia in a Akabane virus belongs to a family of single-stranded
cranium of normal size.2 The cavity that remains is filled ribonucleic acid (RNA) viruses that are transmitted by
with CSF and surrounded by a thin layer of cerebrum.This arthropods. It is responsible for causing arthrogryposis
condition also is termed normotensive hydrocephalus and with hydrocephalus and hydranencephaly in lambs. The
results from the neurologic tissue not developing as it virus is considered exotic to North America but is present
 Chapter 11 Diseases of the Neurologic System • 313

in Australia, Japan, Israel, and Korea. The virus multi- the peripheral cortex.12 Bluetongue virus causes cy-
plies in extra-fetal tissues in the host, producing viremia totropic changes in the undifferentiated cells and results
of 1 to 9 days’ duration.8 During this time an arthropod in a necrotizing encephalopathy with cavitation hydran-
can bite the host and transmit the virus to another if suf- encephaly and retinal dysplasia. Infections that occur
ficient viremia is present. After the host is infected and between 70 and 80 days of gestation result in poren-
develops viremia, transplacental infection of the endothe- cephaly or cerebral cysts, but no ocular lesions. After 100
lial cells of the placenta occurs, followed by sustained days of gestation, infection results in focal areas of
replication in the trophoblastic cells of the fetus.8 The meningoencephalitis without destructive lesions.
placentome appears to be an essential route for hema- Pestivirus infections in pregnant ewes also have been
togenous spread of virus from the dam to the fetus,9 and implicated in causing hydranencephaly in fetuses. Both
the timing of infection seems to be an important factor border disease (BD) and bovine viral diarrhea virus
in determining whether the fetus develops congenital (BVDV) belong to this family. BD and BVDV in sheep
abnormalities. cause several pathologic problems that result in abortions,
If the dam is infected with Akabane virus around day infertility, and deformities in lambs. Sheep that are in-
30 or 31 of gestation (before the fetus develops immuno- fected with BD virus develop a short transitory viremia
competence at days 65 to 70), the fetus will develop neu- that apparently is self-limiting and then become immune
rologic damage. At day 30 the chorioallantoic membrane to reinfection. It is transmitted both vertically and hori-
is formed, as is the interdigitation of the fetal cotyledon zontally by the secretions of infected seronegative animals
with the maternal caruncle. The virus appears to spread that act as reservoirs in a flock.
rapidly to the fetus at this time. The most severe lesions Hydranencephalic lambs affected with BD are born
are found in a fetus that is infected during the early stages with normal-sized heads, fine fleece, and no obvious
of organogenesis after placental attachment and before tremors; some may have arthrogryposis. Grossly the cere-
the development of immunocompetence. During this bral hemispheres are composed of a thin, delicate mem-
time vulnerable cell populations are dividing rapidly, es- brane that is filled with fluid and attached to the
pecially in the central nervous system.10 The extent of meninges. The olfactory lobes, basal ganglia, hippocam-
fetal malformation determines whether the fetus can be pus, and mesencephalon may all be normal.13 The lesions
sustained in utero to term. The virus has a predilection to that occur in BD-infected fetuses with hydranencephaly
accumulate in neural tissue and skeletal muscle. Neonates result from necrosis and inflammation in ependyma.
tend to exhibit primarily nonsuppurative encephalo- Histopathologically, BD is associated with hypomyelina-
myelitis and polymyositis. Hydranencephaly results from tion, which is believed to result from the virus somehow
necrosis of the subventricular zones in the cerebrum that diverting glial cell precursors away from myelin-forming
prevent the outward migration of neuroblasts; the areas of oligodendroglial cells.13 BD also inhibits the thyroid
necrosis then quickly become filled with CSF. Because gland from producing thyroid hormone, which is neces-
sheep attain immunocompetence at day 70 of gestation, sary for proper myelin formation. Thyroidectomized fetal
they are often born without the virus. Arthrogryposis lambs have been experimentally demonstrated at parturi-
appears to be a consequence of a primary necrotizing tion to have hydranencephaly.14
polymyositis, with viral replication occurring in the my- Cache valley virus (CVV) causes outbreaks of lambs
otubule during the early stages of gestation and myofiber born with congenital arthrogryposis and hydrocephalus
development.9 or hydranencephaly throughout the United States. It is a
Bluetongue virus is a double-stranded RNA virus that bunyavirus and is spread by arthropods in a similar
is a member of the genus Orbivirus and family Reoviridae. manner to Akabane virus. Although the clinical signs ex-
Vaccination of pregnant ewes with modified live vaccines hibited by animals infected with CVV are similar to those
and natural infections during gestation are responsible for seen in BD and infection with BVDV, arthrogryposis is a
cerebral malformations, including hydranencephaly. An consistent feature of this disease that is rare in animals in-
arthropod vector, most notably Culicoides species, trans- fected with the other two types of viruses.15 The lesions
mits the virus. It is primarily endemic in tropical areas, observed both grossly and histologically are indistin-
where warm, moist climates prevail; however, it has been guishable from those caused by Akabane virus.
reported in the United States in association with vaccina- Sporadic reports implicate a variety of factors that can
tion using modified live virus.11 A variety of clinical signs result in hydranencephaly. Nutritional deficiencies of
can occur in infected sheep, but the discussion here is copper and thiamine produce hydranencephaly in fetuses.
confined to the deformities it produces in the fetus. In sheep and goats with PEM, thrombosis of the middle
The type of fetal deformity observed depends on the cerebral artery leads to infarction of a large portion of the
stage of gestation during which the ewe becomes in- cerebrum, which causes CSF to accumulate in the area of
fected. Fetal lambs that are between 55 to 60 days of ges- necrotic tissue.1 One report describes a concurrent in
tation do not have neurons or glial cells, only precursor utero infection of a fetal lamb with Toxoplasma gondii and
cells in the subependymal plates that begin to migrate to E. coli that resulted in hydranencephaly.16
314 • Sheep and Goat Medicine
TABLE 11-8

PLANTS ASSOCIATED WITH NEUROLOGIC DISEASES*

DISEASE PLANT SYMPTOMS

Paralysis Astragalus, Oxytropis—locoweed Emaciation, proprioceptive deficits, staggering,

paralysis
Delphinium—larkspur Rapid onset, nervous muscle twitching,
paralysis, death
Seizures or central Apocynum—Indian hemp Convulsions, weakness, coma
nervous system Asclepias—milkweed Convulsions, coma, death
stimulation Cicuta—water hemlock Rapid onset, extremely toxic, convulsions,
muscle spasms, grinding teeth, coma, death
Conium—poison hemlock Trembling, incoordination, respiratory paralysis
Corydalis—fitweed Rapid onset, ataxia, seizures, twitching facial
muscles, chewing movements
Delphinium—larkspur Excitability, staggering, vomiting, convulsions
Lupinus—lupines Nervousness, convulsions, coma
Central nervous system Aesculus—buckeye, horse Vomiting, ataxia, trembling, convulsions,
stimulation and depression chestnut hyperesthesia, excitement or depression
or mixed central nervous Datura—Jimson weed Ataxia, tremors, hallucinations, mydriasis,
effects tachycardia, tachypnea
Eupatorium—white snakeroot Trembling in the muzzle and legs after exercise,
weakness, difficulty breathing
Haplopappus—rayless goldenrod Depression, stiff gait, trembling, weakness,
recumbency, coma, death
Kalmia, Rhododendron—mountain Convulsions, vomiting, weakness, paralysis,
laurel, rhododendron, azaleas death
Leucothoe—fetterbush Incoordination, vomiting, weakness, spasm,
coma, death
Lupinus—lupines Nervousness, depression, twitching,
convulsions, death
Ricinus—castor bean Diarrhea, dullness, weakness, trembling,
incoordination
Solanaceae—ground cherry, Depression, mydriasis, bradycardia,
nightshade, horsenettle, soda apple incoordination
Veratrum—false hellebore Vomiting, arrhythmias, weakness, convulsions,
coma
Zigadenus—death camus Weakness, staggering, convulsions, coma,
excess salivation
Depression or weakness Halogeton Rapid and shallow breathing, coma
Helenium—sneezeweed, bitterweed Depression, weakness, chronic vomiting
Hymenoxys—rubberweed Depression, weakness, bloat, green nasal
discharge
Oxytenia—copperweed Depression, weakness, coma
Sarcobatus—greasewood Dullness, nasal discharge, drooling, weakness
Tetradymia—horsebrush Depression, weakness, swelling around head,
peeling skin

*Cyanogenetic plants such as Triglochin (arrowgrass) and Prunus (wild cherry), as well as plants that contain nitrates, may cause signs that mimic
neurologic deficits. Treatment of animals that have ingested any of these toxic plants should include oral charcoal (0.5 kg PO) and diazepam (0.25
to 0.5 mg/kg) to control seizures, maintenance of hydration status, and nutritional support.
 Chapter 11 Diseases of the Neurologic System • 315

Clinical signs. The clinical signs in animals with hy- 8. Charles JA: Akabane virus, Vet Clin North Am Food Anim Pract
drocephalus and hydranencephaly are similar and can vary 10:525, 1994.
depending on severity and whether the animal has bilat- 9. Parsonson IM, Della-Porta AJ, Snowdon WA: Akabane virus in-
eral or unilateral cerebral involvement. Neonates are often fection in the pregnant ewe. 2. Pathology of the fetus, Vet Micro
born dead or die shortly after birth. If they are born alive 6:209, 1981.
10. Kirkland PD et al: The development of Akabane virus–induced
and are unable to stand, the animals often succumb to sep-
congenital abnormalities in cattle, Vet Rec 122:582, 1988.
ticemia because of an inability to nurse. If they survive 11. Osborn BI, Silverstein AM: Hydranencephaly, porencephaly, cere-
more than a few months, they display poor growth charac- bral cyst, retinal dysplasia, CNS malformations, Am J Path 67:211,
teristics and have difficulty keeping up with the herd and 1972.
socializing. The mental status of the animals can range 12. Osborn BI: Bluetongue virus, Vet Clin North Am Food Anim Pract
from depressed to comatose, and the animals’ craniums 10:547, 1994.
may be grossly enlarged with open fontanelles. Motor dis- 13. Barlow RM: Morphogenesis of hydranencephaly and other in-
turbances include spastic paresis, strabismus, conscious tracranial malformations in progeny of pregnant ewes infected
proprioceptive deficits, ataxia, tremors, and blindness. with pestiviruses, J Comp Path 90:87, 1980.
Unilateral involvement of one cerebral hemisphere results 14. McIntosh GH: Foetal thyroidectomy and hydranencephaly in
in a head tilt, circling, and unilateral hyperreflexia. lambs, Aust Vet J 54:408, 1978.
15. Edwards JF et al: Ovine arthrogryposis and central nervous system
malformations associated with in utero cache valley virus infection:

R EFERENCES
1. de Lahunta A: Cranial nerve—lower motor neuron: general
spontaneous disease, Vet Path 26:33, 1989.
16. Woods LW, Anderson ML: Scoliosis and hydrocephalus in an
ovine fetus infected with Toxoplasma gondii, J Vet Diagn Invest
somatic efferent system, special visceral efferent system. In de 4:220, 1992.
Lahunta A, editor: Veterinary neuroanatomy and clinical neurology,
Philadelphia, 1983, WB Saunders.
2. Leipold HW, Dennis SM: Examination of the bovine nervous OTHER NEUROLOGIC
system, Vet Clin North Am Food Anim Pract 3:163, 1987.
3. Icenogle DA, Kaplan AM: A review of congenital neurologic mal- DISEASES
formations, Clin Pediatr 20:565, 1981. Neurologic diseases seen in small ruminants have many
4. George LW: Diseases of the nervous system. In Smith BP, editor: other causes. These include lidocaine toxicity (see
Large animal internal medicine, St Louis, 1996, Mosby.
Chapter 16), hypermagnesemia and hypocalcemia (see
5. Pritchard GC et al: Multiple cases of Dandy-Walker malforma-
tion in three sheep flocks, Vet Rec 135:163, 1994.
Chapter 2), hypovitaminosis A (see Chapter 12), and
6. James LF et al: Effect of natural toxins on reproduction, Vet Clin heat stress (see Chapter 6). Toxic plants also can cause
North Am Food Anim Pract 10:587, 1994. neurologic dysfunction. Some of these are listed in Table
7. Braund KG: Neurologic examination and diagnostic plan. In 11-8. Grasses associated with staggers or ataxia are de-
Oliver JE et al, editors: Veterinary neurology, Philadelphia, 1987, scribed in Table 11-9. Table 11-10 covers many of the in-
WB Saunders. herited storage diseases seen in sheep and goats.

TABLE 11-9

GRASS STAGGERS

PLANT TOXIN SIGNS CONTROL

Perennial ryegrass Fungus produces Trembling, stiff gait, hypermetria Remove from toxic pasture;
(Lolium perenne) tremorgenic toxin of limbs; worsens when excited; ammoniation of hay cut
animals collapse, struggle, and from affected pasture may
then recover reduce toxicity
Annual ryegrass Corynetoxin (?) Trembling, stiff gait, hypermetria Toxin concentrated in seed
(Lolium rigidum) of limbs; worsens when excited; head and during warm season;
animals collapse, stagger, and therefore mowing or burning
then recover reduces toxicity
Bermuda grass Alkaloid Tremors Mow
(Cynodon dactylon)
Dallas grass, Bahia Ergot (“honey rust” Head tremors, Toxin concentrates on seed head;
(Paspalum species) on seed head) muscle fasciculations, mow or burn pastures that have
ataxia seeded out
316 • Sheep and Goat Medicine
TABLE 11-10

INHERITED LYSOSOMAL STORAGE DISEASES OF SHEEP AND GOATS

DISEASE BREEDS INHERITANCE CLINICAL DIAGNOSIS

AFFECTED

b-Mannosidosis Nubians, Autosomal • Unable to stand • Reduced plasma

Nubian recessive • Carpal contraction b-mannosidase activity
crosses • Hindlimb extension • Abnormal oligosaccharides in
• Pastern hyperextension urine
• Intention tremors • Histopathology
• Nystagmus • Vacuolization of neurons and
• Deafness other cells
• Bilateral Horner’s syndrome • Demyelinization
• Domed head
• Thickened skin
GM1 Suffolks Autosomal • Normal at birth • Histopathology
gangliosidosis recessive • Ataxic at 4 to 6 months • Vacuolization
Generalized • Prostrate within 2 months • Marked distension of neuronal
glycogenosis cytoplasm, periportal
b-Galactosidase hepatocytes, and renal
deficiency epithelial cells
Globoid cell Polled Believed • Pelvic limb incoordination • Decreased brain
leukodystrophy Dorsets to be progressing to tetraplegia galactocerebrosidase activity
Krabbe’s disease autosomal destruction • Histopathology
Galactocerebrosidosis recessive • Myelin
• Loss of oligodendroglia
• Astrogliosis
• Accumulation of PAS*-
positive globoid cells

Modified from Kumar K et al: Caprine b-mannosidosis: phenotypic features, Vet Rec 118:325, 1986; Smith MC, Sherman DM: Nervous system. In
Smith MC, Sherman DM, editors: Goat medicine, Philadelphia, 1994, Lea & Febiger; Jolly RD: Lysosomal storage diseases in livestock, Vet Clin
North Am Food Anim Pract 9:41, 1993; George LW: Diseases of the nervous system. In Smith BP, editor: Large animal internal medicine, ed 2, St
Louis, 1996, Mosby; Murnane RD, Ahern-Rindell AJ, Prieur DJ: Ovine GM1 gangliosidosis, Small Rumin Res 6:109, 1991; Pritchard DH,
Napthine DV, Sinclair AJ: Globoid cell leukodystrophy in polled Dorset sheep, Vet Path 17:399, 1980.
*Periodic acid–Schiff reaction.
 Chapter 12

Diseases of the Eye

BRYAN M. WALDRIDGE AND CARMEN M.H. COLITZ

OCULAR ANATOMY layer and is attached near the optic foramen and the apex
Understanding the normal anatomy of the eye is impor- of the muscle cone at the exit of the optic nerve from
tant when attempting to identify abnormalities. Few phy- the orbit.3 The superficial muscular fascia lies within the
logenetic differences occur among species. Eyes have periorbita and encloses the lacrimal gland and the levator
largely retained the same basic components and embry- palpebrae superiors. The deep muscular fascia is more
ologic development over the course of evolution. Varia- fibrous than the other two fascial layers and originates at
tions are additive to the basic design and have occurred the superior and inferior palpebrae and from the limbus.
largely because of ecological factors such as light intensity It sheaths the extraocular muscles and optic nerve.3 The
and duration and feeding habits.1 Goats and sheep are ar- orbital fat fills the orbital dead space and provides a
rhythmic ruminants—they are equally active diurnally cushion that protects the globe and extraocular muscles.
and nocturnally.
Extraocular muscles. Seven extraocular muscles sus-
pend the globe and move the eye. The four rectus muscles
Adnexa include the dorsal, ventral, medial, and lateral recti; they
Orbit. Sheep and goats have an enclosed orbit, typical move the globe in the direction indicated by their names.
of most grazing animals. Both species have lacrimal, zy- The recti originate from the orbital apex. The dorsal
gomatic, frontal, sphenoid, and palatine bones compris- oblique originates from the medial orbital apex, passes
ing the bony fossa of the orbit. In addition, sheep have a anteriorly on the dorsomedial wall of the orbit, and is
maxillary bone and goats have an ethmoid bone that then deflected around the trochlea to insert on the dorso-
forms part of the orbit. The size, shape, and position of lateral aspect of the globe beneath the tendon of the
the orbit are closely associated with visual activity and dorsal rectus muscle.3 The trochlea is a cartilaginous
feeding behavior.1 In general, prey species such as sheep pulley that is attached to the anterior aspect of the medial
and goats have eyes that are located more laterally on the wall of the orbit.4 The dorsal oblique muscle rotates the
skull and have mostly monocular vision.1 Nerves and dorsal aspect of the globe medially and ventrally. The
blood vessels travel into the orbital region by the rostral ventral oblique muscle originates from a depression in the
alar, ethmoidal, lacrimal, orbital, ovale, optic, rotundum, ventromedial wall of the orbit, specifically the anterolat-
and supraorbital foramina or fissures. The pterygopala- eral margin of the palatine bone. It passes laterally
tine region has nerves and vessels associated with the beneath the globe, crossing the ventral rectus tendon
orbit as well, including the caudal palatine, maxillary, and before inserting on the ventrolateral aspect of the globe.1,3
sphenopalatine foramina. Glands of the infraorbital sinus The ventral oblique muscle moves the globe medially and
are present only in sheep and are better developed in rams dorsally. The retractor bulbi muscle originates from the
than in ewes. These are specialized cutaneous glands that orbital apex and inserts posterior to the equator beneath
produce pheromones; their secretions exit from the infra- the recti muscles, forming an almost complete cone
orbital sinus in a depression just rostral to the eye.2 around the optic nerve. The retractor bulbi muscle re-
tracts the globe for additional protection. The oculomo-
Orbital fascia and fat. The globe is surrounded by tor nerve (cranial nerve III) innervates the dorsal, ventral,
three fascial layers. The periorbita is the most external and medial recti. The dorsal oblique is innervated by the
• 317 •
318 • Sheep and Goat Medicine
trochlear nerve (cranial nerve IV), and the lateral rectus layer of the preocular tear film. The palpebral conjunctiva
and retractor bulbi muscles are innervated by the ab- continues onto the globe as the bulbar conjunctiva where
ducens nerve (cranial nerve VI). it meets and is continuous with the corneal epithelium.
The palpebral and bulbar conjunctivae meet at the fornix,
Eyelids and conjunctiva. The superior and inferior and this region is lined with stratified cuboidal epithe-
palpebrae (eyelids) are two musculofibrous folds of thin lium. The potential space created by the conjunctivae is
skin continuous with the facial skin. The superior eyelid the cul-de-sac. The palpebral, bulbar, and nictitans con-
is more mobile than the inferior eyelid. The opening junctivae are named based on their anatomic locations,
formed by the free edges of the eyelids is the palpebral but they are continuous. The vascular supply to the con-
fissure.1,3,4 Histologically, the eyelids have four tissue junctiva is from the anterior ciliary arteries (branches of
layers: the skin, the orbicularis oculi muscle, the tarsus the external ophthalmic artery).1 Ventromedially, the
and stromal layer, and the palpebral conjunctiva. The lacrimal caruncle is seen as a small mucosal elevation that
palpebral skin is thin and elastic and is covered by a dense may or may not be pigmented.
coat of short hairs with small tubular and sebaceous The nictitating membrane (third eyelid, nictitans) is
glands. The superior palpebrae have a row of cilia, and located ventromedially between the lacrimal caruncle and
vibrissae are present a short distance from the superior the globe. It is completely lined by conjunctiva and con-
and inferior palpebral margins in goats and sheep. The tains a T-shaped cartilaginous plate with a gland (gland of
arrectores ciliorum are bundles of smooth muscle fibers the nictitating membrane or nictitans) at its base. The
that extend from the eyelash follicles toward the tarsus horizontal part of the T lies at the free edge of the fold.
and are present in ruminants, but not in carnivores.1 The The gland of the nictitating membrane surrounds the
superior palpebral skin receives sensory innervation by stem of the cartilage. The anterior and posterior aspects of
the ophthalmic branch of the trigeminal nerve (cranial the nictitating membrane are lined with nonkeratinized
nerve V), and the inferior palpebral skin is innervated by stratified squamous epithelium. The nictitating mem-
the maxillary branch of the trigeminal nerve. The orbicu- brane moves passively over the eye in a dorsolateral direc-
laris oculi muscle encircles the entire palpebral fissure and tion when the globe is retracted by contraction of the re-
functions to close the palpebral fissure. It receives motor tractor oculi muscle and displacement of the orbital fat.1
innervation by the palpebral branch of the facial nerve
(cranial nerve VII). The superior eyelid is elevated by the
levator palpebrae superioris muscle, which receives motor
Lacrimal and Nasolacrimal Systems
innervation from the oculomotor nerve. The levator The lacrimal system consists of the lacrimal gland, the
palpebrae superioris originates at the orbital apex and gland of the third eyelid, the accessory glands of Krause
extends along the dorsal half of the mid-stroma. The and Wolfring, the glands of Zeis, the tarsal glands, and
sympathetically innervated Müller’s muscle complements the nasolacrimal duct system.1,3,4 The lacrimal gland lies
the function of the levator palpebrae superioris. Other in the dorsolateral wall of the orbit between the dorsolat-
muscles that are associated with eyelid function include eral wall of the orbit and the globe. Histologically, the
the corrugator supercilii muscle, which assists in elevating lacrimal gland of the sheep and goat is a compound tubu-
the superior eyelid, and the retractor anguli oculi muscle, loalveolar mixed gland.6,7 The lacrimal gland receives its
which lengthens the lateral palpebral fissure. Both of blood supply from the lacrimal artery. The lacrimal nerve
these muscles are innervated by the facial nerve. The sends sensory innervation to the gland, and the secretory
tarsus is a poorly developed narrow layer of dense collage- portion of the gland is sympathetically innervated by
nous connective tissue that separates the eyelid muscles postganglionic fibers from the cranial cervical ganglion.
from the palpebral conjunctiva. The tarsus is continuous Two large and four to five small excretory ducts originate
with the septum orbitale in both the superior and inferior from the central surface of the lacrimal gland in both
palpebrae. The septum orbitale is attached to the perios- sheep and goats.7 The lacrimal fluid drains into the dorsal
teum of the bony orbital rim.5 Near the margin of both fornix of the conjunctival sac and mixes with the secre-
eyelids are the tarsal gland openings. The tarsal glands are tions of the accessory glands.3 The glands of Zeis and the
sebaceous glands that produce the lipid component of the tarsal glands produce the outer lipid layer of the preocular
preocular tear film. These glands open onto the edge of tear film. The lacrimal gland, the gland of the third
both eyelids through small openings arranged longitudi- eyelid, and the accessory glands of Krause and Wolfring
nally. The tarsal glands are parasympathetically inner- produce the middle aqueous component of the preocular
vated by the oculomotor nerve.1 The palpebral conjunc- tear film. The inner mucin layer is produced by the con-
tiva is the mucous membrane that lines the inner aspect junctival goblet cells.1 The three layers of the preocular
of the eyelids. It consists of stratified columnar epithe- tear film are continuously spread across the eye’s surface
lium that becomes more stratified and squamous as it by the eyelids and nictitating membrane during blinking.
nears the eyelid margin. The stratified columnar epithelia Unlike cattle, sheep and goats have lysozyme, an antibac-
have numerous goblet cells that contribute to the mucus terial enzyme, in their tears.8 Excess preocular tear film
 Chapter 12 Diseases of the Eye • 319

pools in the lacrimal lake at the ventromedial angle of the and choroid. The inner nervous tunic includes the retina
eye. Mechanical pumping action draws the tear fluid into and optic nerve. The three tunics surround the aqueous
the superior and inferior puncta lacrimale (lacrimal humor, lens, and vitreous humor.
puncta). The puncta are located on the palpebral conjunc-
tiva, just inside the edge of the eyelid and medial to the
last tarsal gland.1 Smooth muscle in the puncta contract
Fibrous Tunic
during blinking to remove pooled tear fluid. The superior Cornea. The cornea is the transparent, avascular, and
and inferior lacrimal puncta continue as the superior and colorless anterior 20% of the fibrous tunic. It is composed
inferior canaliculi. The canaliculi coalesce at the naso- of dense collagenous connective tissue arranged in a
lacrimal sac located in the lacrimal fossa of the lacrimal regular lamellar pattern. This lamellar pattern, combined
bone.1 The lacrimal sac empties into the nasolacrimal with the physiologic pump of the posterior epithelium,
duct, which initially continues rostrally through the maintains the cornea’s transparency and deturgescence.
osseous lacrimal canal and the osseous lacrimal groove of The nonkeratinized anterior surface epithelium and the
the maxilla. It then parallels the mucous membrane of the small diameter of the collagen fibrils also contribute to
middle meatus and opens on the nasal mucous membrane the cornea’s transparency.9
at the junction of pigmented and nonpigmented skin.7 The cornea is the most powerful refractive surface of
the eye. In sheep and goats the shape of the cornea is el-
liptical, with its horizontal diameter greater than its verti-
Vascular Supply of the Eye cal diameter. In sheep the average width of the cornea is
In domestic mammals the majority of the ocular and 22.4 mm and the average height is 15.4 mm.1 The sheep
adnexal vascular supply is from the external ophthalmic cornea is thickest at its center (0.8 to 2.0 mm) and
artery, a branch of the maxillary artery. The arteries sup- thinnest at its edge (0.3 to 0.5 mm).1 The cornea is inner-
plying the globe originate from the external ophthalmic vated by the long ciliary nerves, which derive from the
and the malar artery, a smaller branch of the maxillary ophthalmic branch of the trigeminal nerve.
artery. The nasal and lateral long posterior ciliary arteries In domestic animals the cornea has four layers. The
(LPCAs) branch off of the external ophthalmic arteries. anterior, nonkeratinized, stratified, squamous epithelium
The lateral and nasal LPCAs branch to the choroid and (epithelium corneae) covers the outermost corneal surface
ciliary processes; in the periphery, each LPCA divides and is continuous with the conjunctival epithelium. The
again into dorsal and ventral branches that form the most posterior layer of the anterior epithelium consists of
major arterial circle of the iris. The LPCAs give off the a monolayer of columnar basal cells that lie on a thin
short posterior ciliary arteries (SPCAs). The SPCAs pen- basement membrane. The basement membrane of the
etrate the globe adjacent to the optic nerve to supply the anterior epithelium is made up of primarily types IV, VI,
inner layers of the retina and then ramify into the and VII collagen.1 Anterior to the basal layer are numer-
choroidal vasculature. The SPCAs also branch to the peri- ous layers of polyhedral or wing cells, and anterior to
limbal region and the anterior ciliary body. The smaller these are numerous layers of nonkeratinized squamous
internal ophthalmic artery supplies the optic nerve and epithelial cells. Hemidesmosomes, arranged in a linear
anastomoses with the external ophthalmic artery or one manner, attach the basal cells to the basal lamina of the
of its branches.1 The external ophthalmic artery then basement membrane (lamina limitans).1,4 The stroma
gives off two muscular branches: the ventral and the (substantia propria) forms the bulk of the cornea (90%).
dorsal branches. These branches supply the extraorbital The stroma is composed of extracellular matrix and a
muscles, the gland of the nictitating membrane, the lamellar arrangement of collagen fibrils oriented in paral-
lacrimal gland, and the levator palpebrae superiors. lel lamellae positioned at oblique angles to each other and
separated by less than a wavelength of light.10 Interwoven
between the collagen fibrils and extracellular matrix are
Globe keratocytes. Keratocytes possess cellular extensions that
The globe (bulbus oculi) is nearly spherical in shape. The help maintain the stromal lamellae. After a deep corneal
average anterior to posterior axis of the sheep globe is injury, keratocytes can differentiate into fibroblasts and
26.85 mm; that of the goat globe has not been reported. contribute to scar formation.1 Descemet’s membrane
The globe is composed of three tunics or coats: the (lamina elastica), located on the posterior aspect of the
fibrous, vascular, and nervous tunics. The external fibrous cornea, is homogeneous and acellular and functions as a
tunic is made up of dense collagenous connective tissue protective boundary within the cornea. It is produced
that resists the eye’s internal pressure and gives the globe throughout life by the corneal endothelium and is made
its round shape. The fibrous tunic is composed of the up of types I, III, IV, V, VI, and VIII collagen. Descemet’s
cornea and sclera, which coalesce at the corneoscleral membrane terminates at the apex of the trabecular mesh-
junction or limbus. The middle vascular tunic is com- work in the area of the limbus.1 The endothelium is a
prised of the uvea, which includes the iris, ciliary body, monolayer of flattened polygonal cells lining the most
320 • Sheep and Goat Medicine
posterior aspect of the cornea. In the adult the endothe- basic ways. The collagen fibrils of the sclera are irregularly
lium rarely undergoes mitosis and has an age-dependent arranged. The scleral epithelium is thicker than the
loss of endothelial cells. corneal epithelium. It has small basal cells with scanty cy-
toplasm.1 Scleral thickness at the entry point of the optic
Lens. The lens further focuses light entering the eye nerve in the sheep is 1.0 to 1.2 mm. It thins at the equator
to allow for sharp focus of visualized images. The lens is to 0.25 to 0.30 mm and thickens at the corneoscleral
a transparent, biconvex, almost spherical structure that is junction to 0.4 to 0.5 mm.1
located posterior to the iris and anterior to the vitreous.
It is held in position by the zonular ligaments (zonula
ciliaris) that arise from the ciliary epithelium and are
Vascular Tunic (Tunica Vasculosa Oculi)
composed of fibrillin.11 Other structures that support The vascular tunic is comprised of the iris, ciliary body,
the lens include the patellar fossa of the vitreous and the and choroid. These structures are highly vascularized and
iris. Herbivorous animals have a marginally functional usually pigmented.
accommodative mechanism and therefore have poor
near vision. Iris. The iris is the smallest component of the uvea. It is
The lens is transparent and avascular and receives the a muscular diaphragm suspended between the cornea and
majority of its nutrients from the aqueous humor. The the lens. It is attached to the sclera at its periphery by the
lens grows throughout life at a slow, regulated rate pectinate ligaments and to the ciliary body. The iris
because of continued division and differentiation of the divides the space between the cornea and the lens into the
lens epithelial cells into lens fiber cells. The average diam- anterior and posterior chambers of the anterior segment.
eter of the sheep lens is between 14.5 to 15.53 mm; it Its central aspect has an aperture, the pupil (pupillae),
weighs approximately 2.3 g.1 that changes in size to adjust the amount of light entering
The lens is enveloped in a basement membrane of pri- the eye and reaching the retina. The muscles that regu-
marily type IV collagen. The anterior lens capsule is sig- late pupil size are the sphincter pupillae and the dilator
nificantly thicker than the posterior lens capsule and pupillae. The sphincter muscle lies concentrically near
thickens with age. The lens capsule is produced by the the pupillary margin and the dilator muscle has fibers
lens epithelial cells, which are only present on the ante- arranged radially from the sphincter to the ciliary border.
rior aspect of the lens. The lens epithelial cell population The pupil is oval in a horizontal plane in sheep and goats
is made up of three regions. The most central cells are and has several round, variably sized black masses at the
squamous in appearance and rarely undergo mitosis. The superior and inferior aspects of the pupillary border called
cells in the germinative region, which encircles the granula iridica. The granula iridica are extensions of the
central epithelium, are more cuboidal in appearance and posterior pigmented epithelium of the iris. They enhance
undergo mitosis at a slow rate. The lens epithelial cells in the effect of pupillary constriction or miosis. In goats the
the equatorial region elongate into lens fiber cells, lose myocytes of the sphincter muscle are occasionally found
their nuclei by a process called denucleation, and attach in the basal portion of the granula iridica.1
at the anterior and posterior lens sutures. The fiber cells The iris is grossly divided into two regions divided by
are continually being formed—the newest fiber cells are the collarette. The central region is the pupillary zone,
located peripherally and the oldest become the most cen- and the peripheral region is the ciliary zone. The periph-
tralized and compressed lens fibers. Nearly 80% of eral half of the ciliary zone contains a circumferential
glucose metabolism in the lens occurs primarily by gly- artery, the annular major arterial circle. The major arterial
colysis. The tricarboxylic cycle accounts for 5%, the circle is an incomplete circle that originates from the
pentose monophosphate shunt accounts for 15%, and the dorsal and ventral branches of the medial and lateral
sorbitol pathway accounts for a negligible portion of LPCAs. The major arterial circle branches into radial ar-
glucose metabolism. teries that nourish the rest of the iris. Radial vessels
provide venous drainage for the iris. They empty directly
Vitreous. The vitreous also refracts light that enters into the anterior choroidal circulation.
the eye and passes through the lens to focus light on The three cellular layers of the iris are the anterior
the retina. The vitreous is gel-like and lies posterior border layer, the middle stroma (which contains the
to the lens and anterior to the retina. The vitreous is 98% sphincter muscle), and the posterior epithelial layers.
water that is suspended in collagen fibers and gly- The anterior border layer consists of fibroblasts and
cosaminoglycan matrix. The vitreous body physically melanocytes, and their processes form an incomplete
holds the retina against the choroid. No continuous layer across the surface of the iris. No continuous layer of
turnover of the vitreous occurs. epithelium extends across the iris’s anterior surface.1 The
iris stroma is loosely arranged and consists of fibroblasts,
Sclera. The sclera comprises the posterior 80% of the fine collagenous fibers, chromatophores, and melano-
fibrous tunic. The sclera differs from the cornea in three cytes. Iris color depends on the density of the pigmenta-
 Chapter 12 Diseases of the Eye • 321

tion in the stroma. The iris sphincter muscle of sheep and becular meshwork and the uveal trabecular meshwork
goats is probably very similar to that of the horse, another form a delineated angular aqueous plexus.13 The ciliary
ungulate with an oval pupil in a horizontal direction. In cleft and pectinate ligaments are smaller in sheep and
the horse the iris sphincter lies in the main portion of the goats than in cattle and horses because of their smaller
central stroma and is covered by the granula iridica.1 It is globe size. Aqueous humor can take two pathways to exit
parasympathetically innervated. The iris dilator muscle is the eye: the conventional and the unconventional outflow
located in the posterior aspect of the iris stroma. It is in- pathway. The majority of aqueous humor exits the eye in
nervated by sympathetic fibers and is continuous with the most species by the conventional pathway. Specifically,
pigmented epithelium of the ciliary body. The posterior following its production by the ciliary body, aqueous
pigmented epithelium of the iris is continuous with the humor passes into the posterior chamber, through the
nonpigmented epithelium of the ciliary body. Both the pupil, into the anterior chamber, between the pectinate
iris dilator muscle and the posterior pigmented epithe- ligaments, through the trabecular meshwork, into the
lium form the granula iridica in herbivores. The size of scleral venous plexus, and then the systemic circulation.
the dilator muscle in the sheep and goat is probably Aqueous humor can also exit the eye by a number of an-
similar to that of the horse.1 cillary pathways. It can drain anteriorly within the iridal
stroma and across the cornea, it can flow posteriorly into
Ciliary body (corpus ciliare). The ciliary body is the the vitreous humor, or it can flow exteroposteriorly along
middle portion of the uvea that joins the choroid (poste- a supraciliary-suprachoroidal space into the adjacent
rior uvea) to the peripheral iris (anterior uvea). It consists sclera.1 The uveoscleral (unconventional) pathway is the
of two sections: the anterior pars plicata (corona ciliaris) most prominent of the ancillary routes of aqueous
and the posterior pars plana. The pars plicata consists of drainage. Aqueous humor is absorbed from the ciliary
radial folds called ciliary processes that are “thick and club- cleft into the anterior face of the ciliary body and diffuses
like with shallow valleys in herbivores.”12 The ciliary into the sclera and the systemic venous circulation. The
processes connect the zonular fibers to the lens equator percentage of outflow by the uveoscleral pathway has
that holds the lens in place. In ungulates the processes been determined for many species but not for cattle,
have numerous arterioles and veins within the processes’ sheep, or goats. This outflow pathway is thought to be the
core. The ciliary processes also have well-developed capil- major aqueous outflow pathway in the horse and may be a
lary beds that produce the majority of the aqueous major pathway in other ungulates.
humor.1 The pars plana is the flat portion of the ciliary
body that terminates in the pars ciliaris retinae, the junc- Choroid (choroidea). The choroid is a dense network
tion of the ciliary body and the retina. The pars plana of blood vessels and pigmented stroma between the retina
varies in width because the retina extends more anteriorly and the sclera. The choroid supplies nutrition to the pos-
medially and inferiorly in most species. Aside from the terior layers of the retina. The total choroidal blood
ciliary processes the ciliary muscles comprise the majority supply far exceeds the need for retinal nutrition and it
of the ciliary body. The ciliary musculature is composed may also serve as a heat exchange mechanism to prevent
of meridional smooth muscle fibers coursing close to the the retina from overheating. Morphologically the choroid
sclera. This musculature is poorly developed in ungulates, can be divided into four layers: suprachoroidea, large-
accounting for their poor accommodative ability. Evolu- vessel layer, medium-sized vessel and tapetum layer, and
tion has allowed herbivores to develop large corneas, hor- choriocapillaris. The suprachoroidea is the potential
izontally oval-shaped pupils, and large anterior chambers space between the choroidal stroma and is attached
for better night vision and good motion detection. loosely to the sclera by the lamina fusca. The LPCAs and
However, these evolutionary changes also have led to the nerves travel in the suprachoroidea along the horizontal
loss of ciliary musculature development. meridian. The large-vessel layer (lamina vasculosa) is the
posterior stromal layer. It has large cavernous vessels, pri-
Iridocorneal angle. The iridocorneal angle (ICA) is marily veins, that drain the choriocapillaris and some
the most anterior aspect of the ciliary body. The most an- branches of the SPCA. The medium-sized vessel and ta-
terior region of the ICA is the termination of Descemet’s petum layer is the anterior stromal layer of the choroid. It
membrane.13 The ICA is bordered by the limbus, the has smaller vessels connecting the choriocapillaris to the
base of the iris, and the ciliary cleft. The ciliary cleft is a large-vessel layer. Within this inner stromal layer lies the
triangular region that is the posterolateral extension of tapetum. In ungulates the tapetum is fibrous (tapetum fi-
the anterior chamber into the ciliary body. Pectinate liga- brosum) and composed of regularly arranged collagen
ments are present in the ciliary cleft from the pigmented fibers and occasional fibrocytes. Herbivores are born with
limbus to the root of the iris.1 The ICA and ciliary mus- mature eyes and well-developed tapeta. Sheep have
culature of sheep and goats are similar to those of cattle. several hundred layers of well-arranged collagen lamel-
The outflow tract has a large ciliary cleft with prominent lae.14 Capillaries penetrate the tapetum at right angles to
spaces of Fontana. The large, semi-oval corneoscleral tra- the collagen lamellae, connecting the choriocapillaris to
322 • Sheep and Goat Medicine
the medium-sized vessels; when visualized end-on, they
are referred to as the “stars of Winslow.”1 The choriocap-
illaris is the single layer of capillaries between the
choroidal stroma and the retinal pigmented epithelium
(RPE). These capillaries are fenestrated, and external to
their endothelium they have a basement membrane that
forms the outermost layer of Bruch’s membrane separat-
ing the choroid from the RPE.

Neural Tunic
The neural tunic includes the retina and optic nerve,
both derivatives of the forebrain. The retina and optic
nerve are the only portions of the brain that can be seen
on a physical examination and can provide clinical infor-
mation about an animal’s physical status. The retinal vas-
culature, derivatives of the SPCAs, provides the inner
layers of the retina with the majority of its nutrients. The
choriocapillaris provides the outer layers of the retina
with nutrients, and the vitreous plays a minor role in pro-
Figure 12-1 Normal fundus of a sheep.
viding nutrition to the inner layers of the retina. The
retinal metabolic rate is one of the highest in the body,
and therefore if either the retinal or choroidal vasculature
is even marginally compromised, the retina can become visual streaks—a horizontal streak and a vertical streak.15
ischemic.1 The rod-to-cone ratio for sheep is 301 to 401.16 No
The retina has 10 layers, the outermost of which is the rod-to-cone ratio has been reported in goats. Both sheep
RPE; the inner nine layers are known as the sensory and goats have two types of cones, allowing these animals
retina. The five layers of clinical importance (from poste- dichromatic color vision.17
rior to anterior) are as follows: The RPE is a single layer of cells between the sensory
retina and the choriocapillaris. It is nonpigmented in the
1. RPE
dorsal half of the fundus, allowing the tapetum exposure
2. The photoreceptors
to light. The primary functions of the RPE are metabo-
3. The inner nuclear layer (nuclei of the bipolar cells)
lism of retinol for phototransduction and phagocytosis of
4. The ganglion cell layer
waste products from the sensory retina. The RPE has
5. The nerve fiber layer (axons of the ganglion cells)
tight interepithelial junctions that form part of the blood-
The photoreceptors include the rods and cones. Rods retinal barrier.
function in dim-light vision. Cones function in bright Sheep and goat retinae have a holangiotic vascular
light and play roles in color recognition and visual acuity. pattern. The term holangiotic means that all quadrants of
Photoreceptors are composed of inner and outer seg- the retina are vascularized with vessels extending from
ments. The outer segments have rhodopsin embedded in the optic nerve to the periphery. Sheep retinae have three
their membranes. Bipolar cells synapse with photorecep- or four major venules and numerous branching arterioles.
tors on one side and with ganglion cells on the opposite Occasionally the superior arteriole and venule wrap
side. They transfer the electrical potential generated by around each other. Goat retinae have five to eight
the photoreceptors to the ganglion cells. The ganglion primary venules.
cells are the innermost cell layer of the retina. Projecting The tapetal fundus is triangular, can be yellow to
axons run parallel to the retinal surface in the innermost bluish-purple, and is stippled with the stars of Winslow.
nerve fiber layer and converge at the optic disc. These The dorsomedial tapetal fundus has more pigment than
axons turn posteriorly to form the optic nerve (cranial the other sections. The nontapetal fundus is pigmented
nerve II). Optic nerve fibers exit the eye through the because the RPE contains pigment and is located ventral
lamina cribrosa. The density of the ganglion cells has to the tapetal fundus. The tapetal-nontapetal junction
been determined in the area centralis and visual streak of separates the two fundi. In sheep the optic nerve is located
goats. The area centralis is the area of maximal cone within the nontapetal fundus just ventral to this junction.
density and the visual streak is the area of maximal gan- Sheep have a kidney bean–shaped optic disc and goats
glion cell density. The central retina of sheep is similar to have a rounder optic disc that is often located within the
that of other mammals with an area centralis and a single tapetal fundus (Figure 12-1). Goats also have a pigmented
visual streak. Goats have an area centralis and also two ring that surrounds the optic disc (Figure 12-2).18
 Chapter 12 Diseases of the Eye • 323

6. Gargiulo AM et al: Ultrastructural study of sheep lacrimal glands,

Vet Res 30(4):345, 1999.
7. Sinha RD, Calhoun ML: A gross, histologic, and histochemical
study of the lacrimal apparatus of sheep and goats, Am J Vet Res
27(121):1633, 1966.
8. Brightman AH, Wachsstock RS, Erskine R: Lysozyme concentra-
tions in the tears of cattle, goats and sheep, Am J Vet Res 52(1):9,
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9. Whitley RD, Gilger BC: Diseases of the canine cornea and sclera.
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10. Maurice DM: The structure and transparency of the cornea, J
Physiol 136:263, 1957.
11. Mir S et al: A comparative histologic study of the fibrillin microfib-
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12. Duke-Elder S: The eyes of mammals in the eye of evolution, St Louis,
1958, Mosby.
13. Samuelson DA: A reevaluation of the comparative anatomy of the
eutherian iridocorneal angle and associated ciliary body muscula-
ture, Vet Comp Ophthalmol 6(3):153, 1996.
Figure 12-2 Normal fundus of a goat. 14. Bellairs R, Harkness LR, Harkness RD: The structure of the
tapetum of the eye of the sheep, Cell Tissue Res 157(1):73, 1975.
15. Gonzalez-Soriano J et al: A quantitative study of ganglion cells in
the goat retina, Anat Histol Embryol 26(1):39, 1997.
The optic nerve is composed of the axons of the retinal 16. Braekevelt CR: Retinal photoreceptor fine structure in the domes-
ganglion cells. The optic nerve is located ventrolateral to tic sheep, Acta Anat 116(3):265, 1983.
the posterior pole of the globe. It is myelinated in all 17. Jacobs GH, Deegan II JF, Neitz J: Photopigment basis for dichro-
species; in sheep and goats the myelin is maintained as matic color vision in cows, goats, and sheep, Vis Neurosci 15(3):581,
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the fibers enter the globe through the lamina cribrosa.
18. Whittaker CJG, Gelatt KN, Wilkie DA: Food animal ophthal-
The optic nerve has a small dark central depression called mology. In Gelatt KN, editor: Veterinary ophthalmology, ed 3,
the physiologic cup or pit. The orbital portion of the optic Philadelphia, 1999, Williams & Wilkins.
nerve is enveloped in the thick dura mater and fuses ante-
riorly with the sclera. Internal to the dura mater is the
arachnoid sheath, and within this layer is the pia mater.
Herbivores, including sheep and goats, exhibit more than
OPHTHALMIC EXAMINATION
80% decussation at the optic chiasm to form the optic A thorough ophthalmic history should include a descrip-
tracts. Each optic tract is composed of pupillary and tion of signalment, type of environment in which the
visual fibers. The pupillary fibers travel to the pretectal animal is housed, present and previous diet, ophthalmic
nucleus to control the pupillary light reflex (PLR), complaint, vaccination status, previous medical therapy,
whereas the visual fibers travel to the lateral geniculate and concurrent medical problems. Ophthalmic changes
nucleus and then to the visual cortex for visual perception. can be clues to an animal’s physical status, and therefore
questions concerning the animal’s ophthalmic problems

R EFERENCES
1. Samuelson DA: Ophthalmic anatomy. In Gelatt KN, editor: Vet-
should be accompanied by inquiries into the animal’s
physical condition. The examiner should avoid asking
questions that may lead the owner to over-interpret the
erinary ophthalmology, ed 3, Philadelphia, 1999, Williams & clinical signs they have observed.
Wilkins. After taking the history, the examiner should observe
2. Shively MJ: Integumentary. In Shively MJ, editor: Veterinary the animal’s movements in a small area before beginning
anatomy, College Station, TX, 1984, Texas A & M University the ophthalmic examination. The animal should be en-
Press. couraged to maneuver around obstacles in bright and dim
3. Dyce KM, Sack WO, Wensing CJG: The sense organs. In Dyce
light. Because sheep and goats have laterally placed eyes,
KM, Sack WO, Wensing CJG, editors: Textbook of veterinary
anatomy, ed 2, Philadelphia, 1996, WB Saunders.
unilateral blindness is less likely to be compensated for by
4. Sisson S, Grossman JD: The sense organs and common integu- the contralateral eye. An animal often turns its head in an
ment. In Grossman JD, editor: The anatomy of domestic animals, ed attempt to see in front of it when visual acuity is compro-
4, Philadelphia, 1953, WB Saunders. mised on one side. If the examiner still harbors doubts
5. Martin CL, Anderson BG: Ocular anatomy. In Gelatt KN, editor: concerning vision, he or she can cover each eye individu-
Veterinary ophthalmology, Philadelphia, 1981, Lea and Febiger. ally for better assessment.
324 • Sheep and Goat Medicine
The ophthalmic examination can be performed under by first applying topical anesthetic (0.5% proparacaine) to
manual restraint in sheep while they are seated on their the globe and puncta. The distal blunt end of the cannula
rumps; goats can stand for the examination. Before is inserted into the superior puncta, and saline solution is
touching the head, the examiner should assess the eyes injected until fluid is seen to exit the inferior puncta. The
for symmetry in size and position, note the presence of cannula is then inserted into the inferior puncta and
abnormal ocular discharge, observe the eyelids as they saline solution is gently injected until fluid is seen exiting
pass over the ocular surface, and record any rubbing, the distal naris.
blepharospasm, or other abnormalities. The menace test The conjunctiva should not be hyperemic, thickened,
can be used to evaluate the optic nerve (cranial nerve II) or edematous (chemosis). Examination for hemorrhage,
and facial nerve (cranial nerve VII) for presence of vision foreign bodies (especially beneath the nictitating mem-
and ability to blink, respectively. If the palpebral fissures brane), and lymphoid follicle hyperplasia should be per-
do not close completely, a palpebral reflex test should be formed. Samples from the conjunctiva for culture and
performed by touching the skin around the eye. This test sensitivity, cytology, immunofluorescent antibody (IFA),
assesses the trigeminal nerve (cranial nerves V) and facial and biopsy can be obtained in physically restrained
nerve (cranial nerve VII). Both pupils should be assessed animals after the application of topical anesthetic so-
for size, shape, and symmetry under both light and dark lution. Fluorescein dye should not be applied before
conditions without direct stimulation. Shining a focal sample collection for IFA because it may result in a false
bright light source into one eye allows assessment of the positive result.1
PLR. After the response from the stimulated eye is ob- The cornea is examined with a focal light source for
served, the contralateral eye should be quickly evaluated clarity. A bluish hue is indicative of edema, white opaci-
for the consensual pupillary response. The consensual ties may indicate scarring, a yellow-white color is often
pupillary response is slower and more incomplete com- associated with white blood cell infiltrate, and red is con-
pared with the stimulated eye because of unequal cross- sistent with neovascularization (this condition is generally
over of the optic nerve fibers at the optic chiasm. The more prominent at the limbus). Corneal edema can result
PLR is a subcortical response that requires normal func- from injury to the superficial corneal epithelium or
tion of the retina, optic nerve (cranial nerve II), midbrain, corneal endothelium. Corneal ulcers result in focal cor-
oculomotor nerve (cranial nerve III), and iris sphincter neal edema and positive uptake of fluorescein dye. Flu-
muscle. Cortically blind animals can have a normal PLR. orescein is a hydrophilic dye that binds exposed corneal
The dazzle response assesses the visual pathway between stroma, but not epithelium or Descemet’s membrane. The
the optic nerve and the midbrain. A very bright light slit beam on a direct ophthalmoscope can be used to
source directed toward the eye usually causes a bilateral assess the depth of a corneal ulcer by how deeply the beam
blink or turning of the head away from the light stimulus. is projected on the ulcer. If the ulcer is deep and fluores-
This is a subcortical response that reaches the rostral col- cein dye uptake is not evident, a descemetocele is likely. A
liculus and also stimulates the facial nucleus to cause the perforated corneal ulcer may have aqueous humor drain-
blink reflex. ing from the perforation or the iris; fibrin may occlude the
Abnormalities of the orbit can be assessed by palpation perforation. These ulcers should not be manipulated and
of the bones of the orbital rim for fractures and asymme- minimal diagnostics should be performed because surgi-
try or by skull radiography. Difficulty in retropulsing the cal intervention is the treatment of choice.
globe (with the eyelids closed) may indicate a retrobulbar The anterior chamber is evaluated for clarity and
space-occupying mass or other orbital disease. Difficulty depth. Damage to the blood-aqueous barrier allows
or pain on opening of the mouth may indicate inflamma- protein and cells into the aqueous humor, creating turbid-
tory orbital disease. Retrobulbar neoplasia usually does ity or the Tyndall effect (aqueous flare). The slit beam or
not cause pain on opening of the mouth. The involved the smallest circle on a direct ophthalmoscope can be
orbit or globe should always be compared with the con- used to identify aqueous flare. The beam of light is
tralateral side. The eyelids should be evaluated for entro- focused directly on the cornea and then observed at 90° to
pion or ectropion, complete closure of the palpebral fis- the direction of the beam as it passes through the anterior
sures, increased wetness or ocular discharge on the hair chamber. There should be no evidence of light absorption
adjacent to the eyelid margins, and distichiasis or trichia- within the anterior chamber. Aqueous flare is seen when
sis. The patency of the nasolacrimal apparatus can be as- protein and cells absorb light and the light beam is re-
sessed by determining whether fluorescein dye passes flected in the aqueous humor. Iris bombé and intumes-
from the lacrimal lake to the nares after it is placed on the cent cataracts can cause the anterior chamber depth to
globe and flushed with saline solution. If fluorescein dye appear decreased, and hypermature cataracts can cause
is not evident at one or both nares, the examiner can use a the anterior chamber depth to appear increased.2
22- or 23-gauge cannula attached to a 6-ml syringe filled The iris is examined for abnormal shape (dyscoria),
with sterile saline solution to flush the nasolacrimal ducts color, thickness, miosis, or mydriasis inconsistent with
in an orthograde direction. This procedure is performed the level of ambient light. Dyscoria can result from lens
 Chapter 12 Diseases of the Eye • 325

luxation or subluxation, synechia (adhesions), or a mass is inverted and reversed. The advantages of using indirect
caudal to or within the iris. Pupil size should be examined ophthalmoscopy include a larger field of view (approxi-
in bright and dim light, and the examiner should deter- mately 40% of the entire fundus depending on the
mine direct and consensual PLRs. The color and thick- strength of the lens), which allows the peripheral fundus
ness of the iris should be compared with the contralateral to be examined more completely, and stereopsis (use of
side; increased iridal thickness may be obvious in cases of both of the examiner’s eyes). Disadvantages include the
cellular infiltrate and anterior uveitis. The granula iridica need for a relatively dilated pupil. Examination in a dark-
should be examined for size and symmetry because severe ened room and use of a dimmed light source and a 28-
acute or chronic uveitis can cause them to atrophy. diopter lens often allow fundic evaluation without dila-
Intraocular pressure (IOP) in most species is between tion in herbivores through their horizontally oval pupils.
15 and 25 mm Hg. The average IOP in sheep and goats Another limitation of indirect ophthalmoscopy is that it
has not been established but is likely similar to that of requires practice for the examiner to become proficient
other species. IOP can be measured in small ruminants with the technique. When examining the fundus by indi-
using a Schiotz tonometer or a TonoPen. The footplate of rect ophthalmoscopy, the examiner should move his or
the Schiotz is curved for use on human corneas and is her head in the direction that is to be visualized within
probably not accurate in sheep or goats. Applanation the fundus. The examiner should have a pattern for ex-
tonometers such as the TonoPen are more accurate than amining the fundus beginning with the optic nerve, di-
indentation tonometers and are easier to use in domestic viding the fundus into quadrants, and examining each
animals because the head does not have to be in a nose- one by evaluating the vessels and color of the tapetal and
up position, the footplate is only 3.22 mm in diameter, nontapetal fundi.
the footplate is not curved, and the reading does not have
to be converted.2 After administering topical anesthesia,
the examiner gently taps the cornea with the TonoPen.
Auriculopalpebral Nerve Block
The instrument takes a number of readings and then pro- The auriculopalpebral nerve is a branch of the facial nerve
vides the average of those readings in mm Hg. A high and provides motor function to the eyelids. Local anes-
reading is consistent with glaucoma. Excessive neck re- thesia of the auriculopalpebral nerve combined with
straint should be avoided during the use of either instru- topical anesthesia (0.5% proparacaine) facilitates removal
ment because this elevates the IOP. of foreign bodies and subconjunctival injections. The au-
The lens, vitreous, and fundus are best evaluated riculopalpebral nerve can be palpated along the zygomatic
through a dilated pupil. The pupil can be dilated with a arch near the base of the ear. Using a 25-gauge, 5⁄8-inch
short-acting topical parasympatholytic such as 1% tropi- needle, the examiner injects 1 to 2 ml of local anesthetic
camide.Time to effect for tropicamide is 10 to 20 minutes, perineurally to produce akinesia of the eyelids.3
and the effect lasts between 4 and 8 hours.2 The lens
should be evaluated for position and clarity. Nuclear scle- SPECIALIZED DIAGNOSTIC
rosis is an aging change that does not preclude evaluation
of the fundus but must be differentiated from cataracts. TESTS
The fundic examination can be performed by either
direct or indirect ophthalmoscopy. Direct ophthalmos- Corneal and Conjunctival Scrape
copy is performed at a distance of 2 to 3 cm from the Conjunctival scrapings for cytologic examination and
patient’s eye. The large circle is used when the pupil is aerobic bacterial culture are valuable for the diagnosis of
dilated, and the smaller circles are used when the pupil is infectious keratoconjunctivitis. Collection of samples for
not dilated. The instrument is set at either 0 or the red 2 culture should be performed before other diagnostic pro-
to begin the examination. The numbers are sequentially cedures. Sterile swabs should be moistened with sterile
changed to bring a lesion into focus depending on its lo- saline or transport media before application. The palpe-
cation. The disadvantages of direct ophthalmoscopy bral margins should not be scraped to reduce the possibil-
include the small field of view (approximately 2% of the ity of contamination. Anaerobic bacteria and fungi are
entire fundus) and difficulty in examining the peripheral rare ocular pathogens in sheep and goats.4 Fungal cul-
fundus. The advantages of direct ophthalmoscopy include tures are best obtained using a sterile, blunt instrument
greater magnification and the ability to alter the dioptric such as a Kimura spatula or the flat handle end of a
strength of the ophthalmoscope.2 scalpel blade. The culture sample should be placed di-
Indirect ophthalmoscopy requires a focal light source rectly onto fungal culture media.4
to be held adjacent to one of the examiner’s eyes and an The cornea and conjunctiva should be anesthetized
indirect lens (held at arm’s length) positioned 2 to 4 cm in with topical 0.5% proparacaine before the procedure is
front of the patient’s eye after the tapetal reflex has been performed, and a palpebral nerve block may be beneficial.
identified. A relatively inexpensive ophthalmic indirect If conjunctival follicles are present, these areas should be
lens ($50 to $75) is effective. The image seen is virtual but avoided to obtain a more representative sample. The
326 • Sheep and Goat Medicine
sample should be very gently rolled or smeared onto a
slide before staining with Diff-Quick or Wright’s or
Gram’s stains.4-6 Viral, mycoplasmal, or chlamydial or-
ganisms are poorly identified by Gram’s staining.4 Healthy
conjunctiva is characterized cytologically by numerous
epithelial cells, occasional lymphocytes, and rare neu-
trophils. Melanin granules may be observed in dark-faced
breeds and can be mistaken for bacteria. Goblet cells are
more common in animals with acute keratoconjunctivitis
but also are present in unaffected animals. In acute kera-
toconjunctivitis, neutrophils become more numerous and
plasma cells may be observed. Small numbers of eosino-
phils in otherwise normal sheep probably indicate a local
reaction to environmental irritants.6

R EFERENCES
1. da Silva-Curieal JMA et al: Topical fluorescein dye: effects on im-
munofluorescent antibody test for feline herpesvirus keratoconjunc-
tivitis, Prog Vet Comp Ophthalmol 1(2):99, 1991. Figure 12-3 Entropion of the lower eyelid and secondary keratitis
in a goat. Dorsal corneal neovascularization and central corneal
2. Strubbe DT, Gelatt KN: Ophthalmic examination and diagnostic
edema with a superficial corneal ulcer also are present. (Courtesy Dr.
procedures. In Gelatt KN, editor: Veterinary ophthalmology, ed 3,
Mary B. Glaze, Baton Rouge, Louisiana.)
Philadelphia, 1999, Williams & Wilkins.
3. Skarda RT: Local and regional anesthetic techniques: ruminants
and swine. In Thurmon JC, Tranquilli WJ, Benson GJ, editors: Vet-
erinary anesthesia, ed 3, Baltimore, 1996, Williams & Wilkins. keratoconjunctivitis. Initially epiphora may be present,
4. Ramsey DT: Surface ocular microbiology in food and fiber- but ocular discharge becomes mucopurulent as secondary
producing animals. In Howard JL, Smith RA, editors: Current vet- bacterial keratoconjunctivitis develops (Figure 12-3).1-4
erinary therapy, food animal practice, ed 4, Philadelphia, 1999, WB Secondary entropion is usually unilateral and may affect
Saunders. either the upper or lower eyelid. Animals of any age may
5. Pickett JP: Ophthalmic examination techniques for food animals. be affected.3,4
In Howard JL, Smith RA, editors: Current veterinary therapy, food
animal practice, ed 4, Philadelphia, 1999, WB Saunders. Treatment. Initial treatment of entropion is generally
6. Dagnall GJR: Use of exfoliative cytology in the diagnosis of ovine conservative and involves the administration of topical
keratoconjunctivitis, Vet Rec 135(6):127, 1994.
antibiotic ointments and attempts to evert the affected
eyelid(s). Antibiotic ointments should be applied at least
PATHOLOGY OF THE EYELIDS every 8 to 12 hours; more severe cases may require more
frequent administration. Topical 1% atropine is indicated
AND NASOLACRIMAL DUCTS in animals with severe ocular pain and ciliary spasm. At-
ropine is administered every 8 to 12 hours until the pupil
Entropion is dilated, after which the frequency of administration
Entropion is an inward deviation or rolling of the eyelid may be reduced.3
that causes a contact irritation of the cornea and conjunc- Nonsurgical eversion of the affected eyelid may be at-
tiva by the eyelashes and periocular hair. Entropion has tempted using a variety of methods. Subcutaneous palpe-
been reported to be the most common ocular disease of bral injection of benzathine or procaine penicillin imme-
neonatal lambs.1 If entropion is congenital (or primary), diately corrects entropion and acts as a local irritant that
which is common, usually only the lower eyelid is affected often causes sufficient fibrosis to correct the problem.
and the condition is bilateral.2-4 Secondary (or acquired) Approximately 1 to 2 ml of penicillin (sufficient to evert
entropion may result from trauma, severe dehydration, the eyelid) is injected in a linear fashion just parallel to
loss of retrobulbar fat because of emaciation, old age, mi- the affected eyelid margin.1-3,5,6 The skin of the affected
crophthalmia, phthisis bulbi, or painful ocular conditions eyelid may be clamped with a mosquito hemostat to
that cause contraction of the retractor bulbi muscle and create swelling and resultant fibrosis that may perma-
blepharospasm. nently correct the entropion. The hemostat is applied just
below and parallel with the eyelid margin and left in place
Clinical signs. Clinical signs are ordinarily observed in for 30 seconds.1,3,4,7 Another method involves the place-
lambs during the first few days to weeks of life and may ment of two or three vertical mattress sutures, skin
include blepharospasm, photophobia, eye rubbing, and staples, or Michel wound clips to evert the eyelid.1-7 In
 Chapter 12 Diseases of the Eye • 327

most cases entropion is effectively treated with these ommended, using techniques as described for other
techniques, and surgical correction should be considered species.1,3
only when temporary eversion techniques have not been
successful.6 Some authors suggest that surgical proce-
dures should be performed only on older animals (at least
Viral Blepharitis
4 to 6 months of age).6 Blepharitis has numerous etiologies, and several of these
Surgical correction of entropion is best undertaken are systemic diseases that are likely to affect other body
with the animal anesthetized and placed in lateral recum- systems. Viral causes of blepharitis include cutaneous
bency (see Chapter 16). A crescent-shaped flap of skin is ecthyma (orf ), ulcerative dermatosis, and bluetongue.3,4
removed from the affected eyelid using a #15 scalpel
blade and sharp dissection. The flap of skin to be Clinical signs. Lesions of contagious ecthyma are
removed is incised 1 to 2 mm distal to the eyelid margin characterized by vesicles or pustules that rapidly progress
and 3 to 4 mm wider than the affected area. The underly- to proliferative, scab-like crusts.10 Owners and clinicians
ing section of the orbicularis oculi muscle also should be should wear gloves when treating animals with clinical
excised. Placement of a sterile tongue depressor, Jaeger signs of cutaneous ecthyma virus because of its zoonotic
lid plate, or scalpel handle underneath the eyelid in the potential. Similarly, ulcerative dermatosis virus causes en-
conjunctival fornix facilitates incision and dissection of crusted ulcerations of the eyelids of sheep. Clinical signs
the eyelid. The skin is closed in one layer with a simple of bluetongue virus infections are more likely to be ob-
interrupted pattern. Closure should begin in the middle served in sheep than goats and include blepharitis,
of the incision and proceed to the edges to ensure even blepharospasm, and conjunctivitis.3,4 Other ocular lesions
skin tension across the suture line. Soft (silk or monofila- of bluetongue include hyperemia and eczema of the
ment nylon), fine (3-0 to 4-0) suture material is sug- adnexal skin and retinal dysplasia.3
gested. The clinician should take care to tie knots away
from the cornea to prevent irritation. Sutures should be Treatment. Treatment of viral blepharitis is largely
removed in 10 to 14 days. Topical antibiotics should be symptomatic and may involve the administration of anti-
continued for several days after surgery or until any inflammatory agents and topical ophthalmic antibiotics
corneal ulcers have healed. to prevent secondary bacterial infections.3 Affected animals
should be isolated, and contamination of ointment tubes
Prevention. Congenital entropion is suspected to be a must be avoided.3
heritable trait, and affected animals should not be used for
breeding purposes.2,3,6,7 The genetic factors resulting in
congenital entropion are unknown, but the trait is believed
Bacterial Blepharitis
to be multifactorial and caused by more than a simple, au- Bacterial blepharitis may be caused by Dermatophilus con-
tosomal recessive inheritance.2,4,8 Dusty or windy condi- golensis, Actinobacillus lignieresii, and Clostridium novyi.3,4
tions may contribute to the development of entropion in A. lignieresii infections are characterized by pyogranulo-
genetically predisposed animals.6 From 4% to 80% of a matous nodules with draining tracts. Impression smears
flock may be affected with congenital entropion, and of exudate reveal clumps of filamentous gram-negative
usually several lambs are affected in the new lamb crop.9 In bacteria and inflammatory cells.3 Bighead (C. novyi in-
contrast, secondary entropion (e.g., that resulting from de- fection) usually occurs in rams as a sequela to head
hydration) normally affects only single animals.4 trauma during fighting and butting. Affected animals
have extensive facial and cervical swelling that may affect
the eyelids.3,4 Blepharoedema may be severe enough to
Ectropion obliterate the palpebral fissure and blind the animal or
The most common etiologies of ectropion include iatro- cause exposure keratitis because of an inability to close
genic overcorrection of entropion and trauma.1,3,4 Ectro- the eyelids fully.4
pion is relatively rare in sheep and goats.3,4
Treatment. Treatment of C. novyi infection requires
Clinical signs. Clinical signs of ectropion include intensive therapy with systemic antiinflammatory ther-
drooping of the affected eyelid, epiphora, and exposure apy, antimicrobial agents (e.g., penicillin, florfenicol), and
keratoconjunctivitis.4 Some sheep have mild drooping of topical antibiotic ointments.4
the eyelids as a normal conformational variation. Mildly
affected animals may be predisposed to conjunctivitis but
most have no clinical signs of ocular disease.1
Fungal Blepharitis
Clinical signs. Clinical signs of dermatophytosis include
Treatment. If surgical correction is necessary, a V to facial alopecia and crusting that may affect the eyelids.
Y blepharoplasty or eyelid shortening procedure is rec- Young goats are most commonly affected, and cases are
328 • Sheep and Goat Medicine
most likely to occur during late winter and early spring.3 coma, and melanoma.3,5 Papilloma virus infection causes
Diagnosis may be based on fungal culture, fungal growth eyelid warts.3,5 In immunocompetent animals, warts are
on dermatophyte test media, and microscopic examina- generally fairly benign and self-limiting. Papillomas that
tion of affected hairs after application of potassium hy- interfere with eyelid function or irritate the cornea should
droxide (KOH). Dermatophytes are potentially zoonotic be removed.3
and people should wear gloves when treating infected
animals. Treatment. Treatment of eyelid neoplasms is deter-
mined by the invasiveness of the tumor but may involve
Treatment. Fungal blepharitis is usually self-limiting, surgical removal, cryotherapy (possible complications
and most animals recover in the spring with improved include eyelid fibrosis and corneal damage), CO2 laser ex-
pasture conditions and increased dietary vitamin A con- cision, or local hyperthermia therapy. Topical antibiotic
centrations. Symptomatic therapy may involve the admin- ointments should be administered for several days after
istration of topical antifungal ointments or shampoos.3 surgery.

Parasitic Blepharitis Facial Nerve Paralysis

A variety of external parasite infestations can cause Locoweed (Astragalus and Oxytropis species) produces
blepharitis. Blepharitis may be caused by the parasites di- paralysis of the palpebral nerve and secondary exposure
rectly or may result from rubbing or scratching in pruritic keratoconjunctivitis sicca (KCS).6 Locoweed toxicity also
animals. Psoroptes, Psorergates, and Chorioptes infestations causes marked cytoplasmic vacuolization of the lacri-
may cause intense itching and rarely involve only the mal gland secretory epithelium. The resultant decrease in
facial area.3 Diagnosis is based on clinical signs and con- tear production further contributes to KCS and may
firmed by microscopic examination of skin scrapings. cause animals to have a “dull-eyed” appearance.11 Liste-
riosis should be ruled out as a possible cause of cranial
Treatment. Other external parasites that may cause nerve abnormalities, especially in animals with unilateral
blepharitis include sheep keds, lice, and ticks.3,4 Mite in- deficits.
festations are treated by ivermectin administration, dip-
ping in insecticides, and local application of insecticides
as necessary.3
Nictitating Membrane
Abnormalities of the nictitating membrane are uncom-
mon. Lymphoid follicles of the third eyelid may be very
Elaeophoriasis (Sorehead) prominent in cases of infectious conjunctivitis, especially
Elaeophora schneideri (sorehead) may aberrantly infect if the condition is caused by chlamydial organisms. Carci-
sheep and goats. Sorehead occurs in the high mountain nomas and adenocarcinomas affecting the third eyelid
regions of the western United States where small ruminants may be treated by local excision or preferably by removal
are pastured near deer.1,6 Clinical signs of E. schneideri of the entire nictitating membrane.3
infection in small ruminants and elk include facial swelling,
blepharospasm, keratoconjunctivitis, alopecia, ulceration,
and encrusted lesions of the face.1,6 Sorehead most com-
Nasolacrimal Duct Disease
monly affects adult sheep during the fall and winter.1,6 Disease of the nasolacrimal duct of sheep is most com-
Diagnosis is based on consistent clinical signs in small ru- monly caused by larvae of the nasal bot (Oestrus ovis).
minants in endemic areas and the demonstration of Normally the larvae of the nasal bot fly mature in the
E. schneideri microfilaria in skin or conjunctival biopsies. frontal and nasal sinuses until they are sneezed out to
complete their life cycle. Occasionally, larvae may aber-
Treatment. Reported effective treatments include pi- rantly migrate into the nasolacrimal duct or ocular
perazine (50 mg/kg by mouth [PO]) and diethylcarba- mucous membranes. Clinical signs of ocular or naso-
mazine (100 mg/kg PO). The efficacy of ivermectin lacrimal infection include epiphora and conjunctivitis.
against the parasite is unknown.6 Affected animals also may exhibit frenzied behavior to
Other causes of blepharitis and blepharoedema include avoid adult botflies, stomp, sneeze, and may have a nasal
photosensitization, solar dermatitis, contact hypersensi- discharge.
tivity dermatitis, and cutaneous myiasis.3,5
Treatment. Treatment involves removal of visible larvae,
flushing of the nasolacrimal ducts, and administration
Neoplasia of ivermectin (200 mg/kg PO). Nasal bot infections
Neoplasms reported to affect the eyelids of sheep and are most effectively treated in the fall when larvae are
goats include squamous cell carcinoma, fibroma, fibrosar- smaller.3,6
 Chapter 12 Diseases of the Eye • 329

R EFERENCES
1. Moore CP, Wallace LM: Selected eye diseases of sheep and goats.
atitis. The most common ocular foreign bodies are small
particles of plant material that become embedded in the
conjunctiva or corneal stroma.
In Howard JL, editor: Current veterinary therapy, food animal prac-
tice, ed 3, Philadelphia, 1993, WB Saunders. Treatment. Removal of small, superficial foreign bodies
2. Miller TR, Gelatt KN: Food animal ophthalmology. In Gelatt is often accomplished with topical anesthesia using 0.5%
KN, editor: Veterinary ophthalmology, ed 2, Philadelphia, 1991, Lea proparacaine and manual restraint. Foreign bodies are
and Febiger.
usually easily removed using cotton-tipped applicators or
3. Moore CP, Whitley RD: Ophthalmic diseases of small domestic
ruminants, Vet Clin North Am Large Anim Pract 6(3):641, 1984.
ophthalmic forceps. After foreign body removal, topical
4. Wyman M: Eye diseases of sheep and goats, Vet Clin North Am antibiotics should be administered every 6 to 8 hours for
Large Anim Pract 5(3):657, 1983. several days. Nonpenetrating corneal lacerations may be
5. Lavach JD: Disorders of the eyelids, conjunctivae, and naso- treated as simple corneal ulcers with topical antibiotics
lacrimal system. In: Large animal ophthalmology, St Louis, 1990, and 1% atropine.1 Chemical injuries to the cornea and
Mosby. conjunctiva are caused by insecticide dips or sprays,
6. Pickett JP: Selected eye diseases of food and fiber-producing shampoos, and disinfectants. In the case of chemical in-
animals. In Howard JL, Smith RA, editors: Current veterinary juries, immediate lavage with large volumes of isotonic
therapy, food animal practice, ed 4, Philadelphia, 1999, WB Saun- saline or ordinary tap water is essential to flush the con-
ders. junctival sac and dilute the offending agent. After lavage
7. Rook JS, Cortese V: Repair of entropion in the lamb, Vet Med
the affected eyes should be treated with topical antibiotics
Small Anim Clin 76(4):571, 1981.
8. Taylor M, Catchpole J: Incidence of entropion in lambs from two
and atropine. Topical anticollagenase preparations such as
ewe flocks put to the same rams, Vet Rec 118(13):361, 1986. acetylcysteine may be beneficial to reduce ongoing
9. Gelatt KN: Congenital entropion in a Hampshire lamb, Vet Med corneal degeneration. Systemic antiinflammatory agents
Small Anim Clin 65(8):761, 1970. are indicated to control secondary uveitis.1
10. Smith MC, Sherman DM: Skin. In Smith MC, Sherman DM,
editors: Goat medicine, Philadelphia, 1994, Lea and Febiger.
11. Van Kampen KR, James LF: Ophthalmic lesions in locoweed poi-
Infectious Conjunctivitis
soning of cattle, sheep, and horses, Am J Vet Res 32(8):1293, 1971. Reports describing the normal conjunctival flora of sheep
and goats are scarce. In clinically normal sheep, 60%
PATHOLOGY OF THE of eye swabs were negative for bacterial growth.2 In
sheep the most commonly isolated bacteria were similar
CONJUNCTIVA AND CORNEA to Branhamella (Neisseria) ovis and were recovered in
low numbers. Other frequently isolated organisms were
Conjunctival Trauma Micrococcus and Streptococcus species. Less commonly iso-
Goats and sheep have large, prominent eyes that may be lated bacteria were of the genera Corynebacterium, Achro-
traumatized by fencing, feeders, and coarse forage during mobacter, Bacillus, Neisseria (other than N. ovis), Staphy-
browsing. Dusty or windy conditions also may cause an lococcus, Pseudomonas, Moraxella, and Escherichia coli.2,3
irritant conjunctivitis. Moraxella bovis is not a cause of infectious keratocon-
junctivitis in goats.3 However, conflicting reports indi-
Clinical signs. Animals with conjunctival trauma often cate the possible pathogenicity of Moraxella in ovine
have conjunctival hemorrhage and swelling. If the globe keratoconjunctivitis.4,5 Other known ocular pathogens,
appears soft (decreased IOP) or the anterior chamber is including Mycoplasma conjunctivae and Chlamydia psittaci,
shallow or flat, a scleral or corneal laceration is likely. can be cultured from the eyes of sheep and goats after
Subconjunctival hemorrhage is often an incidental finding resolution of keratoconjunctivitis and in clinically normal
in neonates and is caused by minor trauma during animals.3,6-10
parturition.

Treatment. Uncomplicated cases of conjunctival irrita-

Mycoplasma Conjunctivitis
tion and minor trauma can be treated with topical broad- Mycoplasma species are important and frequent patho-
spectrum antibiotic ointments (e.g., triple antibiotic) to gens causing keratoconjunctivitis in sheep and goats. Re-
prevent secondary bacterial infections and to provide ported mycoplasmal pathogens include M. conjunctivae,
corneal lubrication.1 M. mycoides subsp. mycoides, M. capricolum, M. agalactiae,
and M. arginini.
Corneal Trauma Clinical signs. Clinical signs of ocular mycoplasmal
Corneal trauma may be caused by penetrating foreign infections are hyperemia of the conjunctival blood
bodies, lacerations, and abrasions causing ulcerative ker- vessels, photophobia, blepharospasm, and epiphora that
330 • Sheep and Goat Medicine
may become mucopurulent (Figure 12-4).8-15 Corneal Diagnosis. Diagnosis of mycoplasmal infection is
neovascularization and opacity beginning at the limbus based on clinical signs, IFA staining of conjunctival
and progressing centrally may occur in some cases scrapings, and positive culture of lacrimal secretions,
(Figure 12-5).8,10-12,14,15 Severely affected animals may blood, or milk.8,11 Conjunctival scrapings stained with
develop iridocyclitis, corneal ulcers, or blindness because Giemsa-type stains may reveal basophilic, coccobacillary
of intense corneal opacity.3,9-13 Some authors state that organisms within the cytoplasm of the epithelial cells.8,11,12
clinical signs are more common and severe in adult sheep Conjunctival neutrophils, lymphocytes, and plasma cells,
than in lambs.8,12 as well as necrotic epithelium also may be observed
(Figure 12-6).11 Culture and cytology results are more
likely to be positive when obtained soon after the onset of
clinical signs.12

Treatment. Many cases of mycoplasmal keratocon-

junctivitis are self-limiting and resolve completely within
a few weeks without treatment.10,13,15 Both systemic and
topical antibiotic therapy have been recommended, and
antibiotics may speed the recovery of affected animals.15,16
Systemic tylosin, oxytetracycline (10 to 20 mg/kg intra-
muscularly [IM] or subcutaneously [SC]), chlortetracy-
cline (80 mg/head/day in the feed), and streptomycin
have been found to be effective in vitro against isolates
taken from sheep.16 Topical tetracycline alone12 or com-
bined with polymyxin B15 also is reported to be effective.
The prophylactic use of long-acting oxytetracycline (20
mg/kg every 48 to 72 hours IM or SC) may prevent the
appearance of clinical signs in other members of the herd
or flock.12

Prevention. Affected animals should be isolated to

Figure 12-4 Keratoconjunctivitis with conjunctival hyperemia, prevent the spread of disease.11 Carrier animals and ap-
chemosis, epiphora, and corneal neovascularization. (Courtesy Dr. Ron parently uninfected animals are an important source of
Ofri, Rehovot, Israel.) infection because M. conjunctivae may persist for months

Figure 12-5 Keratoconjunctivitis in a goat. Periocular swelling, Figure 12-6 Photomicrograph of a conjunctival scraping from the
epiphora, and generalized corneal edema with circumlimbal deep goat in Figure 12-5. Neutrophils, erythrocytes, and conjunctival
neovascularization also are present. (Courtesy Dr. M.A. Salisbury, epithelial cells with basophilic coccobacillary pleomorphic bodies
Sarasota, Florida.) within the cytoplasm are present, consistent with Mycoplasma
infection. Wright’s stain, 250 magnification. (Courtesy Dr. M.A.
Salisbury, Sarasota, Florida.)
 Chapter 12 Diseases of the Eye • 331

in the conjunctival sac and nares after recovery.8 Recently

affected herds or flocks often have a history of introduc-
tion of new members that were inapparent carriers of M.
conjunctivae.3,8,12,15 The infection is spread by direct
contact with infective ocular secretions, fomites, and face
flies.3,11,12 Some authors recommend isolation and pro-
phylactic treatment of new animals before they are added
to the herd or flock11 (see Chapter 5).

Chlamydia psittaci Conjunctivitis

Ocular C. psittaci infections in sheep and goats cannot be
distinguished from M. conjunctivae infections based on
clinical signs alone because they appear similar clinically.3
Two strains of C. psittaci exist and are characterized by
their ability to cause keratoconjunctivitis alone or as part
of a systemic disease process such as pyrexia, polyarthritis,
respiratory tract infection, and abortion.3,11 Keratocon-
junctivitis in lambs caused by C. psittaci is more likely to
be bilateral than M. conjunctivae infection.3
Figure 12-7 Corneal stromal abscess in a sheep. Corneal cellular
Clinical signs. As many as 80% of lambs are affected infiltrate, deep neovascularization, and severe conjunctival hyperemia
bilaterally, but lesions may be asymmetric.3,11,17,18 In one also are present. (Courtesy Dr. P. Lybaert, Brussels, Belgium.)
report,17 all affected lambs with polyarthritis also had
some degree of conjunctivitis. Clinical signs are generally
more severe in lambs than adult sheep and as many as fected animals these cells are found in sheets of several
90% of lambs may become infected.3,11 Initial clinical cells.18 Chlamydial inclusions are usually juxtanuclear17
signs of ocular C. psittaci infection include conjunctival and may be found in approximately 50% of conjunctival
petechiae and hyperemia, corneal edema, neovasculariza- scrapings if Giemsa stain is used.8,11
tion, and ocular discharge that may vary from serous to
mucoid or purulent. As the condition progresses, severe Treatment and prevention. Treatment of C. psittaci in-
conjunctival hyperemia, neovascularization, and corneal fection is as described for mycoplasmal infections. Sys-
ulceration occur, along with a neutrophilic corneal infil- temic and topical tetracycline is reportedly effective.3,11
trate (Figure 12-7).3,11,17-20 A characteristic clinical sign In uncomplicated cases the disease is usually self-limiting
of chlamydial keratoconjunctivitis is the formation of and recovery can be expected within 2 to 3 weeks.11,18,20
conjunctival lymphoid follicles. Lymphoid follicles begin Transmission of C. psittaci occurs by infective secretions,
as small, discrete, pale, elevated areas in the conjunctiva direct contact, and insects.11,18 Recovered animals may
that gradually enlarge and coalesce to form pink to red shed C. psittaci in tears and nasal secretions for several
folds in the lower conjunctival fornix. The follicles can months after the resolution of clinical signs.11 In 8- to
protrude as much as 8 to 10 mm to fill the conjunctival 10-month-old lambs a degree of resistance appears to
fornix and become confluent with the follicles on the develop.18 Although some authors12,20 state that some
surface of the nictitating membrane.18 sheep are carriers for C. psittaci, others report that
chlamydial organisms cannot be cultured from the eyes of
Diagnosis. Diagnostic tests for C. psittaci keratocon- clinically normal animals3 (see Chapter 5).
junctivitis include culture of blood or ocular secretions,
serology using complement fixation tests, and specific
IFA staining or microscopic examination of conjunctival
Colesiota conjunctivae Conjunctivitis
smears.3,8,11,12,17-19 A four-fold or greater rise between Colesiota conjunctivae is a member of the family Chlamydi-
acute and convalescent serum samples (taken 2 weeks aceae, and similar to C. psittaci it also can cause conjunc-
apart) using the complement fixation test may confirm tivitis in sheep. Previously C. conjunctivae was presumed to
the diagnosis.8 Organisms are more likely to be found be a Rickettsia-like organism based on its morphologic
using culture or cytologic methods early in the disease appearance.11,20,21 However, this classification was proba-
process.12,20 Conjunctival scrapings reveal numerous bly based on misidentification of epithelial inclusions of
neutrophils with some lymphocytes and plasma cells.18 In C. psittaci as rickettsial organisms.11,20 The bacterium has
chlamydial infections, conjunctival epithelial cells are not been cultured and has only been identified from con-
shed singly or in groups of two or three, whereas in unaf- junctival scrapings.11
332 • Sheep and Goat Medicine
Branhamella ovis Conjunctivitis Mycotic Keratitis
Branhamella (Neisseria) ovis may cause conjunctivitis, Mycotic keratitis is rare in ruminants.27 If fungal ele-
epiphora, injected scleral blood vessels, photophobia, and ments are cultured or observed in conjunctival scrapings,
corneal neovascularization in sheep and goats.11,22 Only a their presence as possible contaminants should be care-
small number of affected sheep develop keratitis.11 The fully considered. Saprophytic fungi such as Aspergillus
role of B. ovis as a primary pathogen is unclear and the and Mucor species have been isolated from both diseased
bacteria may be primarily opportunistic with infections and unaffected eyes in sheep and goats.15,18
by other organisms such as M. conjunctivae and C.
psittaci.3,8,11,12 Diagnosis of B. ovis infection is based on Treatment. Treatment involves the application of topical
bacterial culture results and Gram’s staining of conjuncti- antifungal agents, including natamycin, miconazole, itra-
val scrapings, which reveals a predominance of gram- conazole/dimethyl sulfoxide (DMSO), or ketoconazole.
negative diplococci.22 Topical miconazole is usually the most cost-effective
therapy and should be administered every 4 to 6 hours.
Treatment. Successful treatment of B. ovis infection in Superficial keratectomy can be used for both therapeutic
goats involves parenteral tylosin for 5 days combined with and diagnostic purposes. Keratectomy removes diseased
topical application of bacitracin-neomycin-polymyxin B corneal material, providing tissue for fungal culture
ointment. Animals without any corneal involvement and cytology while increasing the penetration of topical
recover within 48 hours.22 B. ovis may be cultured from medications.
the eyes of both diseased and unaffected sheep and
goats3,6,8,10-12 but has been isolated more frequently from
the eyes of affected sheep.10,12
Parasitic Keratitis
Thelazia rhodesii, the eye worm, causes widespread infec-
tion in North America. However, clinical disease is un-
Acholeplasma oculi Conjunctivitis common.28,29 Eye worm infections may cause conjunc-
Clinical signs of Acholeplasma oculi (or A. oculusi) infection tivitis, conjunctival cysts, and keratitis. In severe cases,
in sheep and goats include conjunctivitis, keratitis, bleph- corneal edema, ulceration, and neovascularization may
arospasm, epiphora, and pannus.23,24 occur.29 Face flies and other Musca species are intermedi-
ate hosts for the parasite, and therefore fly control is es-
Treatment. Treatment of A. oculi infection in ewes is sential for reducing infections.
successful with subconjunctival injections of oxytetracy-
cline; a second treatment is necessary in only a few Treatment. Therapy can involve manual removal of
animals.23 worms after the application of topical anesthestics29,30
or organophosphate (echothiophate iodide, phospholine
iodide)31 and irrigation of the conjunctival sac. In
Listeria monocytogenes Conjunctivitis cattle, both ivermectin (200 mg/kg SC)30 and do-
In sheep, Listeria monocytogenes may cause conjunctivitis ramectin (200 mg/kg SC)32 have greater than 99% effi-
as well as encephalitic disease.25 Infections tend to be cacy against eye worms. Levamisole (5 mg/kg PO) also
unilateral and are characterized by blepharospasm, appar- may be efficacious.31
ent blindness, hypopyon, corneal edema, and catarrhal O. ovis larvae can aberrantly migrate into the conjunc-
conjunctivitis. Clinical signs may resolve within 2 weeks tiva or nasolacrimal duct of sheep, causing epiphora and
without corneal scarring. Animals may be infected by conjunctivitis.28 Keratoconjunctivitis, blepharospasm, and
feeding on contaminated silage. blepharoedema may occur in small ruminants as sequelae
to E. schneideri infection.28 Treatment of O. ovis and E.
Treatment. Response to antibiotics, including topical schneideri infection is described in the section on pathol-
oxytetracycline and systemic ampicillin, appears to be ogy of the eyelid.
poor.
Conjunctivitis Therapy
Viral Keratoconjunctivitis Most of the bacterial ocular pathogens of sheep and goats
Severe conjunctivitis, keratoconus, corneal opacity, and are susceptible to tetracycline. Combination therapy with
blindness has been reported in two goats naturally af- long-acting injectable (20 mg/kg IM or SC) and topical
fected with infectious bovine rhinotracheitis virus.26 The tetracycline (every 6 to 8 hours) is usually effective for
virus was isolated from the nasal secretions of both goats. most bacterial infections.33 Topical ophthalmic oint-
The goats had clinical signs of respiratory tract disease ments are generally preferred over solutions because of
before ocular involvement was noted, and both recovered. their prolonged contact time and because less drug is
Bluetongue virus infection may cause conjunctivitis, bleph- likely to be lost in ocular secretions. For these same
aritis, and blepharoedema.27 reasons, ointments are administered less frequently than
 Chapter 12 Diseases of the Eye • 333

solutions. However, ointments should be avoided if a per- grasses. Contaminated stall bedding should be removed,
forating corneal ulcer is suspected because they are very and water troughs and feeders should be cleaned and dis-
irritating to intraocular structures. Powdered preparations infected. Affected animals may have visual deficits and
are not recommended for topical ophthalmic use because should be either confined or kept near readily accessible
they are extremely irritating and have low drug bio- feed and water sources.
availability. Topical administration of therapeutic agents
provides higher drug levels in the cornea, conjunctiva,
aqueous humor, iris, and ciliary body.33
Miscellaneous
Another method to achieve high local concentrations Dermoids (choristoma) are ectopic patches of epidermal
of therapeutic agents is subconjunctival injection. Before tissue and can be found on the conjunctiva, limbus, and
injection an auriculopalpebral nerve block and sedation cornea. They rarely occur in sheep and goats.28 Dermoids
may be necessary. The conjunctiva should be anesthetized affecting the conjunctiva or palpebral mucosae are often
with 0.5% proparacaine. In sheep and goats a maximum easily removed with sharp dissection under topical or re-
volume of 0.5 ml may be administered in the dorsal con- gional anesthesia. Corneal dermoids are removed by su-
junctival fornix with a 25-gauge needle. Subconjunctival perficial lamellar keratectomy. Regeneration can occur if
injection of antibiotics may be used to achieve initial high the entire lesion is not removed.34
concentrations of antibiotics but should not be adminis-
tered in place of topical antibiotics.33

Third eyelid flaps. Third eyelid flaps may be used in

R EFERENCES
1. Whitley RD: Ocular trauma. In Smith BP, editor: Large animal in-
some cases of ulcerative keratitis as a temporary oph- ternal medicine, ed 2, St Louis, 1996, Mosby.
thalmic bandage. The clinician applies a topical anes- 2. Spradbrow PB: The bacterial flora of the ovine conjunctival sac,
thetic to the eye and performs a line block over the dorsal Aust Vet J 44(3):117, 1968.
aspect of the upper eyelid. The third eyelid is sutured to 3. Ramsey DT: Surface ocular microbiology in food and fiber-
the dorsal fornix of the upper eyelid with two or three producing animals. In Howard JL, Smith RA, editors: Current vet-
simple interrupted horizontal mattress sutures using mono- erinary therapy, food animal practice, ed 4, Philadelphia, 1999, WB
filament suture (00) material. The sutures are placed Saunders.
using a curved cutting needle directed through the skin of 4. Baker JR, Faull WB, Ward WR: Conjunctivitis and keratitis in
sheep associated with Moraxella (Haemophilus) organisms, Vet Rec
the upper eyelid 1 cm from the palpebral margin; the
77(14):402, 1965.
needle is then passed into the third eyelid 2 to 3 mm from 5. Wood DR, Watson WA, Hunter D: Conjunctivitis in sheep, Vet
its edge on the palpebral side before being passed parallel Rec 77(19):551, 1965.
to the eyelid margin into the fibrous tissue of the third 6. Dagnall GJR: Use of exfoliative cytology in the diagnosis of ovine
eyelid to obtain a 3- to 4-mm piece of tissue. The clini- keratoconjunctivitis, Vet Rec 135(6):127, 1994.
cian next passes the needle through the palpebral con- 7. Trotter SL et al: Epidemic caprine keratoconjunctivitis: experi-
junctiva and skin and ties it off to complete the suture. mentally induced disease with a pure culture of Mycoplasma con-
The suture should not penetrate the bulbar mucosa of the junctivae, Infect Immun 18(3):816, 1977.
third eyelid, and the nictitating membrane should be 8. Hosie BO: Infectious keratoconjunctivitis in sheep and goats, Vet
seated as deeply as possible in the dorsal conjunctival cul- Ann 29:93, 1989.
de-sac to avoid corneal injury by the sutures. If absorbable 9. Jones GE et al: Mycoplasmas and ovine keratoconjunctivitis, Vet
Rec 99(8):137, 1976.
suture material such as chromic gut is used, sutures
10. Egwu GO et al: Ovine infectious keratoconjunctivitis: a microbio-
usually dissolve in 2 or 3 weeks. Nonabsorbable sutures logical study of clinically unaffected and affected sheep’s eyes with
should be removed as soon as ocular disease has re- special reference to Mycoplasma conjunctivae, Vet Rec 125(10):253,
solved.31 One large disadvantage of third eyelid flaps is 1989.
that the cornea and intraocular structures cannot be ex- 11. Moore CP, Wallace LM: Selected eye diseases of sheep and goats.
amined. Third eyelid flaps should be avoided in cases of In Howard JL, editor: Current veterinary therapy, food animal prac-
melting corneal ulcers, ulcers deeper than three quarters tice, ed 3, Philadelphia, 1993, WB Saunders.
of the corneal stromal thickness, and infected ulcers. 12. Greig A: Ovine keratoconjunctivitis, In Practice 11(3):110, 1989.
13. McCauley EH, Surman PG, Anderson DR: Isolation of My-
coplasma from goats during an epizootic of keratoconjunctivitis,
Prevention of Conjunctivitis Am J Vet Res 32(6):861, 1971.
14. Dagnall GJR: Experimental infection of the conjunctival sac of
In epizootic cases of suspected bacterial keratoconjunc-
lambs with Mycoplasma conjunctivae, Br Vet J 149(5):429, 1993.
tivitis, several control measures have been suggested to 15. Baas EJ et al: Epidemic caprine keratoconjunctivitis: recovery of
reduce the spread of disease.31 Infected animals and Mycoplasma conjunctivae and its possible role in pathogenesis,
animals in direct contact with them should be isolated. Infect Immun 18(3):806, 1977.
Exposure to environmental irritants such as flies, dust, 16. Egwu GO: In vitro antibiotic sensitivity of Mycoplasma conjuncti-
pollen, and wind should be avoided. Pastures should be vae and some bacterial species causing ovine infectious kerato-
mowed to eliminate long-stemmed or rough weeds and conjunctivitis, Small Rumin Res 7(1):85, 1992.
334 • Sheep and Goat Medicine
17. Stephenson EH, Storz J, Hopkins JB: Properties and frequency of failure of passive transfer. Mycoplasma species often cause
isolation of chlamydiae from eyes of lambs with conjunctivitis and septicemia and systemic disease in both neonates and
polyarthritis, Am J Vet Res 35(2):177, 1974. adult animals. In addition to ocular disease, clinical signs
18. Hopkins JB et al: Conjunctivitis associated with chlamydial poly- of mycoplasmal infections include polyarthritis, mastitis,
arthritis in lambs, J Am Vet Med Assoc 163(10):1157, 1973. and agalactia.1,2,4 Animals infected with mycoplasmal or-
19. Wilsmore AJ, Dagnall GJR, Woodland RM: Experimental con-
ganisms should be isolated because bacteria are transmit-
junctival infection of lambs with a strain of Chlamydia psittaci iso-
lated from the eyes of a sheep naturally affected with keratocon-
ted by direct contact with infected animals, infective se-
junctivitis, Vet Rec 127(9):229, 1990. cretions, and fomites.1
20. Cello RM: Ocular infections in animals with PLT (Bedsonia) L. monocytogenes infections can result in septicemia in
group agents, Am J Ophthalmol 63(5):1270, 1967. 4- to 6-month-old feedlot lambs fed silage-based rations.
21. König CDW: Keratoconjunctivitis infectious ovis (KIO), “pink Lambs may have clinical signs of uveitis, conjunctivitis,
eye” or “zere oogjes” (a survey), Vet Q 5(3):127, 1983. and endophthalmitis, as well as cranial nerve deficits.2,5,6
22. Bulgin MS, Dubose DA: Pinkeye associated with Branhamella ovis Toxoplasma gondii is an uncommon cause of anterior
infection in dairy goats, Vet Med Small Anim Clin 77(12):1791, uveitis in sheep and goats.6 In sheep, ocular toxoplas-
1982. mosis most frequently involves the iris, ciliary body,
23. Arbuckle JBR, Bonson MD: The isolation of Acholeplasma oculi and retina, and a nonsuppurative iridocyclitis is often
from an outbreak of ovine keratoconjunctivitis, Vet Rec 106(1):15,
present.7
1979.
24. Al-Aubaidi JM et al: Identification and characterization of Achole-
plasma oculi spec. nov. from the eyes of goats with keratoconjunc- Diagnosis and treatment. Antibiotic and antiinflam-
tivitis, Cornell Vet 63(1):117, 1973. matory therapy are indicated for treatment of anterior
25. Walker JK, Morgan JH: Ovine ophthalmitis associated with Liste- uveitis. In septicemic neonates, blood culture and sensi-
ria monocytogenes, Vet Rec 132(25):636, 1993. tivity results are valuable to determine appropriate an-
26. Mohanty SB et al: Natural infection with infectious bovine rhino- timicrobial agents. Culture of ocular secretions or blood
tracheitis virus in goats, J Am Vet Med Assoc 160(6):879, 1972. may identify pathogenic Mycoplasma species. Both topical
27. Wyman M: Eye diseases of sheep and goats, Vet Clin North Am and systemic antibiotics should be administered for bac-
Large Anim Pract 5(3):657, 1983. terial septicemia and secondary uveitis. Topical 1% at-
28. Pickett JP: Selected eye diseases of food and fiber-producing ropine ointment is indicated to promote pupillary dila-
animals. In Howard JL, Smith RA, editors: Current veterinary
tion, relieve iris and ciliary muscle spasm, and thereby
therapy, food animal practice, ed 4, Philadelphia, 1999, WB Saun-
ders.
decrease intraocular pain.1,3,5 If corneal ulceration is not
29. English RV, Nasisse MP: Ocular parasites. In Smith BP, editor: present, topical, subconjunctival, or parenteral cortico-
Large animal internal medicine, ed 2, St Louis, 1996, Mosby. steroids may be administered for their antiinflammatory
30. Soll MD et al: The efficacy of ivermectin against Thelazia rhodesii effects.1,3,5 Nonsteroidal antiinflammatory drugs (NSAIDs)
(Desmarest, 1828) in the eyes of cattle, Vet Parasitol 42(1-2):67, are often beneficial to reduce the intraocular inflamma-
1992. tory response and provide analgesia. Mycoplasma species
31. Moore CP, Whitley RD: Ophthalmic diseases of small domestic are usually susceptible to tetracycline, erythromycin, and
ruminants, Vet Clin North Am Large Anim Pract 6(3):641, 1984. tylosin.1,5 Penicillin or tetracycline5 is generally effective
32. Kennedy MJ, Phillips FE: Efficacy of doramectin against eye- against L. monocytogenes. Systemic pyrimethamine and
worms (Thelazia spp.) in naturally and experimentally infected sulfadiazine in combination with topical 10% sulfa-
cattle, Vet Parasitol 49(1):61, 1993.
cetamide, atropine, and steroid ointments have been rec-
33. Ramsey DT: Ophthalmic therapeutics. In Howard JL, Smith RA,
editors: Current veterinary therapy, food animal practice, ed 4,
ommended for treatment of ocular toxoplasmosis.5
Philadelphia, 1999, WB Saunders.
34. Miller TR, Gelatt KN: Food animal ophthalmology. In Gelatt Cataracts
KN, editor: Veterinary ophthalmology, ed 2, Philadelphia, 1991,
WB Saunders. Cataracts are the most common lens abnormality of
sheep and goats. The majority of cataracts are congeni-
tally acquired.6 Any opacity in the lens is a cataract,
PATHOLOGY OF THE UVEAL except nuclear sclerosis, which is an aging change that
results from compression of the oldest lens material.
TRACT AND LENS Cataracts are described by their appearance, location, and
size. The smallest cataracts (less than 5% of the total lens)
Uveitis are incipient. Immature cataracts can be subdivided into
Clinical signs. Clinical signs of uveitis may include early immature (6% to 50% lens coverage) and late imma-
miosis, photophobia, iris hyperemia, aqueous flare, hy- ture (51% to 99% lens coverage). Mature cataracts involve
popyon, hyphema, blindness, and fibrin deposition within the entire lens (Figure 12-8). Hypermature cataracts are
the anterior chamber.1-5 Uveitis is a frequent clinical sign characterized by lens fiber liquefaction, wrinkling of the
of septicemia and is often observed in neonates with lens capsule, and the development of dense plaques on
 Chapter 12 Diseases of the Eye • 335

pigmented foci over the anterior lens capsule. Focal opac-

ities may be present in the cornea or on the anterior lens
capsule in areas where the persistent pupillary mem-
branes adhere. An essential iris atrophy has been reported
in Shropshire sheep.13 Affected sheep are born normal
but develop ocular lesions by 1 to 11⁄2 years of age.
Lesions are bilateral but not symmetric and include
partial- or full-thickness holes in the iris stroma and an
absent or a rudimentary corpora nigra. Pupils are pear-
shaped and respond poorly to both light and the admin-
istration of topical tropicamide.

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1. Moore CP, Wallace LM: Selected eye diseases of sheep and goats.
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ruminants, Vet Clin North Am Large Anim Pract 6(3):641, 1984.
3. Lavach JD: Lens, uvea, and glaucoma. In: Large animal ophthal-
Figure 12-8 Mature cataract in a sheep. In this animal, cataracts mology, St Louis, 1990, Mosby.
were bilateral and caused by an unknown etiology. (Courtesy Dr. Brad 4. Whitley RD, Albert RA: Clinical uveitis and polyarthritis associ-
Nadelstein, Chesapeake, Virginia.) ated with Mycoplasma species in a young goat, Vet Rec 115(9):217,
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5. Wyman M: Eye diseases of sheep and goats, Vet Clin North Am
the anterior and posterior lens capsules.8 Cataracts with Large Anim Pract 5(3):657, 1983.
an autosomal dominant inheritance have been described 6. Pickett JP: Selected eye diseases of food and fiber-producing
animals. In Howard JL, Smith RA, editors: Current veterinary
in New Zealand Romney sheep.9 These cataracts were
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bilateral and the majority of them developed in animals ders.
between 2 to 4 months of age; however, some lambs were 7. Piper RC, Cole CR, Shadduck JA: Natural and experimental
affected at birth. Congenital, nonprogressive nuclear ocular toxoplasmosis in animals, Am J Ophthalmol 69(4):662, 1970.
cataracts that do not interfere with vision have been ob- 8. Colitz CMH et al: Histologic and immunohistochemical charac-
served in sheep and goats.3 Incipient cataracts and con- terization of lens capsular plaques in dogs with cataracts, Am J Vet
firmed diabetes mellitus have been reported in twin male Res 61(2):139, 1999.
lambs.10 Cataracts also may occur as sequelae to ocular 9. Brooks HV et al: An inherited cataract in New Zealand Romney
trauma and severe uveitis.3,6 Any uveitis can potentially sheep, N Z Vet J 30(2):113, 1982.
cause cataracts. Septicemic infection such as that caused 10. Mattheeuws D et al: Diabetes mellitus in two twin male lambs, Vet
by Mycoplasma agalactiae can result in uveitis-induced Q 4(3):135, 1982.
11. Abdelbaki YZ, Davis RW: Ophthalmoscopic findings in
cataracts.6 Intraocular E. schneideri infection may cause
elaeophorosis of domestic sheep, Vet Med Small Anim Clin
posterior synechia and cataract formation.11 67(1):69, 1972.
12. Rubin LF: Fundus of ox, sheep, and other ruminants and pig. In:
Miscellaneous Atlas of veterinary ophthalmoscopy, Philadelphia, 1974, Lea and
Febiger.
Persistence of the hyaloid artery may be an incidental 13. Aguirre G, Greene B, Gross S: Essential iris atrophy in sheep, Proc
finding during ophthalmoscopic examination of sheep Am Coll Vet Ophthalmol 12:84, 1981.
and goats.12 In the embryo the hyaloid artery supplies
blood to the lens and normally atrophies after birth.
However, as many as 30% of sheep between 1 and 3 years
PATHOLOGY OF THE RETINA
of age and approximately 40% of goats may have unilat- Many infectious organisms and septicemic conditions
eral or bilateral persistent hyaloid arteries. The remnant can cause retinitis or retinal changes. Septic neonates and
of the hyaloid artery appears as a tight linear structure ex- feedlot lambs with listeriosis may develop chorio-
tending from the posterior lens capsule to the optic disc. retinitis.1 In sheep, toxoplasmosis frequently causes focal
Persistent pupillary membranes have been reported in retinal necrosis and cyclitis or iridocyclitis.2
sheep.3 The remnants of the embryonic pupillary mem- E. schneideri infections in sheep can result in retinal
brane appear as pigmented strands of iris tissue extending disease. An ophthalmoscopic examination can greatly aid
from the iris collarette to the anterior lens capsule or in the identification of this parasite.3 Reported ophthal-
corneal endothelium. Mild cases may appear only as small moscopic changes include chorioretinal atrophy with
336 • Sheep and Goat Medicine
proliferation of tapetal pigment, attenuation of retinal
Inherited Retinal Degeneration
vasculature, and optic nerve atrophy.3 The optic discs of Ceroid lipofuscinosis (Batten’s disease) is an inherited
affected animals may have a hazy outline and appear lysosomal storage disease that causes blindness, ataxia,
edematous and pale gray. In contrast to elk, affected sheep and tremors in South Hampshire sheep.12 Blindness
do not become blind.3 occurs by two mechanisms. Early loss of vision results
A necrotizing retinopathy and retinal dysplasia occurs from atrophy of the cerebral cortex. A concurrent retinal
in lambs if their dams are naturally infected with blue- dystrophy also occurs in the rod and cone outer seg-
tongue virus or a modified live vaccine is administered ments as the retinal cells accumulate ceroid lipofuscin
during the first half of gestation.4 Lambs born to infected pigment.13,14 Affected animals have abnormal elec-
or vaccinated ewes have visual impairment and central troretinograms.13,14 Retinal degeneration characterized
nervous system defects.1 Goats are more resistant to blue- as a rod-cone dysplasia has been reported in a 4-month-
tongue virus than sheep.5 Modified live bluetongue old Toggenburg doe.15 Clinical signs of blindness became
vaccine should not be administered to pregnant ewes, apparent after weaning and included bumping into
particularly during the first half of gestation.6 objects, decreased weight gain, horizontal nystagmus, and
Scrapie has been shown to be a rare cause of blind- poor PLRs.
ness.7 In one report7 affected sheep lacked a menace
reflex and walked into objects, although they main-
tained a PLR to bright light. Ophthalmoscopy revealed
Vitamin A Deficiency
several oval-shaped, blister-like lesions scattered through- The retina requires a constant supply of vitamin A to
out the tapetum lucidum; these lesions ranged from one maintain vision. Phototransduction depends on vitamin
to three quarters of the size of the optic disc. Histolog- A and progressive retinal degeneration results from a
ically the lesions were caused by an accumulation of dietary deficiency.16 Rhodopsin initiates the cascade of
lipid pigment between the RPE and photoreceptors in phototransduction and is made up of opsin (a protein that
the retina. determines the wavelength of the photon the pigment
will absorb) and retinol (a vitamin A derivative).16 After
light stimulation, rhodopsin undergoes a series of confor-
Plant Toxicity mational changes and activates transducing activating
If it is chronically grazed, bracken fern (Pteridium aquil- phosphodiesterase, which results in hyperpolarization in
inum) causes a progressive retinal degeneration in sheep the outer segments of the photoreceptors.16 Ruminants
colloquially called bright blindness.8-10 The majority of are efficient in converting dietary beta-carotene into
affected sheep are noticed to be blind between Septem- vitamin A if they have access to good-quality green
ber and November,8 several months after they begin to forage sources. Vitamin A is stored in the liver, and
graze bracken fern.10 Most sheep are affected between 3 hepatic stores may prevent vitamin A deficiency disease
and 4 years of age.8 The earliest detectable clinical sign for many months if dietary deficiency occurs.
of bright blindness is an increased hyperreflectivity from
the tapetum lucidum.8Affected sheep are permanently Clinical signs. Clinical signs of vitamin A deficiency
blind and very alert. The pupils are dilated and rounded may not become apparent for at least 3 months in
and the PLR is poor.8,10 Ophthalmoscopic examination goats17 and 200 days in sheep18 if they have previously
may reveal attenuated retinal vessels that appear more been grazing good-quality pasture. Under the same con-
widely separated than normal. In advanced cases the ditions of dietary vitamin A deficiency, male animals are
nontapetal fundus is pale with small cracks and gray foci. apparently more susceptible to developing clinical signs
The optic disc may appear pale or gray-pink in color.8,10 of deficiency than females.19 Nyctalopia (night blind-
Choroidal vessels may be visible in some areas of the ness) is a consistent clinical sign of vitamin A deficiency
fundus.10 The exact toxin responsible for bright blind- in sheep and goats, along with anorexia and poor body
ness remains unknown, but retinal lactate dehydrogenase condition.20,21 Severely affected animals may be com-
activity in experimentally affected sheep is significantly pletely blind and lack a PLR.19,21 Ophthalmoscopy
lower than in controls.9 Platelet and leukocyte counts reveals papilledema, papillary and peripapillary retinal
also are significantly lower in affected sheep.9 Micro- hemorrhages, and depigmentation of the nontapetal
scopic lesions are limited to the retina and are character- retina.19,22 In young animals, vitamin A deficiency
ized by a complete destruction of the outer nuclear layer induces bony remodeling, narrowing of the optic canal,
and photoreceptors.8 and thickening of the dura mater, which in turn causes
Locoweed (Astragalus and Oxytropis species) toxicity an ischemic necrosis of the optic nerves.19,23 Remodel-
causes marked cytoplasmic vacuolization of the retinal ing of the optic canal does not occur in skeletally
ganglion and bipolar cells, which may result in visual mature animals and blindness is likely caused by retinal
deficits.11 degeneration.19,23
 Chapter 12 Diseases of the Eye • 337

Treatment. Nyctalopia is reversible with vitamin A re- 19. Paulsen ME et al: Blindness and sexual dimorphism associated
placement. However, completely blind animals probably with vitamin A deficiency in feedlot cattle, J Am Vet Med Assoc
will not respond to therapy.19,22 Allowing free access to 194(7):933, 1989.
green forages or parenterally administering a commer- 20. Schmidt H: Vitamin A deficiencies in ruminants, Am J Vet Res
cially available vitamin A product is usually preventive in 2(5):373, 1941.
21. Eveleth DF, Bolin DW, Goldsby AI: Experimental avitaminosis A
areas in which dry, brown hay is fed for extended periods
in sheep, Am J Vet Res 10(36):250, 1949.
and the inclusion of vitamin A in a feed or mineral sup- 22. Divers TJ et al: Blindness and convulsions associated with vitamin
plement is required. A deficiency in feedlot steers, J Am Vet Med Assoc 189(12):1579,
1986.

R EFERENCES
1. Pickett JP: Selected eye diseases of food and fiber-producing
23. Hayes KC, Nielsen SW, Eaton HD: Pathogenesis of the optic
nerve lesion in vitamin A-deficient calves, Arch Ophthalmol
80(6):777, 1968.
animals. In Howard JL, Smith RA, editors: Current veterinary
therapy, food animal practice, ed 4, Philadelphia, 1999, WB Saun-
ders. BLINDNESS
2. Piper RC, Cole CR, Shadduck JA: Natural and experimental
Severely ill or septicemic animals may appear blind as a
ocular toxoplasmosis in animals, Am J Ophthalmol 69(4):662, 1970.
3. Abdelbaki YZ, Davis RW: Ophthalmoscopic findings in
result of depression or systemic disease. Evaluation of
elaeophorosis of domestic sheep, Vet Med Small Anim Clin vision is difficult in neonatal animals because they nor-
67(1):69, 1972. mally lack a menace reflex for several days after birth.
4. Silverstein AM et al: An experimental, virus-induced retinal dys- Blindness can be caused by neurologic diseases such as
plasia in the fetal lamb, Am J Ophthalmol 72(1):22, 1971. hydrocephalus, intracranial neoplasia, and any encephali-
5. Wyman M: Eye diseases of sheep and goats, Vet Clin North Am tis, including caprine arthritis-encephalitis, scrapie, toxo-
Large Anim Pract 5(3):657, 1983. plasmosis, cerebral abscesses, and aberrant parasite mi-
6. Moore CP, Wallace LM: Selected eye diseases of sheep and goats. gration (Parelaphostrongylus tenuis).1-3 L. monocytogenes
In Howard JL, editor: Current veterinary therapy, food animal prac- infections may cause blindness as a sequela to septicemia,
tice, ed 3, Philadelphia, 1993, WB Saunders. which generally causes severe endophthalmitis and hy-
7. Barnett KC, Palmer AC: Retinopathy in sheep affected with
popyon or (less commonly) meningoencephalitis.3,4 Other
natural scrapie, Res Vet Sci 12(4):383, 1971.
8. Watson WA, Barnett KC, Terlecki S: Progressive retinal degener-
clinical signs of listeriosis are optic neuritis, amaurosis,
ation (bright blindness) in sheep: a review, Vet Rec 91(27):665, decreased PLRs, head tilt, and unilateral cranial nerve
1972. deficits.3 Pituitary abscesses or neoplasia may lead to
9. Watson WA et al: Experimentally produced progressive retinal de- blindness if the optic chiasm is compressed. Pregnancy
generation (bright blindness) in sheep, Br Vet J 128(9):457, 1972. toxemia and ketosis may produce clinical signs of blind-
10. Watson WA, Barlow RM, Barnett KC: Bright blindness—a con- ness because of cerebral energy deprivation and swelling.5
dition prevalent in Yorkshire hill sheep, Vet Rec 77(37):1060, 1965. Lightning strike, trauma, and improper use of debudding
11. Van Kampen KR, James LF: Ophthalmic lesions in locoweed poi- irons may damage the cerebral cortex and cause second-
soning of cattle, sheep, and horses, Am J Vet Res 32(8):1293, 1971. ary blindness.2,4,6
12. Jolly RD, West DM: Blindness in South Hampshire sheep: a neu- Central blindness is a clinical syndrome characterized
ronal ceroid-lipofuscinosis, N Z Vet J 24(6):123, 1976.
by ophthalmoscopically normal eyes, absence of the
13. Mayhew IG et al: Ceroid-lipofuscinosis (Batten’s disease): patho-
genesis of blindness in the ovine model, Neuropathol Appl Neurobiol
menace reflex, absent dazzle response, and a normal
11(4):273, 1985. PLR.2 Etiologies of central blindness in sheep and goats
14. Graydon RJ, Jolly RD: Ceroid-lipofuscinosis (Batten’s disease) se- include polioencephalomalacia, lead poisoning, and sodium
quential electrophysiologic and pathologic changes in the retina of toxicosis and water deprivation (see Chapter 11).
the ovine model, Invest Ophthalmol Vis Sci 25(3):294, 1984.
15. Buyukmichi N: Retinal degeneration in a goat, J Am Vet Med Assoc
177(4):351, 1980.
16. Ofri R: Optics and physiology of vision. In Gelatt KN, editor: Vet-
R EFERENCES
1. Lavach JD: Ophthalmoscopic anatomy and disorders of the optic
erinary ophthalmology, ed 3, Philadelphia, 1999, Williams & nerve, retina, and choroid. In: Large animal ophthalmology, St Louis,
Wilkins. 1990, Mosby.
17. National Research Council: Nutrient requirements. In National 2. Collins BK: Neuro-ophthalmology in food animals. In Howard JL,
Research Council, editor: Nutrient requirements of goats: Angora, editor: Current veterinary therapy, food animal practice, ed 3,
dairy, and meat goats in temperate and tropical countries, Washing- Philadelphia, 1993, WB Saunders.
ton, DC, 1981, National Academy Press. 3. Miller PE: Neurogenic vision loss. In Howard JL, Smith RA,
18. National Research Council: Nutrient requirements and signs of editors: Current veterinary therapy, food animal practice, ed 4,
deficiency. In National Research Council, editor: Nutrient require- Philadelphia, 1999, WB Saunders.
ments of sheep, ed 6, Washington, DC, 1985, National Academy 4. Moore CP, Whitley RD: Ophthalmic diseases of small domestic ru-
Press. minants, Vet Clin North Am Large Anim Pract 6(3):641, 1984.
338 • Sheep and Goat Medicine
5. Smith MC: Polioencephalomalacia in goats, J Am Vet Med Assoc
174(12):1328, 1979.
6. Smith MC, Sherman DM: Ocular system. In Smith MC,
Sherman DM, editors: Goat medicine, Philadelphia, 1994, Lea and
Febiger.

PATHOLOGY OF THE ORBIT

Glaucoma
Glaucoma in sheep and goats usually results from ocular
inflammatory conditions such as severe keratoconjunc-
tivitis, corneal ulcers, anterior uveitis, ocular trauma, and
septicemia.1,2 Glaucoma develops from a decreased outflow
of aqueous humor, which may result from extensive an-
terior synechia or filtration angle obstruction with in-
flammatory cells or fibrin.1
Figure 12-9 Cyclopia and facial malformations in a lamb.
Clinical signs. Clinical signs of glaucoma include con- (Courtesy Dr. Robert Poppenga, Kennett Square, Pennsylvania, and
gestion of conjunctival and episcleral blood vessels, corneal the University of Pennsylvania Poisonous Plants Home Page,
http://cal.nbc.upenn.edu/poison/)
edema, buphthalmos, blindness, exposure keratitis, lens
luxation, and cataracts.2
skunk cabbage.6 Occasionally only one lamb of twins is
Treatment. Buphthalmic eyes should be enucleated, affected.5,6
especially if exposure keratitis is present.1,2 A silicone in-
traorbital prosthesis may be implanted in some cases if a
cosmetic appearance is desired and the animal is unilat-
Miscellaneous Ophthalmic Problems
erally affected.1 If the animal retains vision in the af- Congenital microphthalmia, along with other ocular
fected eye, diode laser cycloablation can be performed to defects such as aphasia, aniridia, and optic nerve hypopla-
destroy some of the ciliary body epithelial cells, which sia, may be inherited as an autosomal recessive trait in
decreases aqueous humor production. Medical therapy of Texel sheep.7 Several ocular abnormalities may occur in
glaucoma may be attempted and is similar to that used lambs born to ewes grazing seleniferous pastures.8 Mi-
in horses.3 crophthalmia, conjunctival cysts, aphasia or displacement
of the lens, aniridia or rudimentary iris, and a lack of a di-
vision between the cornea and sclera have been reported.
Exophthalmos Some 75% of affected lambs died at birth.
Exophthalmos can be caused by retrobulbar abscesses or
neoplasia, especially lymphoma and squamous cell carci-
noma. Orbital cellulitis is rare but may result from perioc-
R EFERENCES
1. Moore CP, Whitley RD: Ophthalmic diseases of small domestic ru-
ular puncture wounds, plant awns migrating from the oral minants, Vet Clin North Am Large Anim Pract 6(3):641, 1984.
cavity, and caseous lymphadenitis abscesses.4 2. Lavach JD: Lens, uvea, and glaucoma. In: Large animal ophthalmol-
ogy, St Louis, 1990, Mosby.
Cyclopia 3. Lavach JD: Glaucoma. In: Large animal ophthalmology, St Louis,
1990, Mosby.
Cyclopia in fetal lambs, a developmental anomaly charac- 4. Pickett JP: Selected eye diseases of food and fiber-producing
terized by the presence of only one orbit, has been associ- animals. In Howard JL, Smith RA, editors: Current veterinary
ated with the consumption of Veratrum californicum therapy, food animal practice, ed 4, Philadelphia, 1999, WB Saunders.
(skunk cabbage, corn lily, or false hellebore) by ewes on 5. Binns W et al: Chronologic evaluation of teratogenicity in sheep fed
the fourteenth day of gestation.5,6 The plant grows in the Veratrum californicum, J Am Vet Med Assoc 147(8):839, 1965.
6. Binns W et al: A congenital cyclopian-type malformation in lambs
mountain ranges of the western United States. Other
induced by maternal ingestion of a range plant, Veratrum califor-
congenital defects attributed to grazing V. californicum nicum, Am J Vet Res 24(103):1164, 1963.
include anophthalmia, shortening or absence of the max- 7. Moore CP, Wallace LM: Selected eye diseases of sheep and goats.
illary and nasal bones, cebocephalus (monkey face), hy- In Howard JL, editor: Current veterinary therapy, food animal prac-
drocephalus, and harelip (Figure 12-9).5,6 The incidence tice, ed 3, Philadelphia, 1993, WB Saunders.
of congenital deformities may range from 1% to 25% 8. Rosenfeld I, Beath OA: Congenital malformations of eyes of sheep,
of lambs in flocks grazing pastures contaminated with J Agri Res 75(3):93, 1947.
 Chapter 12 Diseases of the Eye • 339

ENUCLEATION tating membrane. Because enucleation is often per-

Enucleation is indicated for removal of eyes damaged by formed to remove severely infected and ruptured globes,
severe keratitis, perforating injury, glaucoma, and intraoc- the transpalpebral approach is most often indicated to
ular neoplasia. Exenteration may be necessary in cases of reduce surgical contamination. After induction of general
severe ocular infections or neoplasia; this procedure in- anesthesia or sedation and retrobulbar anesthesia, the
volves removal of the entire globe, extraocular muscles, patient is placed into lateral recumbency with the eye to
and adnexa. The contralateral eye should be carefully be enucleated toward the surgeon. The affected orbit
evaluated to ensure normal vision before enucleation or should be lavaged with a 1:50 dilution of povidone iodine
exenteration is performed. If keratitis or endophthalmitis solution and isotonic saline. Before clipping and aseptic
is present, systemic and topical antibiotics should be ad- preparation of the surgical field, the affected eyelids
ministered preoperatively. should be sutured closed using a monofilament, nonab-
sorbable suture material in a simple continuous pattern.
A tail of suture should be left at each end of the incision
Retrobulbar Anesthesia
to facilitate manipulation of the eye during surgery. The
General anesthesia or sedation (see Chapter 16) with palpebral skin is incised 3 to 4 mm from the eyelid
local retrobulbar anesthesia may be used for enucleation margins using a #15 or #10 scalpel blade. Blunt dissec-
in sheep and goats.1 In small ruminants a 3.75-cm, 22- tion is then performed circumferentially, using curved
gauge, slightly curved needle may be used for retrobulbar scissors and proceeding deeply into the eyelids and exter-
anesthesia. A four-site retrobulbar injection technique nal to the extraocular muscles. The optic nerve and
desensitizes the optic nerve, extraocular muscles, and vessels should be clamped with a curved hemostat, then
sensory portions of the eye and adnexa. Landmarks for ligated and transected. The bony orbit should be gently
the injections are the dorsal, ventral, medial, and lateral lavaged several times with sterile saline solution contain-
edges of the bony orbit. Topical ophthalmic anesthetic ing a broad-spectrum antibiotic. Closure of the remain-
(0.5% proparacaine) should be applied before injection to ing soft tissues may be attempted to reduce postoperative
desensitize the cornea and conjunctiva. The surgeon’s sinking of the eyelids; however, this is often difficult in
index finger should be used to deflect the globe and small ruminants because of their rather deep and wide
protect it from the needle as each injection is adminis- bony orbit. The subcutaneous tissues are closed using ab-
tered. The clinician palpates the wall of the bony orbit sorbable suture (2-0 to 3-0) in a simple continuous or
and inserts the needle from the conjunctival fornix until it subcuticular pattern. The skin is closed using nonab-
encounters the apex of the orbit. Approximately 1 to 2 ml sorbable suture (2-0) in a simple interrupted pattern.
of local anesthetic (2% lidocaine) or mepivacaine is in- Systemic antibiotics and antiinflammatory drugs should
jected at each site as the needle is advanced. be continued for several days after surgery. Some sur-
geons place a modified head bandage for a few days to
compress the enucleated orbit and decrease postoperative
Surgery
swelling. All enucleated eyes should be submitted for
Enucleation may be performed using the subconjunctival histopathologic examination to determine the exact cause
or transpalpebral technique. The subconjunctival ap- of ocular disease.
proach removes only the globe and usually causes less
hemorrhage. If a prosthesis is to be placed for a more cos-
metic result, the subconjunctival approach should be
used. The transpalpebral approach is indicated in cases of
R EFERENCE
1. Skarda RT: Local and regional anesthetic techniques: ruminants
ocular infection or neoplasia; it involves removal of the and swine. In Thurmon JC, Tranquilli WJ, Benson GJ, editors: Vet-
entire globe, conjunctiva, extraocular muscles, and nicti- erinary anesthesia, ed 3, Baltimore, 1996, Williams & Wilkins.
 Chapter 13

DMammary
iseases of the
Gland
DAVID E. ANDERSON, BRUCE L. HULL, AND D.G. PUGH

Diseases of the teats and udders of sheep and goats are terial blood supply to the udder is provided by the exter-
less extensively discussed in the veterinary literature than nal pudendal artery. Blood from this artery courses
those of dairy cattle. However, these diseases are no less through the inguinal ring after originating from the ab-
important or significant to the dairy or meat goat or dominal aorta and traveling through the external iliac
sheep farmer. Mastitis is a significant problem for the artery, deep femoral artery, and pudendal epigastric trunk.
goat and sheep dairy industries and can result in poor The venous blood from the udder is drained by the exter-
milk production and low weaning weights among meat nal pudendal veins, the caudal superficial epigastric veins,
breeds. Problems of the teat and udder that require and the perineal veins. The iliohypogastric and ilioin-
surgery seem to be much less common in small rumi- guinal nerves innervate the cranial udder. The gen-
nants than in cattle. This is especially true in sheep, itofemoral nerve innervates the caudal udder.
where the most common teat and udder surgeries include The teat wall is composed of five layers. The inner-
udder amputation following a gangrenous mastitis and most layer is very thin and is made up of epithelium and
removal of large, fibrotic udders so that the genetic po- mucosal tissue. A layer of connective tissue, rich in blood
tential of the animal is preserved. Indications for teat supply, surrounds the inner layers. External to the con-
surgery may change as the dairy sheep industry grows in nective tissue layer is the muscular layer, which is com-
the United States. posed of both circular and longitudinal muscle fibers.
Externally the teat is covered by stratified squamous
epithelium. The teat mucosa surrounds a teat cistern (teat
ANATOMY sinus, lactiferous sinus) that is filled with milk during lac-
The mammary system of sheep and goats includes two tation. The teat cistern is continuous proximally with the
glands, each of which have one teat.1,2 The principal gland cistern but is demarcated from it by a distinct
support for the udder is the medial and lateral suspensory annular ring. This annular ring contains a large vein that
ligaments. The medial suspensory ligament is elastic in encircles the base of the teat and is occasionally referred
nature; each half of the udder has a medial suspensory to as Furstenberg’s venous ring. Located at the distal end
ligament, and they adhere tightly to each other. The of the teat and connecting the teat cistern to the outside
medial laminae are composed of elastic sheets of tissue is the streak canal (teat canal, papillary duct). This struc-
arising from the ventral abdominal wall and dividing the ture is lined by longitudinal folds of stratified squamous
udder into two halves. The lateral suspensory ligament epithelia that produce keratin plugs. At the junction of
arises from the pelvic symphysis, subpelvic tendon, and the teat cistern and the streak canal is the rosette of
prepubic tendon. Secondary laminae arise from the Furstenberg. This rosette is created when the epithelium
medial and lateral laminae to support lobes of the udder. of the teat cistern meets the stratified squamous epithe-
The indentation formed between the two halves of the lium of the streak canal. The circular teat sphincter
udder is associated with the medial laminae and is re- muscle lies directly beneath the rosette of Furstenberg at
ferred to as the intermammary groove. the proximal end of the streak canal. The streak canal
The two halves of the udder are distinct and are sup- varies from 0.5 to 1.0 cm in length and ends externally at
plied by separate arteries, veins, and nerves. The main ar- the teat orifice.
• 341 •
342 • Sheep and Goat Medicine
MILK PRODUCTION all types of equipment have their limitations. On ultra-
Much of the emphasis on milk and milk production has sound examination, the normal udder displays a uniform
traditionally dealt with feeding meat and fiber sheep and mixture of hyperechogenic and hypoechogenic material.
goats for optimal milk production to maximize weaning Abscesses, tumors, and fibrotic tissue are hyperechogenic,
weights. Chapter 2 addresses some of the feeding con- and milk is hypoechogenic. If the clinician is in doubt
cerns in this area with dairy goats and sheep. Other pro- about the status of a female’s udder, comparing the results
duction concerns include the length of lactation and the with ultrasound images of a normal female’s udder can
amount of milk produced, the effects of machine milking, greatly aid in assessment. The anatomy of the gland,
and production-related diseases. Dairy goats that kid an- annual ligament, and teat cistern can all be evaluated.
nually lactate for 305 days of the year. Similar to sheep,
dairy goats experience peak milk production at 6 to 8
weeks after giving birth.3 As with their dairy cow coun-
BIOPSY
terparts, they usually “dry off ” 60 days before giving birth. Mammary biopsies are not commonly performed. In rare
Goats allowed a shorter dry period may experience de- cases in which mammary tumors are suspected, a clini-
pressed production in the following lactation.3 The lacta- cian can sedate the animal, anesthetize and aseptically
tion curve of meat goats and sheep is much steeper than scrub the skin over the area, insert a biopsy instrument
that of dairy goats.3 (14 gauge) through the skin, and collect the tissue. The
As a general rule, feeding the dairy goat (and to some area to be biopsied should be carefully palpated for proper
extent the dairy sheep) is similar to feeding dairy cows. placement of the biopsy needle. This procedure is en-
Similar to cows, high-producing dairy goats are in a neg- hanced by first measuring the depth of the abnormality
ative balance for energy and some other nutrients during with real-time ultrasound equipment or using ultrasound
early lactation.4 As production begins to taper off, they to help guide the operator in collecting the biopsy. If a
begin to replete their body stores. As with dairy cows, the seepage of milk occurs, the biopsy site was located too
three basic problems limiting productivity of dairy goats close to a superficial duct or cistern. In this case a purse-
and sheep are nutrition, reproduction, and mastitis (see string suture should be applied around the biopsy site
Chapters 2 and 6). after the biopsy has been taken. However, these rare milk
Inflammation of the mammary gland can result from leaks usually heal without intervention.
trauma, infective organisms (viruses, bacteria, fungi), and
environmental insults (freezing temperatures, irritating MILK CULTURE AND
substances). When treating a doe or ewe with a mammary
disease, unless an emergency situation such as excessive ANTIBIOTIC SENSITIVITY
hemorrhage exists, the clinician should gather a complete Whenever milk is encountered that is abnormal in color,
history and perform a thorough physical examination. consistency, or odor or comes from a hot and inflamed
The gland should be uniformly soft and symmetric. It udder, it should be collected from the affected half for
should have a similar temperature to the rest of the body microbial culture and antibiotic sensitivity patterns. After
and be free of swelling, edema, and pain. The superficial a standard washing and drying of the teat, the teat end
inguinal (supramammary lymph) node should be barely should be scrubbed with an alcohol swab or pad (70%
palpable, not excessively hot, and pain-free on light pal- ethanol), the teat should be expressed and “first n fore”
pation. Careful palpation alone is an excellent diagnostic milk should be discarded, and then several milliliters of
tool; teats should be thin, uniform, and normal in appear- milk should be aseptically collected into a sterile milk
ance. Milk should be easily expressed or stripped out culture tube or container. The sample should be refriger-
without overt signs of pain. If the female is lactating, the ated (4° C or 39° F) if it is not immediately cultured,
examiner should express some milk into a black plate or but it should be swabbed onto a blood agar plate within
strip cup to evaluate it for abnormal color, consistency, 24 hours. Samples should be frozen if more than 24
and clots or flakes. Other diagnostic tests to augment the hours will elapse before submission to the laboratory.
assessment of the mammary gland include the California Mycoplasma may be a cause of mastitis, and when it is
mastitis test (CMT). suspected Mycoplasma-specific culture media may be
employed.
ULTRASOUND
Real-time ultrasonography may be useful for identifying
SOMATIC CELL CULTURE
tumors, abscesses, granulomas, and excessive fibrosis. Cells in the milk are somatic cells and can be assessed
Many practitioners only have access to 5 MHz linear with somatic cell culture (SCC). Infection that results in
array ultrasound equipment, but this equipment can be an increase in inflammatory cells increases the cells noted
successfully employed. A sector scanning machine usually on SCC. SCCs in goats are less reflective of subclinical
provides a wider view of the udder, and a 3.5 MHz trans- intramammary infection than an SCC of cow’s milk.3
ducer allows for deeper udder visualization. Obviously, The cytoplasmic droplets produced by the goat’s apocrine
 Chapter 13 Diseases of the Mammary Gland • 343

secretion of milk result in an artificially elevated SCC if usually much smaller. When supernumerary teats are
electronic counting methods are used. Methods of deter- found in rams and bucks, these teats are usually located
mining the SCC that measure deoxyribonucleic acid cranial to the scrotum. A distinction must be made between
(DNA) or involve direct microscopy are more applicable supernumerary and bifid teats (see the next section).
for the goat. Still, an increased SCC may be used to indi-
cate an inflammatory response in the goat. Treatment. Supernumerary teats are usually removed
with serrated scissors when the kid or lamb is young.
Teats should always be removed so the resultant cut is
CALIFORNIA MASTITIS TEST craniocaudal and the scar blends with the normal folds
The CMT is a commonly used method of estimating the of the udder. If supernumerary teats are not removed
cellularity of milk in cows, sheep, and goats. Milk (2 to 3 until the animal is older, they should be dissected and
ml) is stripped into the CMT paddle, an equal volume of sutured after tranquilization and local anesthesia.
reagent is added, and the changes in viscosity of the After tranquilization and the administration of local
mixture of milk and CMT reagent is graded a negative, anesthesia, the supernumerary teat should be dissected
trace, 1, 2, and 3. The greater the degree of viscos- with an elliptic incision in a cranial-to-caudal orienta-
ity (or the higher the number), the more cellular the milk tion. This dissection provides visualization of the glan-
and possibly the greater the degree of inflammation. This dular epithelium and mucosa from which the super-
test is a good screen to predict the potential for infection numerary teat arose. This tissue is closed with a simple
and to compare the two halves.3 continuous suture of fine (3-0 or 4-0) absorbable
monofilament material. The adjacent connective tissue
should also be closed with a continuous suture of fine ab-
DISEASES sorbable material. The skin should then be closed with
interrupted sutures of nonabsorbable material (polymer-
Supernumerary Teats ized caprolactam, polypropylene). An alternate method is
Accessory teats or supernumerary teats may be separate to crush the teat base with a Burdizzo emasculatome and
and not connected to the primary mammary gland, or cauterize the base with silver nitrate.
they may be connected to the primary teat or gland.
However, usually they are separate and have a function-
ally separate mammary gland.1,2 Small supernumerary
Bifid Teats
teats that are completely separate from the main teats are Bifid teats (fused teats, forked teat) may be fused for a
rarely observed in goats. When seen, supernumerary teats variable distance but always have two teat sphincters and
are generally located caudal to the main teats and are two teat orifices (Figure 13-1). They are considered to be

Figure 13-1 Bifid teat in a goat. Note the presence of two orifices.
344 • Sheep and Goat Medicine
an inherited defect, and surgical correction of them is itary component of this defect must be considered, al-
considered unethical. Therefore unless an extra teat is though no breeding studies have been done to date.
clearly a separate and distinct teat the kid or lamb should
not be used as a dairy or meat replacement animal. These
abnormalities appear to be more common among pygmy
Poor Suspensory Ligament Support
goats and other non-dairy goat breeds.2 The suspensory ligaments of the udder may become pre-
maturely disrupted or may be congenitally malformed, re-
sulting in abnormal udder conformation. The base of the
Weeping Teats udder is abnormally low, the teats may be splayed (angled
Weeping teats (Figure 13-2) are probably a variation of laterally), and the walls of the teats may expand (balloon
what is called a web teat in dairy cattle. In goats these teat) if connective tissue damage includes the teats. Ab-
small masses of secretory tissue, which are usually numer- normalities of udder conformation are undesirable, and
ous, are commonly located on the teat near its base, but affected animals and their offspring should not be se-
may be located on the udder near the base of the teat.2 lected for use as replacement stock.
These masses of secretory tissue usually communicate to
the outside through small pores in the side of the teat.
Ultrasound examination (real-time, B-mode) is useful
Uneven (Asymmetric) Udders
to confirm the diagnosis (Figure 13-3). These tissues An asymmetric udder is seen occasionally in goats, but
become obvious in early lactation because of contamina- rarely in sheep. This abnormality should not be the sole
tion of the teat skin with the secretions. Occasionally one reason to cull an affected animal. Goats seem to be more
or two of these small masses of secretory tissue does not prone to this type of udder problem than other domestic
have an opening and accumulates milk to form a milk species. Asymmetric udder abnormality may occur at
cyst in the wall of the teat (usually near its base). In rare freshening, in which the udder is more developed on one
cases, gland development may be extensive with a true side than the other (Figure 13-4). This is more common
web teat formation (see Figure 13-3). in primiparous animals, but affected animals may have
Although chemical cauterization using silver nitrate normal udder conformation in subsequent lactations. The
has been suggested to treat these cystic structures, this abnormality may be caused by unsynchronized or uneven
treatment is often not satisfactory because of the wide- udder development.
spread nature of the extraneous secretory tissue.2 A hered-
Precocious Udder
Udder development in non-pregnant goats is not uncom-
mon2 (see Figure 13-5). Examination of precocious
udder development should be aimed at differentiating
between udder enlargement because of fat deposition,
high estrogen concentrations in feeds (e.g., moldy corn,

Figure 13-2 Weeping teat in a goat. Note the presence of cystlike Figure 13-3 An ultrasound image of the teat in Figure 13-2. Note
structures at the base of the teat. the presence of cysts (*) in the wall of the base of the teat.
 Chapter 13 Diseases of the Mammary Gland • 345

clover), intersex, and true milk production associated result from the vascular fragility associated with hydro-
with persistent corpus luteum or natural prolactin-like static congestion.
substances. Response to empirical treatment with prosta-
glandin F2a (5 mg intramuscularly [IM]) suggests the in- Treatment. Udder edema usually resolves with time,
fluence of a persistent corpus luteum. These goats should but treatment is occasionally warranted. When needed,
not be milked because they are at an increased risk of treatment may involve the administration of antiinflam-
mastitis. If milking is required to relieve pain, infusion of matory drugs (flunixin meglumine 1 to 2 mg/kg intra-
an intramammary product may be advisable to guard venously [IV] or IM), diuretics (furosemide 2 to 10
against the development of mastitis. Also, feeding man- mg/kg IV or IM), steroids (dexamethasone 0.1 to 1
agement to attempt “dry off ” should be done. This may mg/kg IV or IM), as well as more frequent milking and
include eliminating grain sources and feeding poor- possibly hydrotherapy. If edema recurs in subsequent
quality roughage but should not include water depriva- lactations, viral involvement (ovine progressive pneu-
tion. In rare cases the precocious udder may become pen- monia virus [OPPV] or caprine arthritis-encephalitis
dulous, self-traumatized, or mastitic or may suffer teat [CAE] virus) or genetic influences should be suspected.4
damage severe enough to warrant udder amputation (see These animals should be selected for culling when
Chapter 7). possible.

Udder Edema Gynecomastia

Udder edema occurs sporadically in dairy breeds of sheep Some male goats from heavy milk-producing lines of
and goats. It can be diagnosed by finding pitting edema certain breeds (e.g., Saanen, Alpine) can experience udder
around the external aspect of the mammary glands, espe- development, lactate, and on occasion develop mastitis.
cially cranial to the udder. Affected animals do not Excessive udder development in these males more com-
exhibit hot udders or changes in milk quality. Udder monly occurs in the summer months. Energy and protein
edema may be present before or can develop after partu- intake in these males should be reduced during times of
rition.4 If prepartum udder edema is present, the glands the year when they are prone to lactate (spring and
should not be milked out. Prepartum milking increases summer) or when these animals begin to lactate. Affected
the risk of hypocalcemia and mastitis, which may con- males appear to be of normal fertility. A mastectomy,
tribute to the failure of passive transfer of colostral anti- when necessary, can be performed as described for
bodies to lambs or kids. Udder edema is most common in females.
primiparous females and may be associated with inade-
quate development of venous and lymphatic drainage
from the udder. Inadequate drainage may be caused by
Skin Diseases
rapid engorgement of the udder in the final stages of ges- Diseases affecting the skin of the udder are discussed in
tation without venous and lymphatic adaptation. Occa- Chapter 7.
sionally blood is seen in the milk and is presumed to
OBSTRUCTION TO MILK FLOW
Blind Half
Rarely, “blind” mammary glands may be observed when
females begin their first lactation. Blind glands usually
occur on one side only and may be caused by congenital
defects of the mammary gland or by granulomatous or
viral mastitis early in the development of the udder. A
Saanen goat was determined to have a congenitally blind
udder because the milk ducts failed to unite with the
gland cistern.5

Hard Milker
“Hard milkers,” as seen in the cow, are rarely encountered
in sheep or goats. However, when they are observed they
may be treated in a similar manner as affected cattle. A
hard milker in a sheep or goat may be caused by trauma to
Figure 13-4 An asymmetric udder in a young goat. the teat end or may just be due to a congenitally small
346 • Sheep and Goat Medicine
(tight) teat sphincter. When trauma occurs it is usually in syringe and a 27-gauge needle. The goal of this procedure
the form of a crushing injury and is often self-inflicted. is to tighten the teat sphincter by stimulating scar tissue
Animals occasionally crush their teat between their leg development. Unfortunately, this is often unrewarding.
and the floor when trying to rise. Obviously, because of The owner should be warned that injecting Lugol’s might
their small udder size this injury is extremely rare in result in sloughing of the tissues because goats’ teats seem
sheep. Other causes for this type of trauma are poor to be even more sensitive than those of cattle.
milking machine function (delivering excess vacuum to
the teat end) and frostbite of the teat end. Frostbite is ob-
viously a seasonal event. Any traumatic insult to the area
Teat “Spider” and Lactoliths (Milk Stones)
of the teat sphincter causes the formation of scar tissue in The term teat spider is usually used to describe scar tissue
this area, which may lead to a small stream of milk and from the wall of the teat that hinders complete and rapid
slow milking. This type of injury is therefore often self- milking. As such, teat spiders seldom occur in small ru-
perpetuating. The typical history is that one half of the minants. However, small ruminants are somewhat prone
udder takes a lot longer to milk out than the other half in to small floating pieces of scar tissue that have broken off
dairy breeds or that one half of the udder is never milked from within the secretory tissue of the udder as a sequela
out in meat breeds. This longer milking effort increases to mastitis. Goats also occasionally get lactoliths, which
the trauma to the end of the teat and may in time increase are small, mineralized deposits. Lactoliths, or milk
the amount of scar tissue and make the animal even more stones, are concretions formed within the teat cistern.
difficult to milk. The trauma to the teat end coupled with These concretions are most likely caused by incomplete
incomplete milking may lead to mastitis. milking and may be formed by precipitation of debris and
mineral composites contained in the milk. In either case
Treatment. If surgery is indicated to increase the size these small floating objects may occlude the streak canal
of the milk stream, the use of a small teat knife is prefer- and obstruct milk flow.
able to other methods of opening a hard milker because
most other instruments (designed for cattle) open the Treatment. If the offending mass is small it may be
sphincter too far and create permanent leakage. Surgery manually massaged out of the streak canal with a combi-
for a stenotic teat sphincter should be performed before nation of hydrostatic pressure (forceful milking) and ma-
the morning milking so that surgical response can be nipulation of the teat end. If this is not possible and the
monitored and proper aftercare can be initiated through- mass is small or pliable it can be extracted with an alliga-
out the day. After aseptic preparation of the teat skin and tor forceps inserted into the teat cistern through the
end, the surgeon inserts a teat knife through the streak streak canal.
canal, taking care to avoid cutting the entire length of the If neither procedure works, the teat must be opened
streak canal. The surgeon angles the knife at 45 degrees (thelotomy) to remove the offending foreign object. Elec-
and makes a cut at the rosette of Furstenberg (area of the tive thelotomy does not carry the high risk of incision
sphincter muscle) before gently removing the knife from failure that is commonly observed after laceration sutur-
the teat. The teat is forcefully milked to assess progress. If ing. The success of thelotomy results from its minimal
necessary the teat sphincter is cut 180 degrees from the tissue damage, limited contamination, and the short time
first cut. These cuts can be repeated at 90 degrees separa- interval between incision and closure. The teat should be
tion if necessary. Milk flow should be evaluated after each opened along its long axis. At this point the teat cistern
cut. Evidence of the correct amount of cut is provided by can be explored and the offending foreign body or scar
the teat dripping a fine stream of milk for a minute or two tissue removed. The teat is then closed as described for
after a forceful stream of milk is expelled from the teat. teat lacerations in the following section.
After surgery the quarter should have several streams
of milk expressed every 15 minutes for the next 2 or 3
hours and then once every hour until the next milking.
Teat Lacerations
This stripping must be forceful because the goal is to Teat lacerations in sheep and goats appear to be less
prevent closure of the incisions. The owner or clinician common than teat lacerations in cattle, but they can be
can help break down any fibrinous adhesions that may just as devastating if left untreated. If repair of teat lacer-
start to form between the cut edges by rolling the end of ations is to be attempted, the clinician should tranquilize
the teat between the thumb and finger. the animal and use ring block of a local anesthetic (2% li-
Overzealous treatment of the hard milker may cause docaine hydrochloride); general anesthesia may be prefer-
permanent leakage and increase the risk of mastitis. An able in some cases. The prognosis for teat laceration treat-
enlarged teat orifice is very difficult to treat. Treatment ment depends on several factors and can vary from good
may be attempted by injecting 0.1 ml of Lugol’s iodine at to hopeless.6-11 Needless to say, full-thickness lacerations
four places around the teat end (each at 90 degrees’ sepa- (into the teat cistern) have a much poorer prognosis than
ration). The solution is injected using a tuberculin (TB) partial-thickness lacerations. The fresher a laceration is,
 Chapter 13 Diseases of the Mammary Gland • 347

the better it heals. The prognosis is poorer for lacerations titis detection is performed. If she is being hand milked
that are more than 4 hours old, and after about 12 hours the owner or clinician may choose to prepare the teat
the prognosis is extremely poor. Because of the nature of carefully with alcohol and drain the milk with a teat tube
the blood supply of the teat, vertical (longitudinal) lacer- for 4 or 5 days before resuming hand milking.
ations heal far better than horizontal lacerations and lac- If a horizontal laceration that is not full thickness
erations near the base of the teat (its attachment to the results in a ventrally based skin flap, the blood supply
udder) heal better than lacerations of the distal teat. Lac- should be carefully evaluated. If the blood supply is inad-
erations that involve the teat sphincter and streak canal equate, the flap should be trimmed to healthy tissue. The
have a much poorer prognosis than those that do not remaining wound may be closed in some cases or left to
involve these structures because anatomic repair and granulate if the remaining tissue is inadequate for closure.
return to complete function are more difficult to achieve Any full-thickness teat laceration or laceration that
in this area. damages the teat end should be treated as though it
were a case of mastitis. Culture and sensitivity tests are
Treatment. Before attempting repair the clinician must probably indicated and certainly appropriate antibiotics
clean and thoroughly evaluate the laceration for any (both intramammary and systemic) should be employed.
small, deep holes that may be covered by fibrin clots. However, the clinician should be careful during intra-
Even small fistulas change the method of repair and the mammary infusion to avoid damaging the repair. Because
prognosis. If the clinician is to attempt repair of a lacera- the teat has an excellent blood supply the skin sutures can
tion of unknown duration or a laceration known to be usually be removed in 10 days.
more than 4 hours old, extensive débridement may be
necessary. Any tissue that is infected, necrotic, or devital-
ized must be completely removed. Often, however, very
Teat Fistula
little “extra” tissue is available and delicate dissection is Teat fistulas are rare in sheep and goats and usually result
necessary to remove desiccated tissue while preserving all from the unsuccessful repair of a teat laceration or from a
the normal tissue possible. Débridement should continue laceration in which no repair was attempted.
until fresh bleeding tissue is uncovered.
After anesthesia and débridement have been accom- Treatment. If the initial repair fails, the laceration
plished, suturing with fine (4-0 or smaller) absorbable should be allowed to granulate until the swelling and in-
suture increases the chance of success. If full-thickness fection subside. During this period the wound should be
lacerations are not sutured but rather left to granulate, the cleaned daily and mastitis prevention measures instituted
majority will heal by second intention with fistula forma- for 2 to 4 weeks.
tion. The lining tissue should be sutured with a simple After the wound has granulated to an end-stage
continuous pattern using fine (4-0 or 5-0) absorbable fistula, surgery should be performed to correct it.6-11
suture material with a swaged-on atraumatic needle. The After preparation and administration of a ring block, the
tissue must be sutured carefully to obtain a milk-tight entire fistulous tract is dissected out of the surrounding
seal. After completely closing the tissue the clinician may tissue. This may be accomplished with an elliptic incision
wish to insert a teat cannula through the teat sphincter (around the fistula) parallel to the long axis of the teat.
and gently probe the suture line to check for holes or This dissection must be performed all the way to the teat
weak areas. If the inner lining is not sutured, granulation cistern. After the dissection has been completed, the
tissue may proliferate into the lumen of the teat cistern defect is closed as described for teat lacerations (three-
and obstruct milk flow. When suturing full thickness in layer closure).
the mucosal surface the clinician is more certain to seal Dissection of teat fistulas is extremely difficult if not
the mucosa completely and prevent milk fistulas. Because impossible in sheep or goats with small teats. In these
this inner surface tissue is very thin and delicate it should cases, teat size precludes surgery because insufficient teat
be supported by another simple continuous layer of fine tissue is available to dissect the fistula and close the
absorbable suture placed in the submucosa. The submu- wound adequately.
cosa of a teat is not a distinct layer, but rather the tissue
directly adjacent to the mucosa and epithelial lining. The
remainder of the teat wall should be closed with vertical
Udder Amputation
mattress sutures of a non-capillary material. A deep “bite” Udder amputation is perhaps the most common mam-
of the vertical mattress suture is placed adjacent to the mary surgery in small ruminants. This surgical proce-
submucosal suture line to give it support. If the animal is dure is performed when an owner wishes to keep the
being machine milked she can be put back on the animal (either for genetic potential or as a pet) after the
machine at the next scheduled milking. Research in cattle udder has become too pendulous for normal function. In
suggests that one quarter can be rested for 7 days and still sheep of exceptional value the udder may be amputated
return to function if daily palpation of the gland for mas- after long-term chronic mastitis has left a non-secretory
348 • Sheep and Goat Medicine

Figure 13-5 Large udders are a common finding in goats. These illustrations show an enlarged
injured udder of a pregnant 6-year-old Boer-cross goat. She had been grazing and doing well (body
condition score 3) until the owner noticed her dragging something behind her.

fibrotic mass for an udder. In these cases the animal is

often a “poor doer” because of the chronic infection. In
goats, udders may be amputated because of chronic fi-
brotic mammary tissue (as with sheep) or excessive size
(Figure 13-5) resulting from inappropriate lactation syn-
drome (see Chapter 7). Goats are more prone to preco-
cious milking than any other domestic species. Although
many medical therapies have been attempted to cease this
milking, they are seldom successful. Often these are pet
animals that the owner does not wish to milk. In other
cases the owner gets tired of milking the animal on a con-
tinual basis. Regardless, without milking the udder in
some cases increases in size over time until it grows large
enough to become uncomfortable for the animal and un-
sightly for the owner. At this point the owner of a pet Figure 13-6 Circumferential incision made around the base of
sheep or goat often elects udder amputation. the udder.
Udder amputation is not a procedure to be undertaken
lightly because the animal is often in poor physical condi-
tion and/or anemic as a result of the chronic nature of the animal should be positioned in dorsal recumbency to fa-
infectious process.12 Additionally, the clinician must con- cilitate working on both sides of the udder. If dorsal re-
sider the mass of the udder to be removed and the poten- cumbency is not possible the animal will need to be rolled
tial for serious hemorrhage. The owner should be made from one side to the other during surgery and the appro-
aware of these potentially serious consequences. General priate preparations should be made. The ventral abdomen
anesthesia, although not an absolute necessity, is certainly is clipped and aseptically prepared for surgery.
preferable. The external pudendal artery should be ligated before
A blood donor should be available or blood should be any of the venous system is occluded. This allows the
drawn and banked in case a blood transfusion is needed. blood contained by the udder to drain back into the cir-
Most of the time, udder amputation is an elective proce- culation before the udder is removed. The surgeon makes
dure. Therefore the animal should be fasted for 24 to a skin incision parallel to the base of the udder and about
48 hours, and broad-spectrum antibiotics should be ad- 3 to 5 cm ventral to the dorsal edge of the mammary
ministered up to 4 hours before surgery. Although this tissue (Figure 13-6). Eventually this incision will extend
surgery can be attempted on a heavily sedated animal completely around the udder in an elliptic manner. Hem-
with lumbosacral epidural anesthesia, general anesthesia orrhage can be controlled by either cautery or ligation.
is usually required (see Chapter 16). If possible the After incising the skin, the surgeon carefully extends the
 Chapter 13 Diseases of the Mammary Gland • 349

incision through the lateral suspensory ligament of the and/or suppressing local immune function (secondary to
udder. Care should be taken at this point because the ex- increased stress-related cortisol output).13 Grazing im-
ternal pudendal artery and vein lie directly beneath the proved pastures and implementing feeding practices that
lateral suspensory ligament. The external pudendal artery favor excessive milk production may predispose to masti-
and vein course from the inguinal ring in a tortuous tis.13 Surveys of goat dairy herds indicate that mastitis
manner. They should be ligated separately where they exit may occur in 13% to 20% of lactating does.14,15 Sheep,
the inguinal ring. The clinician should exercise extreme goats, and cattle share many pathophysiologic processes,
caution during this procedure. If separation is difficult, and diagnostic and treatment principles established for
the artery and vein can be ligated or double-ligated to- cattle can easily be adapted to use on sheep and goats.
gether. This raises the possibility of an arteriovenous Replacement livestock and animals with mastitis
shunt, but this rarely occurs. After the artery and vein should be examined for predisposing factors, including
have been ligated on one side, the procedure should be re- teat fistula, accessory teats, trauma, pendulous udder, and
peated on the opposite side unless only half of the udder udder edema. Dairy animals are most susceptible to
is being amputated. mammary infections at parturition but may be infected
At this point the clinician extends the incisions (each through lactation or even after drying off. Brood ewes
side) cranially and ligates the subcutaneous abdominal and does most commonly develop mastitis between par-
veins. Traditionally reports have suggested that there is one turition and weaning. Ewes have the same risk factors as
subcutaneous abdominal vein for each half of the udder, goats, but after their lambs are 4 to 6 weeks of age, if milk
more commonly these veins have numerous branches as needs (such as those of twins) exceed production, teat
they approach the udder. Each branch must be individu- trauma can result from hungry lamb bites, particularly in
ally ligated or double-ligated. After the subcutaneous ab- poor producers.3 With mastitis the udder becomes hot,
dominal veins have been ligated, the skin incisions are ex- swollen, and painful; however, affected animals also may
tended caudally and the perineal veins are ligated. There display few or no outward signs. Nevertheless, meat and
should be one perineal vein on each side, although this is fiber animals suffering from mastitis and referred for
somewhat variable. treatment are usually sick, anorexic, and febrile and are
After ligating all the major vessels, the clinician cuts often toxic. Animals affected with subclinical mastitis
the median suspensory ligament near the body wall. often fail to produce enough milk to raise their young or
Ideally, about 1 to 2 cm of medial suspensory ligament wean smaller young and have increased scar tissue on
should remain on the body to provide a place to anchor some areas of the udder. Whenever possible, owners or
the skin and help obliterate dead space during closure. If clinicians should palpate udders before purchase, before
only half of the udder is being amputated, the right and breeding, and at parturition. Herd problems from masti-
left half of the median suspensory ligament can be sepa- tis or increased somatic cell counts should be thoroughly
rated, with the half of the median suspensory involved investigated. With dairy animals, milking technique,
with the amputated half being severed. milking hygiene, milking machine function (proper vac-
After amputating the udder, the clinician closes the uum pressure), environmental risk factors, and personnel
skin, obliterating the dead space if possible. This usually should all be evaluated.16
includes placing some of the sutures into the median sus-
pensory ligament while closing the skin. The surgeon
may choose to place a drain in the dead space for several
Agalactia
days after surgery. Agalactia has many causes in sheep and goats, including
After surgery first intention healing is desired, but age of the female, poor prepartum gestation, genetics, and
second intention healing seems to be more common. Al- some diseases. Some infectious causes include CAE and
though umbilical tape has been traditionally used as the ovine progressive pneumonia (OPP); previous bouts of
ligature of choice, postoperative infection is much less of mastitis that destroyed mammary tissue also can predis-
a problem with absorbable ligatures. If absorbable sutures pose to agalactia. Whenever agalactia is encountered
are used, the clinician should be aware of the large vessels females should undergo a complete physical examination
that are being ligated and employ appropriately sized and be tested for these diseases. Affected animals should
sutures. Antibiotics should be continued as needed, and be quarantined or, if genetics is the probable cause, culled.
any postoperative pain should be managed.
Acute Mastitis
Mastitis Acute mastitis may be recognized by the presence of heat,
Mastitis is common among all dairy and meat production redness, pain, swelling of the udder, and/or lameness or
livestock. Cold or wet environments and climatic condi- stiff walking. Palpation of the udder may reveal edema,
tions, muddy areas, and nutritional stress all may predis- firmness of the gland, and enlargement of the supramam-
pose to mastitis by reducing the blood flow to the udder mary lymph nodes. Milk stripped from the gland may
350 • Sheep and Goat Medicine
have an abnormal color, contain flakes or clots (garget),
and be thinner (serous) or thicker than normal. Bacteria
such as Escherichia coli and Mycoplasma species also may
cause septicemia or toxemia in the affected animal. This
may be recognized by increased rectal temperature, ele-
vated heart rate, decreased appetite, and marked reduc-
tion in milk production.14

Coliform Mastitis
Coliform mastitis seems to be less common among small
ruminants when compared with cattle. E. coli and Kleb- Figure 13-7 A goat with gangrene mastitis. Note the dark color of
the distal portion of the left (far) gland.(Courtesy Dr. Tom Powe,
siella species are the most common coliform bacteria im- Auburn, Alabama.)
plicated in mastitis.2,5 Coliform mastitis is more common
in the post-parturient period and is associated with severe
systemic disease. It can be either a persistent or transient from an alteration in mammary blood flow during the
infection.3 disease process that causes a change in udder color. The
most common pathogens isolated from affected udders
Clinical signs. Affected animals may have fever, are Staphylococcus aureus and Pasteurella haemolytica.18 S.
anorexia, apparent depression, lethargy, and high heart aureus is most commonly associated with the gangrenous
rate; shock and death may ensue if the infection is not form of the disease. P. haemolytica may be more common
treated. Milk changes to a small volume of a watery among range ewes. Mastitis can occur as an acute, a sub-
serosanguineous secretion. Palpation of the gland reveals acute, or a chronic infection. The disease may progress
heat, swelling, edema, and pain. Endotoxin and inflam- rapidly and be severe enough to result in the death of af-
mation may cause vascular thrombosis and gangrene, fected animals. The incidence of this infection increases
which can appear clinically similar to bluebag. with age and the number of lactations and is most
common during lactation.
Treatment. Treatment should include antiinflamma- S. aureus is a non-motile, non-encapsulated, non–
tory drugs (e.g., flunixin meglumine, 1 to 2 mg/kg IV), spore-forming, gram-positive, coagulase-positive, coccoid,
systemic antibiotics (oxytetracycline 10 mg/kg IV), and aerobic bacterium. Milk cytology reveals bacteria as
IV fluid therapy (see Appendix II) as needed. Use of singles, pairs, or chains of cocci. This bacterium is
aminoglycoside antibiotics should be avoided in food- common on the skin and mucous membranes of normal
producing animals because of prolonged and unpre- sheep and goats. It can be destroyed by heat (60° to 80° C
dictable drug elimination times. Intravenous administra- for 30 minutes) and some antiseptic agents (1% phenol
tion of 5% hypertonic saline solution (HSS) (dosed at 5 for 35 minutes contact time; 0.5% mercuric chloride for
ml/kg body weight over 5 minutes) is useful as a form of 60 minutes; 10% formalin for 10 minutes).18
shock therapy to improve cardiac output. P. haemolytica is a non-motile, non–spore-forming, en-
capsulated, gram-negative, bipolar, pleomorphic, aerobic
Prevention. Coliform bacteria are environmental patho- rod bacterium. It is found in the upper respiratory tract of
gens. Therefore control measures should be aimed at normal sheep and goats. This bacterium is more easily
proper hygiene. Bedding should be kept clean and dry. destroyed than S. aureus and is susceptible to heat (60° C
Other prevention measures include milking clean, dry for 10 minutes) and antiseptic chemicals (0.5% phenol
teats; providing teat dips (0.25 0 0.5 iodine) before and for 15 minutes). P. haemolytica can survive for weeks in a
after milking; wiping teats with a towel (used only on that favorable environment. This infection is more common in
animal); and maintaining optimal milking machine func- sheep than in goats, but outbreaks of P. haemolytica have
tion to avoid teat end injury.3 Post-milking dips should been documented in goats.19 In sheep, P. haemolytica
contain ingredients that are effective but do not result in often results from lamb-induced teat injuries, but some
milk residues. Vaccination against gram-negative “core ewes may be chronic carriers.
proteins” may be beneficial. These bacteria are most likely inoculated onto the teat
end by flies, excessive or aggressive nursing that causes
teat end damage, poor milking machine hygiene, or con-
Bluebag taminated bedding and pastures. Infection is followed
The bluebag form of mastitis is an infectious disease that rapidly by a severe inflammatory response. Pain and in-
is only rarely contagious.15 It is a common concern for flammation cause a marked decrease in milk production.
sheep and goat farmers (Figure 13-7). Its name comes S. aureus toxins cause vascular thrombosis and subsequent
 Chapter 13 Diseases of the Mammary Gland • 351

gangrene and tissue sloughing. P. haemolytica infection Treatment. Response to therapy is often poor, but if
may lead to abscess formation; these abscesses may treatment is instituted it should be based on culture and
rupture through the skin of the udder. sensitivity results.
Arcanobacterium pyogenes may cause infection in non-
Clinical signs. The acute form of bluebag produces the lactating animals. Development and rupture of udder ab-
clinical signs of fever (41° to 42° C), decreased feed scesses are typical of this infection. Milk becomes puru-
intake, refusal to lay down, and lameness because of udder lent and has a foul odor. Although susceptible to a
pain. Animals infected by P. haemolytica may exhibit variety of antibiotics, infection with this bacterium is dif-
lameness of the rear legs early in the course of the disease. ficult or impossible to cure because of the formation of
Typically only half of the udder is infected. The skin is udder abscesses. Therefore these animals serve as carriers
initially erythematous and hot, but becomes cyanotic of infection in the herd. Affected animals should be
(hence the name bluebag) and cold as the infection pro- culled to prevent continued contamination of the milking
gresses.17 The udder may become very edematous. equipment and/or herd mates. Affected halves in geneti-
Animals that survive may slough the udder or the af- cally superior animals may be treated to cease milk pro-
fected half. Milk decreases in volume and becomes a duction by the infusion of some caustic solutions (60 to
serous and watery or bloody and brown secretion with 120 ml of a 2% chlorhexidine solution twice a day for 2
fibrinous debris. In cases of mastitis caused by P. haemo- to 3 days).
lytica, concurrent lamb pneumonia may be encountered. Streptococcal mastitis is caused by a variety of Strepto-
In sheep flocks, 5% of sheep may be infected. Mortality coccus species. Streptococci may cause individual or herd
rates approach 50% for P. haemolytica and 80% for S. outbreaks of mastitis. Some streptococci (e.g., S. zooepi-
aureus infection if no treatment is provided. Toxemia and demicus) may cause udder abscesses, atrophy, and chronic
shock may cause death in either case. The affected gland mastitis. S. agalactiae causes mastitis sporadically in goats.
usually does not return to complete milk production in Infection with this bacterium may result in fibrosis and
surviving sheep and goats. loss of milk production but is often not associated with
systemic signs. S. dysgalactiae and S. uberis are more
Treatment. Antimicrobial drug therapy should be common causes of mastitis. These bacteria are spread by
based on culture and sensitivity results, but empirical se- poor milking machine or personnel hygiene.
lection of b-lactam or tetracycline antibiotics based on Bacillus cereus and other Bacillus species cause mild to
historical susceptibility patterns is justified. In cases of S. severe (gangrenous) mastitis in goats. This organism is a
aureus infection, antibiotics do not appear to reach the or- soil and water contaminant.3 Other pathogens rarely re-
ganism and are therefore of limited value. Toxemia may ported in sheep include Clostridium perfringens and Lep-
be treated with fluid therapy (see Appendix II) and nons- tospira hardjo. C. perfringens is associated with an acute
teroidal antiinflammatory drugs (NSAIDs; flunixin meg- gangrenous mastitis, whereas L. hardjo may result in a
lumine 1 to 2 mg/kg IV or IM). However, in most cases sudden depression in milk output.
therapy is unrewarding. Affected animals that survive
should be culled. In severe cases of gangrenous mastitis, Clinical signs. Acute mastitis produces udder swelling,
udder amputation may be the treatment of choice. If a pain, decreased milk production, and abnormal milk.
chronic problem exists in a flock, the production and use
of an autogenous bacterium should be considered. Treatment. Treatment includes a combination of sys-
temic and intramammary antibiotics based on culture and
sensitivity tests. Empirical systemic antibiotic therapy
Miscellaneous Bacterial Mastitis may be instituted with trimethoprim-sulfadimethoxine,
Pseudomonas species have been associated with mastitis and intramammary treatment may be instituted with
and are usually spread by a contaminated water supply or cephalosporin-based products.
teat dips.3 Mastitis may be severe enough to cause sys-
temic clinical signs, including septicemia and hemor-
rhagic milk. P. aeruginosa and P. pseudomallei have been
Subclinical Mastitis
isolated from animals with clinical cases of mastitis. In Subclinical mastitis is one of the most common causes
one study, P. aeruginosa was associated with purulent mas- of culling animals from the flock. As the name implies,
titis that progressed to gangrene and death in some it is a form of mastitis or inflammation of the mam-
goats.5 Experimental inoculation with the isolated bacte- mary gland that insidiously drains the animal’s produc-
ria caused hemorrhagic mastitis in some goats and a tive ability. Subclinical mastitis in sheep and goats is
watery greenish secretion in others; severe inflammation caused by a variety of bacteria, including Bacillus species,
in the udder, fever up to 41° C (106° F), and decreased Staphylococcus epidermidis, E. coli, P. aeruginosa, A. (Actin-
milk production also were observed. omyces, Corynebacterium) pyogenes, A. pseudotuberculosis,
352 • Sheep and Goat Medicine
BOX 13-1

P ATHOGENS I SOLATED FROM M ASTITIC M S ILK AMPLES IN G OATS

SUBCLINICAL MASTITIS MASTITIS CHRONIC MASTITIS

(FREQUENCY %) (FREQUENCY %) (FREQUENCY %)
Staphylococcus species Staphylococcus epidermidis (24.6%) Culture positive (66.7%)
(59.1%; 12 species): Escherichia coli (11%) Staphylococcus aureus
S. aureus (17.2%) Pseudomonas aeruginosa (8%) Beta-hemolytic Streptococcus
S. epidermidis (14.2%) Staphylococcus aureus (7%) Streptococcus agalactia
S. capitis (12.8%) Arcanobacterium pyogenes (3%) Coagulase negative
Bacillus species (29.9%) Arcanobacterium pyogenes (3%) Staphylococcus
Coliforms (4.3%) Enterobacter cloacae (3%) Arcanobacterium pyogenes
Micrococcus species (2.6%) Streptococcus species (3%) Pseudomonas species
Streptococcus species (1.9%) Pseudomonas putida (1%) Pasteurella species
Corynebacterium, Bacillus species (1%) No growth (33.3%)
Arcanobacterium (1.5%) Klebsiella pneumoniae (1%)
Pseudomonas species (0.7%) Gram-positive rods (1%)
No growth (35.6%)

From Turner CW, Berousek ER: Blind halves in a goat’s udder, J Dairy Sci 25:549, 1942; Kalogridou-Vassiliadou D: Mastitis-related pathogens in
goat milk, Small Rumin Res 4:203, 1991; Lerondelle C, Richard Y, Issartial J: Factors affecting somatic cell counts in goat milk, Small Rumin Res
8:129, 1992; Chineme CN, Addo PB: Chronic caprine mastitis: clinical, microbiological and pathological findings in spontaneously occurring cases
in Nigerian goats, Intl Goat and Sheep Res 3:266, 1984; Rowe JD: Milk quality and mastitis, Proceedings of the 1998 Symposium on the Health and
Disease of Small Ruminants Western Veterinary Conference, 1998, Las Vegas, NV; Van Tonder EM: Notes on some disease problems of Angora goats
in South Africa, Vet Med Rev 1:109, 1975.

Klebsiella species, and other environmental pathogens presence of DNA-containing cells. The test solution lyses
(Box 13-1).21,22 cells to release DNA, which then coagulates to a visible
gelatin- or mucus-like material. The pH detector turns
Clinical signs. Subclinical mastitis may be recognized dark purple in alkaline milk and tan to yellow in acidic
by poor lamb or kid growth, neonatal malnutrition, and milk. The CMT is not interpreted as stringently in sheep
neonatal death caused by starvation in meat breeds. In and goat milk because these species typically have higher
dairy breeds, low daily milk production is the most somatic cell counts; a CMT of trace or 1 should be con-
common finding. Occasionally, udder abscesses are recog- sidered within normal limits for this test (Table 13-2).
nized by swelling, edema, or rupture and subsequent pu- Sheep and goat milk contains relatively higher somatic
rulent exudate. cell counts compared with that of cattle. A typical
somatic cell count range for sheep and goats is 0 to
Diagnosis. Diagnosis of subclinical mastitis is by pal- 500,000 cells/ml (see Table 13-2). Mild inflammation in-
pation of the udder and/or milk culture. Other tests help- creases the count to the 500,000 to 2,000,000 cells/ml
ful for identifying animals with subclinical mastitis are range. The somatic cell count is inversely related to milk
SCCs and CMTs. Herd managers should be encouraged production. As milk production decreases in late lacta-
to perform routine udder palpation and milk tests when tion, the somatic cell count increases because a similar
animals freshen and at appropriate intervals according to number of cells are diluted in a lesser volume of milk.23
the management system. Differentiation of various types The count approaches 5,000,000 cells/ml in normal
of pathogenic bacteria has become easier and may be per- goats near the end of lactation. A more useful applica-
formed in a general practice without submitting samples tion of CMT and SCC is to compare results between
to commercial laboratories (Table 13-1). However, accu- udder halves. In one study, udder halves infected with
rate identification of species of bacteria may require the coagulase-negative Staphylococcus had a mean somatic cell
use of a commercial microbiology laboratory. Whenever count of 932,000 cells/ml, udder halves infected with
culturing halves, the clinician should communicate to the other major pathogens had a mean somatic cell count
diagnostic laboratory that non-hemolytic Staphylococcus of 2,443,000 cells/ml, and uninfected udder halves had
may be a cause of subclinical mastitis and should be in- a mean somatic cell count of 272,000 cells/ml. If milk
cluded in any findings. The CMT is based on pH and the from one half of the udder scores markedly higher on the
 Chapter 13 Diseases of the Mammary Gland • 353

TABLE 13-1

DIFFERENTIATION OF BACTERIAL CULTURE ISOLATES

GRAM-POSITIVE ORGANISMS GRAM-NEGATIVE ORGANISMS

Cocci Rods Yeast Rods Cocci

Uncommon Rare
Catalase Catalase Oxidase
Positive Negative Positive Negative Positive Negative
Staphylococcus Streptococcus Bacillus Actinomyces Pasteurella Escherichia coli
Corynebacterium pyogenes Pseudomonas Klebsiella
Pseudotuberculosis Enterobacter
Serratia
Proteus
From Smith MC, Sherman DM: Mammary gland and milk production. In Smith MC, Sherman DM, editors: Goat Medicine, Baltimore, 1994,
Williams & Wilkins.

TABLE 13-2 Treatment and Prevention

of Bacterial Mastitis
MILK TESTS AND INTERPRETATION
A variety of regimens have been used to treat mastitis in
CALIFORNIA sheep and goats. Response to therapy varies with the type
MASTITIS SOMATIC CELL of pathogen causing the disease. Difficulties with par-
TEST RESULT CULTURE (CELLS/ML) INTERPRETATION enteral treatment of mastitis during lactation are dis-
cussed by Pyorala et al.26 In this study, 452 dairy cows
Negative 0 to 480,000 Normal were treated with either parenteral procaine penicillin G,
Trace 0 to 640,000 Normal spiramycin, or enrofloxacin; 35 cows were treated with
1 240,000 to 1,440,000 Normal supportive care only (all 35 had E. coli infection). The cure
2 1,080,000 to 5,850,000 Mastitis rate was 34% for S. aureus, 76% for coagulase-negative
3 More than 10,000,000 Mastitis Staphylococcus, and 65% for Streptococcus. Heifers experi-
From Smith MC, Sherman DM: Mammary gland and milk encing their first lactation had higher cure rates than
production. In Smith MC, Sherman DM, editors: Goat medicine, older cows. Mastitis caused by E. coli was cured in 74% of
Baltimore, 1994, Williams & Wilkins. cows receiving procaine penicillin G and 71% of cows re-
ceiving supportive care only. Cows affected with mastitis
early in the course of lactation suffered more severe clini-
CMT or SCC compared with the contralateral gland, a cal signs when infected with coagulase-negative Staphylo-
diagnosis of subclinical mastitis is justified and culture coccus or E. coli. The authors of the study concluded that
should be performed. Research investigating improved penicillin therapy may be beneficial in heifers in their first
diagnostic tests for mastitis continues. Some recent tech- lactation, but not in older cows and not for coliform mas-
niques include measuring electrical conductivity, anti- titis.26 The results of this study appear to be applicable to
trypsin, N-acetyl-b-D-glucosaminidase (NAGase), fat, sheep and goats.
and protein content.15,22-25 In cases of toxic or gangrenous mastitis, treatment
S. epidermidis is commonly associated with mastitis in consists of hydration maintenance with either IV or oral
dairy goats and may be the most common bacterium im- fluids (see Appendix II) or hypertonic saline (4 ml/kg
plicated in chronic progressive mastitis.3 This bacteria is IV), administering NSAIDs (flunixin meglumine 1 to 2
spread from the skin of goats or milking personnel and mg/kg), and milking out every 2 to 3 hours.27 Oxytocin
may cause acute mastitis. administered at each milk-out may aid in milk removal.
The use of antibiotics is controversial. Still, many owners
Prevention. Preventive measures include keeping all and clinicians include broad-spectrum antibiotics in their
housing and dry lots clean and avoiding muddy areas. treatment protocols. If the mastitis is not associated with
When “drying off ” or at weaning, the owner or clinician systemic signs, stripping the affected half out every 2 to 3
may choose to infuse halves with a “dry cow” infusion. If hours may be all that is required.27 If the animal survives
halves were treated during lactation, a different class of and the udder does not slough, a partial mastectomy (pre-
antibiotics should be used for “dry off ” infusion. viously discussed) can be performed. An alternative pro-
354 • Sheep and Goat Medicine
cedure to surgery is the infusion of the udder with Lugol’s Where possible, identification (by milk culture or
iodine or chlorhexidine solution. Infusion with either of CMT) and culling of all affected animals should be
these results in drying and “killing” the half.28 carried out because these animals may serve as sources of
Intramammary infusions are an accepted practice at continuing flock infection. As previously stated, milking
dry-off in dairy cattle and may be of some value in sheep technique, milking machine function, and diet should all
and goats.26-28 In one study, 49 does with bacterial mas- be carefully evaluated. Ewes or does that are thin (body
titis (coagulase-negative Staphylococcus, C. bovis, S. uberis) condition score less than 2.5) should be fed enough to
had the infected udder half treated at dry-off with ensure adequate milk output. This may help minimize
cephapirin benzathine intramammary infusion.29 Udder teat and udder trauma from hungry lambs or kids. Lambs
halves were monitored for treatment success or the devel- or kids whose dams are poor milkers should be identified
opment of new infection. Also, antibiotic residues were and fed a supplement. Hungry lambs and kids may trans-
determined at freshening. At the time of freshening, mit infection if they are “bumming” or nursing milk from
78.9% of infected quarters had been cured. All treatment numerous ewes and does. This may be more of a problem
failures occurred in udder halves infected with coagulase- in lambs infected with bacterial respiratory disease (Pas-
negative Staphylococcus (8 of 40 were not cured). Fewer teurella species) (see Chapter 5). Contagious ecthyma
than 7% of udder halves not infected at dry-off were should be prevented because it may predispose to bacter-
found to be infected at the time of freshening. This study ial or fungal mastitis. Providing proper shelter; clean,
emphasized the possibility of selective treatment of udder non-muddy paddocks; and clean, uncontaminated bedding
halves at dry-off rather than the standard practice of dry are all paramount in preventing both clinical and non-
treatment of all udders (current recommendations for clinical mastitis. All handling, lounging, or feeding areas
dairy cows include the use of nonselective dry cow infu- should be well drained. Dry ewe or doe teat infusion and
sion). Antibiotic residues were detected in only one goat, possibly post-infusion teat dipping at weaning or drying
suggesting that prolonged antibiotic residues may remain off also can reduce flock infection rates.13,20,28 If teat
when bovine intramammary preparations are used in or udder infusion with antibiotics is used, good aseptic
goats. Another study evaluated the effect of intramam- technique should be emphasized. The drastic practice of
mary infusions on bacterial infection and somatic cell withholding feed and/or water 24 to 48 hours before
count in goats. Treatments included infusion of a combi- weaning is probably of only marginal value. Still, decreas-
nation product after the last milking (penicillin, nafcillin, ing feed intake to meet but not exceed maintenance at or
dihydrostreptomycin) and no infusion at dry-off.30 Only just before weaning may be of some value in decreasing
19.8% of control goat udder halves were culture-negative milk output and reducing mastitis cases. All ewes and
2 weeks after freshening, compared with 71% of udder does should be closely monitored for signs of mastitis for
halves treated by intramammary infusion. One study31 the first 2 weeks after weaning.
evaluated the effect of intramammary infusion of ewes
that were infused at the time of lamb weaning and cul-
tured again 1 to 3 weeks after freshening. Untreated
Mycoplasma Mastitis
control ewes were 2.6 times more likely to develop new Mycoplasma species are increasingly recognized as signifi-
intramammary infections compared with treated ewes. cant pathogens in the udder.33-41 Mycoplasma-induced
Interestingly, the presence of one infected udder half was mastitis should be suspected when clinical signs support a
associated with a higher risk of the other half of the diagnosis of mastitis but repeated attempts to culture bac-
udder becoming infected.31 In a Canadian study,32 tilmi- teria fail to identify a significant pathogen. Diagnostic
cosin given parenterally to multiparous ewes 1 month laboratory techniques have improved greatly in recent
before lambing was shown to improve the growth of their years, and identification of Mycoplasma species pathogens
lambs compared with lambs from untreated control ewes. is performed more readily. Mycoplasma-infected milk may
Lambs from tilmicosin-treated ewes were 0.52 kg heavier be a significant source of infection for young animals,
at 50 days of age, compared with lambs from untreated which then develop arthritis and keratoconjunctivitis.
ewes. The tilmicosin treatment resulted in a 43% de- Feeding of mastitic milk to young kids and lambs is dis-
crease in palpable udder abnormalities compared with couraged because it may result in lifelong infection (see
the controls. However, no difference in the incidence of Chapters 5 and 9).
clinical mastitis was noted between the two groups. M. agalactiae (the causative organism of contagious
Therefore a management protocol of giving tilmicosin agalactia) may produce acute or chronic mastitis in sheep
(10 mg/kg IM) at the time of prelambing vaccination and goats.2 This pleomorphic gram-negative bacterium
may improve lamb weaning weights by decreasing the in- is hemolytic on blood agar. Contagious agalactia is most
cidence of subclinical mastitis.32 Tilmicosin is not ap- common in European and Middle Eastern countries and
proved for use in sheep in the United States, but it is ap- rare in the United States; it is a federally reportable
proved in Canada. Its use should be avoided in goats (see disease. Infective organisms contaminate the environ-
Appendix I). ment through milk, urine, nasal and ocular secretions,
 Chapter 13 Diseases of the Mammary Gland • 355

exudate from joints, and secretions from the reproduc- are variable, prognosis is poor, and a carrier state may
tive tract. persist.

Clinical signs. Clinical cases are observed most often Prevention. Because udder damage is considered per-
during spring months. Often infection of the udder manent, culling of infected sheep and goats is advised.
occurs during the final trimester of gestation. After being Carrier animals may remain clinically normal and shed
ingested, M. agalactiae invades the intestinal wall, where organisms for months or years during times of stress (e.g.,
it multiplies and then gains entry into the bloodstream, parturition, relocation). Herd control measures may
causing a sustained septicemia. During the septicemic include serologic testing (if available for the specific strain
period the animal’s temperature may rise to 41° or 42° C identified), intermittent bulk tank cultures to detect dairy
(105° to 107° F) and the affected animal becomes anorec- animals with subclinical disease, culture of colostrum at
tic. Foci of infection may become established in the freshening, pasteurization of milk before feeding to
udder, uterus, eyes, and joints. Clinical signs may be ob- young stock, isolation or culling of clinically affected
served as soon as 5 to 7 days after inoculation of infective animals, use of individual towels for each udder when
organisms or as late as 60 days after ingestion of infective cleaning in the dairy parlor, and close attention to
organisms from the environment. Interstitial mastitis hygiene by personnel. Vaccination with strain-specific
causes fibrosis and reduced milk production. Milk from vaccines may be useful, but concerns about the persistence
infected udders is more alkaline than normal, has a of carrier animals in the herd remain (see Chapter 5).
yellow color, segregates into layers on standing with a Because milk is the major route for infection for My-
green-yellow supernatant, and exhibits granular sedimen- coplasma in kids, many of the same protocols for preven-
tation in the bottom of the receptacle. As the disease pro- tion of CAE are useful in preventing Mycoplasma masti-
gresses, the udder atrophies and milk production is se- tis.37 Removing kids from dams at birth and feeding
verely decreased. them heat-treated colostrum (60 minutes at 56° C) helps
M. arginini, although considered non-pathogenic, has prevent this disease. Identifying carrier animals through
been associated with mastitis in goats.39,40 Affected culture testing, removing them from the herd or flock,
goats suffer marked decreases in milk production and and implementing proper milking hygiene practices also
exhibit purulent exudate and large numbers of leukocytes are crucial to preventing Mycoplasma mastitis.37,38
in the milk.
M. putrefaciens has been isolated from cases of acute
and subclinical mastitis. Acute mastitis caused by this or-
ZOONOTIC PATHOGENS
ganism may be associated with agalactia, abortion, and Raw milk consumption poses certain risks for the trans-
arthritis. However, glandular fibrosis is not a common mission of zoonotic disease (Box 13-2). Listeria monocyto-
finding despite the marked leukocyte increases in milk. genes rarely causes interstitial mastitis. However, this bac-
M. mycoides subspecies capri, M. mycoides subspecies
mycoides, and M. capricolum have been associated with
mastitis in goats.2,41 Mastitis caused by these pathogens
is characterized by purulent exudate in the milk, thicken- BOX 13-2
ing of the milk, markedly decreased milk production, en-
larged supramammary lymph nodes, and systemic dis-
eases such as arthritis, pneumonia, and conjunctivitis. A
Z OONOTIC P P
ATHOGENS OTENTIALLY

6-year-old French Alpine goat exhibited decreased ap-

petite and milk production, fever (41° C), an auricular
C ONTAMINATING R S AW HEEP OR G MOAT ILK

abscess, and mastitis.41 In this case the milk was watery SECRETED INTO MILK CONTAMINANTS
and yellow. Serology confirmed a diagnosis of M. mycoides Brucellosis Campylobacter
subspecies mycoides.37 Corynebacterium Escherichia coli
Agalactia caused by Mycoplasma species infection is pseudotuberculosis Listeria monocytogenes
followed by udder atrophy. However, resolution of the Leptospirosis Listeria monocytogenes
udder may be followed by normal lactation after the next Salmonella
parturition because glandular fibrosis is not common with Coxiella burnetii
Mycoplasma-induced mastitis. Mycobacterium bovis
Mycobacterium avium
Treatment. Although treatment for mastitis caused by subsp. paratuberculosis
Mycoplasma may be attempted with tiamulin, tylosin (20
mg/kg IM twice a day [BID]), erythromycin (3 to 5 From Smith MC, Sherman DM: Mammary gland and milk
mg/kg IM BID), or tetracycline (10 mg/kg IV once a day production. In Smith MC, Sherman DM, editors: Goat medicine,
[SID] to BID or 20 mg/kg every 48 hours), success rates Baltimore, 1994, Williams & Wilkins.
356 • Sheep and Goat Medicine
terium is occasionally isolated from milk cultures. The tinues, but total production levels are generally depressed.
zoonotic potential of this pathogen is of great concern Milk production was evaluated in a herd of Alpine goats
and affected animals should either be treated until proven infected with CAE.44 Approximately 36% of the herd
free of disease or culled from the herd. However, the was seropositive to CAE by agar gel immunodiffusion
owner and clinician should bear in mind that proving an (AGID). Production parameters were higher for seroneg-
animal free of disease is difficult. Mycobacterium bovis, M. ative goats (696 kg milk, 24 kg butterfat, and 21 kg of
tuberculosis, and M. avium may cause subacute or chronic nonfat solids) than for seropositive goats (656 kg milk, 20
mastitis. Palpation of the udder reveals hard nodules in kg butterfat, 20 kg nonfat solids). Diagnosis is by thor-
the parenchyma. Infection is confirmed by an intradermal ough palpation of the udder, failure to yield Mycoplasma
tuberculin skin test, and affected animals are culled under species or other bacteria on culture, observation of mono-
federal supervision. nuclear infiltrates on histology, and positive serology or
immunofluorescent antibody tests. Affected goats should
be culled because treatment response is poor. Kids born to
Fungal Mastitis affected does should be removed immediately from the
Fungal infection of the udder is infrequently diagnosed. doe and given colostrum and milk free of CAE virus and
Most often, fungal infection is associated with prolonged Mycoplasma species (see Chapters 6, 9, and 14).
or repeated administration of antimicrobial drugs into the
udder by intramammary infusion. A variety of infective
fungi have been identified, including Candida albicans,
Prevention of Mastitis
Aspergillus fumigatus, A. terreus, Cryptococcus albidus, C. Prevention of mastitis is best accomplished by close at-
neoformans, Yersinia pseudotuberculosis, Nocardia species, tention to hygiene, milking equipment maintenance,
Rhodotorula glutinis, and Geotrichum candidum. Treatment optimal nutrition, and proper animal care and housing.37
of fungal mastitis is not generally recommended because Various guidelines have been established for the preven-
it requires the administration of drugs not approved for tion of mastitis (Table 13-3). Maintaining clean, dry
use in food-producing animals. bedding and properly cleaning lambing jugs helps
prevent the spread of some organisms (e.g., P. haemolyt-
ica). If milking machines are used on sheep or goat
VIRAL MASTITIS dairies, careful monitoring and maintenance of equip-
ment is required.5 Post-milking teat dipping, dry doe or
Chronic Indurative Mastitis of Sheep ewe treatment, and identification of all infected animals
Sheep flocks infected with OPPV suffer high morbidity (by culture testing) are paramount in control of the more
but low mortality.2 The udder appears full but has a firm contagious pathogens (S. aureus and Mycoplasma spe-
texture on palpation. Milk production is markedly cies).3 Dry doe or ewe teat infusion can be based on cul-
reduced and the teats fail to fill up with milk.38 Although ture and antibiotic sensitivity testing, but broad-spectrum
the disease may be present at first lactation, the incidence infusions without culture and sensitivity testing are com-
is highest among ewes older than 3 years. Milk color and monly administered with good response. When My-
content appear normal. This viral infection causes coplasma infection is suspected, removing kids at birth
periductal lymphoid proliferation and lymphoid follicle and feeding them only pasteurized colostrum are good
formation, which results in alveolar atrophy. Milk flow is preventive techniques. Clipping or burning udder hair,
inhibited; fibrosis of the parenchyma results in firmness cleaning the teats before and after milking (using a sepa-
on palpation. Clinical signs among meat breeds include rate towel for each animal), and dipping before and after
poor lamb or kid growth. Dairy breeds suffer decreased milking are good procedures in problem herds.3 Perform-
milk production. Diagnosis is made by virus isolation or ing CMTs, identifying infected animals, maintaining
serology (see Chapters 6 and 14). them in a separate area from uninfected animals, and
milking them last helps minimize the spread of disease.
Ewes and does that are marginal milk producers near
Hard Udder of Goats weaning should be provided a palatable creep feed for
Hard udder is a chronic fibrosing mastitis of goats caused their young (see Chapter 2) to help minimize udder
by the CAE virus, which is nearly identical to OPPV in trauma caused by aggressive nursing. Whenever chronic
sheep.2,18,42 This viral infection causes an interstitial mastitis occurs or chronically high somatic cell counts are
mastitis characterized by periductal lymphocytic infiltra- encountered, the dietary adequacy of energy, protein,
tion and subsequent fibrosis. Although the udder is ex- water, macronutrients, and micronutrients should be in-
tremely firm on palpation and little milk can be expressed, vestigated. Adequate dietary selenium (0.2 to 0.3 ppm),
udder edema, erythema, and heat are not evident. Super- copper (7 to 11 ppm in sheep; 10 to 15 ppm in goats),
ficial inguinal lymph nodes may become enlarged. This zinc (more than 25 ppm), molybdenum (a copper-to-
form of mastitis is seen in some animals at puberty.43 molybdenum ratio of 6:1), and vitamin E should be made
Milk production may increase as the lactation cycle con- available.
 Chapter 13 Diseases of the Mammary Gland • 357

TABLE 13-3

TECHNIQUES USED TO PREVENT MASTITIS IN DAIRY ANIMALS

RISK FACTOR INTERVENTION

Pathogen exposure Provide clean, dry bedding

Eliminate overcrowding
Bedding material Provide sand or crushed limestone for bedding material
Avoid wood shavings and straw unless excellent management is available
Milking procedures Maintain a clean, stress-free parlor
Check foremilk, California mastitis test (CMT), black plate, strip cup, and milk
Identify affected animals (CMT, culture, somatic cell culture testing) and milk them last or with
a separate claw
Wash teats and udder
Strip milk
Dry teats with single-use towels
Pre-dip teats (optional)
Dry teats again with single-use towels
Attach teat cup as soon as teats are full of milk
Adjust and monitor milking unit
Vacuum off before removing teat cups
Dip teats after milking
Disinfect teat cups between animals
Check milking machine vacuum and function periodically
Herd health Provide teat infusion for the doe or ewe using appropriate antibiotics at “dry off ”
Adapted from Turner CW, Berousek ER: Blind halves in a goat’s udder, J Dairy Sci 25:549, 1942; Sharma SP, Iyer PKR: Pathology of chronic
lesions in the mammary glands of goats (Capra hircus). 2: Fibrocystic disease and intraductal carcinomas, Ind J Anim Sci 44:474, 1974; Nickerson
SC: Mastitis management: strategies to combat mastitis, Agri-Pract 16:17, 1995.

Neoplasia gently with dairy industry personnel to achieve milk

Neoplastic conditions of the udders of sheep and goats quality assurance.
are rare. Skin tumors are most common and include squa- Treatment recommendations should respect guidelines
mous cell carcinoma and papilloma. Saanen goats have a described in the Animal Medicinal Drug Use Clarifica-
breed-specific predisposition to udder papillomatosis.6 tion Act (AMDUCA) to avoid residue contamination of
This condition also is associated with white udder skin meat and milk. Sheep and goats differ from cattle in
color. One selection criterion for replacement dairy goats many drug dosages and drug elimination times. There-
should be darker skin color (tan versus white). Teat and fore, whenever possible, drug withdrawal times should be
udder papillomas may progress to squamous cell carci- drawn from research performed specifically on sheep or
noma or erode into the teat cistern and cause mastitis and goats. One author has recommended doubling the with-
permanent loss of the affected udder half. The most drawal times established for cattle when applying the
common mammary neoplasia reported in goats is intra- same products in goats.2 The main component in avoid-
ductal carcinoma, but the prevalence of this neoplasm is ance of drug resistance is proper record-keeping and
very rare (0.08% in two studies).45,46 Mammary adeno- identification of treated animals.
carcinoma also has been diagnosed in a goat.47 Both ade-
nocarcinoma and fibroepithelial hyperplasia have been
diagnosed in goats.43 R EFERENCES
1. Pasquini C, Spurgeon T: Anatomy of domestic animals, ed 5, Pilot
Point, TX, 1989, Sudz Publishing.
Drug Residue Avoidance 2. Smith MC, Sherman DM: Mammary gland and milk production.
In Smith MC, Sherman DM, editors: Goat medicine, Baltimore,
Preservation of a wholesome milk product that is free 1994, Williams & Wilkins.
of contaminants is paramount to the dairy sheep and 3. Rowe JD: Milk quality and mastitis, Proceedings of the 1998 Sympo-
goat industry. Nearly all treatments for mastitis and sium on the Health and Disease of Small Ruminants Western Veteri-
udder diseases are performed in an extra-label manner nary Conference, 1998, Las Vegas, NV.
because relatively few drugs are approved for use in 4. East NE, Birnie EF: Diseases of the udder, Vet Clin North Am Food
either sheep or goats. Veterinarians must work dili- Anim Pract 5:591, 1983.
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5. Turner CW, Berousek ER: Blind halves in a goat’s udder, J Dairy 28. Matthews JG: Outline of clinical diagnosis in the goat, London,
Sci 25:549, 1942. 1996, Wright Publishing.
6. Arighi M et al: Invasive teat surgery in dairy cattle II. Long-term 29. Fox LK, Hancock DD, Horner SD: Selective intramammary an-
follow-up and complications, Can Vet J 28:763, 1987. tibiotic therapy during the nonlactating period in goats, Small
7. Bristol DG: Teat and udder surgery in dairy cattle—Part I, Comp Rumin Res 9:313, 1992.
Cont Ed Pract Vet 11:868, 1989. 30. Poutrel B et al: Control of intramammary infections in goats:
8. Bristol DG: Teat and udder surgery in dairy cattle—Part II, Comp impact on somatic cell counts, J Anim Sci 75:566, 1997.
Cont Ed Pract Vet 11:983, 1989. 31. Hueston WD, Boner GJ, Baertsche SL: Intramammary antibiotic
9. Ducharme NG et al: Invasive teat surgery in dairy cattle I. Surgi- treatment at the end of lactation for prophylaxis and treatment of
cal procedures and classification of lesions, Can Vet J 28:757, 1987. intramammary infections in ewes, J Am Vet Med Assoc 194:1041,
10. Modransky P, Welker B: Management of teat lacerations and 1989.
fistula, Vet Med 88:995, 1993. 32. Croft A et al: The effect of tilmicosin administered to ewes prior
11. Trent AM: Teat surgery, Agri-Pract 14:6, 1993. to lambing on incidence of clinical mastitis and subsequent lamb
12. Kerr HJ, Wallace CE: Mastectomy in a goat, Vet Med 72:1177, performance, Can Vet J 41(4):306, 2000.
1978. 33. DaMassa AJ: Recovery of Mycoplasma agalactiae from mastitic
13. Bruere AN, West DM: The sheep: health, disease and production, goat milk, J Am Vet Med Assoc 183:548, 1983.
Palmerston North, New Zealand, 1993, Massey University Press. 34. DaMassa AJ et al: Caprine mycoplasmosis: acute pulmonary
14. Lewter MM et al: Mastitis in goats, Comp Cont Ed Vet Pract disease in newborn kids given Mycoplasma capricolum orally, Aust
6:S417, 1984. Vet J 60:125, 1983.
15. Vihan VS: Determination of NA-Gase activity in milk for diagno- 35. DaMassa AJ, Brooks DL, Holmberg CA: Induction of mycoplas-
sis of subclinical caprine mastitis, Small Rumin Res 2:359, 1989. mosis in goat kids by oral inoculation with Mycoplasma mycoides
16. Kalogridou-Vassiliadou D, Manolkidis K, Hatziminaoglou J: subsp. mycoides, Am J Vet Res 47:2084, 1986.
Changes in mastitis pathogens in goat milk throughout lactation, 36. DaMassa AJ, Wakenell PS, Brooks DL: Mycoplasmas of goats and
Small Rumin Res 4:197, 1991. sheep, J Vet Diagn Invest 4:101, 1992.
17. Kimberling CV: Diseases of ewes. In Kimberling CV, editor: 37. East NE: Mycoplasma mycoides polyarthritis of goats. In Smith BP,
Jensen and Swift’s diseases of sheep, ed 3, Philadelphia, 1988, Lea & editor: Large animal internal medicine, ed 2, St Louis, 1996,
Febiger. Mosby.
18. Van Tonder EM: Notes on some disease problems of Angora goats 38. East NE et al: Milkborne outbreak of Mycoplasma mycoides sub-
in South Africa, Vet Med Rev 1:109, 1975. species mycoides infection in a commercial goat dairy, J Am Vet Med
19. Chineme CN, Addo PB: Chronic caprine mastitis: clinical, micro- Assoc 182:1338, 1983.
biological and pathological findings in spontaneously occurring 39. Prasad LN, Gupta PP, Singh N: Isolation of mycoplasmas from
cases in Nigerian goats, Intl Goat and Sheep Res 3:266, 1984. goat mastitis, Ind J Anim Sci 54:1172, 1984.
20. Clarkson MJ, Winter AC: A handbook for the sheep clinician, ed 5, 40. Prasad LN, Gupta PP, Singh N: Experimental Mycoplasma argi-
Liverpool, UK, 1997, Liverpool University Press. nine mastitis in goats, Aust Vet J 62:341, 1985.
21. Kalogridou-Vassiliadou D: Mastitis-related pathogens in goat 41. Blikslager AT, Anderson KL: Mycoplasma mycoides subspecies my-
milk, Small Rumin Res 4:203, 1991. coides as the cause of a subcuticular abscess and mastitis in a goat, J
22. Lerondelle C, Richard Y, Issartial J: Factors affecting somatic cell Am Vet Med Assoc 201:1404, 1992.
counts in goat milk, Small Rumin Res 8:129, 1992. 42. Bulgin MS: Ovine progressive pneumonia, caprine arthritis-
23. Park YW: Interrelationships between somatic cell counts, electri- encephalitis, and related lentiviral diseases of sheep and goats, Vet
cal conductivity, bacteria counts, percent fat and protein in goat Clin North Am Food Anim Pract 6:691, 1990.
milk, Small Rumin Res 5:367, 1991. 43. Dawson M: Caprine arthritis encephalitis. In Boden E, editor:
24. Maisi P: Analysis of physiological changes in caprine milk with Sheep and goat practice, London, 1991, Bailliere Tindall.
CMT, NAGase, and antitrypsin, Small Rumin Res 3:485, 1990. 44. Smith MC, Cutlip R: Effects of infection with caprine arthritis-
25. Maisi P: Milk NAGase, CMT, and antitrypsin as indicators of encephalitis virus on milk production in goats, J Am Vet Med Assoc
caprine subclinical mastitis infections, Small Rumin Res 3:493, 193:63, 1998.
1990. 45. Sharma SP, Iyer PKR: Pathology of chronic lesions in the
26. Pyorala SHK, Pyorala EO: Efficacy of parenteral administration mammary glands of goats (Capra hircus). 2: Fibrocystic disease and
of three antimicrobial agents in treatment of clinical mastitis in intraductal carcinomas, Ind J Anim Sci 44:474, 1974.
lactating cows: 487 cases (1989-1995), J Am Vet Med Assoc 212:407, 46. Singh B, Iyer PKR: Mammary intraductal carcinoma in goats
1998. (Capra hircus), Vet Path 9:441, 1972.
27. Gessert ME: Flock health, Part II. Nutritional and infectious dis- 47. Anderasen CB, Huber MJ, Mattoon JS: Unilateral fibroepithelial
eases, Proceedings of the 1998 Symposium on the Health and Disease of hyperplasia of the mammary gland in a goat, J Am Vet Med Assoc
Small Ruminants Western Veterinary Conference, 1998, Las Vegas, 202:1279, 1993.
NV.
 Chapter 14

DImmunologic,
iseases of the Hematologic,
and Lymphatic
Systems (Multisystem Diseases)
CHRISTOPHER CEBRA AND MARGARET CEBRA

BASIC HEMATOLOGY skin into the vein at an approximate 30-degree angle. The
An adequate volume of blood for hematologic and bio- blood should not come out of the vessel in pulsatile
chemical analysis is best obtained from the jugular vein of waves; this is suggestive of an arterial stick. After asepti-
sheep and goats. The animal should be restrained in a cally obtaining an adequate volume of blood, the collector
standing position (goats or sheep) or tipped up (sheep removes the needle and releases the pressure on the vessel
only) with the head turned away from the jugular vein to near the thoracic inlet. Pressure should be applied to the
be used. Ideally the animal should be restrained by site of puncture for a minute or more to prevent extravas-
someone other than the blood collector, although the cular leakage of blood and hematoma formation. The
same person may be able to both restrain a sheep and blood should be carefully transferred to a vial containing
collect blood if the animal is tipped up or a halter is used the appropriate anticoagulant to prevent red blood cell
(Figure 14-1). The animal should be at rest, with minimal (RBC) rupture. Goat erythrocytes are small and particu-
excitement. The collector parts or clips the wool or hair to larly prone to hemolysis. To minimize this problem, goat
visualize the jugular vein and then uses the hand not blood should be collected with a needle and syringe, not a
holding the needle to apply digital pressure proximally Vacutainer. White blood cell (WBC) differential distri-
just above the thoracic inlet to block blood movement bution, individual blood cell staining characteristics, and
through the vein. The vessel may take a second or more to morphology may be assessed by microscopic examination
distend after pressure is applied. The collector may then of a stained blood film. The differential distribution pro-
use the needle-bearing hand to “strum” the vessel and vides more information than total WBC count because
cause the blood to oscillate. If in doubt about whether the inflammatory conditions in sheep and goats often result
distended vessel is the jugular vein, the collector can in a shift in neutrophil populations toward more degener-
release the hand placing pressure on the vessel and ate, toxic, or immature forms without changing the
observe whether the distended vessel disappears; if it overall WBC count.1 The preferred anticoagulant for a
does, the distended vessel was probably the jugular vein. complete blood count (CBC) is ethylenediaminetetraac-
The collector should avoid vessels that pulsate because etate (EDTA), and tubes should be filled to capacity to
these are likely the carotid arteries. The area should be ensure the proper blood-to-anticoagulant ratio. Blood
cleaned with alcohol or other disinfectant, water, or a samples should be processed as soon as possible after col-
clean, dry gauze sponge. An 18- or 20-gauge, 1- to 1.5- lection. If a delay is anticipated, the blood sample should
inch needle is usually adequate to collect blood from an be refrigerated (4° C) and an air-dried blood smear
adult sheep or goat, whereas a 22-gauge needle may be should be made because prolonged contact of blood with
used in a neonate. The skin of adults or males may be EDTA causes changes in WBC morphology and the sep-
thicker and more difficult to penetrate with the needle. A aration of some RBC parasites. Blood can be refrigerated
syringe or evacuated tube attached to a Vacutainer for 24 hours and still yield an accurate CBC.
(Becton Dickinson Inc., Rutherford, NJ) can be used to A reference range for hematologic data for sheep and
collect blood. The needle should be plunged through the goats is provided in Table 14-1. Goats tend to have a low
• 359 •
360 • Sheep and Goat Medicine
TABLE 14-1

NORMAL HEMATOLOGIC PARAMETERS FOR SHEEP AND GOATS

PARAMETER (UNITS) ADULT SHEEP ADULT GOAT

Hematocrit (%) 27 to 45 22 to 36
Hemoglobin (g/dl) 9 to 15.8 8 to 12
Red blood cell count (106/ml) 9 to 17.5 8 to 17
Mean corpuscular volume (fL) 28 to 40 15 to 26
Mean corpuscular hemoglobin
concentration (g/dl) 31 to 34 29 to 35
Platelet count (105/ml) 2.4 to 7.0 2.8 to 6.4
Total white blood cell count (/ml) 4000 to 12,000 4000 to 13,000
Segmented neutrophils (/ml) 1500 to 9000 1400 to 8000
Band neutrophils (/ml) 0 0
Lymphocytes (/ml) 2000 to 9000 2000 to 9000
Monocytes (/ml) 0 to 600 0 to 500
Eosinophils (/ml) 0 to 1000 0 to 900
Basophils (/ml) 0 to 300 0 to 100
Total plasma protein (g/dl) 6.2 to 7.5 6.0 to 7.5
Fibrinogen (mg/dl) 100 to 600 100 to 500

BONE MARROW
Bone marrow aspirates and core biopsy samples taken
from sites of active erythropoiesis can be useful to evalu-
ate erythrocyte production and determine the cause of
anemia and other hemogram abnormalities. The sites of
biopsy in sheep and goats include the sternebra, femur,
and ileum. The procedure should be done under chemical
sedation or anesthesia. The area over the biopsy site is
clipped and surgically prepared; the sampler should wear
sterile gloves to maintain asepsis. Aspirates can be ob-
tained by inserting a sterile needle attached to a 3- or 6-
cc syringe containing one or two drops of EDTA through
the bone and into the bone marrow. Drawing back on the
syringe plunger several times may aid in the procurement
of an acceptable sample; such a sample may consist of as
little as 0.5 ml of bone marrow. If the sample is going
to be processed immediately, no anticoagulant is re-
Figure 14-1 Placement of a needle into the jugular vein to attain quired. Core biopsies are obtained using a Jamshidi or
a blood sample. Westerman-Jensen biopsy needle. The skin is incised
with a scalpel and the biopsy needle is inserted into the
bone and turned several times to obtain a core sample.
mean corpuscular volume (MCV) because of their small More than one site may be used. The sampler then closes
erythrocytes. Small ruminants younger than 6 months the skin with sutures or staples. Biopsy samples are pre-
old tend to have lower hematocrit, RBC count, hemoglo- served by placing them in 10% neutral buffered formalin
bin, and plasma protein concentrations, as well as a solution. Impression smears can be made from these
higher total WBC count. Neonates often have a high samples by gently rolling them on a clean glass slide
hematocrit at birth that decreases with colostral inges- before placing them in the formalin solution (Figure
tion. Lactating animals may have decreased hematocrits, 14-2). Information obtained from bone marrow samples
RBC counts, and hemoglobin concentrations. Animals includes subjective data regarding cell density, megakary-
grazing at high altitude (mountain goats and Bighorn ocyte numbers, abnormal cells, maturation patterns of
sheep) tend to have increased RBC counts, hematocrits, RBCs and WBCs, and the ratio of erythroid to myeloid
and hemoglobin concentrations. cells. Prussian blue stain can be used on bone marrow to
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 361

dog bites, severe lacerations, and complications of castra-

tion or dehorning. CBC values appear normal immedi-
ately after acute blood loss. However, after a few hours of
fluid redistribution, anemia and hypoproteinemia are
evident. Evidence of red cell regeneration (macrocytosis,
reticulocytosis, nucleated red cells) should appear within
a day or two of the blood loss.
Hemolysis occurs most commonly after ingestion of
toxic plants, RBC parasitism, intravenous (IV) injection
of hypotonic or hypertonic agents, contact with bacterial
toxins, water intoxication, or immune-mediated destruc-
tion of opsonized erythrocytes. Ingested toxins include
Figure 14-2 After collection of the bone marrow aspirate, a few sulfur compounds from onions and Brassica plants (kale,
drops are placed on clean slides for cytologic evaluation.
canola), nitrates, nitrites, and copper. Except for that
caused by copper, hemolysis usually occurs within a day
or two after ingestion. Copper toxicosis can occur after
acute overingestion but more commonly is seen in
demonstrate iron stores. Bone marrow aspirates and animals that are chronically overfed copper and suffer
biopsies are painful and invasive procedures. Therefore some stressful event. Goats are more tolerant of excess
animals should be placed on antibiotics and antiinflam- copper than sheep, and certain breeds of sheep, particu-
matory drugs prophylactically. larly the Suffolk, are highly sensitive to copper toxicosis
(see Chapters 2, 4, and 10).
Hemolytic bacterial toxins include those from Clostrid-
BLOOD CULTURES ium perfringens type A, C. haemolyticum and Leptospira in-
Blood cultures can be useful in diagnosing bacteremia in terrogans. Intraerythrocytic parasites include Anaplasma
an intermittently or persistently febrile sheep or goat or species, Eperythrozoon ovis, and Babesia species. Immune-
an animal with numerous sites of organ infection. Ideally mediated RBC destruction is very uncommon except
the clinician should obtain the sample before instituting with parasitemia, the administration of certain drugs
antimicrobial therapy. However, if this is impossible, an- (penicillin), or bovine colostrum to small ruminant
timicrobial therapy should be discontinued 48 to 72 neonates. Rapid reduction of plasma osmolality can lead
hours before sampling. Samples should be taken before to osmotic lysis of erythrocytes. This can occur locally as
and during febrile episodes. The jugular vein is most a sequela to rapid IV injection of hypotonic substances
commonly used to attain a blood culture. As described or after ingestion of a large quantity of water following
previously, the skin over the jugular vein should be a period of water deprivation and dehydration (water
clipped and surgically prepared. The person collecting the intoxication).
blood sample should wear sterile gloves and use a sterile Parasite infestation, opsonization, and ingestion of
needle and syringe. Blood samples should be placed im- toxic plants typically cause extravascular hemolysis. In
mediately in a blood culture flask. The chances of attain- these cases damaged erythrocytes are removed by cells of
ing a positive culture from bacteremic animals increases the reticuloendothelial system, resulting in anemia, pallor,
with the size of the sample up to about 30 ml, but adding weakness, depression, icterus, and dark urine. Bacterial
more than the recommended amount to any one culture toxins, changes in plasma osmolality, and copper toxicosis
vial may overwhelm the capacity of the specialized cause intravascular hemolysis, resulting in the additional
antibiotic-absorbing resins within the flasks. The clini- signs of hemoglobinemia and hemoglobinuria. Other
cian should change the needle on the sample syringe after signs such as fever, neurologic symptoms, and sudden
collecting the blood and before putting the sample in the death may be seen with specific diseases. Signs of regen-
culture medium. Samples should be refrigerated until eration should be seen on the hemogram 1 to 2 days after
they can be sent to a diagnostic laboratory, where aerobic the onset of hemolysis.
and sometimes anaerobic cultures are made. Anemia that is not related to the loss or destruction
of erythrocytes usually results from a lack of production.
By definition, these anemias are nonregenerative. Al-
CHANGES IN THE HEMOGRAM though mild forms may exist in pregnant sheep and
The most common and significant abnormality of the he- goats and those deficient in vital minerals (e.g., iron, se-
mogram is anemia. In sheep and goats, anemia occurs lenium, copper, zinc), the most common cause of nonre-
most commonly after blood loss, hemolysis, and chronic generative anemia is chronic disease. Under these condi-
disease. Blood loss is usually covert and commonly caused tions, iron is sequestered in an unusable form in the bone
by gastrointestinal or external parasites. Overt blood loss marrow; staining a marrow sample with Prussian blue
is usually caused by major trauma such as that caused by stain reveals large iron stores, differentiating this disease
362 • Sheep and Goat Medicine
from iron-deficiency anemia. The causes of anemia of nants, and inflammation is almost always a sequela of in-
chronic disease are numerous and include infectious con- fection. An increase in neutrophil numbers and their pro-
ditions (e.g., pneumonia, footrot, caseous lymphadenitis), portional contribution to the total WBC count is usually
malnutrition, and environmental stressors.1 seen in mild gram-positive, subacute, or chronic bacterial
infections. Animals with more severe disease may exhibit
high or normal counts, but a greater proportion of the
TREATMENT OF ANEMIA neutrophils will have toxic changes or be immature forms
Most anemia does not require treatment. Unless loss of (band cells, metamyelocytes, or myelocytes). In severe,
RBC volume is rapid and severe, the animal is usually acute inflammation and many diseases caused by gram-
able to compensate to the decreased oxygen-carrying negative bacteria, a temporary reduction in neutrophil
capacity by decreasing activity. It is important to remem- numbers is observed, often with a concurrent shift toward
ber in this regard that anemia often first becomes ap- more toxic or immature forms. If the animal survives the
parent to the manager of a sheep or goat flock when peracute disease, neutropenia should resolve over 3 to 4
animals appear overly stressed or die during movement or days, first through an increase in immature cells, and later
handling. through a mature neutrophilic response. The most im-
If possible, the cause of the anemia should be ad- portant cause of increased total and relative neutrophil
dressed. This can involve trying to control internal and counts is stress (or glucocorticoid administration), which
external parasites, changing the diet, and treating infec- inhibits neutrophil margination and extravasation and
tious diseases. Maintaining adequate hydration is essen- thereby increases the number of these cells in the mid-
tial in animals with intravascular hemolysis to avoid stream blood.
hemoglobin-induced renal tubular damage. Specialty Increases in eosinophil counts are usually related to ex-
compounds such as molybdenum salts for copper toxico- posure to eukaryotic parasites. Decreases are rarely of
sis and methylene blue for nitrate toxicity are usually too clinical significance and may be seen as part of the stress
expensive or difficult to be used on a flock-wide basis, but response. Idiopathic allergic-type reactions also are indi-
may be useful in valuable individual animals. cators of pathology but are very rare. Increases in ba-
Animals with severe acute blood loss or hemolysis may sophils are rarely clinically significant.
benefit from a whole blood transfusion. Because transfu- Increases in lymphocyte counts often reflect chronic
sion reactions are rare and strong erythrocyte antigens inflammatory disease such as that seen with internal ab-
have not been identified in sheep and goats, almost any scesses. In rare cases, lymphocytosis may consist of ab-
donor of the same species is acceptable for a first transfu- normal, blast-type cells and indicate a lymphoprolifera-
sion. Cross-matching can be done to ensure compatibil- tive neoplasm. Lymphopenia is an important part of the
ity, which becomes more important if the animal receives stress response; nevertheless, the clinician must keep in
more than one transfusion. Blood should be withdrawn mind that many diseases stimulate a stress response.
aseptically from the donor and collected by a bleeding Therefore lymphopenia and neutrophilia may represent
trocar into an open flask or by a catheter into a special either stress or inflammation, and an examination of neu-
collection bag. Blood should be mixed at a 41 ratio with trophil morphology and plasma fibrinogen concentra-
acid-citrate dextrose, sodium citrate, or another suitable tions may be useful in distinguishing the two situations.
anticoagulant and administered through a filtered blood A high fibrinogen concentration, toxic changes, and high
administration set. If the jugular vein is not accessible, counts of immature neutrophils indicate inflammation
blood may be infused into the peritoneal cavity, but the under those circumstances. Blood monocyte counts also
slower absorption from that site makes it less effective for may indicate stress or chronic inflammation. The difficul-
treating acute blood loss. The first 15 to 30 minutes of ties in interpreting individual cell count abnormalities
administration should be slow. If no reaction is seen highlight the importance of obtaining a differential
(fever, tenesmus, tachypnea, tachycardia, shaking), the WBC count and description of cellular morphology in
rate may be increased. Transfused erythrocytes may only assessing sick sheep and goats.
survive a few days, and therefore the original cause of the Leukogram abnormalities are rarely given specific
anemia must be addressed.1 treatment. It is far more common and useful to use the
information from the leukogram to develop a plan to
treat the disease responsible for the abnormality.
CHANGES IN THE LEUKOGRAM
Peripheral WBCs include granulocytes (neutrophils, ASSESSMENT OF THE
eosinophils, and basophils) and mononuclear cells (lym-
phocytes and monocytes). Immature forms of neutrophils LYMPHATIC SYSTEM
and lymphocytes may be seen during severe inflammatory Palpation of external lymph nodes is part of the thorough
diseases. Abnormalities of the neutrophil line are usually physical examination. Lymph nodes that can be found
the best cellular evidence of inflammation in small rumi- in normal sheep and goats include the submandibular,
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 363

prescapular, and prefemoral nodes. None of these should Diagnosis. Postmortem lesions include homogeneous
be prominent or painful on palpation. Additional nodes white to tan masses that bulge on the cut surface. They
that may be palpated occasionally in normal animals may be small or large. Less commonly, diffuse paleness of
include the parotid, retropharyngeal, supramammary, the reticuloendothelial organs is noted. Microscopic ex-
perirectal, and popliteal nodes. Internal lymph nodes that amination of these tissues reveals infiltrates of abnormal
may be identified during specialized diagnostic proce- cells of the lymphocyte line.
dures include the mediastinal, mesenteric, and other ab-
dominal nodes. Prevention. Avoiding exposure to the bovine leukemia
Enlargement of lymph nodes may be focal, multifocal, virus and avoiding the use of instruments contaminated
or generalized. Identification of a single enlarged superfi- with blood on more than one animal may help prevent
cial node does not always rule out a multifocal or general- the spread of lymphosarcoma. However, most animals
ized disorder because the status of the internal nodes appear to develop this neoplasm spontaneously.
often cannot be determined. Enlargement generally indi-
cates either inflammation or neoplasia. Inflammatory en-
largement is generally related to an associated disease
Failure of Passive Transfer
with an infectious component. Small ruminants are par- Pathogenesis. Lambs and kids are born with func-
ticularly sensitive to lymph node–based infections (e.g., tional lymphocytes that are capable of producing endoge-
caseous lymphadenitis), so the search often does not nous immunoglobulin. These cells develop the ability to
extend beyond aspirating or draining the lymph node respond to foreign antigens in the fetus at approximately
itself. Neoplastic enlargement almost always results from 80 days of gestation. However, because of a lack of in
lymphosarcoma. utero exposure, basal concentrations of immunoglobulin
are low at birth. Therefore these cells respond too slug-
gishly to new challenges to provide an adequate defense
DISEASE OF THE LYMPHATIC against acute infection for approximately the first 6 weeks
SYSTEM of life. Additionally, as with other ruminants, no transpla-
cental passage of immunoglobulin to fetal sheep and
goats occurs. Lambs and kids depend on intestinal ab-
Lymphosarcoma sorption of ingested colostral antibodies to provide a
Pathogenesis. Neoplastic transformation of a member ready supply of immunoglobulin and allow opsonization
of the lymphocyte cell line leads to unregulated clonal ex- of pathogens for the first months of life.
pansion of that cell. The cause of transformation is Adequate passive transfer requires delivery of a suffi-
usually unknown; in rare cases, especially in flock out- cient quantity of good-quality colostrum into the gas-
breaks in sheep, it can be linked to exposure to the bovine trointestinal tract as well as adequate absorption of anti-
leukemia virus, which has occurred experimentally and as bodies from the colostrum into the blood. In general, this
a result of the administration of whole blood Anaplasma is left to chance: the quality of the colostrum, amount in-
vaccines. Whether the bovine leukemia virus can induce gested, and adequacy of absorption are rarely monitored.
lymphosarcoma in goats is still unclear. Proliferation of Problems in colostral quality can arise from young, sick,
lymphocytes leads to mass lesions and infiltration of undernourished, and poorly vaccinated dams. Problems
viscera. These cause physical obstruction (to breathing, in availability can arise from prepartum leakage or
blood flow, urination, defecation), ulceration of mucosal nursing by another lamb or kid. Problems in ingestion
surfaces (blood loss, bacterial invasion), immune system can arise from weak or sick neonates, competition with
dysfunction, organ failure, and generalized malaise and other lambs or kids, and separation of the neonate from
cachexia. Tissues masses may be internal or visible on ex- the dam. Problems in absorption can arise from weak-
ternal examination. ness, sickness, hypothermia, hypoxemia, dehydration,
previous exposure of the gut to protein, delay in inges-
Clinical signs. Signs vary according to the site of tion, and other factors that affect gut function in the
the masses. Slowly progressive weight loss is the most neonate. Sheep and goats are especially prone to many of
common finding. In some cases, expansile masses are these causes of failure of passive transfer because of their
noted; at first they usually are presumed to be caseous tendency to have numerous offspring; the earliest-
lymphadenitis abscesses. Most masses form at the sites nursing, most vigorous offspring may ingest more than
of internal or external lymph nodes. Leukemia is rare. their share of colostrum.
The most common abnormalities are those of chronic Extrapolating from equine research, a finding of 800
disease and cachexia, and include nonregenerative ane- mg/dl of immunoglobulin in the plasma of a 1-day-old
mia and hypoalbuminemia. Bone marrow examina- lamb or kid is considered indicative of adequate passive
tion may reveal clonal expansion of lymphoid precursor transfer. No research has been done to show that this par-
cells. ticular concentration is significantly protective in small
364 • Sheep and Goat Medicine
ruminants, and it is probably more important that Colostral substitutes generated from slaughterhouse
immunoglobulin against specific opportunistic and pri- blood are becoming available, but their absorption and ef-
mary pathogens be absorbed than any bulk amount. ficacy remains largely untested. After the window for im-
Moreover, this amount should be considered mini- munoglobulin absorption has closed, plasma adminis-
mally acceptable—most healthy small ruminant neonates tered intravenously or intraperitoneally is the best way to
achieve immunoglobulin concentrations that are 50% to raise the neonate’s blood immunoglobulin concentra-
200% higher. tions. Adult donor plasma contains approximately 2.5 to
In addition to immunoglobulin, colostrum also con- 3.5 g of immunoglobulin per dl, so a volume equivalent to
tains large quantities of fat-soluble vitamins that do not 10% of body weight is necessary to achieve similar con-
cross the placenta. The most important of these are vita- centrations as with normal passive transfer. If plasma is
mins A, D, and E, which are important in bone develop- used instead of colostrum, administration of vitamins A,
ment and the immune or inflammatory response. Neo- D, and E also may be beneficial.
nates that have not ingested enough colostrum are likely If colostrum and plasma are unavailable or cost pro-
to be deficient in these vitamins. hibitive, “closing” the gut as quickly as possible with milk,
maintaining high standards of hygiene, and possibly ad-
Diagnosis. A diagnosis of failure of passive transfer can ministering prophylactic antibiotics offer the greatest
be deduced from the history if the neonate is known not prospects for preventing infectious disease. Vaccination of
to have ingested colostrum in the first day of life or the the neonate or the administration of antitoxin hyperim-
dam is known not to have had colostrum. Owners mune serum should not be considered protective, but may
occasionally pick a lamb or kid up, hold it at ear level be of value.
while carefully cradling the head and neck, and shake the
abdomen in order to hear milk in the abomasum. A Prevention. Ensuring colostral quality is best done
presumptive diagnosis can be made if the neonate shows through good nutrition, health care, and vaccination of
signs of undernourishment or sepsis in the first few dam (see Chapter 2). Administration of vaccines 6 weeks
days after birth. A definitive diagnosis can be made prepartum, followed in 2 weeks with a booster, provide
by direct laboratory measurement (radioimmunoassay) the highest quantity of protective immunoglobulin in the
of immunoglobulin concentrations. Numerous semi- colostrum. Prepartum leakage is rarely the problem in
quantitative methods of estimating immunoglobulin exist, small ruminants that it is in horses and cattle. However,
including various agglutination (glutaraldehyde) and pre- in a flock or hard environment, still-pregnant dams may
cipitate assays (sodium sulfate) and measurement of blood steal babies from other sheep or goats. To prevent theft
protein fractions. The use of a hand-held refractometer to and the resultant loss of colostrum by the “adopted”
measure total protein in a well-hydrated animal may be neonate, owners may choose to keep pregnant stock sep-
used as a quick screen. A total protein of 5.5 to 6 mg/dl or arate from those that have already delivered. If complete
greater is usually suggestive of successful transfer of separation is not possible, the dam and her offspring
colostral antibodies in a normally hydrated neonate. These should be allowed to bond to each other in a private pen
methods may be relied on to give an overall flock (“jug” or “crate”) for at least 24 hours before being placed
assessment of adequacy of passive transfer, but they are back with the flock. Clipping excessive wool or mohair
rarely accurate enough to provide definitive information from around the perineal area and udder before lambing
on individual animals (see Chapter 6).2 or kidding, expressing the teats to ensure they are not
plugged, and having extra colostrum when placing preg-
Treatment. Failure of passive transfer is not by itself a nant females in jugs or crates are other good preventive
disease, but it greatly increases the neonate’s susceptibility measures.
to infectious diseases. The amount of colostrum absorbed
across the gut decreases with time, especially in animals
that have been ingesting other proteins (e.g., the casein in
Neonatal Sepsis
milk); it also decreases with illnesses that decrease gas- Pathogenesis. Sepsis is the condition resulting from
trointestinal function. Sufficient immunoglobulin likely systemic bacterial infections or toxemia. Most systemic
cannot be absorbed more than 24 hours after birth. bacterial infections are caused by opportunistic infections
Therefore oral colostrum is the best treatment in the im- in immunocompromised animals or the overwhelming of
mediate postpartum treatment in still-healthy neonates. a competent immune system with massive challenge.
Same-species colostrum is best: hemolysis has been re- Rarely, small numbers of aggressive primary pathogens
ported in lambs receiving cattle colostrum. To make up are the cause. The most common cause of immune dys-
for complete failure, approximately 5% of the neonate’s function in neonates is failure of passive transfer. Less
body weight by volume of colostrum (or about 1.25 g of common causes include nutritional deficiencies (notably
immunoglobulin per kg of body weight) should be ad- in selenium, copper, or vitamin E), stress, and other
ministered on two separate occasions, 4 to 12 hours apart. illnesses.
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 365

Bacteria enter the body through the gastrointestinal or chemical analysis may be helpful in assessing overall con-
respiratory tracts or through a break in the skin (e.g., um- dition.2 Definitive diagnosis of sepsis is achieved by iso-
bilicus, castration site, docked tail, wound). The role of the lating the bacteria. Blood culture or postmortem internal
umbilicus is usually overemphasized over the other, more organ culture are the best diagnostic tools for acute, un-
common routes. Bacteria proliferate locally and either treated bacteremia. Aspirates of abscesses or infected
enter the circulation or produce toxins that enter the cir- joints are more accurate if sepsis is long-standing, partic-
culation. After entering the bloodstream, bacteria seed ularly if the animal has been treated with antibiotics.
various body sites, including the lungs, kidneys, liver,
central nervous system, joints, umbilicus, lymphoid tissue, Treatment. Treatment for neonatal sepsis is most
and body cavities. Toxins tend to damage blood cells, rewarding when initiated early in the infection.
vascular endothelium, and various organ tissues. Over- Although cost and residues are always a concern when
whelming bacteremia or toxemia is usually fatal; less treating young food animals, their small size and long
severe disease is associated with localization of the bacte- time interval until slaughter or milk production gives the
ria to one or more sites of chronic infection such as the clinician greater leeway in choosing appropriate anti-
umbilicus, lymph nodes, organ abscesses, and joints. The microbial agents. Because both gram-positive and gram-
greater the immune responsiveness of the animal, the negative infections are possible, broad-spectrum cov-
more likely it is to prevent invasion and clear the infection. erage through single antibiotics or combinations of them
The major opportunistic causes of neonatal sepsis is preferred (ceftiofur 1 to 2.2 mg/kg intramuscularly
include most Escherichia coli, Streptococcus, Actinomyces (Ar- [IM] once a day [SID] to twice a day [BID]). Treatment
canobacter), and other organisms (often gram-negative should be continued for at least 5 days to ensure
enteric bacteria). Most of these organisms are normal in- clearance of the infection. Nonsteroidal antiinflamma-
habitants of the ruminant gastrointestinal tract or soil and tory drugs (NSAIDs) also are beneficial in their anti-
therefore are likely to be found in the highest concentra- pyretic, antiinflammatory, and antiendotoxic roles (flu-
tions around areas with the poorest hygiene. The major nixin meglumine 1 to 2 mg/kg IV or IM).
primary causes of neonatal sepsis include some E. coli, Sal- If the neonate is severely dehydrated or obtunded, fluid
monella dublin or S. typhimurium, and Erysipelothrix rhu- treatment should be initiated. Because septic neonates are
siopathiae. These organisms may be associated with illness often deficient in immunoglobulin as a result of failure of
in adults and outbreaks in neonates in spite of good nutri- passive transfer or consumption of milk, plasma transfu-
tion, hygiene, and adequate passive transfer. sions are often beneficial. Plasma should come from the
same species; whole blood can be used in an emergency
Clinical signs. The clinical signs of acute sepsis are the situation. Adverse reactions are rare.
same as those of shock. Fever is present in the most acute
phase but is transient, and the absence of fever should Prevention. Methods to improve colostral quality and
not be taken as evidence against bacterial infection. passive transfer are helpful in preventing sepsis. Decreas-
Hypothermia is often present in advanced cases. Other ing overcrowding, separating neonates from most adult
common clinical signs include obtundation; anorexia stock (except their dams), and decreasing fecal and soil
with a weak suckle reflex; cold extremities; dry or contamination of facilities decrease the amount of bacte-
tacky mucous membranes with purple-blue discoloration rial challenge. Sanitizing common equipment and mini-
(buccal) or enlarged, engorged blood vessels (sclera); mizing contamination of tail docking and castration sites
tachycardia; tenting skin; and poor filling of the jugular also are important. Dipping the umbilicus is of question-
veins. Diarrhea, swollen joints, tachypnea, and specific able importance and is probably unnecessary in well-
neurologic signs may be present if the pertinent organs managed, clean flocks. However, the procedure is harm-
are affected. less and provides an opportunity to examine the newborn,
so current recommendations include dipping the umbili-
Diagnosis. A presumptive diagnosis can be made on cus with dilute iodine or chlorhexidine solutions.2
finding a neonate with the previously described clinical
signs. Other disorders that can produce these signs
include hypothermia, hypoxemia, congenital cardiovascu-
Neonatal Uncomplicated Diarrhea
lar or nervous system anomalies, and starvation. These Pathogenesis. Uncomplicated diarrhea may be caused
other disorders often coexist with sepsis as predisposing by viral, bacterial, and protozoan pathogens. They differ
factors or complications of the infectious disorder. Clini- from the causative agents of complicated diarrhea in that
cal pathology data that support a diagnosis of sepsis they do not invade beyond the gut wall or result in sys-
include evidence of failure of passive transfer, hyperfib- temic toxemia (see Chapter 4).
rinogenemia, and left shift of the leukogram, particularly The net result of such an infection is that a large volume
when neutropenia, toxic changes to neutrophils, or my- of isotonic intestinal fluid is lost into the bowel with the
elocytes and metamyelocytes are present. Serum bio- unabsorbed ingesta. If enough fluid and electrolytes are
366 • Sheep and Goat Medicine
lost, dehydration and metabolic acidosis induce systemic proper treatment of infected animals. To identify the
clinical signs similar to those seen in complicated diar- causative agent, feces should be examined by electron mi-
rhea. This disease in kids is one component of “floppy kid croscopy to identify the viruses, by culture to determine a
syndrome.” bacterial cause, by light or fluorescent microscopy after
sugar flotation, acid-fasting, auramine, or fluorescent an-
Clinical signs. Profuse, watery diarrhea without fever tibody staining for C. parvum.
is the hallmark clinical sign. With severe dehydration
or acidosis, affected lambs and kids become weak and Treatment. The immediate goals of treatment are re-
dull and lack appetite. Mucous membranes become hydration, replacement of lost electrolytes, and restora-
tacky, and skin tenting becomes prolonged. Shock signs tion of acid-base balance. Less immediate goals are provi-
may develop. Physical assessment often has to take the sion of nutrition and replacement of ongoing losses. The
place of clinical pathology analysis in lambs and kids. aggressiveness of treatment is dictated by the severity of
Mild, nonclinical uncomplicated diarrhea is character- the condition as well as economic considerations3:
ized by profuse diarrhea with minimal systemic signs.
1. Rehydration: Calculate the percentage of
The animal is bright and alert. Minimal skin tenting is
dehydration. Example: 10% dehydration in a 3-kg
evident. The animal is able to stand and eat readily and
lamb: 0.1  3 kg  1 kg/L  0.3 L, or 300 ml
has a strong suckle reflex. The animal is less than 5% de-
2. Replace lost electrolytes—Sodium, chloride,
hydrated, with a blood pH of 7.35 to 7.50 and a bicar-
bicarbonate, and potassium are lost roughly in
bonate deficit of 0 mEq/L.
proportion to extracellular fluid; replace in roughly
Moderate uncomplicated diarrhea is characterized by
the same proportions (except provide more
profuse diarrhea in a dull but responsive animal. Skin
bicarbonate and less chloride; see next step). Replace
tenting is prolonged, but eye luster is normal. The sheep
with fluid that is similar in composition to
or goat is able to stand and eat, but eats slowly and has a
extracellular fluid.
weak suckle reflex. The animal holds its head down. It is
3. Restore the acid-base balance—Estimate bicarbonate
5% to 7% dehydrated, with a blood pH of 7.10 to 7.25
deficit by blood gas analysis (24, measured) or physical
and a bicarbonate deficit of 5 mEq/L.
assessment. Then calculate the whole-body deficit.
Severe uncomplicated diarrhea is characterized by
Example: Assessment suggests a deficit of 16 mEq/L
profuse diarrhea. The sheep or goat is dull and minimally
bicarbonate in a 3-kg, comatose lamb with prolonged
responsive with a very long skin tent and dull, sunken
skin tenting (0.5 is the multiplier for extracellular
eyes. It can only stand with assistance and prefers to stay
fluid in a neonate)—0.5  (16 mEq/L)  3 kg 
in sternal recumbency with its head up. The animal eats
1 kg/L  24 mEq bicarbonate
very slowly, if at all, and has a minimal suckle reflex. It is
8% to 10% dehydrated, with a blood pH of 6.90 to 7.10 Therefore the immediate goal is to provide 300 ml of
and a bicarbonate deficit of 10 mEq/L. fluid and 24 mEq of bicarbonate to this lamb in a fluid
Very severe uncomplicated diarrhea is characterized by that resembles normal extracellular fluid (ECF). Fluids
profuse diarrhea and profound weakness. The animal’s can be given by various routes:
skin remains tented for more than a minute and its eyes
are very sunken and dull. It is nonresponsive with no Oral
suckle response. It is unable to maintain sternal recum- • Advantages: Oral fluids are inexpensive (non-sterile)
bency (lateral). The animal is 10% to 12% dehydrated, and easy to give. They are less likely to cause fatal
with a blood pH of 6.8 to 7.0 and a bicarbonate defi- arrhythmias or neurologic disease than IV fluids.
ciency of 15 to 20 mEq/L. • Disadvantages: An animal receives a maximum of its
gastric volume (5% of body weight) and good gastric
Clinical pathology. The leukogram should be normal motility is required. Oral fluids may not be well
or have abnormalities compatible with stress. Serum bio- absorbed by a damaged gut. Absorption also is slow.
chemical or blood gas analysis may reveal evidence of in-
testinal electrolyte loss (hyponatremia, hypochloremia, Intravenous
metabolic acidosis) and dehydration (hyperalbuminemia, • Advantage: This method allows rapid correction of all
azotemia). deficits, even in moribund animals.
• Disadvantages: It is expensive (sterile), requires venous
Diagnosis. A presumptive diagnosis may be based on access, and can rapidly lead to overcorrection.
the characteristic clinical signs and exclusion of causes of
complicated diarrhea (“scours”). Response to conservative Subcutaneous
treatment also is supportive of this diagnosis. Identifica- • Advantages: This method does not require venous
tion of the specific causative agent is less important than access or good gut motility.
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 367

• Disadvantages: It is expensive (sterile) and the fluids 2. Consideration of the addition of milk to the
may not be well absorbed in very dehydrated animals. treatment regimen:
Absorption is not as quick as by IV administration.
Animals should only be given hypotonic or isotonic • Milk has more energy but fewer electrolytes per
fluids. unit of fluid.
• Milk can be used for up to half of the feedings:
Intraperitoneal
Lambs fed milk lose less weight with scours.
• Advantages: This method does not require venous
Free water helps prevent hypernatremia.
access or gut motility. Fluids are absorbed quickly by • Milk should not be mixed with electrolytes because
this route.
they inhibit curd formation (although acetate is
• Disadvantages: It is expensive (sterile) and can cause
allegedly safe).
peritonitis. Isotonic fluids are best used in this route. • Milk may exacerbate diarrhea in the early stage:
Only a limited volume can be given.
Large intestine fermentation leads to osmotic
In general, lambs and kids with good appetites (espe- diarrhea and further fluid loss. Withholding milk
cially those being fed by bottle) and those that have re- for 24 hours may help, but longer delays lead to
cently lost their appetites (including those being fed by cachexia.
tube or working the bottle) may be treated with oral • Milk is a good potassium source.
fluids, but those that have a lack of appetite coupled with
severe dehydration should be treated with IV or subcuta Other Causes of Weakness and Depression in
neous (SC) fluids. SC fluids are most useful as an
adjunct: the owner or clinician can give a few hundred ml
Neonates
to a neonate treated with an IV bolus to provide a pro- Ruling out infectious causes of depression and weakness
longed effect. If oral fluids have not produced an im- is difficult, and clinicians often do well to assume that an
provement within 2 to 4 hours, IV treatment should be infectious disease is contributing to clinical signs when
strongly considered. making treatment decisions. However, a number of non-
Many good commercial oral fluids are available. These infectious systemic disturbances also can depress neuro-
contain electrolytes (sodium similar to plasma), an alka- logic and muscular function. Successful treatment often
linizing agent (bicarbonate, propionate, acetate, citrate; requires identification and correction of each of these dis-
most good ones have about 80 mEq/L of base), and turbances. Among the more common abnormalities
glucose or glycine to slow gastric emptying and aid in leading to depression in neonates are hypoxemia, meta-
sodium absorption. The amount of carbohydrates varies; bolic or respiratory acidosis, hypothermia, hyperthermia,
it is higher in “high-energy” solutions. Less carbohydrate hypoglycemia, dehydration, azotemia, and imbalances in
is needed in less severely affected animals because they some electrolytes.
are less likely to have severe hyponatremia. Fluids to be Hypothermia and hyperthermia can easily be diag-
avoided include medicated milk replacers and unbuffered nosed with a rectal thermometer. Hypothermia is far more
saline solutions. common and can result from weakness, shock, and envi-
IV treatment should be provided with a sterile com- ronmental stress. Cold, windy weather or tube feeding
mercial product. These typically contain 25 to 30 mEq/L with cold milk replacer or fluids can lead to a rapid drop in
of base. Additional sodium bicarbonate solution or core body temperature, especially in neonates that are
powder can be added (12 mEq of bicarbonate per g of small or weak or have been inadequately licked off or re-
powder, or 1 mEq/ml of 8.4% solution) to replace the base jected by their dams. Strong, vigorous neonates usually are
deficit. The bicarbonate deficit should be replaced over 4 protected by heat produced during muscular activity and
hours to avoid the development of neurologic signs. are able to seek food and shelter. Clinical signs begin when
After deficits are replaced, the following continued the rectal temperature drops to 98° F or below. Protection
treatments and adjuncts may be considered: from wind and cold such as an individual ewe jug or pen,
heat lamps (positioned far enough away so as not to burn
1. Continued administration of fluids (oral rather than IV
the neonate), hot water bottles, blankets, and warm fluids
if possible) to replace ongoing losses (see Appendix II):
are helpful in treating and preventing hypothermia. Shear-
• A volume equal to 5% of the body weight can be ing the ewe before lambing is of value because it forces the
given orally at a time; feedings can be increased ewe to seek shelter. If this management technique is used,
from two (normal) to three to six feedings a day. care should be taken to avoid inducing severe hypothermia
After 24 hours, less hypertonic fluids can be used. in the dam.
• IV fluids can be continued at twice the maintenance Environmental hyperthermia is much less common
fluid rate until appetite is restored. than fever in neonates. Therefore treatment for infectious
• More bicarbonate may be necessary. diseases in young animals with high temperatures is
368 • Sheep and Goat Medicine
usually warranted. Providing cool shelter with good ven- acids, transient neonatal renal tubular acidosis, and lactic
tilation, minimizing stressful events, ensuring adequate acidosis following toxic impairment of cardiovascular
fluid intake, and shearing the adults are the best defenses function. Overgrowth of C. perfringens type A is often
against environmental heat stress. suggested as a source of the toxin. Because of the high
Hypoglycemia also is easy to diagnose with the aid of anion gap, a pathologic condition that leads to overpro-
an inexpensive, portable glucose meter. Lambs and kids duction of an organic acid should be considered more
typically develop hypoglycemia under the same circum- likely than one that leads to bicarbonate loss. The disease
stances as hypothermia. Administering 50 ml/kg of dex- can occur in individuals or in outbreaks; although parity
trose (approximately 3.5 fl oz/lb, or 5% of body weight) in of the dam and number of offspring have not been asso-
warm milk replacer or 1 ml/kg of 50% dextrose IV or by ciated with the disease, aggressively feeding kids are more
mouth (PO, diluted to 5% dextrose) should provide likely to suffer from milk fermentation or clostridial over-
ample energy to correct hypoglycemia. IV treatment may growth. An infectious etiology appears more likely in
be necessary if gut motility is absent. Follow-up treat- herds that have an increased incidence as the kidding
ment may be necessary if the neonate does not regain its season progresses. The disease also is reported to be more
appetite. common in meat goats than dairy goats. Incidence can
Except during severe conditions, normal lambs and vary tremendously from year to year in a single flock or
kids should be able to maintain normal body core tem- region. A similar disease has been reported in calves and
perature. Therefore they should be examined for an un- llama crias, and lambs also are likely to be susceptible
derlying disorder if they exhibit signs of hypothermia or under the right conditions.
hyperthermia. Clinicians and owners should not assume Because blood gas analysis and exclusion of other dis-
that warming and feeding a cold, weak neonate will eases often are impractical, the term floppy kid syndrome
always correct its condition. frequently is used by owners to refer to any kid that is
Hypoxemia is much more difficult to diagnose. Port- weak and does not have an overt, organ specific sign (e.g.,
able blood gas meters for arterial analysis and radiography diarrhea). Different pathologic processes are grouped to-
units for thoracic imaging are available but still uncom- gether by their common clinical endpoint (as with “thin
mon in small ruminant practice. For those reasons, hyp- ewe syndrome”), and the veterinarian is charged with de-
oxemia is usually under-diagnosed. Hypoxemia can result termining the etiology in a specific flock. Most possible
from prematurity or dysmaturity, infection, depression or causes are found in the previously provided list of condi-
weakness (decreased ventilation), meconium aspiration, tions that cause weakness and depression in neonates.
bullous emphysema, hernias, and other thoracic fluid or Sepsis and hypoxemia are the most important items on
tissue masses. It is likely to be a contributing factor to that list and therefore also must be considered important
illness and death in most weak neonates younger than 3 causes of possible floppy kid syndrome. Treatment and
days old. Such animals benefit from the provision of sup- prevention of floppy kid syndrome currently follow the
plemental oxygen, either through a nasal insufflation tube same lines as the treatment and prevention of neonatal
or oxygen tent. In addition to its direct effect on attitude, sepsis or enteritis. Spontaneous recovery of animals with
hypoxemia at birth leads to poor gut function and subse- floppy kid syndrome may occur. However, in valuable
quent poor colostral absorption. Many animals that kids, quick assessment of blood chemistry and base
exhibit failure of passive transfer and subsequent sepsis deficits allows correction of electrolyte and blood pH ab-
had a previous bout of hypoxemia. normalities with 1.3% sodium bicarbonate.4
Azotemia, metabolic acidosis, and electrolyte imbal-
ances are difficult to diagnose without clinical pathology
analysis. Therefore they are best treated in animals
showing signs of dehydration with the administration of
R EFERENCES
1. Morris DD: Anemia. In Smith BP, editor: Large animal internal
a balanced, physiologic electrolyte solution. Metabolic medicine, ed 2, St Louis, 1996, Mosby.
2. Koterba AM, House JK: Neonatal infection. In Smith BP, editor:
acidosis is usually accompanied by either obvious evi-
Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
dence of bicarbonate loss (diarrhea) or severe dehydra- 3. Naylor JM: Neonatal ruminant diarrhea. In Smith BP, editor: Large
tion. However, neither of these conditions is present with animal internal medicine, ed 2, St Louis, 1996, Mosby.
floppy kid syndrome. This descriptive title is applied to 4. Rowe JD, East NE: Floppy kid syndrome (metabolic acidosis
muscle weakness, anorexia, and depression in kids in the without dehydration in kids), Proceedings of the 1998 Symposium on
first 2 weeks of life. By its strictest definition, floppy kid the Health and Disease of Small Ruminants Western Veterinary Confer-
syndrome refers to metabolic acidosis with a high anion ence, 1998, Las Vegas, NV.
gap without dehydration or any known cause in young
kids that were normal at birth. A variety of etiologies
have been proposed for metabolic acidosis without dehy-
Tissue-Invading Clostridia
dration, including intestinal fermentation of milk in well- Tissue-invading Clostridia are large, straight, gram-
fed kids with subsequent absorption of volatile fatty positive rods that are 3 to 10 mm in length. C. perfringens
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 369

and C. haemolytica are smaller bacteria and C. novyi, C. handling stresses, feed changes, and an overabundance of
chauvoei, and C. septicum are larger. The bacteria grow high-energy feeds are thought to promote overgrowth.
best under anaerobic conditions and produce waste gases. Milk, bakery products, and cereal grains are the most
Clostridia bear spores that may be the only viable form in common high-energy feeds associated with outbreaks.
soil. Identification of these spores within bacteria on mi- Toxin production occurs with overgrowth and precipi-
croscopic examination is useful to identify Clostridia. tates disease. Other enteric infections that disrupt the
Spores in C. perfringens are central and do not affect the mucosal border may increase systemic absorption of
shape, whereas most other species have the spore toward toxins.
one end and appear slightly club-shaped. C. perfringens type A occurs worldwide and is the most
Clostridia cause infectious, noncontagious disease. The common type of this species isolated from soil. It causes
bacteria inhabit the intestinal tract and are present in the “yellow lamb disease” in younger animals, a condition re-
feces of many healthy animals. Small numbers of organ- ported much more commonly in sheep than in goats.
isms in their dormant spore form also may reside in Risk factors for infection have not been established. This
tissues such as the liver and skeletal muscle. They can be disease occurs most commonly in lambs 2 to 6 months
isolated from soil, where most are thought to have short old. Under favorable conditions the organisms proliferate
life spans. Soil concentrations are highest in locations re- and cause a corresponding increase in alpha toxin produc-
cently contaminated with ruminant feces, especially tion. The alpha toxin causes minor gastrointestinal
crowded, overused facilities such as feedlots and lambing lesions and is absorbed across the gut wall to cause he-
sheds. Environmental contamination also appears highest molysis and vasculitis. The clinical course is usually less
during cool, damp times of the year such as late winter than 24 hours (see Chapter 4).
and spring.
The concentration of organisms and their toxins found Clinical signs. The clinical signs include weakness, de-
in the feces, gut contents, and internal organs of most pression, fever, icterus, anemia, hemoglobinuria, tachyp-
adult ruminants is usually small. Competition and peri- nea, and terminal recumbency. Laboratory evaluation
stalsis prevent overgrowth in the gut and aerobic condi- reveals evidence of intravascular hemolysis. Necropsy
tions prevent overgrowth in other tissues in live animals. reveals evidence of hemolysis, hyperemic intestines, and
However, rapid overgrowth and tissue invasion occur multifocal internal petechial hemorrhages. Positive diag-
after death, making rapid postmortem examination es- nosis is based on identification of the alpha toxin and the
sential to ascertain whether clostridial organisms are re- absence of other toxins by newer enzyme-linked im-
sponsible for the death. munospecific assay (ELISA) tests or older live-animal
Pathogenic clostridial organisms all produce heat- assays. Morbidity in a flock is lower than for many of the
labile protein exotoxins. Most make a variety of toxins, other enteric clostridial diseases, but the mortality rate is
and the relative contribution of each toxin to the disease very high.
state is not known. The major exotoxins of C. perfringens Adult animals also are susceptible to hemolytic disease
are alpha, a phospholipase that lyses mammalian cells; and vasculitis caused by C. perfringens type A infection.
beta, a trypsin-labile necrotizing toxin; epsilon, a trypsin- The organism has been isolated from sites distant from
activated necrotizing toxin; and iota, another trypsin- the infection, including muscle and the mammary gland.
activated necrotizing toxin. Toxin production is used to Fatal abomasitis and rumenitis in neonates and juveniles
classify C. perfringens organisms according to type. All also has been blamed on C. perfringens type A, but the
five types of C. perfringens make alpha toxin. Types B and rapid postmortem proliferation of the organism makes
C also make beta toxin (with B making epsilon toxin as substantiation of this claim difficult.
well), Type D makes epsilon toxin, and Type E makes iota
toxin. Because the necrotizing toxins cause more promi- Clinical pathology. The most characteristic change is
nent lesions than alpha toxin, they are used to character- neutrophilic leukocytosis with a left shift. Other evidence
ize diseases caused by C. perfringens infection with types of systemic toxemia (metabolic acidosis, azotemia, in-
other than A. Other tissue-invasive clostridial organisms creases in liver and muscle enzymes) also may be seen.
make toxins similar to those produced by C. perfringens in
addition to various other necrotizing and hemolyzing Treatment. Administration of antibiotics such as peni-
toxins. In many cases these toxins can be chemically cillin and Clostridium antitoxin are the mainstays of treat-
altered to produce antigenic toxoids.1-4 ment, although animals may die acutely before treatment
can be instituted.
Enteric Infections Prevention. A toxoid against the clostridial alpha tox-
Pathogenesis. Enteric clostridial organisms are thought in is available in some countries, but not in the United
to proliferate under conditions of decreased peristalsis States. Prevention efforts should focus on environ-
and poor ruminal and abomasal function. Weather and mental hygiene and avoiding favorable gut conditions
370 • Sheep and Goat Medicine
for proliferation of the organism. Because this type agents may be indicated as well. Usually the condition is
appears to survive better in soil than other types, not recognized until the animal is dead or dying.
preventing ingestion of soil may be important in
preventing disease. Prevention. A beta toxoid is available in the United
C. perfringens types B and C cause very similar diseases States and other countries. It is usually packaged with an
called lamb dysentery and hemorrhagic enterotoxemia, re- epsilon toxoid. The best protection is achieved by vacci-
spectively. Both lambs and kids can be affected. With nating pregnant dams twice, with the second dose admin-
both diseases the beta toxin is important, and inactivation istered approximately 3 to 4 weeks before lambing or
of this toxin after maturation of pancreatic trypsinogen kidding. Juveniles also should be vaccinated twice, start-
secretion effectively limits the susceptible population to ing around weaning time. Adults should receive an
neonatal animals. Older animals may become susceptible annual booster.
as a result of overwhelming infection or trypsin inhibition C. perfringens type D produces epsilon toxin, which is
by some soy and sweet potato products. The reported ge- responsible for increasing gut permeability and wide-
ographic range of both neonatal diseases appears to be spread tissue damage. The organism proliferates best and
limited (type B to the United Kingdom and South Africa produces the most toxin in the duodenum under condi-
and type C to the United Kingdom and North America), tions of excess fermentable starch, such as occurs after
even though infection with C. perfringens type C appears over-ingestion of high-energy feeds (milk, grain, lush
to occur worldwide. pasture). Overindulgence can be a primary condition or
The diseases initially affect lambs and kids less than reflect failure of the ruminal flora to adjust to an abrupt
3 days old, with illness occasionally occurring in older feed change such as increasing the grain portion of the
lambs. Because of the age of the animals, fecal contam- ration or moving a flock onto an ungrazed, lush pasture.
ination of teats, hands, and equipment that enter the In addition to providing substrate for the organisms,
mouths of the neonates (orogastric tubes, nipples) is a these rapidly fermentable diets may decrease peristalsis,
major cause of infection. Severely affected animals or allowing the toxin to accumulate. Because of the need for
those at the beginning of an outbreak are usually found trypsin cleavage of the protoxin, animals less than 2
dead. Less acutely affected animals display yellow, fluid weeks of age are rarely affected. The disease occurs
feces that may contain brown flecks of blood; splinting worldwide.
of the abdomen, especially when handled; colic signs; Natural disease caused by C. perfringens type D differs
and feed refusal. The clinical course is usually short, and between sheep and goats, possibly because of a difference
the disease is almost always fatal. Terminal convulsions in relative local and systemic action of the toxin, al-
and coma are occasionally noted, especially with the though experimental models have demonstrated that
disease in the United States. Postmortem examination both species develop similar lesions. Sheep tend to
reveals small hemorrhagic ulcers in the small intestine develop enterotoxemia. Peracutely affected sheep may die
with type B infection and diffuse reddening with hem- before or shortly after illness is noted and may have no
orrhage and necrosis of the abomasum and the entire in- postmortem lesions. Acutely affected sheep develop
testine with type C infection. Animals that die very tachypnea, tachycardia, fever, colic signs such as lateral re-
rapidly may have minimal or no gross abnormalities of cumbency and splinting of the abdomen, anorexia, and
the intestine. neurologic signs that begin as dullness and progress to
C. perfringens type C in older sheep causes “struck.” seizures or coma. Yellow, watery diarrhea may be evident
Temporary suppression of pancreatic trypsin production terminally and is a more prominent sign in subacutely or
may be important in the development of this disease. Af- chronically affected lambs. Postmortem lesions include
fected animals are usually found dead or with signs of subendocardial hemorrhage around the mitral valve and
toxemia. Specific antemortem signs of gastrointestinal pericardial effusion. The disease is more common in ewe
disease are rare. Postmortem changes include neu- lambs; in single, rapidly growing lambs 3 to 8 weeks of
trophilic leukocytosis with a left shift. Other evidence of age; and in feedlot lambs 2 to 3 weeks after they enter the
systemic toxemia (metabolic acidosis, azotemia, increases lot. Tail docking, castration, and other forms of interven-
in liver and muscle enzymes) also may be seen. tion are thought to decrease the incidence of this disease
by temporarily decreasing appetite. The disease also
Diagnosis. Diagnosis of these diseases is made by affects unvaccinated adult sheep, even without any
identification of characteristic lesions and positive toxin history of stressors or feed changes.
assays. Because the beta toxin is very labile, negative toxin Goats tend to develop more severe enteritis but fewer
assays are less significant than negative assays with other neurologic and systemic signs. Postmortem findings
tissue-invading Clostridia. include pseudomembranous enterocolitis with mucosal
ulceration, as well as fibrin, blood clots, and watery con-
Treatment. If identified early in the disease course, an- tents in the bowel lumen. Evidence of systemic toxemia,
tibiotics such as penicillin products and Clostridium anti- including multifocal petechial and ecchymotic hemor-
toxin may be beneficial. Fluids and antiinflammatory rhage, proteinaceous exudates in body cavities, pul-
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 371

monary edema, and cerebral malacia with perivascular serohemorrhagic exudates, and local tissue necrosis.
cuffing, is seen after both natural and experimental infec- Wounds appear and smell gangrenous. Systemic toxemia
tions but is less common and less pronounced than may affect internal organs, leading to the death of the
lesions seen in sheep. animal. C. sordelli causes identical disease.

Clinical pathology. Characteristic changes include Diagnosis. Laboratory analysis may reveal an increase
neutrophilic leukocytosis with a left shift. Other evidence in enzymes of muscle or liver origin as well as neu-
of systemic toxemia (metabolic acidosis, azotemia, in- trophilic leukocytosis with many immature and toxic
creases in liver and muscle enzymes) also may be seen. neutrophils. Postmortem findings include local necrosis
around the injury site. Diagnosis is usually made by iden-
Treatment. If identified early in the disease course, an- tifying characteristic lesions.
tibiotics such as penicillin products and Clostridium anti-
toxin may be beneficial. Fluids and antiinflammatory Treatment. Wound management (disinfection, dé-
agents may be indicated as well. Usually the condition is bridement) and administration of antibiotic products
not recognized until the animal is dead or dying. (penicillin G sodium 20,000 IU/kg IV every 6 hours) are
important treatment considerations.
Prevention. Vaccination of pregnant ewes with two
doses of toxoid, with the second dose coming 3 to 4 Prevention. Ram management may aid in prevention
weeks before lambing, and adequate ingestion of colos- of head-butting wounds. Annual vaccination with multi-
trum are the best methods of protecting newborn lambs. valent clostridial toxoids also may be helpful. In flocks
Vaccination of the lamb itself before it is 6 weeks old pro- with a high prevalence of this disorder, a booster vaccine
vides minimal protection. Lambs should be vaccinated given to rams 1 month before the breeding season may
twice around weaning or at entrance to a feedlot. Males provide additional protection.6
and adult females that are not part of the breeding
program may be vaccinated annually. Vaccination has
been shown to protect goats from experimental disease,
Black Disease
but clinical evidence suggests that well-vaccinated goats Pathogenesis. Sporulated organisms within Kupffer’s
are still susceptible to developing clostridial enteritis. The cells and spores of the organism present in the liver are
toxoids may not protect against local action of the toxins thought to proliferate and begin secreting toxins when
in the goat, which appears to play a greater role in their migrating fluke larvae create adequate anaerobic condi-
disease than it does in sheep1-4 (see Chapter 4). tions. Infective organisms also may be brought into the
liver by the flukes. Necrotizing toxins cause local hepatic
NON-ENTERIC CLOSTRIDIAL necrosis and systemic toxemia.
INFECTIONS Clinical signs. Affected sheep are debilitated, fail to
C. novyi (black disease, necrotic hepatitis, bighead) is keep up with the flock, and exhibit weakness, recum-
found worldwide in the soil, feces, and gastrointestinal bency, separation, and anorexia. Tachypnea and tachycar-
tracts of healthy ruminants. The organism also can be dia may be seen; fever occurs early in the disease. The
found in the liver of some healthy ruminants. It is a very patches of subcutaneous hemorrhagic edema that give
large, straight, rod-shaped organism with terminal oval this disease its name are less likely to develop in sheep
spores. Two types exist: type A secretes alpha, gamma, than in cattle, and therefore are rarely noted before the
and epsilon toxins and is one of the organisms responsible animal dies. The clinical course usually lasts less than 1
for bighead and a minor contributor to malignant edema day, and the disease is uniformly fatal. The short course
(see the later section on C. septicum); type B secretes alpha often prevents producers from noticing any abnormalities
and beta toxins and is responsible for black disease. The before the death of the animal.
temporal and geographic distributions of black disease
resemble those of fascioliasis, with the greatest incidence Diagnosis. The most characteristic clinical pathology
of disease occurring in milder, moister months in many changes are neutrophilic leukocytosis with a left shift.
countries. Black disease is less common in sheep than in Other evidence of systemic toxemia (metabolic acidosis,
cattle, and also is rare in goats.5,6 azotemia, increases in liver and muscle enzymes) also may
be seen. Postmortem findings include multifocal hepatic
necrosis, straw-colored body cavity exudates, and patches
Bighead of subcutaneous hemorrhagic edema.
Pathogenesis and clinical signs. Fecal and soil con-
tamination of wounds received during head-butting leads Treatment and prevention. Although black disease is
to proliferation of C. novyi type A in damaged head and rarely identified before the animal dies, it is best treated
neck tissues. Secreted toxins lead to swelling, edema, with flukicides (clorsulon 7 mg/kg PO) and antibiotics
372 • Sheep and Goat Medicine
(penicillin G sodium 20,000 to 40,000 IU/kg IV every 6 treatments such as fluids, antiinflammatory agents (flu-
hours). Supportive care, including nutritional support, nixin meglumine 2 mg/kg IV), nutritional support, and
fluids, and stress reduction, may be beneficial. Efforts to blood transfusions may be necessary. Hygiene during in-
control fluke infestation are the most effective way to vasive procedures such as castration, obstetric manipula-
prevent this disease. Annual administration of multiva- tion, shearing, tail docking, and administering injections
lent clostridial vaccines also may be helpful. In flocks at is helpful in preventing malignant edema. Multivalent
high risk for developing this disorder, a booster vaccine clostridial toxoids may provide some protection and
given 1 month before fluke exposure may provide addi- should be given annually to animals at risk.7,8
tional protection.5,6
Blackleg
Malignant Edema and Braxy C. chauvoei is the most important cause of blackleg.
C. septicum is the most important cause of malignant However, other tissue-invasive Clostridia can cause this
edema. However, other tissue-invasive Clostridia can disease, and mixed infections are common. The patho-
cause this disease, and mixed infections are common. The genesis of infection is often similar to that seen with
pathogenesis of infection is often similar to that seen with bighead and malignant edema: soil or fecal Clostridia in-
bighead and blackleg: soil or fecal Clostridia invasion of a vasion of a contaminated wound. Tail-docking, castra-
contaminated wound. Activation of dormant bacteria in tion, and shearing wounds appear to be especially impor-
damaged tissue similar to that seen in clostridial necrotic tant sites of infection in sheep. Activation of dormant
hepatitis also occurs. In both cases, bacterial toxins lead to bacteria in damaged tissue, similar to that seen in
local tissue necrosis and systemic toxemia. The alpha, clostridial necrotic hepatitis, also occurs, and the original
beta, gamma, and delta toxins are lecithinase, deoxyri- cause of tissue damage such as a wound is not always
bonuclease, hyaluronidase, and hemolysin, respectively. evident. In some cases, bacterial proliferation appears to
Commonly affected sites include castration, dehorning, occur in a site distant from the original wound (fetal in-
and injection sites; the umbilicus; and the postpartum fections after shearing of a ewe). Bacterial toxins lead to
uterus. Invasion through the lining of the abomasum local tissue necrosis and systemic toxemia. This bacterium
causes braxy. Factors that promote braxy have not been produces similar toxins to those produced by C. septicum,
identified, although ingestion of frozen feedstuffs in year- and the disease is seen worldwide. C. chauvoei also causes
lings has been implicated. Both forms of the disease have severe gangrenous mastitis in postparturient ewes.
worldwide distribution and are described more com-
monly in sheep than goats. Clinical signs. Blackleg is characterized by local to re-
gional painful, edematous swelling; fever; and signs of
Clinical signs. Malignant edema is characterized by shock. Focal signs such as lameness, udder swelling, and
local or regional pain, edematous swelling, fever, and subcutaneous swelling are more commonly seen with this
signs of shock. Evidence of subcutaneous gas production disease than with malignant edema. Evidence of subcuta-
is less common in this infection than in blackleg. Uterine neous gas production is common. Uterine and mammary
infections may cause a fetid vaginal discharge. Death infections may cause a fetid vaginal or mammary dis-
occurs within hours to a few days after the onset of signs. charge. Death often occurs within hours to a few days
Braxy usually causes death before any abnormalities are after the onset of signs, but the focal nature of this disor-
noted. On rare occasions, signs of depression, weakness, der gives affected animals a better prognosis than those
and colic may be seen. affected by other nonintestinal clostridial disorders.

Diagnosis. Characteristic clinical pathology changes Diagnosis. Characteristic clinical pathology changes
include neutrophilic leukocytosis with a left shift. A de- include neutrophilic leukocytosis with a left shift. A de-
crease in WBC and RBC counts also is possible because crease in WBC and RBC counts also is possible because
of the leukocidal and hemolytic effects of the toxins. of the leukocidal and hemolytic effects of the toxins.
Other evidence of systemic toxemia (metabolic acidosis, Other evidence of systemic toxemia (metabolic acidosis,
azotemia, increases in liver and muscle enzymes) also may azotemia, increases in liver and muscle enzymes) also may
be seen. Postmortem changes with malignant edema be seen. Postmortem changes with blackleg most com-
include dark red, swollen muscle filled with hemorrhagic, monly consist of focal, crepitant, red, brown, or black
proteinaceous exudate and little or no gas. With braxy the areas of myonecrosis. Other regions such as the fetus, tail
abomasal wall is hemorrhagic and necrotic. Both diseases head, or mammary gland also may be affected. Degener-
cause rapid postmortem decomposition of the carcass. ative changes can occur in internal organs, especially if
postmortem evaluation is delayed. Diagnosis is made by
Treatment and prevention. Wound management and isolating the organism. Fluorescent antibody tests are
antibiotics are important in treating braxy. Ancillary available to differentiate C. chauvoei from C. septicum.
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 373

Treatment and prevention. Wound management, ad- to 40,000 IU/kg IV every 6 hours) and flukicides (clorsu-
ministration of antibiotics (penicillin G sodium 20,000 to lon 7 mg/kg PO) and the provision of supportive care
40,000 IU/kg IV every 6 hours), and supportive care (nu- (nutritional support and administration of antiinflamma-
tritional support, fluids, antiinflammatory agents) are im- tory agents, blood transfusions, and fluids). Efforts to
portant. Hygiene during invasive procedures such as cas- control liver flukes and prevent other causes of liver
tration, obstetric manipulation, shearing, tail docking, damage are most important. Polyvalent clostridial toxoids
and administering injections is helpful in preventing may provide some protection. In addition to the annual
blackleg. Multivalent clostridial toxoids may provide booster, a second or biyearly booster vaccination given 1
some protection and should be given annually to animals month before fluke exposure may provide additional pro-
at risk7 (see Chapter 9). tection to flocks at high risk for developing this disorder.9

Red Water Disease Noninvasive Clostridia

C. haemolyticum is the etiologic agent associated with red Both tetanus and botulism are important diseases in small
water disease. The organism appears to be related closely ruminant medicine. These two diseases are covered in
to C. novyi and may be referred to as type D of that species. Chapter 11.
The major difference between the two organisms is that
C. novyi type B produces a phage-associated alpha toxin in
addition to the beta toxin produced by both species.
C. haemolyticum has a similar life cycle to other Clostridia
R EFERENCES
1. Hagan WA, Bruner DW, Timoney JF: Clostridium perfringens. In
and appears to thrive on alkaline pastures with standing Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
water. It colonizes the livers of healthy animals and prolif- microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
erates after liver damage, including damage caused by mi- NY, 1988, Comstock Publishing.
grating flukes or liver biopsies. The beta toxin causes 2. Blackwell TE: Clinical signs, treatments, and postmortem lesions in
intravascular hemolysis and damages the capillary en- dairy goats with enterotoxemia: 13 cases (1979-1982), J Am Vet Med
dothelium. Anemia, hepatic infarction, hemorrhagic Assoc 200:214, 1992.
enteritis, and hemoglobin-induced tubular nephritis are 3. Uzal FA, Kelly FA: Enterotoxemia in goats, Vet Res Comm 20:481,
1996.
the primary results. The disease is seen worldwide and
4. Uzal FA, Kelly FA: Experimental Clostridium perfringens type D en-
is more commonly reported in sheep than in goats. terotoxemia in goats, Vet Pathol 35:142, 1998.
Seasonality varies with the life cycle of the flukes. 5. Hagan WA, Bruner DW, Timoney JF: Clostridium novyi. In Hagan
WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s microbi-
Clinical signs. Affected animals appear weak and de- ology and infectious diseases of domestic animals, ed 8, Ithaca, NY,
pressed and produce red urine and feces. Heart and respi- 1988, Comstock Publishing.
ratory rates are high and become much higher with any 6. Hamid ME et al: First report of infectious necrotic hepatitis (black
sort of effort or stress. Fever and icterus are seen early and disease) among Nubian goats in Sudan, Rev Elev Med Vet Pays Trop
late, respectively, in the course of the disease. Death 44:273, 1991.
occurs within hours to a few days after the onset of signs. 7. Hagan WA, Bruner DW, Timoney JF: Clostridium septicum. In
Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
Diagnosis. Hematologic evaluation reveals evidence of
NY, 1988, Comstock Publishing.
intravascular hemolysis, including severe anemia, hemo- 8. Eustis SL, Bergeland ME: Suppurative abomasitis associated with
globinemia, and hemoglobinuria. Mature neutrophilia Clostridium septicum infection, J Am Vet Med Assoc 178:732, 1981.
with a degenerative left shift (immature forms of neu- 9. Hagan WA, Bruner DW, Timoney JF: Clostridium haemolyticum. In
trophils and toxic changes) is often present. Serum bio- Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
chemical evaluation may reveal evidence of organ failure microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
and shock. The most characteristic postmortem finding is NY, 1988, Comstock Publishing.
a large pale center of necrosis in the liver that results from
bacterial proliferation and regional infarction of the
portal vein. Microscopic evaluation reveals numerous
Juvenile and Adult Sepsis
Clostridia-like organisms within the necrotic region. Pathophysiology. Older animals are generally more re-
Hemorrhagic polyserositis with blood-tinged body cavity sistant to sepsis than neonates because they have larger
exudates also are common. A presumptive diagnosis can amounts of circulating antibodies. However, this resis-
be made based on the lesions. Positive diagnosis is made tance can be overwhelmed by aggressive bacteria, or loss
by isolating the organism. of immune function can allow invasion by opportunistic
bacteria. Malnutrition, parasitism, transport, overcrowd-
Treatment and prevention. Treatment includes the ing, other diseases, extreme weather conditions, and other
administration of antibiotics (penicillin G sodium 20,000 stressors are the major causes of immune suppression.
374 • Sheep and Goat Medicine
Clinical signs. Sepsis may produce peracute, acute, or of initial recognition that the animal is sick. Prophylactic
chronic disease signs. Peracute signs include fever, in- antibiotic treatment of healthy animals (oxytetracycline
jected mucous membranes (including the sclera), tachy- 10 mg/kg IV SID) may decrease spread and mortality
cardia, tachypnea, dyspnea, swollen joints, lameness, during outbreaks. The disease is reportable in many areas.
splinting of the abdomen, weakness, depression, anorexia, Local forms of anthrax also occur, most commonly after
recumbency, seizures, coma, and sudden death. Acute transmission through a skin wound or fly bite. Local heat,
signs are similar, except that they persist for a longer pain, swelling, and necrosis are seen first, and the general-
period and therefore are more likely to be noticed. ized syndrome often follows.2
Chronic signs usually result from the partial clearance of Borrelia burgdorferi is thought to spread to ruminants
infection after an acute episode, which may be clinical or from its mouse host by Ixodes ticks. The condition is
inapparent. zoonotic, causing Lyme disease in humans. The organism
is thought to be responsible for fever, weight loss, and
IMPORTANT BACTERIAL chronic septic arthritis in some ruminants, based on the
finding that these animals are seropositive and occasion-
CAUSES OF SEPSIS ally respond to tetracycline antibiotics. Abundant evi-
Actinobacillus seminis is a gram-negative bacillus or coc- dence for this is lacking, and it is likely that some of those
cobacillus that primarily affects the male and female re- animals have mycoplasmal or other infections. A similar
productive tracts. Infection causes posthitis, epididymitis, organism, possibly Borrelia theileri, is responsible for rare
and orchitis in rams and metritis and abortion in ewes. cases of bacteremia and fever3 (see Chapter 9).
Other sites of infection, including rare occurrences of
chronic sepsis, also are possible. Serologic tests are much
more useful for identifying infected flocks than infected
ZOONOTIC INFECTIONS
individuals within flocks. Definitive diagnosis depends on Brucella melitensis is more common in goats than sheep.
bacteriologic culture of the organism and differentiation Swine, cattle, and other ruminants are common hosts.The
of it from Brucella ovis. The bacillus is common in sheep disease is zoonotic. Infection usually causes inapparent
in some parts of the world but is uncommon in North mammary infection and abortions. Diagnosis is made by
American sheep and goats.1 serology, culture, or agglutination tests4 (see Chapter 6).
Arcanobacterium (Actinomyces) pyogenes is best known Chlamydia psittaci has a life cycle that is not particu-
as an abscess-forming bacterium because of the thick pus larly well understood. It is an obligate intracellular para-
formed in response to infection by it and the fibrinous re- site that spreads from cell to cell in the form of elemen-
sponse it elicits. It occasionally also causes sepsis. Its asso- tary bodies. It colonizes epithelial membranes, including
ciation with chronic sepsis lends credence to the belief the intestinal mucosa, where it may persist within a flock.
that Arcanobacterium is often a secondary invader that Transmission between animals may occur through direct
colonizes tissues damaged by another bacterium (see contact (ocular secretions, abortions), fecal-oral passage
Chapter 8). of infective elementary bodies, and possibly through
Bacillus anthracis is a large, gram-positive, anaerobic insect bites, birds, and breeding (venereal spread). Poly-
bacillus that causes anthrax. It forms spores under aerobic arthritis, conjunctivitis, pneumonia, orchitis, epididymi-
conditions (such as on culture plates) but rarely does so tis, and middle- to late-pregnancy abortion are the most
when oxygen tensions are low, as in carcasses. The organ- common disease manifestations; the different manifesta-
ism affects most mammals, with herbivores being most tions may be caused by different strains. Chlamydial dis-
susceptible. It is usually carried from one area to another eases are more commonly reported in sheep than in goats.
by shedding or dying animals and also can multiply in al- Diagnosis of chlamydial disease is often difficult. Ele-
kaline, nitrogenous soils. Periods of heat and intermittent mentary bodies may be seen on histopathologic examina-
flooding promote overgrowth of the organism. B. an- tion of affected tissues, including the placenta. Serologic
thracis spores may be inhaled or ingested; in rare cases the and cytopathologic assays also exist. Vaccines are available
bacillus itself may be spread by biting flies. After local to prevent chlamydial abortion in sheep5 (see Chapters
replication the organism gains access to the blood, where 6 and 12).
it multiples readily. Large numbers of the organisms col- Coxiella burnetii is a rickettsial organism that is an im-
onize the spleen. B. anthracis secretes a holotoxin made of portant cause of abortion in sheep and goats and also
edema factor (EF), protective antigen (PA), and lethal causes zoonotic disease. It is spread between animals by
factor (LF). This toxin impairs phagocytosis, increases ticks and also possibly by inhalation of aerosolized parti-
capillary permeability, and inhibits clotting. Splenic en- cles or contaminated dust. In addition to abortion, newly
gorgement, generalized edema, circulatory shock, and infected sheep and goats occasionally have mild, transient
bleeding diathesis are the most common lesions and signs fevers. C. burnetii is far more important as the cause of Q
of anthrax. Generalized infection should be considered fever in humans, who become infected after inhaling par-
uniformly fatal. Death may occur before or within hours ticles, handling contaminated animals, or coming into
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 375

contact with contaminated body fluids (uterine fluid, nonspecific inflammatory changes and azotemia may be
milk) from infected animals. Results of vaccination trials seen. Animals dying in the acute hemolytic stage are
in animals have been equivocal both at preventing abor- likely to have dark, discolored urine, bladder, and kidneys.
tion and limiting shedding of the organism. Currently no Spirochetes can be identified on dark-field microscopy of
vaccine is available in the United States6 (see Chapter 6). fresh urine or plasma from infected animals and may be
More common in sheep than goats, E. rhusiopathiae cultured with special techniques. In animals with less
has many hosts (including domestic swine and wild severe infection, a rise in antibody titers can be used to
rodents). It appears to be plentiful in some environments support a diagnosis of leptospirosis.
and is zoonotic by wound infection. The organism
appears to enter through skin breaks such as tail docking, Prevention. Numerous vaccines are available for sheep.
castration, and shearing wounds. Chronic septic arthritis Because protection is serotype-specific, it is important to
is the most common manifestation. Diagnosis is by vaccinate against common serotypes in the area. L.
culture.7 pomona is the most consistent isolate from sheep and
Francisella (Pasteurella) tularensis is more common in goats. Vaccination immunity is thought to be short lived;
sheep than goats. The organism has many hosts, of which boosters should be given at least twice a year in endemic
the most important are wild rabbits and rodents. It can areas10 (see Chapter 6).
contaminate water sources. It is zoonotic, causing tu-
laremia, or rabbit fever. Transmission to sheep is usually
through biting arthropods (ticks, flies) that have previ-
Listeria monocytogenes
ously fed on an infected wild mammal. Acute or chronic Pathogenesis. L. monocytogenes causes disease with
sepsis may be seen, with more widespread and severe similar frequency in sheep and goats. The organism is a
disease occurring in sheep with poor immune function. common soil and fecal contaminant, especially if pH is
Healthy sheep are thought to be resistant to infection. greater than 5.0. It also proliferates in silage that is not
Granulomatous splenitis and hepatitis are seen at nec- properly acidified and in rotting, woody debris. Risk of
ropsy8 (see Chapter 5). exposure depends on the feed and environment of the
animals. Environmental and fecal contamination are
more common sources than silage in small ruminants
Leptospira interrogans overall because most sheep and goats throughout the
Pathogenesis. Leptospires are spirochete bacteria that world are never fed silage. Infection almost always results
live in moist environments. Their survival time outside of from ingestion.
hosts is usually short, so their most important reservoirs Listeria may invade the body through the gastroin-
are the kidneys of infected animals, especially rodents. In- testinal tract. The most common form of listerial infec-
fected animals shed the organisms through urine and tion is sepsis, especially in animals younger than 1 year
most other body fluids. Organisms enter new hosts old. The organism appears to be cleared quickly from the
through mucous membranes and skin breaks and cause blood but causes persistent problems resulting from local-
bacteremia. Signs of sepsis range from severe, especially ized infections. Hepatitis, abortion, and nervous system
in neonates, to inapparent. Intravascular hemolysis may disease are the most common manifestations. Listeria
result from the action of hemolytic toxins or agglutinat- may have a predilection for the central nervous system
ing antibodies. Animals that survive the acute stage local- because many affected animals have clinical signs and
ize the infection in sites such as the kidneys, eyes, and fe- necropsy lesions compatible with diffuse meningoen-
toplacental unit. Abortion may occur a month or more cephalitis or spinal myelitis. Animals with the latter
after acute signs first become evident; renal shedding may lesions appear bright but have hindlimb paresis or tetra-
occur for several months. Leptospirosis is zoonotic, paresis. A better known form of listeriosis in ruminants is
causing flulike signs and encephalitis. Because sheep and a specialized brainstem disease.
goats are not commonly infected, they are less likely to be
sources of infection than other domestic and wild species. Clinical signs. The most common signs are those of
sepsis, with the majority of affected animals also exhibit-
Clinical signs. Acute leptospirosis causes signs of ing neurologic signs. Animals with the brainstem form of
sepsis, including fever, depression, dyspnea, exercise in- the disease display signs that differ according to the nerve
tolerance, weakness, and death. Additionally, many af- nuclei affected.
fected animals show signs of intravascular hemolysis such
as anemia, icterus, and hemoglobinuria. Diagnosis. Diagnosis is made by isolating the organ-
ism from lesions, body fluids, or feeds (silage). A pre-
Diagnosis. Evidence of intravascular hemolysis such as sumptive diagnosis of the brainstem form of the disease
anemia, hyperbilirubinemia, hemoglobinuria, and hemo- can be made by histopathologic identification of the
globinemia is specific to this disease. In chronic infection microabscesses.
376 • Sheep and Goat Medicine
Prevention. No vaccine is available, so efforts to avoid common causes of pinkeye in North American small ru-
infection include providing adequate passive transfer of minants. Mycoplasma are thought to inhibit tracheal
immunoglobulin to neonates, properly fermenting silage, ciliary function and thus have a role similar to viruses in
and removing rotting, woody vegetation from pastures11 “shipping fever pneumonia” in facilitating lower respira-
(see Chapters 6 and 11). tory tract invasion by Pasteurella and Mannheimia. Many
of the major pathogenic serotypes found in other coun-
tries (some of which cause severe pleuropneumonia
Mycoplasmal Diseases without the participation of another bacteria), including
Pathogenesis. Mycoplasma are very small, simple bacte- M. mycoides subsp. mycoides, M. mycoides subsp. capri, M.
ria that parasitize cells of higher species. They are agalactiae, and strain F38, are not found in or have been
common inhabitants of mucous membranes and can have eradicated from North America.
either a commensal or pathogenic relationship with the
host. Transmission between animals is most likely Clinical signs. Keratoconjunctivitis, mastitis, exudative
through direct or indirect contact with infected body vulvovaginitis, fever, cough, dyspnea, exercise intolerance,
fluids from infected animals, inhalation of respiratory abortion, lameness, swollen joints, neonatal death, and
droplets, and arthropod vectors. Common sites for super- depression may all be seen with Mycoplasma infections.
ficial infection include the ocular membranes, lung,
mammary gland, and female reproductive tract. The or- Diagnosis. No specific clinical pathologic findings
ganisms can also enter the blood and cause septicemia, occur with these diseases. Mycoplasma infection should be
abortion, pleuritis, and polyarthritis. Flare-ups often suspected in sheep and goats with severe exudative pleu-
occur during times of crowding and during lambing or ropneumonia in some parts of the world. Mycoplasma can
kidding, when neonates can spread the organisms from be identified by bacteriologic culture or staining of exu-
the mother’s mouth to her udder and in turn become in- dates. Examiners must take care in interpreting positive
fected by ingesting contaminated milk. cultures from body surfaces because nonpathogenic My-
The most important Mycoplasma species in sheep and coplasma are common.
goats in the United States are M. conjunctivae, M. capri-
colum, and the less pathogenic M. ovipneumoniae. They Prevention. Vaccines against mycoplasmal infections
are most commonly associated with keratoconjunctivitis are available in some parts of the world, but not in the
(Figure 14-3), acute or chronic sepsis, and pneumonia, United States. Providing fly control, preventing stress and
respectively. M. conjunctivae and C. psittaci are the most overcrowding, and isolating sick animals from healthy
ones may help prevent the spread of disease12 (see Chap-
ters 5, 12, and 13).

Fusobacterium Infections
Fusobacterium necrophorum causes or is associated with a
variety of diseases in sheep and is likely to cause many
similar diseases in goats. It is best known as a cause of
footrot and hepatic abscesses and also appears to be im-
portant in lip-leg ulceration. It is an enteric gram-
negative anaerobe and as such can cause gram-negative
sepsis after entrance of the bacteria or its toxins into the
circulation.
F. necrophorum has a poor ability to invade healthy
tissue. However, it readily colonizes regions damaged by
trauma, persistent moisture, and infection. In addition to
endotoxin the bacterium produces leukocidal and cytolytic
toxins that form zones of necrosis around bacterial
colonies. This tissue necrosis as well as the foul-smelling
waste gases produced by the bacteria are characteristic of
necrobacillosis, or F. necrophorum infection. Clinical signs
include necrotic, fetid lesions, usually of the mouth or feet,
that can cause ingestion or lameness problems. Efforts to
maintain good hygiene are helpful in preventing fecal con-
Figure 14-3 Keratoconjunctivitis in a goat caused by tamination. Additionally, preventing trauma to foot and
Mycoplasma species. (Courtesy Drs. Tom Powe and D.G. Pugh, Auburn mouth tissues through good surface choices and proper
University, Alabama.) pasture drainage is important9 (see Chapter 9).
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 377

PASTEURELLA AND or less prominent than in pneumonia caused by M.

haemolytica. Samples for bacteriologic culture are usually
PASTEURELLA-LIKE obtained postmortem. Blood or tracheal fluid may be ob-
INFECTIONS tained before death if the value of the animal warrants it.

Prevention. Vaccines are available for control of pneu-

Pasteurella multocida monic pasteurellosis, although they are of questionable
Pathogenesis. P. multocida is a small, gram-negative, efficacy in controlling that infection13 (see Chapters 5
bipolar, ovoid rod that inhabits the pharynx of healthy and 6).
ruminants, similar to other Pasteurella species and
Mannheimia haemolytica. It can survive in soil and water
for varying amounts of time after contamination with ru-
Pasteurella haemolytica
minant nasal secretions. Healthy ruminants shed P. mul- M. haemolytica (P. haemolytica biotype A) is a gram-
tocida much more frequently than M. haemolytica. Disease negative rod that is a common commensal inhabitant of
occurs when bacteria colonize the lower respiratory tract the tonsils of young animals. It is gradually replaced by P.
or enter the blood. Risk factors for pulmonary and sys- trehalosi in older animals. Disease is much more fre-
temic infection include viral or mycoplasmal respiratory quently described in sheep than in goats and occurs when
diseases, temperature extremes, respiratory tract irritants, the organism gains access to the lower respiratory tract.
transport, overcrowding, changes to higher-energy feeds,
and handling stress. These factors are thought both to in- Clinical signs and diagnosis. The most common syn-
crease bacterial replication in the airway and suppress drome is enzootic pneumonia, which is seen in young
mechanisms to clear the infection. Pasteurellosis is a lambs and their dams. Hemorrhagic bronchopneumonia
major problem in feedlot sheep but less common in small is the major lesion and respiratory signs predominate.
breeding or hobby flocks. Pasteurellosis also is a signifi- Gangrenous mastitis (bluebag) is seen in some of the
cant disease in certain wild small ruminants such as dams, presumably after they have been nursed by infected
Bighorn sheep. offspring. Factors that promote respiratory disease, in-
Direct spread of the organism between animals occurs cluding viral infections, airborne irritants, high stocking
with nasal contact, and indirect spread occurs after density, and stress, are thought to promote invasion of the
contact with infected nasal secretions. The organism per- lower airway by these bacteria.
sists in the environment for longer periods during warm,
moist weather. Pasteurella produces a polysaccharide Prevention. Vaccines are available for control of pneu-
capsule that inhibits phagocytosis and an endotoxin that monic pasteurellosis, but they are of questionable efficacy
contributes to clinical signs. Unlike M. haemolytica, P. in controlling that infection14 (see Chapters 5 and 6).
multocida does not appear to produce a leukotoxin that
has a direct lytic effect on host cells and leads to extensive
secondary damage resulting from the release of prote-
Pasteurella trehalosi
olytic enzymes from lysed neutrophils. The major disease P. trehalosi (P. haemolytica biotype T) is a gram-negative
caused by P. multocida is pneumonia. However, Pasteurella rod that gradually replaces M. haemolytica as the major
species also are capable of entering the blood to cause commensal inhabitant of the tonsils. Disease is much
septicemia in neonates and hemorrhagic septicemia in more frequently described in sheep than in goats and
adults. Occasionally focal infections such as septic arthri- occurs when the organism gains access to the lung or
tis and mastitis are found. blood. Replication occurs in the lung and systemic
toxemia or bacteremia result. Hemorrhagic pneumonia,
Clinical signs. Clinical signs of pneumonic and sep- necrotic hepatitis, erosions of the tonsils and gastroin-
ticemic pasteurellosis include bilateral purulent nasal dis- testinal tract, and hemorrhagic serositis are seen. The case
charge, coughing, diarrhea, anorexia, and high fever. The fatality rate is high. Studies have not determined whether
disease course can be short with septicemic pasteurellosis vaccines against M. haemolytica provide any protection
and is usually more insidious with P. multocida pneumo- against P. trehalosi infection14 (see Chapter 6).
nia. Pasteurella mastitis is characterized by the bluebag
condition or gangrene of the udder.
Yersiniosis
Diagnosis. Inflammatory changes in the leukogram Pathogenesis. Yersinia are gram-negative bacteria.
and hyperfibrinogenemia are the most frequent abnor- Y. enterocolitica and Y. pseudotuberculosis both have many
malities. With severe disease and in the septicemic form, mammalian and avian hosts, including humans, and
immature neutrophils may predominate over mature cause clostridial enteritis–like disease in goats. Rodent
cells. Inflammation of the intestine and abomasum also and bird hosts may be important reservoir populations for
may be seen. Hemorrhage and fibrin are usually absent infections in domestic animals. Kids younger than 6
378 • Sheep and Goat Medicine
months old develop enteritis, bacteremia, and diarrhea category, by far the most important genus is Salmonella.
that is watery but not bloody. Severe toxemia and sudden Sources of Salmonella infection are numerous and include
death can occur. Older kids and flocks with chronic expo- carrier animals of the same species, cattle, rodents, birds,
sure tend to have less severe acute disease. Instead, other animals, and possibly feedstuffs. Only one serotype
chronic diarrhea and weight loss are seen, usually in asso- of Salmonella is specifically adapted to sheep (S. abortus
ciation with gut wall and abdominal abscesses. Sheep are ovis), and it is not found in North America. No strain is
rarely affected. known to be host-adapted to goats. Therefore all infec-
tions in sheep and goats have the potential to spread to
Clinical signs. Signs of enteritis or sepsis predominate and from other species, including humans. Serotypes of
in acute disease, whereas signs of wasting are more Salmonella that have caused important infections in sheep
common in chronic disease. or goats include S. typhimurium, S. dublin, and S. montev-
ideo. Most of these infections lead to bacteremia with
Diagnosis. Evidence of acute or chronic inflammation mild systemic signs, followed by abortion. S. dublin and S.
is provided by blood work. Characteristic necropsy typhimurium tend to cause more illness in adults because
lesions include numerous microabscesses in the gut wall of fibrinonecrotic enteritis.
and mesenteric lymph nodes, as well as other evidence of
enteritis or sepsis. Culture of lesions and demonstration Clinical signs. Affected animals can exhibit anything
of a rising antibody titer are diagnostic. from mild depression with a low-grade fever to shock.
Common signs include fever, tachycardia, tachypnea, de-
Prevention. Avoiding exposure to sources and main- pression with slow or absent eating and drinking, weak-
taining overall flock health are helpful in preventing ness or recumbency, and injection or cyanosis of mucous
losses caused by yersiniosis. membranes. Organ-specific signs may betray the source
or at least the primary location of the infection. Fetid dis-
charge may be seen with metritis or abortion; dyspnea
Gram-Negative Sepsis and abnormal lung sounds may be seen with pulmonary
Pathogenesis. Gram-negative bacteria and their toxins infection; and bloat, ruminal atony, abdominal distention,
gain access to the blood from a site of proliferation or de- and diarrhea may be seen with gastrointestinal infections.
struction. The most important toxin is endotoxin, a group
of lipopolysaccharide molecules that reside within the Diagnosis. The most common abnormality identified
wall of the bacteria. Bacteria or endotoxins incite a sys- on a CBC with peracute gram-negative sepsis is pan-
temic inflammatory response, chiefly through activation leukopenia. Over the course of several days this condition
of host macrophages and stimulation of host cytokine may resolve, first through an increase in immature neu-
release. These cytokines cause inflammation, produce trophils and later through an increase in mature neu-
leukocyte recruitment, increase capillary permeability, trophils and restoration of lymphocyte counts. Very im-
induce fever through stimulation of the hypothalamus, mature cells, severe toxic changes, and persistence of
and have regional or diffuse vasomotor effects. neutropenia suggest a poor prognosis. Serum biochemical
Because the ruminant gut has a plentiful population of changes often reflect the severity of the condition; that is,
gram-negative bacteria, it is implicated as the source of the more normal the blood work, the less severe the
most cases of gram-negative sepsis. Grain overload causes disease. The greater the evidence of shock or tissue
a die-off of the normal gram-negative ruminal flora, ul- damage, the worse the prognosis. Metabolic acidosis with
cerative enteric disease allows invasion of bacteria or ab- a large anion gap and azotemia suggest advanced disease.
sorption of their toxins, and ingestion of pathogens pro- Necropsy findings include diffuse evidence of inflamma-
vides a suitable place for proliferation and route for tion, including pulmonary congestion, and polyserositis
invasion of the body. Gram-negative sepsis caused by op- with body cavity exudates. Hemorrhagic pneumonia or
portunistic organisms is best recognized in the immuno- fibrinonecrotic enteritis may be seen and reflect the source
compromised neonate but also can be seen in stressed or of bacterial invasion. In all cases, diagnosis is best con-
immunocompromised sheep or goats of all ages. In those firmed by bacteriologic culture of body tissues or fluids. In
cases a predisposing cause or source of overwhelming the live animal, culture of blood, feces, or tracheal fluid
challenge should be sought. E. coli is commonly found in yields the best results. When numerous animals are in-
fecal material, Klebsiella pneumoniae is found in feces and fected, environmental samples (including feed, water, and
wood products, F. necrophorum lives in the gastrointestinal bedding) should be tested for the presence of the bacteria.
tract and in soil and invades through compromised However, bacteriologic culture of aborted fetuses or pla-
gastric mucosa or footrot lesions, and Pseudomonas aerug- centas frequently yields heavy growth of the organism.
inosa is found in water and wash solutions.
Primary pathogens are relatively more common in Prevention. Maintaining overall good health and hy-
adults. Although some coliform bacteria may fit into this giene is the best means of preventing gram-negative
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 379

sepsis. Anti-endotoxin bacterins are available for cattle in may occur locally, frequently after a wound infection, or
the United States, but their use in small ruminants has at numerous or distant sites from the point of infection.
been too limited to assess their efficacy.15 During a flock For abscesses to occur at the latter sites, the organism
outbreak, the use of autogenous bacterin may help must travel to either by way of the blood or within leuko-
prevent the spread of disease on a farm (see Chapter 6). cytes. Therefore disease characterized by multifocal or in-
ternal abscesses usually results from a low-grade, tran-
TREATMENT FOR SEPSIS sient event of bacteremia.
The best known and most important abscess-forming
(ADULT AND JUVENILE) bacterium in small ruminants is Corynebacterium pseudo-
Bacterial organisms are rarely identified before important tuberculosis, the gram-positive, facultative anaerobic coc-
treatment decisions must be made. Therefore treatment cobacillus that causes caseous lymphadenitis. Infection is
should follow general principles and have a wide spec- usually maintained in a flock by infected animals that
trum of efficacy. Antimicrobial drugs are the cornerstone spread the organism to others through purulent material
of treatment. In meat- or milk-producing small rumi- draining from open abscesses. The organism is very
nants the veterinarian must be careful to use drugs within hardy, so infection can occur through direct contact or in-
label directions or have a rational plan for extra-label drug direct contact with contaminated common instruments
use (see Appendix I). The issue of extra-label drug use is and facilities. Infection is usually introduced into a flock
especially important in goats, because very few pharma- through acquisition of an infected animal, although it
ceutical products have been licensed for them in North also can occur when a naive flock is moved into a con-
America. Cost and convenience of treatment also may taminated area. Horses, cattle, and humans also are minor
dictate the drugs to be used. hosts. Infection is thought to occur after ingestion, in-
Unless the clinician strongly suspects a particular or- halation, or wound contamination. Except for lower re-
ganism (as with clostridiosis or anaplasmosis), he or she spiratory tract invasion, a surface break is thought to be
should use a single antibiotic or combination of antimi- necessary. Contaminated shears, tail-docking knives, and
crobial drugs to provide a broad spectrum of coverage. emasculators readily spread the organisms through a
Penicillins, macrolides, tetracyclines, and cephalosporins flock. Abscesses can form at the site of invasion or more
all provide reasonably effective coverage against gram- commonly at the site of the local lymph node.
positive pathogens, but of these drugs only the newer
cephalosporins are reasonably effective against many sys- Clinical signs. Clinical signs of external abscesses
temic and enteric gram-negative pathogens. The gram- include surface swellings and draining lesions. Drainage
negative pathogens of the respiratory tract are often sen- may be intermittent and usually consists of thick, yellow-
sitive to other classes of antibiotics. Macrolides and white purulent material. Internal abscesses are more diffi-
tetracyclines also are effective against Mycoplasma species cult to diagnose. Thoracic masses may cause inspiratory
and rickettsial organisms (see Appendix I). dyspnea or occlude venous return to the heart. Abdominal
NSAIDs almost always are beneficial in severe infec- lesions may cause tenesmus, stranguria, and occasionally
tious conditions because of their antiinflammatory, an- colic. The most common sign of internal abscesses is
tipyretic, and antiendotoxic effects. They are likely to be weight loss with or without intermittent fever. Common
more effective than corticosteroids because they provide external sites include the submandibular or retromandibu-
benefits without suppressing the immune response. All lar space, preinguinal, prefemoral, and supramammary
such drug use should be considered extra-label and insti- nodes. Head and neck lesions are more common in goats,
tuted accordingly (see Appendix I). Specific antisera are whereas sheep have a more even distribution of cranial and
available for some of the clostridial diseases and may be caudal lesions, presumably as a result of shearing wounds.
beneficial if given before widespread tissue necrosis has External infections rarely cause clinical illness beyond the
occurred. Severely compromised animals should be draining abscess, although some degree of cachexia may be
treated with fluids for shock (see Appendix II). present. More important are internal infections.

Diagnosis. Diagnosis is often made by the characteris-

OTHER CAUSES OF DISEASE tic lesions with their thick, non-malodorous pus. Bacteri-
ologic culture provides a more specific answer, which may
be important for flock management. Serologic tests have
Common Abscess-Forming Bacteria been developed to identify carrier animals and may be
Pathophysiology. Abscess-forming bacteria are usually useful if the manager wishes to eliminate infection from
able to survive phagocytosis and thereby avoid destruc- the flock.
tion by cells of the immune system. Alternatively, they
invoke such an inflammatory response that the host body Treatment. Treatment is often unrewarding: antibiotic
“walls off ” the entire region with fibrous tissue. Abscesses sensitivity profiles do not reflect the degree of protection
380 • Sheep and Goat Medicine
afforded the organisms within the abscesses. Long-term Organisms from ruptured granulomas may be spread
treatment with antibiotics and drainage of any compro- in contaminated respiratory secretions and feces. My-
mising masses may lead to some degree of resolution, but cobacterial infections of all types are uncommon in North
internal abscesses are likely to persist. American sheep and goats, and these species are consid-
ered to be relatively resistant to infection. M. bovis is the
Prevention. Prevention through the use of vaccines has most common organism associated with ovine tuberculo-
been attempted. Vaccines appear to reduce the severity of sis in other countries, but M. avium is more common in
the disease, but do not completely prevent infection. the United States. The most common mycobacterial
Moreover, live attenuated bacterins lead to de facto infec- infection is Johne’s disease (paratuberculosis), whose
tion of all vaccinated animals, and therefore should not be causative organism has been reclassified recently as M.
used in naive flocks16 (see Chapter 8). avium subsp. paratuberculosis. M. tuberculosis is rare in the
Other abscess-forming bacteria are most important as United States (see Chapter 4).
differential diagnoses for caseous lymphadenitis. Ar- Mycobacterial infections are reportable in most
canobacterium (Actinomyces, Corynebacterium) pyogenes is parts of the United States. Some debate is ongoing
another wound contaminant that affects focal areas or re- about human susceptibility to M. avium subsp. paratuber-
gional external lymph nodes. It also commonly colonizes culosis; the other organisms are known to be pathogenic in
damaged internal tissues such as post-pneumonic lungs, people.
post-acidotic livers, and damaged feet and heart valves. It
is thought to be ubiquitous and poorly invasive in rumi- Clinical signs. The most common clinical sign is ema-
nants, and therefore does not have the same flock signifi- ciation. Diarrhea may be seen terminally in both tubercu-
cance as C. pseudotuberculosis. Flocks with outbreaks of losis and paratuberculosis. The disease is insidious, with
this infection often have suboptimal management. signs becoming more apparent over several weeks to
F. necrophorum causes similar disease and often co-infects months. Respiratory signs may be seen, especially with
with A. pyogenes. It is generally more necrotizing and infection by M. bovis or M. avium.
leads to greater systemic signs of acute illness, including
death. F. necrophorum also produces fetid pus, whereas Diagnosis. Reports of clinicopathologic abnormalities
A. pyogenes usually does not. Rhodococcus equi is a rare are rare. Hypoalbuminemia and hypoproteinemia are
cause of pulmonary abscesses in sheep. likely to be common with chronic enterocolitis caused by
Numerous small, coalescent, nodular skin abscesses either tuberculosis or paratuberculosis. The most common
may result from Pseudomonas pseudomallei infection (me- necropsy lesions seen in tuberculosis are nodular lesions of
lioidosis). Infection usually occurs after the sheep or goat the lung, liver, lymph nodes, spleen, and intestines. Histo-
is bitten by an insect that previously fed on an infected logic evaluation reveals the nodules to be granulomas with
rodent. This organism is found in many subtropical giant cells and acid-fast organisms. Frequently the center
regions, including the Caribbean, but is not reported in of the lesion is necrotic and mineralized. Intestinal lesions
North America. appear to be more common than pulmonary lesions in
goats. The lesions of paratuberculosis are centered around
the ileocecocolic junction and the adjacent mesentery. The
Mycobacteria regions may appear normal or be notably thickened. Post-
Pathogenesis. Mycobacteria are small, aerobic, straight mortem diagnosis is made by identifying characteristic
or curved pleomorphic rods with thick lipid cell walls.They lesions and culturing the organisms. Antemortem diagno-
can be stained with acid-fast stains and are usually gram- sis of tuberculosis is best achieved by observing the reac-
positive. The bacteria live within infected animals of many tion to intradermal injection of tuberculin with or without
mammalian species and survive for several years in warm, comparative injection of purified protein derivatives of M.
moist environments. Infection occurs after ingestion or in- bovis and M. avium. All tuberculosis testing should be
halation. An identifying characteristic of the mechanism of done in accordance with local regulations. Antemortem
infection by Mycobacteria is the bacteria’s ability to survive diagnosis of Johne’s disease can be achieved by fecal
within macrophages by preventing fusion of phagosomes culture of the organism, but this test takes several weeks to
and lysosomes. The organisms are carried to local lym- months to complete. Newer serologic tests (e.g., ELISA)
phatic vessels or lymph nodes, where they form granulo- are available and appear to be sensitive and specific for
mas. As they enlarge, granulomas may develop necrotic or Johne’s disease.
mineralized centers surrounded by macrophages and giant
cells. Disease can be local, regional, or generalized, depend- Prevention. Tuberculosis should not be endemic in
ing on the distance the organism is carried from the origi- flocks in the United States because positive animals are
nal site of infection. Granulomatous pneumonia, entero- quarantined or destroyed. Therefore preventing exposure
colitis, and lymphadenitis are the most common local and to wild ruminants and other possible sources is crucial.
regional forms of the disease. Except in goat flocks raised for the production of milk
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 381

that is to be sold unpasteurized, testing is uncommon, so 13. Hagan WA, Bruner DW, Timoney JF: Pasteurella multocida. In
animals are usually not identified until they develop overt Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
disease. microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
NY, 1988, Comstock Publishing.
Paratuberculosis is much more common and may be
14. Hagan WA, Bruner DW, Timoney JF: Pasteurella haemolytica. In
maintained in flocks by carrier animals. No effective
Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
treatment is available for either disease, nor should any be microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
encouraged because efforts should be concentrated on NY, 1988, Comstock Publishing.
eliminating infection from the flock or herd17 (see 15. Hagan WA, Bruner DW, Timoney JF: The genus Salmonella. In
Chapter 4). Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
microbiology and infectious diseases of domestic animals, ed 8, Ithaca,

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WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s micro- Bruner’s microbiology and infectious diseases of domestic animals, ed 8,
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5. Hagan WA, Bruner DW, Timoney JF: Chlamydia psittaci. In
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and the number of red cells infected increases rapidly
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Bruner’s microbiology and infectious diseases of domestic animals, ed 8, against A. ovis lead to opsonization of parasitized
Ithaca, NY, 1988, Comstock Publishing. erythrocytes and their removal by cells of the reticuloen-
10. Hagan WA, Bruner DW, Timoney JF: Leptospira interrogans. In dothelial system; Eperythrozoon infection is thought to
Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s cause more intravascular hemolysis. The result in both
microbiology and infectious diseases of domestic animals, ed 8, Ithaca, cases is hemolytic anemia.
NY, 1988, Comstock Publishing. The protozoon parasites Babesia ovis and B. motasi
11. Hagan WA, Bruner DW, Timoney JF: Listeria monocytogenes. In
have similar life cycles and cause similar diseases, but they
Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
have been eradicated and are reportable in the United
microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
NY, 1988, Comstock Publishing.
States. Babesia affecting small ruminants are generally
12. Hagan WA, Bruner DW, Timoney JF: The genera Mycoplasma less pathogenic than their bovine counterparts.
and Ureaplasma. In Hagan WA, Bruner DW, Timoney JF, editors: Animals that survive the acute hemolytic crisis reduce
Hagan and Bruner’s microbiology and infectious diseases of domestic the parasites to low numbers but rarely clear the infection
animals, ed 8, Ithaca, NY, 1988, Comstock Publishing. completely; they serve as sources of infection for other
382 • Sheep and Goat Medicine
animals. Sheep and goats are susceptible to infection by against it include diminazene, pentamidine, and imido-
either organism; goats generally appear to be more resis- carb dipropionate (1.2 mg/kg IM, repeat in 10 days).
tant to the development of severe parasitemia and clinical Supportive care for all blood parasite infections includes
signs. whole blood transfusions, nutritional support, and ad-
ministration of fluids.
Clinical signs. Animals may have fever after acute in-
fection and during the hemolytic period. Other signs Prevention. Prevention in most cases involves main-
present during the hemolytic crisis may include weak- taining low levels of parasites rather than eliminating
ness, mucous membrane pallor, and dark urine. Urine dis- them entirely. This method ensures continual stimulation
coloration results from increased amounts of bilirubin in of the immune response, whereas eradication often leaves
most cases, although hemoglobinuria may be seen in the animal susceptible to another bout of acute infection.
some sheep with eperythrozoonosis. Icterus is usually Vector control also is important.1,2
present only after the acute hemolytic crisis. Clinical
signs are exacerbated during times of stress, and infection
is often first noted when the animals are moved or
Ehrlichia Infections
handled. Chronically infected animals may appear clini- Pathogenesis. Ehrlichia infections of WBCs cause
cally normal, may have recrudescence of infection after fever, immune suppression, and some organ damage.
stress, or may display signs of ill-thrift such as poor body Their major importance lies in the fact that they cause
condition and fleece (Figure 14-4). Babesiosis occasion- abortion if infection occurs during late pregnancy and
ally causes concurrent central neurologic signs. that they act as facilitators of other infectious diseases.
Ehrlichia (Cytoecetes) phagocytophilia is spread by Ixodes
Diagnosis. The major clinical laboratory finding is re- ticks and causes tick-borne or pasture fever. The inci-
generative anemia with detection of the intraerythrocytic dence of disease is seasonal with the life cycle of the tick.
bodies. Chronically infected sheep often have high The organism infects granulocytes and some monocytes,
counts of nucleated erythrocytes. Because Eperythrozoon leading to severe persistent neutropenia and acute lym-
consumes glucose, hypoglycemia and metabolic acidosis phopenia. Fever occurs 1 to 2 weeks after infection, lasts
may be detected, especially in blood samples that are not as long as 2 weeks, and has occasional relapses. Chronic
processed immediately. Diagnosis is by identification of infection is common. Spleen, lung, liver, and kidney tissue
the organisms on blood smears. Special stains are avail- may show some damage because of immune destruction
able to make the organisms more visible. Postmortem of infected cells, but organ-specific signs are usually the
lesions include pallor or icterus of membranes and result of secondary infection. Establishing ehrlichiosis as
splenomegaly. Some evidence of vasculitis, including a contributor to flock illness often requires looking
edema or exudates in body tissues or cavities, may be seen beyond the obvious clinical signs.
with E. ovis infection.
Diagnosis. E. ovis causes fever (benign ehrlichiosis) 1
Treatment. Eperythrozoon and Anaplasma are sensitive to 2 weeks after infection. Because of this organism’s
to tetracycline antibiotics (oxytetracycline 10 mg/kg IV predilection for mononuclear cells, the degree of immune
SID). Babesia is more difficult to treat. Drugs effective suppression and subsequent importance of this disease
are much less than for E. phagocytophilia infection. Spe-
cific diagnosis is best made by identifying darkly stained
bodies at the periphery of granulocytic cells, as well as oc-
casional large bodies deep within the cytoplasm of some
cells. Stained bodies also can be seen on the periphery of
mononuclear cells from a blood smear during the acute
febrile stage or in tissues during chronic infection.
Lymphadenopathy and splenomegaly may be seen.
Both of these infections affect sheep and goats (E.
phagocytophilia also affects many other ruminants), but
neither has been reported in North America. E. phagocy-
tophilia is found in northwestern Europe, including the
United Kingdom, Scandinavia, and India, and E. ovis is
found mainly in the countries bordering the Indian
Ocean.

Figure 14-4 Chronic weight loss in a goat as a sequela to Treatment and prevention. Treatment and prevention
anaplasmosis. (Courtesy Drs. Tom Powe and D.G. Pugh, Auburn efforts should focus on reducing vectors and bacterial
University, Alabama.) counts during vector season.3,4
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 383

Sarcocystis Species and Neospora caninum with dogs or those living on range land. Anticoccidial
Pathogenesis. Sarcocystis is a protozoon parasite that drugs appear to decrease the chance of clinical disease.5
has a two-host life cycle. Sexual reproduction occurs in
the bowel of a carnivore (mainly dogs and wild canids)
after the carnivore ingests cysts in the muscles of sheep or
Toxoplasma gondii
goats. Sporocysts are passed in the carnivore’s feces and Pathogenesis. T. gondii is a protozoon parasite with a
later ingested by a sheep or goat. The sporocysts hatch in life cycle very similar to Sarcocystis, except that the defini-
the ruminant gut and invade the vascular endothelium tive host is the cat and that a wider range of mammalian
during three phases of asexual reproduction. After the and avian species, including humans, appear to be capable
third phase (approximately 8 to 10 weeks after ingestion), of acting as intermediate hosts. Sporocysts are infective a
merozoites enter the ruminant’s muscle tissue and encyst. few days after passage in cat feces, and most ruminants
Clinical signs are uncommon but can occur during the are infected by eating feed contaminated with cat feces.
stages of reproduction and muscle invasion of the host. People can become infected by ingesting raw meat or
Neospora caninum has a similar life cycle and causes milk from infected animals.
similar disease, except that it appears more likely to cause Abortion, stillbirth, and neonatal death are the most
abortion and affect the central nervous system. common forms of clinical disease in sheep and goats, and
Toxoplasma should be considered one of the most
Clinical signs. Most infections are asymptomatic. How- common causes of perinatal losses in small ruminants.
ever, if a large number of sporocysts are ingested, tissue Abortion usually occurs during the final month of preg-
damage may occur during the intestinal, vascular, and nancy. Fever, vasculitis-induced disease, and neurologic
muscle stages of the Sarcocystis life cycle. Fever, lameness or disease are less common manifestations.
a stiff gait, reluctance to move, and diarrhea may be seen.
Central neurologic signs (blindness, changes in mentation, Clinical signs. Beyond abortion, clinical disease is rare
seizures) may occur if the organisms invade the brain or in adults and resembles systemic sarcocystosis. Clinical
interrupt blood flow to it. Abortion can occur as early as 4 signs include fever, dyspnea, depression, and anorexia.
weeks after ingestion. With severe chronic infections, Neurologic signs are more common than with Sarcocystis
emaciation and anorexia are seen. infection, especially in lambs and kids infected in utero.

Diagnosis. The most characteristic abnormality is an Diagnosis. No specific laboratory abnormalities are as-
increase in muscle enzyme activity (creatine kinase [CK], sociated with toxoplasmosis. Nodular lesions similar to
aspartate aminotransferase [AST]) in the blood. Anemia sarcocysts may be seen in various tissues, including the
is common and may result from extravascular hemolysis. brain. Aborted or stillborn fetuses may appear normal
Cerebrospinal fluid may show mild mononuclear pleocy- except for histologic lesions in the brain, liver, or lung, but
tosis or may appear normal. On necropsy, muscles may more commonly fetuses are macerated. The placenta is
display pale streaks or macroscopic cysts throughout. usually abnormal with gross and microscopic evidence of
Other evidence of vasculitis includes hemorrhagic serosal necrosis of the cotyledons. Microscopic identification of
surfaces, body cavity fluids, and lymphadenopathy. Micro- the organism in body tissues is the most common means
scopic or ultrastructural examination of affected tissues of diagnosis. Serologic tests also are available.
should reveal the presence of organisms. Specific antibody
tests are available and do not cross-react with Toxoplasma Treatment and prevention. Drugs similar to those used
gondii antibodies. Blood antibody titers often peak around to treat Neospora are effective against Toxoplasma. Prevent-
the onset of clinical signs and should be markedly higher ing contamination of feeds with cat feces and preventing in-
than baseline values. Antibody preparations also are avail- gestion of dead animals by cats are the most important ways
able for identification of organisms in tissue preparations. of stemming the spread of this organism. Both methods are
likely to be difficult in most flocks. Direct spread from one
Treatment. Sheep infected with Sarcocystis species can sheep or goat to another is rare. Anticoccidial drugs may
be treated with salinomycin (200 ppm in complete feed), have some prophylactic effect6 (see Chapter 6).
monensin (0.5 to 1 mg/kg PO), or amprolium (25 to 40
mg/kg PO). Drugs such as sulfadiazine or trimethoprim
(25 to 44 mg/kg IM SID), pyrimethamine (0.5 to 1
R EFERENCES
1. Hagan WA, Bruner DW, Timoney JF: Anaplasma ovis. In Hagan
mg/kg PO SID), and clindamycin have shown some
WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s microbi-
success in treating Neospora infections. ology and infectious diseases of domestic animals, ed 8, Ithaca, NY,
1988, Comstock Publishing.
Prevention. Preventing contamination of feedstuffs 2. Hagan WA, Bruner DW, Timoney JF: Eperythrozoon ovis. In
with the feces of infected carnivores and preventing in- Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
gestion of raw meat by carnivores are most important, but microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
these measures may not be possible in flocks handled NY, 1988, Comstock Publishing.
384 • Sheep and Goat Medicine
3. Hagan WA, Bruner DW, Timoney JF: Ehrlichia phagocytophilia. In viruses, and the latter determines the serotype. Sera are
Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s commonly tested with complement fixation, agar gel im-
microbiology and infectious diseases of domestic animals, ed 8, Ithaca, munodiffusion (AGID), or one of several ELISA tests. A
NY, 1988, Comstock Publishing.
competitive ELISA is considered the best serologic test
4. Lepidi H et al: Comparative pathology, and immunohistology asso-
for detecting group antibodies to bluetongue virus. A
ciated with clinical illness after Ehrlichia phagocytophilia–group in-
fections, Am J Trop Med Hyg 62:29, 2000.
direct fluorescent antibody test is available. Polymerase
5. Dubey JP: Sarcocystosis. In Howard JL, editor: Current veterinary chain reaction– (PCR-) based tests for bluetongue have
therapy, ed 3, Philadelphia, 1993, WB Saunders. recently become available and are extremely sensitive and
6. Dubey JP: Toxoplasmosis. In Howard JL, editor: Current veterinary specific.
therapy, ed 3, Philadelphia, 1993, WB Saunders. Other clinicopathologic signs that aid in diagnosis
include leukopenia during the early febrile stage of the
disease and an increase in serum CK corresponding to the
ACUTE VIRAL DISEASES latter phase of muscle stiffness and lameness.
Bluetongue
Treatment. Treatment is nonspecific and consists of
Bluetongue is an acute viral disease of domestic and wild nursing care. Because of the reluctance of animals to eat,
ruminants caused by a ribonucleic acid (RNA) virus in they should be fed a gruel of alfalfa pellets by stomach
the genus Orbivirus and family Reovirus; it is transmitted tube or encouraged to eat soft feeds and green grass.
by the insect vector Culicoides varipennis (gnat)1,2 (see Broad-spectrum antimicrobials (oxytetracycline 5 mg/kg
Chapters 3, 6, and 8). IM SID to BID) are often used to treat secondary pneu-
monia and dermatitis. Animals should be kept on soft
Clinical signs. Bluetongue disease has two different bedding with good footing. Water and shade should be
manifestations—reproductive problems and vasculitis of readily available. NSAIDs (flunixin meglumine 1.1 to 2
several organ systems. A spiked fever often leads to de- mg/kg IV) are commonly used.
pression, anorexia, and rapid weight loss. Leukopenia is
present. Affected animals may develop edema of the lips, Prevention. The Culicoides vector is difficult to elimi-
tongue, throat, ears, and brisket. Other signs include ex- nate, so animals should be kept indoors during periods of
cessive salivation and hyperemia or cyanosis of the oral peak gnat activity (dusk and early evening). Owners
mucosa, including the tongue (hence the name blue- should attempt to eliminate gnat breeding grounds such
tongue). Affected sheep often produce profuse serous as overflowing watering troughs and shallow septic
nasal discharge that soon becomes mucopurulent and systems and should limit exposure of sheep to gnats with
produces crusts and excoriations around the nose and the use of repellent sprays.
muzzle. Oral lesions progress to petechial hemorrhages, Modified live vaccines based on local strains and
erosions, and ulcers. Pulmonary edema is often severe and serotypes are available in some parts of the world. Some
pneumonia may develop. Skin lesions can progress to lo- cross-protection among serotypes does occur. The vac-
calized dermatitis. Affected sheep may exhibit stiffness or cine should be administered at least 2 weeks before
lameness because of muscular changes and laminitis. breeding season to prevent teratogenic effects. Vaccinated
Cyanosis or hemorrhagic changes of the skin of the breeding rams may have a slight risk of decreased fertil-
coronet can extend into the horny tissue. After recovery a ity. Lambs can be vaccinated in the face of an outbreak.
definite ridge in the horn of the hoof may be present for Pregnant animals cannot be vaccinated with modified
many months. Mortality varies widely. In Africa the virus live vaccines.
is much more virulent than in the United States and mor- Sheep that have recovered from an attack of blue-
tality ranges from 2% to 30%. tongue are solidly resistant for months to infection by the
The reproductive or teratogenic form of the disease same viral strain and to some other viral types. Active im-
varies greatly with strain, host, and environmental factors. munity in sheep requires both humoral and cellular
Teratogenic effects include abortions, stillbirths, and immunity.1,2
weak, live “dummy lambs.” Congenital defects may in-
clude hydranencephaly. Peste des Petits Ruminants
Diagnosis. In parts of the world in which the disease is
(Pseudorinderpest)
common, the diagnosis is usually based on clinical signs Etiology. Peste des petits ruminants (PPR) is an acute
alone. The virus can be isolated from blood, semen, or or peracute, febrile, often fatal disease of ruminants
tissues (spleen and brain from aborted fetuses). Viral iso- caused by a virus in the family Paramyxoviridae and genus
lation from blood obtained during the viremic, febrile Morbillivirus. Sheep are less susceptible than goats and
state is the most definitive means of diagnosis. Serologic white-tailed deer. Cattle are only subclinically infected.
evaluation involves two types of viral antigen groups The virus is serologically related to the virus that causes
called P7 and P2. The former is found in all bluetongue rinderpest.
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 385

Pathogenesis. The route of infection is respiratory and and antiinflammatory agents, as well as nutritional
is spread by airborne droplets. All secretions and excre- support. In the United States, state and federal veterinar-
tions of infected animals are contagious throughout the ians should be notified if PPR virus is suspected.
course of the disease, but no carrier state exists. The virus Methods used to eradicate rinderpest are useful in the
targets lymphoid tissue. Lymphocytes are destroyed in eradication and control of PPR. All sick sheep and goats
germinal centers in lymph nodes, Peyer’s patches, tonsils, and those exposed should be slaughtered and disposed of
splenic corpuscles, and cecal lymphoid tissue. Immuno- by burning, burying, or rendering. The premises should
suppression results from lymphoid destruction. Lympho- be decontaminated and the area quarantined. Sheep and
cytes are partially replaced by plasma cells, macrophages, goats can be protected against PPR by immunization
an eosinophilic acellular matrix, and occasionally neu- with rinderpest vaccines or by the simultaneous adminis-
trophils. The epithelial lining of the mouth and digestive tration of PPR hyperimmune bovine serum and virulent
tract is highly vulnerable to the PPR virus. With the loss PPR virus.3,4
of the alimentary tract mucosa, weight loss and diarrhea
become severe. The incubation period is usually 2 to 6
days.
Louping Ill
Pathogenesis. Louping ill is caused by a togavirus
Clinical signs. The clinical disease produced by PPR related to the other arthropod-borne encephalitis viruses.
virus in sheep and goats closely resembles that of rinder- It mainly affects lambs; occasionally also affects grouse,
pest, but the course is much more rapid. With the acute goats, and cattle; and infrequently affects pigs, deer,
form, sheep and goats typically display an abrupt rise in rodents, and humans. Currently, it is thought to occur
temperature to 104° to 106° F (40° to 41° C). Within a only in and near Scotland and Ireland, although a second
few days infected animals develop nasal and lacrimal dis- focus in Eastern Europe is suspected. Transmission is
charge, depression, thirst, anorexia, and leukopenia. Con- most common during tick season, and Ixodes ricinus is
gestion of the conjunctival and other mucous membranes thought to be the most important infective host. Co-
occurs, followed by serous and mucopurulent exudates. infection of sheep with Cytoecetes (Ehrlichia) phagocy-
Sheep and goats develop oral erosions with necrotic foci, tophilia is common and may contribute to central nervous
which results in excessive salivation. Diarrhea that may be system infection.
profuse but is rarely hemorrhagic develops later (within 2 Many sheep clear the infection after a few days of fever
to 3 days) and is accompanied by abdominal pain, tachyp- and viremia, but others develop severe, fatal viral en-
nea, emaciation, and severe dehydration. Bronchopneu- cephalitis. The virus is shed in many secretions, including
monia, particularly that caused by Pasteurella species, may milk, which is an important source of infection for other
be a terminal sequela. Death usually occurs 5 to 10 days animals (and humans). The severity of the disease
after the onset of fever. Pregnant sheep or goats with PPR depends on herd immunity because previous exposure
may abort. gives long-lasting immunity. Colostrum from immune
females is protective for the neonate. High antibody titers
Diagnosis. A presumptive diagnosis of PPR can be also appear to shorten the duration and level of viremia
made on the basis of clinical, pathologic, and epizooti- and thereby prevent invasion of the central nervous
ologic findings. The diagnosis can be confirmed by isolat- system. Naive flocks may have fatality rates as high as
ing the virus from blood or tissues, including lymph 60%.
nodes, tonsils, spleen, and lung. Serologic tests (comple-
ment fixation or AGID) cannot differentiate between Clinical signs. High biphasic fever, anorexia, and de-
PPR and rinderpest. Characteristic postmortem findings pression are seen in most infected sheep. Lambs may die
include necrotic stomatitis that is generally confined to quickly before illness is noted. Some sheep also develop
the inside of the lower lip and adjacent gum, the cheeks central neurologic signs, including hyperexcitability,
near the commissures, and the ventral surface of the free muscle tremors, and rigidity. Abnormal coordination and
portion of the tongue. Abomasal erosions are often muscle activity may cause sheep to move with a bounding
present. In the small intestine, Peyer’s patches are gait (hence the name louping ill).
markedly affected particularly in the first portion of the
duodenum and terminal ileum. The large intestine may Diagnosis. The condition has no characteristic gross
be severely affected. Lesions occurring near the ileocecal lesions. Microscopic examination of animals with neuro-
valve, at the cecocolic junction, and in the rectum are logic signs reveals evidence of viral meningoencephalitis.
often described as zebra stripes that indicate areas of con- Diagnosis is made by history (based on location, signs,
gestion along the folds of the mucosa. and time of year), the identification of characteristic
lesions, virus isolation, or fluorescent antibody staining of
Treatment and prevention. PPR virus infection has no fresh brain tissue. A demonstrated increase in specific an-
specific treatment. Mortality can be reduced by support- tibody titers in survivors strongly suggests the presence of
ive care, including the administration of antimicrobial this infection.
386 • Sheep and Goat Medicine
Prevention. Vaccines are available in endemic areas to flamed with hemorrhage and necrosis. Other signs vary
control infection. Vector control during tick season also is according to the location and severity of the lesions.
important. Lambing season should also be timed so that Lingual and buccal lesions cause salivation, dysphagia,
lambs have high colostral antibody protection at the time and feed refusal. Foot lesions cause lameness and recum-
of exposure to ticks.5,6 bency. Teat lesions cause reluctance to be milked or
nursed and a drop in production. Fever also may be seen
Foot-and-Mouth Disease and Vesicular early in the disease, when vesicles are most apparent. The
fever then usually abates and vesicles are replaced by ero-
Stomatitis sions or ulcers. Abortion may occur, especially with foot-
Pathogenesis. Foot-and-mouth disease is caused by a and-mouth disease, and is probably related to the fever
highly contagious picornavirus and has been eradicated rather than to fetal infection. Except for the malignant
from the United States. Vesicular stomatitis is caused by a form of foot-and-mouth disease and infection compli-
rhabdovirus and is intermittently eradicated from the cated by severe secondary infection, the disease is usually
United States. Both diseases are zoonotic, nearly indistin- self-limiting; most animals recover within 2 to 3 weeks.
guishable from each other, and reportable. Foot-and- Shedding of the virus causing vesicular stomatitis is
mouth disease has a broad host range that includes most thought to subside soon after healing of lesions. Foot-
hoof stock (including pigs but not horses) and several and-mouth disease virus may be shed for as long as 6
other mammalian species. Vesicular stomatitis also affects months and all body secretions and tissues should be con-
many species of hoof stock, including both pigs and sidered contagious, including milk, semen, meat, and
horses. Small ruminants are relatively less susceptible offal. Both viruses have zoonotic potential and cause a
than cattle, particularly to vesicular stomatitis. disease in humans that resembles mild influenza. The dis-
The viruses are spread by aerosol and mechanical eases are self-limiting, but people can shed the viruses in
vectors and primarily colonize skin or mucous mem- sufficient quantities to infect other animals.
branes. Milking machines, flies, birds, and humans all
may be important mechanical vectors. Vesicular stomati- Diagnosis. No characteristic clinicopathologic changes
tis tends to remain at the site of infection, and coloniza- are reported for either virus. Gross lesions resemble those
tion is facilitated by damage to the skin. Oral mucous seen before death and include vesicular, erosive, and ul-
membranes, coronary bands and interdigital skin, and cerative lesions of the mouth, feet, and teat ends; foot-
teat-end skin are common sites of lesions. Vesicular and-mouth disease also causes lesions of the mammary
stomatitis outbreaks in the United States tend to occur in gland and ruminal epithelium. Microscopic findings
the summer or fall and end with the first killing frost. include hydropic degeneration of cells of the stratum
Viremia plays more of a role with foot-and-mouth spinosum of the epidermis without inclusion bodies. Sec-
disease.The virus is present in most body tissues and fluids ondary bacterial infection may lead to deeper ulcers and
in infected animals and can be transmitted through milk, complicate identification of the viral etiology of these
meat, bone, and hide products; semen; equipment that lesions. “Tiger-heart” striping of the myocardium may be
pierces the skin; and biting arthropods. It also tends to seen with the malignant form of foot-and-mouth disease.
spread through the circulation from the site of infection A presumptive diagnosis may be made by identifying
to other susceptible tissues, including the sites of vesicu- characteristic lesions during a season and in an area at risk
lar stomatitis, as well as to the nasal cavity, mammary for one of these infections. In North America, bluetongue
glandular epithelium, and ruminal pillars. A rare “malig- should be considered as an important differential diagno-
nant” form of foot-and-mouth disease also causes fatal sis for ulcerative oral lesions in sheep. A confirmed
myocarditis. diagnosis of foot-and-mouth disease is achieved by a
The basic lesion for both diseases is the vesicle that combination of virus isolation (from vesicles), immuno-
forms and quickly ruptures approximately 2 to 14 days histochemistry, and serology. Identifying the source of in-
after infection. Ruptured vesicles leave deep erosions on fection also is very important. Diagnosis of vesicular
the skin or mucous membranes and appear to cause pain. stomatitis is achieved by complement fixation or fluores-
Tissue damage and inflammation are often compounded cent antibody staining of virus in vesicular fluid or detec-
by secondary bacterial infection, which can cause greater tion of a rise in antibody titers. Flocks with either of these
morbidity and mortality than the original viral infection. diseases in the United States are subject to quarantine
Morbidity is related to feed refusal, increased recum- and possible destruction (especially for foot-and-mouth
bency, and secondary infections of the mouth, udder, disease).
and feet.
Prevention. Meticulous personal hygiene and avoid-
Clinical signs. Vesicles, erosions, and ulcers are seen at ance of contact with new animals are important during
target sites. They may appear mildly inflamed and erythe- outbreaks to prevent spread between flocks. Vaccines
matous; if they are infected, they may appear severely in- against foot-and-mouth disease are available in many
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 387

parts of the world, but not in the United States. Most lesions that are difficult to differentiate from other viral
nations slaughter or quarantine affected animals. Vac- diseases that cause oral proliferative or ulcerative lesions.
cines against vesicular stomatitis are available and are Virus can be isolated from blood or tissues (mainly skin)
most commonly used if the risk of outbreak is high, but during the acute viremic stage and identified by antibody
vaccination does not prevent infection or shedding. Good staining of more chronic lesions. Serologic tests are avail-
hoof and teat care and soft feeds may help prevent spread able to detect rising titers in convalescent animals.
of the virus by providing a healthy, intact barrier against
invasion.7-9 Treatment and prevention. No specific treatment is
available for sheep or goat pox. Antibacterial drugs may
be useful to treat secondary infection. Judicious use of in-
Contagious Ecthyma (Orf, Sore Mouth) secticides and confinement of affected animals may
Contagious ecthyma is caused by a parapoxvirus that has prevent spread. Vaccines are available in some countries,
zoonotic potential. All ages can be affected, but it gener- but not in the United States. Infected flocks are placed
ally only causes clinical disease in young nursing animals. under quarantine or destroyed in regions where the dis-
Papules or pustules on the lips, nose, and udder may last 2 eases are not endemic. These viruses are difficult to erad-
to 4 weeks (see Chapters 3 and 10). icate from flocks because of their environmental persis-
tence and the constant supply of susceptible hosts.10,11
Sheep and Goat Pox
Pathogenesis. Sheep and goat pox are caused by two
closely related poxviruses. Some strains are infective to
both sheep and goats; most are species-specific. They are
R EFERENCES
1. Hagan WA, Bruner DW, Timoney JF: Bluetongue. In Hagan
maintained in populations by infected animals, and trans- WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s micro-
mission occurs by aerosol or direct or indirect contact. biology and infectious diseases of domestic animals, ed 8, Ithaca, NY,
Flies may play an important role as mechanical vectors in 1988, Comstock Publishing.
some flocks. Viruses remain infective in the environment 2. Walton TE: Bluetongue in sheep. In Howard JL, editor: Current
for as long as 6 months. veterinary therapy, ed 3, Philadelphia, 1993, WB Saunders.
3. Hagan WA, Bruner DW, Timoney JF: Peste des petits ruminants.
After infection, viremia and inflammation of the oral,
In Hagan WA, Bruner DW, Timoney JF, editors: Hagan and
nasal, and ocular mucous membranes occur. Erythema- Bruner’s microbiology and infectious diseases of domestic animals, ed 8,
tous papular pox lesions appear a few days later. Mild in- Ithaca, NY, 1988, Comstock Publishing.
fections are characterized by lesions concentrated in the 4. Commission on Foreign Animal Disease: Pest of small ruminants.
non-wooled or hairless regions of the skin. Severe infec- In Commission on Foreign Animal Disease, editor: Foreign animal
tions produce lesions throughout the oral cavity, respira- diseases, Richmond, VA, 1984, US Animal Health Association.
tory tract, and peritoneal cavity. Secondary infection is 5. Hagan WA, Bruner DW, Timoney JF: Louping ill. In Hagan WA,
common with the severe form and mortality is high. Bruner DW, Timoney JF, editors: Hagan and Bruner’s microbiology
Severity varies according to strain pathogenicity, breed and infectious diseases of domestic animals, ed 8, Ithaca, NY, 1988,
susceptibility, and immune status. If the animal survives, Comstock Publishing.
lesions heal in 3 to 4 weeks. Both diseases have been 6. Commission on Foreign Animal Disease: Louping ill of sheep. In
Commission on Foreign Animal Disease, editor: Foreign animal
eradicated from the United States and are reportable.
diseases, Richmond, VA, 1984, US Animal Health Association.
People can develop mild disease on exposure to these 7. Hagan WA, Bruner DW, Timoney JF: Foot and mouth disease. In
viruses. Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
Clinical signs. Fever, inappetence, conjunctivitis, and NY, 1988, Comstock Publishing.
upper respiratory signs are seen in the initial stages. Pox 8. Hagan WA, Bruner DW, Timoney JF: Vesicular stomatitis. In
lesions are visible shortly thereafter. Secondary infection Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
can lead to a variety of more serious signs indicative of microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
respiratory disease, sepsis, and shock. NY, 1988, Comstock Publishing.
9. Commission on Foreign Animal Disease: Foot and mouth disease.
Diagnosis. Characteristic pox lesions are highly sug- In Commission on Foreign Animal Disease, editor: Foreign animal
diseases, Richmond, VA, 1984, US Animal Health Association.
gestive of this disease. Microscopic analysis reveals
10. Hagan WA, Bruner DW, Timoney JF: The genus Capripoxvirus.
eosinophilic intracytoplasmic inclusion bodies, acanthol- In Hagan WA, Bruner DW, Timoney JF, editors: Hagan and
ysis, and pustule formation within the epidermis and oc- Bruner’s microbiology and infectious diseases of domestic animals, ed 8,
casionally the dermis. Viral particles may be seen on ul- Ithaca, NY, 1988, Comstock Publishing.
trastructural examination. 11. Commission on Foreign Animal Disease: Sheep and goat pox. In
Gross and microscopic lesions are characteristic with Commission on Foreign Animal Disease, editor: Foreign animal
the severe form, but mild disease may produce mild diseases, Richmond, VA, 1984, US Animal Health Association.
388 • Sheep and Goat Medicine
CHRONIC VIRAL DISEASES For this reason it is often suggested that kids be at least 6
months old before they are first tested. PCR testing has a
Caprine Arthritis-Encephalitis Virus high specificity and sensitivity and can detect infection
within a day of exposure. Other less commonly used tests
Infection include a Western blot to detect antibodies and a North-
Caprine arthritis-encephalitis virus (CAEV) is an en- ern blot to look for mitochondrial RNA (mRNA).
veloped, single-stranded RNA virus in the subfamily Because of the limitations in interpreting serologic
Lentivirinae. Similar to other retroviruses, CAEV inte- results, CAEV-induced disease can only be definitively
grates into the host chromosomal deoxyribonucleic acid diagnosed by identification of characteristic lesions from
(DNA) before replicating. The virus is able to remain examination of biopsy specimens or postmortem viral
latent or undergo sporadic bouts of productive viral isolation.
replication.
Treatment. No specific treatments are available for any
Clinical signs. Clinical disease may be evident in only of the syndromes associated with CAEV, although
10% of goats from a CAEV- infected herd at any given chemotherapeutics currently used for acquired immunod-
time. As many as 85% of seropositive goats may be eficiency syndrome (AIDS) may be useful (zidovudine
clinically normal. CAEV produces four clinical syn- [AZT], interferon a and g, interleukin-2, and antiviral
dromes: encephalomyelitis, arthritis (Figure 14-5), inter- agents). Young goats suffering from encephalomyelitis
stitial pneumonia, and indurative mastitis. The pattern of may benefit from physical therapy if they are recumbent,
disease usually varies with age. Arthritis is generally seen and bottle feeding may help maintain hydration and
in sexually mature goats, whereas encephalomyelitis is caloric intake. Antibiotics may be beneficial to goats af-
generally seen in kids 2 to 4 months old. Interstitial pneu- fected with interstitial pneumonia or mastitis if secondary
monia and indurative mastitis are more common in adult bacterial infection is present. Generally the prognosis is
goats. Some goats suffer from a wasting disorder charac- poor for the encephalitic form and guarded for the other
terized by poor body condition and rough hair coat. forms.

Diagnosis. A presumptive diagnosis of CAEV can be Prevention. Prevention of CAEV is crucial because in-
made on the basis of history and clinical signs suggestive fection is lifelong. Infected colostrum and milk are the
of one or more of the syndromes. In general, ELISA tests most important sources of infection. Newborn kids
are better for detecting disease in an individual animal should be prevented from ingesting colostrum from in-
because the sensitivity of the test is higher than that of fected does and should instead be fed pasteurized goat’s
the AGID, whereas the AGID is better for herd screen- milk (heated to 56° C for 60 minutes) or milk from
ing that requires high specificity. With the AGID test, CAEV-negative goats. All goats in a herd should undergo
false negatives may occur in goats that have not yet sero- serologic testing twice yearly; seropositive goats should be
converted to recent infection. Individual goats may take segregated or culled to prevent direct contact between in-
months or years to seroconvert or may never do so. Partu- fected and uninfected animals. When no seropositive
rition or advanced stages of disease also may contribute to animals remain after two successive testing periods, the
a false negative result. False positives may occur in goats herd is considered free of CAEV.1,2
younger than 90 days old that have colostral antibodies.
Ovine Progressive Pneumonia Virus
Infection
Ovine progressive pneumonia (OPP) is an ultimately
fatal retroviral disease that causes chronic, progres-
sive, debilitating inflammatory conditions of the lungs
(United States) and central nervous system (other parts of
the world). It also is called maedi- (Icelandic for “short-
ness of breath”) visna (meaning “wasting”). The virus is a
member of the Lentivirinae subfamily of retroviruses and
is closely related to CAEV. The disease has a long incu-
bation period and protracted clinical course.

Pathogenesis. Only sheep older than 2 years are af-

Figure 14-5 This Nubian goat tested positive for CAEV. Note the
large, round carpal joints. This goat appeared to be in a great deal of fected by ovine progressive pneumonia virus (OPPV).
pain and preferred to eat while on its knees. (Courtesy Drs. Tom Powe The virus is spread by direct contact, probably in respira-
and D.G. Pugh, Auburn University, Alabama.) tory and salivary secretions, and by excretion in the milk.
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 389

Transplacental transfer is of minor importance. Infection milking equipment, dehorning instruments, and tail
is established in the monocyte and macrophage cell line docking and castration tools before use and between
and spread by these cells to the lungs, lymph nodes, animals. Contaminated feed and water also are potential
choroid plexus, spleen, bone marrow, mammary gland, routes of infection and should not be shared among in-
and kidneys. Similar to CAEV, OPPV evades the cellular fected and uninfected animals. Serologic testing and sep-
and humoral immune system of the host by incorporation aration or culling of seropositive animals may help reduce
of its provirus in host DNA, low-grade replication of virus infection. Although OPPV can readily be isolated from
only when monocytes differentiate into macrophages (re- ewe colostrum, colostral transmission of OPPV has not
stricted replication), and production of antigenic variants be definitively established. However, many prevention
that are not neutralized by existing antibodies. Continual guidelines recommend that offspring from infected dams
antigenic stimulation of the host by low-grade replication be separated from the dam before they nurse and then be
of OPPV results in chronic inflammation and resultant fed cow colostrum and artificially reared. Quarantine and
lymphoid proliferation in various target tissues. The virus serologic testing of flock additions before placing them
may prevent B lymphocytes from differentiating into with the current flock and purchase of sheep only from
plasma cells in lymph nodes and may thereby impair im- OPPV-free flocks are important to prevent the introduc-
munoregulation. Seroconversion occurs within 2 to 3 tion of new infections. Serologic testing should be per-
weeks after infection. formed at least annually in a flock until two consecutive
negative test results are obtained.3,4
Clinical signs. In the United States serologic surveys
reveal infection rates of between 30% and 67%, but rarely
is more than 5% of a flock lost to OPPV. Icelandic, Texel,
Scrapie
Border Leicester, and Finnish Landrace appear to be sus- Another member of the slow infection group of diseases
ceptible sheep breeds. Goats also are susceptible. Resis- of small ruminants is scrapie (see Chapter 11). It is an
tant sheep breeds include Rambouillet and Columbia. afebrile, chronic, progressive degenerative disorder of the
Various clinical syndromes are associated with OPPV central nervous system of sheep and occasionally of goats.
and include wasting (thin ewe syndrome), pneumonia, The causative agent is poorly characterized and is postu-
mastitis (“hard bag”), posterior paresis, arthritis, and vas- lated to consist of protein fibrils (scrapie-associated
culitis. In North America, pneumonia and indurative fibrils).
aseptic mastitis are common sequelae of infection. Sheep (and goats to a lesser degree) are the natural
hosts for scrapie. Clinical signs often do not appear until
Diagnosis. A presumptive diagnosis can be made on animals are 2 years old and animals as old as 5 years may
the basis of clinical signs, poor response to treatment, exhibit clinical disease. Both vertical and horizontal
characteristic postmortem findings, and serologic testing. transmission have been demonstrated experimentally in
Definitive diagnosis requires isolation of the virus from sheep and goats.
WBCs (buffy coat of whole blood sample) or tissues. Less
expensive and faster serologic tests include AGID, Clinical signs. The onset of scrapie is insidious. Ini-
ELISA, and an indirect immunofluorescence test. The tially, sheep show subtle changes in behavior such as mild
AGID test is frequently used as a flock screening test, but apprehension, staring or fixed gaze, failure to respond to
the ELISA is more sensitive on an individual basis and herding dogs, and boldness around humans. Several
can detect antibodies earlier in the course of the disease. months later, the animals become intolerant of exercise
As with CAEV, false negatives and false positives are and develop a clumsy, unsteady gait and floppy ears. Later
possible (see the section on CAEV, which discusses in- the sheep develop itchy skin that causes them to rub
stances in which each occur). themselves excessively against firm, immobile objects
(origin of the name scrapie). This leads to excoriations and
Treatment. No effective treatment is available for wool damage.
OPPV. Supportive therapy that includes appropriate hus-
bandry and control of secondary infection with antibi- Diagnosis. Histologically the only consistent lesions
otics may prolong life for a few weeks or months but ulti- are degenerative changes in the central nervous system
mately the disease is fatal. Because of the poor prognosis consisting of bilaterally symmetric vacuolation of the
and risk of exposure of naive animals to clinical disease, neurons in the brainstem and spinal cord with accompa-
long-term treatment is not recommended. nying spongy degeneration.5

Prevention. The only known method of preventing

OPPV infection in a flock is to prevent exposure to the
Border Disease Virus
virus. Management practices that help decrease the inci- Border disease virus (BDV) is very similar to the bovine
dence of horizontal transmission include disinfection of viral diarrhea virus (BVD) and hog cholera virus. The
390 • Sheep and Goat Medicine
virus is a helical, enveloped, noncytopathic RNA virus tonic-clonic tremors when awake, which may prevent
that is a member of the Togavirus family and Pestivirus standing or suckling. Most of these lambs die within a
genus. It rarely causes disease in adults and is most im- few days of birth. If they survive, the hair changes disap-
portant as a cause of in utero infection of lambs and kids. pear in 9 to 12 weeks and the central nervous system
The condition gets its name from the fact that it was first signs resolve by 20 weeks. Goats infected at this time
reported in sheep along the Welsh border of the United have similar symptoms except that they rarely exhibit hair
Kingdom. Sheep also are susceptible to BDV. coat changes. If lambs are infected before day 80 of gesta-
tion and are still viable, they may become persistently in-
Pathogenesis. Horizontal transmission of border dis- fected and immunologically compromised. They are
ease virus occurs through contact with secretions and ex- small at birth and generally weak.
cretions of body fluids and tissues from infected animals. Typical outbreaks of border disease cause abortions
The virus crosses intact mucous membranes and can and birth of weak lambs in the first year as the virus
spread rapidly through a flock. The major reservoir is the rapidly spreads throughout a susceptible flock, and then
persistently infected sheep or goat. These reservoirs are insignificant losses in the succeeding years as adult sheep
asymptomatic, congenitally infected, and often seronega- develop immunity.
tive animals that shed large quantities of virus.
If a pregnant animal is infected, the virus may be Diagnosis. Border disease viral antigens can be dem-
transmitted vertically to the embryo or fetus. Depending onstrated in abomasum, pancreas, kidney, thyroid, skin,
on the stage of gestation, embryonic or fetal infection and testicle tissues from aborted fetuses and persistently
may have different outcomes ranging from embryonic re- infected animals using fluorescent antibody tests. The
absorption to normal birth. These infections are the most virus can be isolated from serum, heparinized whole
important aspect of border disease. blood, and tissue taken from brain, spinal cord, spleen,
The major organ system targeted by BDV is the fetal and bone marrow from affected lambs. Whole blood is
central nervous system. The hallmark lesion is hy- better than serum if colostral antibodies are likely to be
pomyelination, or degeneration of oligodendroglial cells. high; serum is an adequate sample in neonates and juve-
Three factors contribute to this lesion. The first is direct niles that have not suckled.
viral damage. The second is viral-induced inhibition of Antibodies to the virus may be quantified by serum
the thyroid gland that causes decreased secretion of neutralization, AGID, and complement fixation with hy-
thyroid hormones. In the absence of these hormones, a perimmune BVD antiserum. Serologic tests are useful to
resultant lowered concentration of a specific nucleotide in detect exposure in late-gestation (after day 80) neonates
the central nervous system also contributes to the hy- and unvaccinated animals, but may be confounded by
pomyelination. The third factor is altered immune func- colostral antibodies in suckling neonates, previous expo-
tion. The virus causes the host to produce a virus-specific sure, and vaccination in older animals. Any titer in a pre-
delayed hypersensitivity reaction that causes inflamma- suckling neonate indicates in utero exposure, whereas a
tion in the central nervous system. It also causes im- serum neutralization titer of 1:20 to 1:320 suggests infec-
munosuppression. Death often results from opportunistic tion in adults. The presence of specific antibodies in the
conditions such as parasitism, diarrhea, and broncho- cerebral spinal fluid suggests border disease virus infec-
pneumonia. tion. Negative presuckling serologic tests do not rule out
exposure because persistently infected lambs tend to be
Clinical signs. Clinical signs depend on the time immunotolerant to the border disease virus and therefore
during gestation when the fetus or embryo is exposed to are born without an antibody titer. These animals may
the virus. Clinical signs also may vary in severity from subsequently develop a titer that is indistinguishable from
animal to animal because different fetuses develop com- that of a normal animal. Although persistently infected
petent immune systems at different times. If the fetus or animals do not respond immunologically to the strain of
embryo is exposed to the virus within 45 days of concep- the virus they carry, they may respond to other strains of
tion, it dies and is resorbed or aborted. These losses are the virus, including vaccine strains.
not usually noticed by the flock manager. The principal Gross postmortem findings include hydranencephaly,
manifestation in the flock is a large number of open ewes porencephaly, microcephaly, cerebellar hypoplasia, abnor-
and a small lamb crop. Infection of the fetus between days mal rib curvature, brachygnathia, doming of the frontal
45 and 80 of gestation causes damage to rapidly growing bones of the skull, narrowing of the distance between the
systems such as the skin and nervous, lymphoid, thyroid, orbits, shortening the crown-to-rump length, shortening
and skeletal systems. Congenital malformations are seen of the diaphyseal length, retention of secondary hair
at birth. Lambs have abnormal fleece (hairy rather than fibers, and abnormal skin pigmentation. The major
woolly in consistency), small stature, domed heads, short- histopathologic changes include hypomyelination and
ened legs, and dark pigmentation of the skin, particularly hypercellularity of the white matter. Glial cells appear
on the dorsal aspect of the neck. The lamb may exhibit normal.
 Chapter 14 Diseases of the Hematologic, Immunologic, and Lymphatic Systems • 391

Treatment. No treatment is available for border disease more effective at preventing clinical disease in vaccinated
infection. Supportive care may include assistance in animals than in preventing in utero infection because
nursing and standing for affected lambs, provision of they do not prevent transient viremia. Vaccination de-
good bedding and solid footing, and treatment of second- creases viremia and fetal infection, but does not eliminate
ary opportunistic infection. them. Therefore vaccines play a role in decreasing eco-
nomic loss but do not replace culling of carrier animals as
Prevention. Control is primarily achieved by eliminat- the major method of control. 6,7
ing persistently infected carrier animals from the flock
and preventing the addition of new carrier animals. This
is easiest in a closed flock but especially difficult in small
ruminant flocks because of the frequent desire to import
R EFERENCES
1. Hagan WA, Bruner DW, Timoney JF: Caprine arthritis-
new genetics. To identify carriers, virus isolation must be
encephalitis. In Hagan WA, Bruner DW, Timoney JF, editors:
performed on every animal in the flock; carrier animals Hagan and Bruner’s microbiology and infectious diseases of domestic
must be culled. Additionally, all unborn animals must be animals, ed 8, Ithaca, NY, 1988, Comstock Publishing.
considered potential carriers and should be tested at 2. Phelps SL, Smith MC: Caprine arthritis-encephalitis virus infec-
birth. After two lamb or kid crops are born without any tion, J Am Vet Med Assoc 203:1663, 1993.
positive animals, the flock is likely to be free of border 3. Hagan WA, Bruner DW, Timoney JF: Maedi-visna. In Hagan WA,
disease. An alternative solution in hobby flocks is to arrest Bruner DW, Timoney JF, editors: Hagan and Bruner’s microbiology
breeding activity until all animals have been shown to be and infectious diseases of domestic animals, ed 8, Ithaca, NY, 1988,
free of infection. New animals should be quarantined and Comstock Publishing.
tested before admission to the flock. Herd screening with 4. Cutlip RC: Maedi-visna. In Howard JL, editor: Current veterinary
the ear skin biopsy test using fluorescent antibody stain- therapy, ed 3, Philadelphia, 1993, WB Saunders.
5. Hagan WA, Bruner DW, Timoney JF: Scrapie. In Hagan WA,
ing to detect virus is less expensive and more convenient
Bruner DW, Timoney JF, editors: Hagan and Bruner’s microbiology
than the whole blood virus isolation test. and infectious diseases of domestic animals, ed 8, Ithaca, NY, 1988,
The role of vaccination in preventing infection is still Comstock Publishing.
unclear. No vaccine against border disease virus is avail- 6. George LW: Diseases of the nervous system. In Smith BP, editor:
able, but some reports suggest that BVD vaccines (inacti- Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
vated or killed products) for cattle may be helpful for 7. Radostits OM, Gay CC, Blood DC: Veterinary medicine, ed 9,
sheep at risk. However, these vaccines have proven to be Philadelphia, 2000, WB Saunders.
 Chapter 15

DSystem
iseases of the Cardiovascular

CHRISTOPHER CEBRA AND MARGARET CEBRA

EXAMINATION OF THE
atrioventricular block, premature and escape beats, and
CARDIOVASCULAR SYSTEM pathologic tachyarrhythmias occur under similar condi-
tions as in other species.
Auscultation of the Heart Assessment of the strength of cardiac contractions is
The most basic method of assessing cardiac health is often subjective. Sounds are louder on the left side than
thoracic auscultation. The clinician places a stethoscope the right side and vary inversely in strength with the body
against the chest wall in the axillary region and then condition of the animal. Both S1 (closure of the atrioven-
assesses heart rate, rhythm, and strength and listens for tricular valves; onset of ventricular systole) and S2
any abnormal sounds. The axillary region, the ventral (closure of the semilunar valves; onset of ventricular dias-
third of the chest between the second and fourth or fifth tole) should be audible.1
rib, has relatively little fleece or hair cover, allowing good
contact between the bell of the stethoscope and the skin.
The clinician should listen to the heart from both sides of
Peripheral Pulses
the chest at two or three intercostal spaces on each side. Assessment of peripheral pulse strength and synchronic-
He or she must take care to push the bell under the elbow ity with cardiac contractions is the simplest way of evalu-
to assess the cranial aspects of the heart and not to push ating the effectiveness of cardiac output. Peripheral arter-
the bell too ventral, where it overlies the sternum and not ies can be difficult to find in sheep and goats, especially in
the thorax. adults. The largest include the femoral artery (medial
Normal heart rate varies with the age of the sheep or thigh) and brachial artery (proximal medial foreleg). The
goat. Neonatal lambs and kids frequently have rates of facial artery (ventrolateral mandible) and carotid artery
120 to 140 beats per minute, whereas adults of both (ventrolateral neck) also can be used for pulse assessment
species often have rates between 66 and 80 beats per in some animals. Weak or absent pulses are consistent
minute. Juveniles typically attain an adult rate by 3 with hypotension and poor cardiac output. Exuberant
months of age. Rates can be increased in stressed or pulses are consistent with hyperdynamic shock or regur-
excited animals; such animals should be given time to ac- gitation of blood from the aorta into the heart (aortic
climate to restraint before the clinician assesses their valve insufficiency) or lung (patent ductus arteriosus with
heart rate. Other reasons for tachycardia include anxiety, left-to-right shunting). Pulses are usually assessed manu-
hypovolemia, venous pooling of blood, arterial hypoten- ally because of the difficulty of placing any sort of mano-
sion, tachyarrhythmia, and poor cardiac function. Causes metric device on a conscious sheep or goat.1
of bradycardia include lesions affecting the vagus nerve,
bradyarrhythmia, and the late stage of shock.
Normal heart rhythm is regular. The most common
Venous Filling, Pulses, and Pressures
rhythm anomaly is sinus arrhythmia, in which the heart Monitoring jugular vein filling and pulses allows the oper-
rate speeds with inspiration and slows with expiration. ator to assess right heart function and blood volume.
Descriptions of other dysrhythmias in sheep and goats Sheep and goats with hypovolemia may have small jugular
are uncommon, but a reasonable presumption is that veins that are not visible or palpable even after manual oc-
atrial and ventricular fibrillation, varying degrees of clusion for several minutes. In contrast, sheep and goats
• 393 •
394 • Sheep and Goat Medicine
with right heart failure or restrictive pericardial disease (methemoglobinemia or sulfhemoglobinemia), and local
may have large jugular veins that are visible or palpable vascular stasis (hypodynamic shock, poor cardiac output,
without being occluded and have positive pressures. Pulses hypothermia). Poor central oxygenation is characterized
in the jugular vein result from backflow of blood during by purple-blue discoloration of all mucous membranes
right atrial or ventricular systole. No valve is present to and possibly of nonpigmented skin, whereas vascular
prevent regurgitation during right atrial systole; slight stasis may only affect certain areas such as the gingival
pulses that disappear when the head is elevated or do not margins. Scleral vessels often become engorged, tortuous,
extend above the level of the heart base are common and and purple during vascular stasis. Approximately one
nonpathologic. Pulses that extend further up the neck third to one half of blood hemoglobin must be deoxy-
even when the head is elevated most commonly result genated for membranes to become cyanotic; therefore
from tricuspid valve insufficiency. Such pulses coincide cyanosis usually only occurs when blood oxygen pressures
with right ventricular systole and are caused by regurgita- (local or central) are already very low.
tion of ventricular blood through the incompetent valve. Accumulation of bilirubin leads to yellow discol-
Tricuspid insufficiency can occur with right heart failure oration of the mucous membranes (jaundice or icterus).
(and jugular distention) or as a separate entity. Icterus can develop as a result of intravascular or extravas-
Monitoring venous pressures requires a manometer. cular hemolysis, decreased hepatic uptake of bilirubin,
The most common form of monitoring involves insert- and decreased biliary excretion; the hemolytic causes are
ing a fluid-filled line into the jugular vein. The line is at- most common in sheep and goats.
tached to a pressure transducer and measuring instru- Hydration can be estimated by the moistness or tacki-
ment. Many electrocardiographs also have the capability ness of the mucous membranes. This is a subjective deter-
of measuring pressures. The venous line may be left in mination that is improved by practice on normal animals.
the jugular vein or advanced into the central veins and A loss of body water suggests that fluids should be part of
heart. The jugular and central veins usually have pres- the treatment protocol. However, dehydration only
sures that are negative to as high as 5 cm H2O. Positive becomes clinically apparent when body fluid loss exceeds
pressures result from hypervolemia (caused by excess 5% of total body weight (see Appendix II).
fluid administration or renal dysfunction), restrictive
pericardial disease, and cardiac dysfunction. If venous hy-
pertension becomes severe, especially over a long period,
Blood Gases
edema develops.1 Analysis of blood gases can provide valuable information
about animals with hypoperfusion. Metabolic acidosis in
sheep and goats without diarrhea, ketonemia, or grain
Mucous Membranes overload often results from lactic acid production by un-
Mucous membranes can be assessed for color, appearance derperfused tissues. The clinician can collect venous
of vessels, hydration, and capillary refill time. The most blood for analysis from any accessible peripheral vein; the
common membranes evaluated are the buccal, conjuncti- blood should be collected anaerobically and stored in a
val, scleral, and vaginal membranes. Normal membranes heparinized container. A determination of whether un-
are pale pink to pale red, although the high frequency of derperfusion is attributable to inadequate blood oxygen
dark-pigmented membranes in some breeds of sheep and content (pulmonary gas exchange) or inadequate tissue
goats sometimes makes this assessment difficult. Overly blood flow (blood volume and pressure) requires arterial
pale membranes can be attributed to anemia or hypoper- blood gas analysis. Arterial blood is most commonly col-
fusion; however, the clinician should keep in mind that ru- lected from the brachial and femoral arteries, but these
minant membranes tend to be paler than many monogas- arteries are poorly accessible in vigorous animals. Clini-
tric species because of their smaller erythrocytes and cians must avoid unnecessary stress when restraining sick
keratinized membranes. Abnormal ruminant membranes animals for blood collection. The auricular arteries and
are often white, not pale pink, and scleral vessels become peripheral limb arteries can be used in anesthetized pa-
very small. In some animals, anemia can be differentiated tients. Inadequate arterial blood oxygen content suggests
from hypoperfusion by observing capillary refill time after right-to-left cardiac shunting (right-to-left patent ductus
slight digital pressure is applied to the buccal or vaginal arterious or septal defect with or without abnormalities of
membranes. In normal animals, color returns in 1.5 to 2 the great vessels) or pulmonary disease. Differentiation of
seconds. A shorter refill time is seen in hyperdynamic the causes of inadequate arterial blood oxygen content re-
shock (which is often accompanied by a reddening of the quires an extensive cardiopulmonary examination.1
membranes) and a longer time is seen in hypoperfusion.
Change of the normal membrane color toward a
purple or blue hue is indicative of cyanosis. Cyanosis
Electrocardiogram
results from poorly oxygenated hemoglobin and can be Electrocardiographic evaluation is most useful for sheep
seen with poor central oxygenation (right-to-left cardiac and goats with cardiac dysrhythmias. The most common
shunting, pulmonary disease), nonfunctional hemoglobin technique uses the base-apex lead: the positive electrode
 Chapter 15 Diseases of the Cardiovascular System • 395

(LA) is placed over the cardiac apex in the left fifth inter- The ECG should be evaluated for regular appearance
costal space at the level of the elbow, the negative elec- of P waves and QRS complexes, regular P-P, R-R, and
trode (RA) is placed in the right jugular furrow at the P-R intervals, appearance of P waves and QRS com-
height of the base of the heart, and the ground (LL) is plexes that are identical in appearance, and appearance of
placed on the dorsal spine or another site distant from the T waves of normal amplitude. The Q-T interval varies
heart. Topical application of alcohol improves skin inversely with heart rate. An absence of P waves indicates
contact and clipping of fleece may be necessary if the atrial fibrillation or ascension of a ventricular or supra-
complexes are small (Figure 15-1). Panting behavior and ventricular pacemaker. The absence of QRS complexes
muscle tremors often lead to baseline interference in indicates atrioventricular block.1
adult sheep.
The electrocardiogram (ECG) should reveal a distinct
P wave (atrial depolarization), QRS complex (ventricular
Echocardiography
depolarization), and T wave (ventricular repolarization). Echocardiography is a diagnostic modality that is safe,
The R component (negative deflection after a positive noninvasive, and convenient to perform in a standing
deflection) of the QRS complex is usually the most animal; however, it is seldom used in small ruminants
prominent and the Q component (negative deflection because of expense. Nevertheless, it is extremely useful
before the first positive deflection) is usually absent. The in sheep and goats to confirm intracardiac and pericar-
T wave can be either positive or negative and may vary on dial diseases, including valvular endocarditis, pericardi-
a single strip (Figure 15-2). tis and pericardial effusions, cardiomyopathy, congestive
heart failure, and congenital heart defects. Echocardiog-
raphy can be used to assess heart chamber size, valve
motion, wall thicknesses, blood flow, and intracardiac
hemodynamics.
Echocardiography has three basic types:
1. M-mode echocardiography is used to evaluate
wall thickness, heart chamber diameters, and valve
motion.
2. Dimensional echocardiography is used to evaluate
anatomic relationships between cardiac structures
and define their movement relative to each other.
3. Doppler echocardiography is used to evaluate
blood flow direction, turbulence, and velocity.
Figure 15-1 Performing an electrocardiogram (ECG) on a goat. Pressure gradients can be estimated within the heart
The leads are attached to the front two legs and the back two legs.
(Courtesy Drs. Hui-Chu Lin and D.G. Pugh, Auburn University, Alabama.)
and great vessels such as the pulmonary artery and aorta.
Pulse wave Doppler and continuous wave Doppler
echocardiography also can be employed. Color flow
Doppler converts the Doppler signals to an arbitrarily
T chosen color scale to semi-quantitatively depict the direc-
L
tion, velocity, and turbulence of blood. The use of color
flow Doppler is mainly restricted to specialty practices
and referral institutions because significant expertise and
P T
experience are required to interpret the image and the
equipment is cost-prohibitive for many practices.
Echocardiography can be performed on a standing or
QRS laterally recumbent small ruminant. The best location for
placement of the transducer is the right third intercostal
space at the level of the elbow; the examiner should use a
T P/N
high-frequency transducer that fits well in the intercostal
Figure 15-2 Normal ECG complex recorded from a conscious space. The same spot on the left side can be used if the
goat using standard limb lead II. The P wave indicates atrial entire heart cannot be visualized from the right side. The
depolarization, whereas the QRS complex and T wave represent examiner may choose to clip the fleece of a sheep or the
ventricular depolarization and repolarization, respectively. (The paper hair of a goat to improve resolution of the image before
speed is 25 mm/sec.) The magnitude and duration of these waveforms
applying the coupling gel.
depend on many factors, including the age of the goat, lead examined,
size of the cardiac chambers, and method of electrical activation. Performing echocardiography involves systematically
ECG can be used to monitor cardiac rhythm and detect cardiac examining chamber size, myocardial function, valve ap-
diseases. (Courtesy Dr. Hui-Chu Lin, Auburn University, Alabama.) pearance and motion, and aorta and pulmonary artery
396 • Sheep and Goat Medicine
blood flow and noting the presence of abnormal struc- cessive trait in Southdown sheep and as a sporadic occur-
tures within or around the heart. Both long- and short- rence in other breeds.
axis views of all cardiac structures should be imaged.1 Rarely a large VSD may cause such severe right ven-
tricular hypertrophy that deoxygenated blood is pumped
into the left side of the heart and out the aorta. This
Other Imaging Modalities “reverse VSD” or “Eisenmenger syndrome” results in
Thoracic radiographs are used diagnostically by many hypoxemia.
private practitioners with access to portable radiographic Tetralogy of Fallot is a more complex abnormality that
equipment or a stationary small animal x-ray machine. includes a VSD, as well as pulmonic stenosis, an overrid-
Most sheep and goats can be treated with the same ing aorta, and right ventricular hypertrophy. The result is
radiographic techniques used for large dogs. Radi- an increase in deoxygenated blood entering the systemic
ographic studies are most helpful if the practitioner sus- circulation, which severely decreases the oxygen content
pects that heart failure, valvular lesions, or abnormal ex- of arterial blood.
tracardiac or intracardiac communication may be causing PDA and atrial septal defects are uncommon and
chamber or great vessel enlargement or dilatation. Some often transient. Both result in recirculation of oxygenated
pulmonary disorders also can be visualized. blood through the lung, without diminishment of the
Lateral thoracic radiographs are easiest to obtain in oxygen content of arterial blood. Unless a large volume of
sheep and goats and may be performed with physical re- blood is recirculated, these lesions often do not cause
straint only. Ventrodorsal (VD) views may require seda- clinical disease. Both may be detected in some neonates
tion and are of limited usefulness in deep-chested small and then resolve spontaneously over the first months of
ruminants. Dirt and foreign bodies in the fleece of sheep life.1
can create artifacts on the radiographic film, so the fiber
should be examined before the radiograph is taken.1 Clinical signs. The major clinical signs associated with
all congenital heart defects include anorexia, reduced
growth rate, exercise intolerance, lethargy, and weakness.
GENERAL CARDIAC DISEASE Other signs such as dyspnea and cyanosis at rest or with
exercise may suggest a specific defect. Signs of congestive
Congenital Cardiac Disease heart failure may predominate. Tachycardia and a heart
Congenital cardiac defects are abnormalities of cardiac murmur may be present. The most common murmur as-
structure or function that are present at birth. Proposed sociated with a VSD is a pansystolic murmur heard best
causes include maternal viral infections leading to fetal on the right side over the tricuspid valve. Often it can be
infection or metabolic dysfunction, fetal anoxia from pla- heard on both sides of the thorax. A PDA murmur also is
cental insufficiency, use of pharmacologic agents in preg- often heard on both sides of the thorax, but it is loudest in
nant dams, exposure to toxins, nutritional deficiencies in the left third or fourth intercostal space at the level of the
early pregnancy, and heredity. The most common defect shoulder. The murmur is described as high-pitched and
in sheep and goats is a ventricular septal defect (VSD). continuous throughout systole and diastole. Its intensity
Other reported defects include atrial hypoplasia, car- increases with increased heart rate, exercise, and excite-
diomegaly, and cardiac anomalies such as patent ductus ment. A tetralogy of Fallot may cause both a VSD
arteriosus (PDA), atrial septal defect, and tetralogy of murmur or a murmur heard best over the pulmonic valve.
Fallot.
Diagnosis. Identification of a murmur in a young
Pathogenesis. A VSD is an opening, primarily in the sheep or goat in conjunction with signs of failure to thrive
membranous portion of the ventricular septum, that sep- is highly suggestive of congenital heart disease. Echocar-
arates the right and left ventricles. The defect is suspected diography is the diagnostic method of choice for nonin-
to occur as a result of failure of the ventricular septum to vasive identification of cardiac anomalies and assessment
fuse during gestation. Blood flows through the hole from of the hemodynamic significance of the shunt. Two-
the left ventricle to the right ventricle and right ventric- dimensional echocardiography can be used to image the
ular outflow tract after birth. This shunting increases the VSD directly and measure the size of the defect. Color
blood flow to the pulmonary circulation and the venous flow Doppler may be useful in observing the jet of regur-
return to the left atrium and ventricle, causing volume gitant blood. A PDA and tetralogy of Fallot may be diffi-
overloading the left heart. Eventually left heart failure cult to visualize with echocardiography. Clinical pathol-
may lead to the backup of blood through the lung into ogy findings are usually unremarkable with VSDs and
the right heart and cause subsequent right heart failure. If PDAs, but tetralogy of Fallot may cause an increase in
the defect is large and a great deal of the blood is shunted, packed cell volume and hemoglobin concentration (poly-
right-sided congestive heart failure may occur first. This cythemia). Radiography may be used to diagnose congen-
defect is thought to be inherited as a simple autosomal re- ital heart defects. Cardiomegaly, decreased pulmonary
 Chapter 15 Diseases of the Cardiovascular System • 397

vascularity, and presence of an overriding aorta may be cowdriosis is relatively rare and occurs most commonly in
some of the radiographic findings. Cardiac catheteriza- naive exotic breeds of ruminants in a heartwater-endemic
tion can be used to provide supplemental information area. Signs include sudden death with no premonitory
about congenital cardiac defects where applicable. signs or fever and convulsions. Occasionally severe diar-
rhea may be seen. The acute form is the most common.
Treatment and prognosis. No treatment to correct Symptoms include a sudden onset of pyrexia (as high as
congenital heart defects is economically viable in small 107° F) followed by anorexia, depression, and respiratory
ruminants. Prostaglandin inhibitors have been used suc- distress, with resultant rapid breathing and cyanosis.
cessfully in humans to close PDAs, although their effi- Clinical signs may develop in a few days and include
cacy has not been evaluated in small ruminants. In the chewing movements, twitching of the eyelids, protrusion
absence of clinical signs, animals can live productive lives of the tongue, behavior changes, circling and high-
with defects, but the prognosis is poor for animals with stepping gait, wide-based stance, and muscle fascicula-
signs of congestive heart failure. tions. Hyperesthesia, nystagmus, frothing at the mouth,
recumbency, seizures, and coma can occur terminally.
Prevention. Because the role of inheritance in congen- Death usually occurs within 1 week of the onset of clinical
ital heart defects is unclear, affected animals should gen- signs. A mild or subacute form (heartwater fever) is seen in
erally not be bred.1 some indigenous breeds of sheep with high natural resis-
tance to the disease. It is more common in older animals.
This form is characterized by a transient fever. Animals
ACQUIRED CARDIAC DISEASES with heartwater fever may serve as sources of infection for
others because the rickettsial organisms do not clear for as
Heartwater Disease (Cowdriosis) long as 223 days in sheep and 8 days in goats.2-4
Heartwater disease is an acute, tick-borne septicemic
disease caused by the rickettsial organism Cowdria rumi- Diagnosis. Heartwater disease can be definitively diag-
nantium. All ruminants are susceptible, particularly nosed by identification of the tick vector and microscopic
Angora goats. The disease is not contagious and is trans- demonstration of C. ruminantium in histologic sections of
mitted by ticks of the genus Amblyomma, particularly A. brain cortex stained with Giemsa stain. Brain biopsies
hebraeum (the bont tick) and A. variegatum. The rick- have been experimentally obtained from goats for ante-
ettsial organism is found in the intestinal epithelial cells mortem diagnosis. The organism also can be found in the
of its vector. The host tick requires three blood meals to intima of large blood vessels and in sections of kidney
complete its life cycle; only the third host must be a large glomeruli and lymph nodes. A common biologic test to
mammal. Infected ewes and does develop ovarian infec- confirm the diagnosis involves inoculation of fresh blood
tions and pass C. ruminantium vertically to their off- from a suspect animal into susceptible sheep. An indirect
spring. The disease is largely confined to areas where ticks immunofluorescence test also is available.
of the genus Amblyomma are prevalent, including sub-
Saharan Africa, Madagascar, some islands in the Indian Treatment. Early in the disease course, oxytetracycline
Ocean, the Caribbean, and Europe. Reports have de- (6 to 10 mg/kg intravenously [IV] every 12 hours for 3 to
scribed the recovery of infected ticks from imported tor- 4 days) may be helpful. Long-acting tetracyclines also are
toises in Florida.2-4 effective but must be used early in disease. Treatment is
less effective in the later, neurologic stages of the disease.
Pathogenesis. C. ruminantium multiplies in reticuloen-
dothelial cells, particularly the capillary endothelial cells Prevention. Tick control in pastures is the mainstay of
of the brain. Regional lymph nodes may serve as the cowdriosis prevention. This is difficult because Ambly-
primary replication sites after infection. Rupture of in- omma ticks have developed ascaricide resistance and
fected neutrophils and macrophages leads to release of because ticks feed off many hosts and have a high rate of
the organism and circulation in the blood (parasitemia reproduction. Complete elimination of tick infestation is
and vasculitis) with subsequent colonization of the vascu- not desirable (or possible in some places) because expo-
lar endothelium of body organs.3,4 sure to low levels of the organism is effective in develop-
ing immunity. In some parts of South Africa, goat herds
Clinical signs. The incubation period in sheep and are given oxytetracycline every 14 days during the
goats varies between 14 and 17 days. Depending on the summer months. Controlled infection followed by antibi-
susceptibility of the animal (Angora goats are exquisitely otic administration has been tried as a means of immu-
sensitive; lambs younger than 8 days and kids younger nizing small ruminants. Such a method is effective in
than 6 weeks are inherently resistant to C. ruminantium) preventing disease caused by a homologous strain of
and the virulence of the organism, three different clinical Cowdria but has no effect against a heterologous strain.
forms of heartwater disease have been identified. Peracute An attenuated live strain of Cowdria is available as a
398 • Sheep and Goat Medicine
vaccine, but it has not been tested in field conditions. Im- Tissue samples of liver can be used to evaluate body
munity after disease is not life-long; susceptibility to rein- stores of selenium. Ration analysis may help support a di-
fection varies between 6 and 58 months. Mortality rates agnosis. Postmortem lesions include white streaks in
in sheep range between 6% and 80% depending on the muscle fibers and pale areas that represent areas of acute
breed (Persian or Africander sheep versus Merino sheep). coagulative necrosis or chronic fibrosis and calcification.
Mortality rates in Angora goats can exceed 90%.2-4 Nonspecific clinical pathology findings that are sugges-
tive of WMD include significant elevations in creatine
Nutritional Myodegeneration kinase (CK), aspartate aminotransferase (AST), and
lactate dehydrogenase (LDH). Evidence of dehydration
(White Muscle Disease) and myoglobinuria may be present.
Nutritional myodegeneration, or white muscle disease
(WMD), produces two distinct syndromes: a cardiac Treatment. The cardiac form of WMD carries a poor
form and a skeletal form (see Chapters 2 and 19). Both prognosis despite appropriate treatment. Injectable vitamin
affect young, rapidly growing farm animals, but the E and selenium preparations should be given parenterally
cardiac form typically affects neonates in the first week of and appropriate supportive care should be provided. The
life. It is caused primarily by a dietary deficiency of vitamin E content of combination supplements is insuffi-
selenium and/or vitamin E. Animals are most often af- cient to correct vitamin E deficiency. Both oral and in-
fected if their dams consumed selenium-deficient diets jectable vitamin E products are available.5,6
during gestation.5,6
Prevention. Prevention is aimed at proper supplemen-
Pathogenesis. Deficiencies of selenium and vitamin E tation of the dam either by salt mix or by total ration sup-
result in the destruction of cell membranes and proteins, plementation (0.1 to 0.3 ppm selenium in the diet).
impairing cellular integrity. Both nutrients are biologic During late gestation, injectable vitamin E and selenium
antioxidants. In their absence, cell damage results from may be necessary5,6 (see Chapters 2 and 9).
the presence of free radicals and peroxides liberated
during normal cellular metabolism. Many animals defi-
cient in selenium and/or vitamin E have no evidence of
Vegetative Endocarditis
WMD, and sometimes both nutrients must be deficient Acquired endocarditis is most common in adult small ru-
to cause signs.5,6 minants and is caused by infection, degenerative changes,
inflammation, trauma, and valvular insufficiency caused
Clinical signs. Clinical signs of both the cardiac and by idiopathic dysfunction of one or more of the four heart
skeletal syndromes range from peracute to subacute. valves. As a result of infectious, neoplastic, or inflamma-
WMD often results in severe debilitation or sudden tory changes, vegetative lesions form on the cardiac valves
death. Small ruminants suffering from the cardiac form and cause vegetative valvular endocarditis. Chronic active
often exhibit referred respiratory signs because the infections such as foot or liver abscesses, rumenitis, and
cardiac, diaphragm, and intercostal muscles are affected. omphalophlebitis can lead to sustained or recurrent
Respiratory signs include dyspnea, tachypnea, foamy or bacteremia that predisposes the animal to develop bacte-
blood-tinged nasal discharge, profound weakness, recum- rial endocarditis. Common bacterial isolates include
bency, and sudden death. Auscultation often reveals Arcanobacter (Actinomyces) pyogenes and alpha-hemolytic
cardiac murmurs and irregular rapid heartbeats. The clin- Streptococcus species.7
ical course is often short, with death often occurring
within 24 hours. Small ruminants that survive the acute Pathogenesis. Vegetative lesions on the valves interfere
phase may fail to thrive because of residual cardiac with normal blood flow and cause cardiac dysfunction.
damage and may exhibit signs of skeletal muscle involve- Dysfunction can result from leakage of blood caused by
ment later in life. the inability of the valve to close properly or from inter-
ference with the ejection of blood by an obstructed
Diagnosis. Definitive antemortem diagnosis of WMD orifice. The vegetative lesions also fragment easily, result-
is based on deficient whole blood levels of selenium and ing in embolic showers that can create abscesses in distant
plasma levels of vitamin E. Plasma selenium concentra- sites such as the lungs, kidney, and joints.
tions are indicative of the current diet or recent injections, Valvular incompetence results in volume overload of
whereas whole blood concentrations (or glutathione per- the recipient heart chamber. Eventually increased end
oxidase analysis) also include selenium incorporated into diastolic volume of this chamber leads to dilatation and
intracellular selenoenzymes several months previously. mild elevations in end diastolic pressure. Compensatory
Therefore plasma is only useful if the diet has not hypertrophy may result. Eventually the contractility of
changed. the chamber is impaired, leading to further elevations in
 Chapter 15 Diseases of the Cardiovascular System • 399

end diastolic pressure and reduced compliance. Depend- tributing to the guarded prognosis. If no abnormalities
ing on the valve involved, other sequelae can include pul- are detected or minimal regurgitation is present on
monary venous hypertension and left-sided heart failure echocardiography, the prognosis is fair to good. Bacterial
(with aortic and mitral regurgitation) or elevated central endocarditis should be treated with long-term broad-
venous pressure and right-sided heart failure (with tricus- spectrum antibiotic administration. Treatment may last
pid regurgitation). for weeks to months. Bactericidal antibiotics are chosen
based on sensitivity patterns and the ability of the drug to
Clinical signs. Affected animals initially show no clini- penetrate tissue. Nevertheless, bacterial endocarditis has a
cal signs but have an audible heart murmur with the point guarded to grave prognosis even with long-term antibi-
of maximum intensity (PMI) over the affected heart valve otic administration.7
in the direction of abnormal blood flow. The intensity of
the murmur is not associated with the severity of the
lesion. Chronic endocarditis can cause the clinical signs of
Plant Cardiotoxicity
cyclic or intermittent fever, weight loss, exercise intoler- Important plants that contain cardioactive glycosides
ance, anorexia, and signs of congestive heart failure (tachy- (cardenolides) capable of poisoning livestock in North
cardia, respiratory distress, cough, jugular venous disten- America include oleander (Nerium oleander), foxglove
tion, subcutaneous edema, and ascites). Cattle may have (Digitalis purpurea), Indian hemp or dogbane (Apoc-
diarrhea, decreased milk production, and lameness; these ynum cannabinum), lily-of-the-valley (Convallaria majalis),
signs also may be encountered in small ruminants. laurels (Kalmia species), milkweed (Asclepias species),
azalea (Rhododendron species), and ornamental succulent
Diagnosis. The best method of diagnosing vegetative (Cotyledon orbiculata). Plant-derived drugs that affect the
endocarditis is a complete echocardiographic examina- autonomic nervous system and cardiac function include
tion. Two-dimensional echocardiography is best for de- atropine derived from Atropa belladonna and Datura
tecting valvular lesions and dysfunction and measuring species, muscarine derived from Amanita muscaria, ephed-
ventricular function. Lesions must be at least 2 to 3 mm rine derived from Ephedra species, ergotamine derived
in diameter to be visible. M-mode ultrasonography may from Claviceps purpurea, and nicotine derived from Nico-
help detect chamber enlargement and a shortening frac- tiana species. Alkaloids found in yews (Taxus species) and
tion. Color flow, pulse wave, or continuous wave Doppler false hellebore (Veratrum species) have both direct and in-
ultrasound may be useful to help quantitate the severity direct cardiac effects.
of valvular regurgitation. Specific antidotes are rarely available for plant toxins.
In the absence of echocardiographic examination, a Therefore prevention is the most effective cure. In
presumptive diagnosis can be based on thoracic ausculta- general, most toxic plants are unpalatable and grow in
tion. Systolic heart murmurs over the left or right heart overgrazed pastures. The plants may be masked in hay,
apex or diastolic murmurs over the left base are suggestive silage, and grain. Most plant toxicoses can be prevented
of valvular incompetence. by feeding adequate amounts of feed that is free of toxic
Bacteriologic culturing of blood samples taken during plants and providing adequate grazing management,
febrile episodes and preferably before antibiotic adminis- weed control, and proper harvest techniques for feeds.
tration may help determine the etiology of bacterial Goats are more inquisitive than sheep and therefore are
endocarditis. Other nonspecific clinical pathology find- more susceptible to plant toxicity through oral explo-
ings include nonregenerative anemia, neutrophilia with or ration of their environment.8,9
without a left shift, hyperglobulinemia, and hyperfibrino-
genemia. Radiographic evidence includes generalized or Pathogenesis. The principal agents responsible for
focal cardiac enlargement and disseminated pneumonia. producing cardiotoxic effects in plants are cardioactive
The ECG may indicate cardiac arrhythmias occurring as glycosides; many varieties exist. The concentration of gly-
sequelae to chamber enlargement or underlying myocar- cosides within the plant varies with season, stage of matu-
dial disease. Nonspecific tests such as cardiac catheteriza- rity, part of the plant, and environmental conditions. Car-
tion for pressure measurements and nuclear angiocardiog- diac glycosides block cellular sodium-potassium ATPase,
raphy may reveal myocardial dysfunction and cardiac leading to sodium accumulation in excitable cells such
enlargement, respectively, but may be cost prohibitive. as those found in nervous tissue and the myocardium.
The result is increased myocardial contraction and altered
Treatment. The treatment and prognosis depend on heart rhythm. These glycosides also are potent gastroin-
the cause, duration, and severity of the valvular lesion. testinal (GI) irritants.
When valvular incompetence is present, the prognosis is As noted previously, agents found in plants that affect the
often guarded to poor. Degenerative lesions may be autonomic nervous system also may affect cardiac function.
asymptomatic and often have a slow progression, con- The alkaloids in yews depress myocardial conduction by
400 • Sheep and Goat Medicine
blocking sodium movement through membranes. The Treatment. Elimination of continued exposure to the
result is arrhythmias ranging from decreased chronotropic poisonous plant is an important part of treatment and
and inotropic effects to ventricular tachycardia or fibrilla- prevention. A rumenotomy may be required to wash out
tion. Nicotinic-acting alkaloids such as Nicotiana species the rumen and remove any remaining cardiotoxic plants
cause toxicity by stimulating ganglions, then blocking them, before significant systemic absorption occurs. Transfau-
leading to paralysis. Sheep are less susceptible to these nation may help to reestablish rumen motility. Supportive
effects than cattle. Tropane alkaloids such as belladonna care should include provision of fluids, minimization of
contain atropine, which blocks acetylcholine at muscarinic stress, and administration of activated charcoal (2 g/kg) as
nerve synapses.The cardiac effect is tachycardia. well as beta-adrenergic blocking agents and antidysrhyth-
mic drugs to treat cardiac dysrhythmias. Fab antibodies
Clinical signs. Many of the clinical signs of acute against cardiac glycosides have been used experimentally
cardiac glycoside toxicosis in sheep and goats are the to treat digitalis and oleander toxicosis.8,9
direct result of hypoxia caused by the inability of the heart
to pump blood, as well as GI irritation. They may include Prevention. Prevention involves vigilant pasture care
nausea, abdominal pain, anorexia, increased salivation, and examination of all feedstuffs. Generally animals do
catarrhal or hemorrhagic diarrhea, coma, convulsions, not consume these plants if other palatable, readily avail-
and sudden death. A variety of cardiac conduction abnor- able food is present.
malities are seen, including bradycardia, tachycardia later
in the disease course, dropped beats, heart block, and
atrial or ventricular arrhythmias. Signs develop 4 to 12
Ionophore Toxicity
hours after ingestion of the plant. If death does not occur, Ionophores include monensin, lasalocid, salinomycin,
signs may persist for 2 or 3 days. Relapses may occur in and narasin. Some are approved for use as coccidiostats
ruminant species because of continued release of the gly- and some are used to improve feed efficiency in sheep,
coside from the rumen. Cardiac toxins often cause death goats, chickens, and cattle. The toxicity of ionophores
before any clinical signs are noted. varies considerably among species, with horses being the
Yew poisoning causes both cardiac and nervous system most sensitive. Toxicoses commonly occur when sensi-
signs. Cardiac signs include bradycardia and cardiac tive species consume ionophore-containing feed formu-
arrest. Nervous system signs include depression, trem- lated for another species and when errors are made in
bling, dyspnea, collapse, and sudden death. Subacute tox- mixing. Ionophore toxicity is potentiated by concurrent
icity causes gastroenteritis and diarrhea. administration of various antibiotics, including erythro-
Belladonna toxicosis causes GI atony, anorexia, rapid mycin, chloramphenicol, and sulfonamides. Even at
heart and respiratory rates, diarrhea, excess urination, therapeutic doses, monensin can potentiate selenium
vision impairment, and delirium. Death is uncommon. toxicity.10
Nicotine-containing plants cause ataxia, weakness, cen-
tral nervous system stimulation, tremors, bloating, and Pathogenesis. Excessive ionophore ingestion causes
death from respiratory paralysis.8,9 preferential transport of specific ions, which results in
altered ionic gradients and disturbed cellular physiology.
Diagnosis. Definitive diagnosis of cardiotoxic plant in- Damage to the myocardium leads to fibrosis and resultant
gestion requires a demonstration of the presence of car- reduced performance or congestive heart failure. As dilated
diotoxic plants in the animal’s pasture and rumen con- cardiomyopathy develops, changes in cellular metabolism
tents. Clinical signs are suggestive of ingestion of occur, leading to ECG abnormalities and reduced cardiac
cardiotoxic plants but are not pathognomonic. Cardiac output.10 Compensation for reduced cardiac output in-
auscultation and electrocardiographic examination may cludes activation of the renin-angiotensin-aldosterone
suggest rhythm and rate disturbances. Necropsy lesions system and increased arterial resistance. The result is in-
also are nonspecific and include hemorrhagic gastroen- creased ventricular preload (venous return) and afterload
teritis and pale mottling of the heart with congestion and (arterial resistance), leading to pulmonary edema and
hemorrhage. Histologic evidence may include myocardial further reduction in cardiac contractility. The ventricle
degeneration and necrosis. A human serum radioim- dilates, further reducing cardiac output, and signs of heart
munoassay is available to assess exposure to digoxin or failure occur.
ouabain, but such tests are often host- and glycoside-
specific and may not be practical for evaluating suspected Clinical signs. Signs in sheep acutely poisoned with
animal poisoning. This test also may cross-react with monensin include lethargy, stiffness, muscular weakness,
oleander glycosides. Alkaloids can be identified by mass stilted gait, mild to moderate dyspnea, mild mucoid diar-
spectral chemistry in samples taken from poisoned rhea, and recumbency. Sudden death may occur after
animals. stress or exercise. Cardiac auscultation may reveal an ele-
 Chapter 15 Diseases of the Cardiovascular System • 401

vated heart rate with or without cardiac arrhythmias.

PERICARDIAL DISEASE
Signs of congestive heart failure such as jugular venous
distention, peripheral edema, and evidence of circulatory
Pericarditis
collapse may be present. Cardiac murmurs may be present Pericarditis is pericardial inflammation that results in
and associated with ventricular dilation. Signs in goats fluid or exudate accumulation between the visceral and
may be similar. Dairy goats may exhibit decreased milk parietal layers of the pericardium. Causes in large animals
production.10 include trauma induced by penetration of an ingested
foreign object (hardware disease), external wounds, hema-
Diagnosis. Diagnosis is made by analyzing suspected togenous spread of infection (septicemia), extension of
feed for inappropriate ionophore concentrations. A pre- infection originating from the pulmonary cavity, and spe-
sumptive diagnosis can be based on clinical signs and cific viral or neoplastic causes. This condition is rare in
clinical pathology findings. These include evidence of sheep and goats.
skeletal and cardiac muscle injury, kidney damage, and
increased erythrocyte fragility. Findings indicative of Pathogenesis. Pericarditis is classified as primarily effu-
erythrocyte fragility include elevated concentrations of sive, constrictive, or a combination of both. Inflammation
alkaline phosphatase, indirect bilirubin, blood urea ni- between the parietal and visceral layers of the pericar-
trogen, CK, creatinine, LDH, and AST. Reductions in dium results in fluid accumulation. Over time, pericardi-
calcium and potassium concentrations and urine pH tis results in decreased cardiac distensibility, which causes
may occur. Abnormal values for the myocardial isoen- increased ventricular end diastolic pressure. This in turn
zymes CK and LDH are highly suggestive of monensin impairs the ability of the heart to fill during diastole. As a
toxicosis in conjunction with historical information. An result, atrial pressures rise and venous return to the heart
ECG may demonstrate sinus tachycardia and other is reduced, impairing the perfusion of the myocardium.
cardiac dysrhythmias. Echocardiography may be normal Reduced perfusion causes a depression in ventricular con-
or show evidence of dilated cardiomyopathy with in- tractility, stroke volume, and ultimately cardiac output.
creased ventricular chamber size, decreased thickness Arterial pressures and renal blood flow decrease. The
of the interventricular septum and left ventricular free heart compensates initially through vasoconstriction, in-
wall, and decreased myocardial function. Increased end- creased heart rate, and sodium retention, increasing vas-
diastolic and end-diastolic dimensions of the left and cular volume to maintain cardiac output.
right ventricles may be apparent, as well as increased left Traumatic reticulopericarditis results from penetration
arterial size and an increased left atrial–to–aortic root of the reticular wall, diaphragm, and pericardial sac by a
dimension ratio. Cardiac catheterization may reveal ele- sharp metal object and ensuing septic inflammation. The
vated intracardiac pressures consistent with dilated car- foreign body is pushed through the cranial wall of the
diomyopathy. Postmortem findings include microscopic reticulum during reticular contractions or episodes of in-
evidence of fibrosis, degeneration of the myocardium, creased abdominal pressure such as parturition. (The peri-
and myocardial necrosis. Myopathy of skeletal muscles cardium and reticulum are in close proximity.) The foreign
may be present. Evidence of congestive heart failure may object allows bacteria from the reticulum to enter the peri-
be reflected in passive congestion of the liver and cardial sac. Cattle are often said to have “splashy” heart
lungs.10 sounds referred to as a washing machine murmur because of
gas and fluid accumulation in the pericardium. Acute, sub-
Treatment. No specific antidote or tested treatment is acute, or chronic fibrinopurulent pericarditis results. After
available for animals that have recently ingested iono- the pericardial sac becomes inflamed, the pathogenesis is
phores. General management consists of administration similar to that of pericarditis from other causes. Because of
of activated charcoal; provision of IV fluids to correct their grazing habits, sheep are only rarely affected by trau-
electrolyte imbalances, preserve renal function, and mini- matic reticulopericarditis. Goats may be slightly more
mize shock (but not in amounts large enough to exacer- prone to the condition because of their inquisitive nature
bate congestive heart failure); specific treatment for dys- and eating habits. Nontraumatic pericarditis usually
rhythmias (digoxin, quinidine, vasodilators, diuretics); results from sepsis.
and stall rest. The prognosis for animals with dilated car-
diomyopathy is poor. Clinical signs. The most consistent clinical signs of
pericarditis on auscultation include muffled heart sounds,
Prevention. Prevention involves careful mixing of tachycardia, and dampened or absent lung sounds in the
feeds containing ionophores and not giving animals feed ventral thorax. Loudness of heart sounds may alternate
formulated for other species. Proper concentrations of between loud and quiet beats (bigeminy). Dorsal lung
selenium in ionophore-treated feed are important to sounds may be more pronounced. Nonspecific clinical
prevent selenium toxicosis. signs include fever, anorexia, depression, and weight loss.
402 • Sheep and Goat Medicine
Signs of congestive heart failure may be apparent and is guarded. Indwelling chest tubes placed in the pericar-
include distended or pulsatile jugular veins, tachypnea or dial sac can enable drainage, lavage, and local infusion of
dyspnea, and exercise intolerance. Signs of chest pain antibiotics. These procedures can be performed once or
such as abducted elbows and grunting or breath-holding twice a day. Treatment with systemic broad-spectrum
on palpation and auscultation may be seen. Clinical signs antibiotics is indicated. Nonsteroidal antiinflammatory
depend on the speed of development of pericarditis and drugs (NSAIDs) are useful adjuncts, as are cortico-
the volume of fluid accumulation. steroids if no evidence of bacterial involvement is present.
Diuretics may be helpful in the short term to relieve some
Diagnosis. Definitive diagnosis of pericarditis is made of the signs of congestive heart disease. Fluids may help
by pericardiocentesis and echocardiography. The former combat dehydration and signs of shock.
technique enhances evaluation of effusion and allows the
clinician to take samples for bacterial and fungal culture. Prevention. In flocks in which this condition is a
It should be performed using echocardiography to guide problem, small magnets can be administered before preg-
aspiration. Echocardiography can be useful to evaluate nancy to help prevent metallic foreign bodies from per-
cardiac function and visualize the site and extent of fluid forating the pericardial sac. However, because of the
and gas accumulation. Common findings include an rare nature of this condition, their routine use is not
echo-free space surrounding the right and left ventricular warranted.
free walls and between the descending aorta and left ven-
tricular posterior wall. If cardiac tamponade is present,
right ventricular diastolic collapse and right atrial collapse
VASCULAR DISEASES
will be apparent. Electrocardiographic findings associated
with pericarditis include decreased amplitude of the QRS
African Trypanosomiasis
complexes, electrical alternans, and S-T segment eleva- People and animals can become infected with trypano-
tion or slurring. A right-axis deviation may be noted in some protozoa. The trypanosomes can complete their de-
the standard limb leads. Clinical pathology findings are velopmental cycle only in tsetse flies (Glossina species).
nonspecific and may include evidence of hemoconcentra- Trypanosomes multiply in blood, tissues, and body fluids
tion, mild anemia, leukocytosis with an absolute neu- of their vertebrate hosts and are transmitted between ver-
trophilia and/or lymphopenia, and hyperfibrinogenemia. tebrate hosts in the saliva of blood-sucking flies as they
Hypoalbuminemia and hyperglobulinemia may be pres- feed. The trypanosome species that are known to infect
ent. Frequently mild elevations in liver enzymes, creati- goats and sheep include Trypanosoma congolense, T. vivax,
nine, bilirubin, and serum urea nitrogen are seen. Eleva- T. brucei subsp. brucei, T. evansi, and T. simiae. The first
tions in the myocardial isoenzymes AST, CK, and LDH three are moderately pathogenic to these small ruminants,
occur. Radiography of the thorax or reticulum and di- whereas the latter two are only mildly pathogenic.11
aphragm may be helpful, particularly for diagnosing
traumatic reticulopericarditis in ruminants. A metallic Pathogenesis. After entering through the skin, try-
foreign body may be seen in the cranial reticulum and/or panosomes reach the bloodstream by way of the lym-
caudal thorax. Cardiomegaly may be seen with pericardi- phatic system. The parasites multiply and the prepatent
tis and is caused by pericardial effusion obscuring the period lasts for 10 to 14 days after infection. The infec-
cardiac silhouette. An obscured vena cava and diaphragm, tion is characterized by periods of parasitemia followed
dorsal displacement of the trachea, and interstitial pneu- by the absence of parasites. This pattern of infection
monia may be noted. occurs because of antigenic variation: trypanosomes vary
the antigenic nature of their glycoprotein surface coat to
Treatment. Treatment of traumatic reticulopericarditis evade the host’s immune system. This ability of try-
is often unrewarding and not economically viable in most panosomes to alter their surface coat prolongs infection
cases. When instituted it is frequently directed toward and is responsible for chronic disease. Some trypano-
salvage and short-term survival. Removal of a foreign somes tend to invade extravascular spaces such as the
body by rumenotomy may prevent further complications ocular aqueous humor and cerebral spinal fluid. The
but rarely is curative. Pericardial drainage can be per- pathogenicity of trypanosomes varies with the different
formed repeatedly by means of pericardiocentesis, fifth host species. Trypanosomes may produce a hemolysin
rib resection, lavage, or pericardiectomy. However, often early in the course of the disease that causes anemia in
heart function does not return to normal after these pro- the host. Later, increased phagocytic activity results in
cedures are performed. Thoracotomy and pericardiec- massive erythrocyte destruction. This may occur in the
tomy by means of a split-rib technique may be effective in absence of parasitemia.11
treating ruminants with traumatic, restrictive pericarditis.
Treatment with long-term antibiotics is required. The Clinical signs. The clinical signs are variable and non-
prognosis for the treatment of nontraumatic pericarditis specific and depend on the speed of onset of anemia and
 Chapter 15 Diseases of the Cardiovascular System • 403

the degree of organ impairment. Entire herds may be af- Treatment. Treatment consists of the use of trypano-
fected. All aspects of production are affected—fertility, cidal agents and supportive care. Animals with acute, suba-
birth weights, lactation, weaning weights, growth, and sur- cute, and subclinical disease respond better to treatment
vival. Trypanosomiasis may predispose the animal to other than animals with chronic disease because of the irre-
diseases that mask the underlying trypanosome infection. versible damage to hematopoiesis caused by chronic infec-
Trypanosomiasis may be acute, subacute, or chronic, tion. The therapeutic indices of trypanocides are low and
with the latter being the most common. Acute disease vary with the host species. Trypanocide efficacy also varies
often causes abortion. Dairy goats may show a sudden with the species of trypanosome present; resistance to
drop in milk production. Depression, anorexia, and a stiff agents is common. Some trypanocides are irritating to the
gait may be present. Physical examination reveals tachy- skin and may cause severe inflammation at the injection
cardia, tachypnea, and a slight fever. Hyperemic mucous site. In sheep and goats with T. brucei infection, the try-
membranes and excessive lacrimation may be noted. panocide of choice is diminazene aceturate, and it should
Animals often become recumbent and anorexic and die be used at a higher dosage rate (7 mg/kg intramuscularly or
within 1 to 3 weeks of the onset of clinical signs. If the subcutaneously) than that recommended for cattle. Protec-
animal survives, it may go on to the subacute phase, tion after trypanocide use usually lasts 2 to 4 months de-
which includes listlessness, weight loss, enlargement of pending on the season. Animals must be rested before and
superficial lymph nodes, and a dull, dry hair coat. Af- after treatment. Supportive care consists of providing
fected animals have similar auscultation findings as those fluids, rest, good nutrition, and possibly blood transfusions.
seen in other acute cardiac disease, as well as pale mucous
membranes and a pronounced jugular pulse. The animal Prevention. Vector control, stress and nutrition man-
may linger for several weeks or months or go on to agement, and selection of trypanosome-tolerant breeds of
develop chronic disease. Affected animals show ill- sheep and goats help control or prevent trypanosomiasis.
thrift—dull, dry hair coats; inelastic skin; lethargy; ema- No vaccine is available. Animals can be treated with in-
ciation; peripheral lymphadenopathy; pale mucous mem- secticides (pyrethroids) to prevent bites by tsetse flies and
branes; and exercise and stress intolerance. Death may other flies. Control consists of strategic use of trypano-
occur many months or even years after infection and cides during the peak season. Constant parasitologic and
usually results from congestive heart failure. Subclinical clinical surveillance is essential to determine the efficacy
trypanosomiasis causes acute episodes when animals are of control measures.11
stressed by inadequate nutrition, increased production
demands, or concurrent disease.11
Shock
Diagnosis. Diagnosis is difficult because the para- Pathogenesis. Shock is the result of many varied
sitemia is intermittent, clinical signs are nonspecific, and pathologic processes and, regrettably, is often the point at
infection is not always synonymous with disease. Al- which veterinary attention is sought. Among the numer-
though a tentative diagnosis can be made on the basis of ous important causes are sepsis, localized bacterial infec-
clinical signs, presence of vectors, and history of try- tions, myocarditis, dehydration, electrolyte and acid-base
panocide use in the herd, a definitive diagnosis requires disturbances, and cardiovascular anomalies. Shock is
the appearance of trypanosomes on a fresh blood smear, a caused by inadequate tissue perfusion and organ dysfunc-
Giemsa-stained blood smear, or less commonly a lymph tion and can result from inadequate vascular tone or in-
smear. Examination of the buffy coat of centrifuged tegrity, poor cardiac output, and pooling of blood within
blood with dark-field phase-contrast spore illumination is capacitance vessels.
the most sensitive direct diagnostic method and is useful Shock begins with a hormone-mediated hyperdy-
when parasite numbers are low. Pathogenic trypanosomes namic phase that is characterized by bounding pulses,
must be distinguished from more ubiquitous, nonpatho- tachycardia with loud heartbeats, and decreased capillary
genic species particularly common in cattle such as filling times of mucous membranes. This phase is tran-
T. theileri. Repeated sampling of individual animals is sient and often unnoticed, but it is quickly followed by
often necessary because parasitemia is intermittent. The the hypodynamic phase of circulatory failure.
diagnosis is supported by evidence of anemia on a com-
plete blood count. Clinical signs. Most clinical abnormalities center
Indirect diagnostic methods include an indirect fluo- around insufficient perfusion of organs or the inability of
rescent antibody test (IFA) and the enzyme-linked im- the cardiovascular system to maintain perfusion. Com-
munospecific assay (ELISA). These tests are less useful mon signs include weakness, obtundation, cold extremi-
for diagnosing a single clinical case but are useful in as- ties, tachycardia with a weak pulse, decreased urination
sessing herd infection. Both T. congolense and T. brucei and defecation, cyanotic or pale mucous membranes, and
readily infect rats and mice and can be used to diagnose shallow breathing. Other signs are possible depending on
the infection indirectly.11 the inciting cause.
404 • Sheep and Goat Medicine
Diagnosis. Most of the clinicopathologic changes
reflect the inciting cause of shock, but others reflect the
R EFERENCES
1. Reef VB, McGuirk SM: Congenital cardiovascular disease. In
changes that occur with shock. The latter include organic Smith BP, editor: Large animal internal medicine, ed 2, St Louis,
acidosis, azotemia, and stress hyperglycemia. Diagnosis is 1996, Mosby.
by recognition of characteristic clinical signs and clinico- 2. Hagan WA, Bruner DW, Timoney JH: Heartwater disease. In
Hagan WA, Bruner DW, Timoney JF, editors: Hagan and Bruner’s
pathologic abnormalities.
microbiology and infectious diseases of domestic animals, ed 8, Ithaca,
NY, 1988, Comstock Publishing.
Treatment. Restoration of organ perfusion and func- 3. Commission on Foreign Animal Diseases: Heartwater. In Com-
tion are the main goals of treatment. This is best accom- mission on Foreign Animal Diseases, editors: Foreign animal dis-
plished through administration of IV fluids. A shock dose eases, Richmond, VA, 1984, US Animal Health Association.
of approximately 8% of the animal’s body weight should 4. Oberem PT: Heartwater. In Howard JL, editor: Current veterinary
be given as an initial bolus. Any isotonic fluid is adequate therapy, ed 3, Philadelphia, 1993, WB Saunders.
in most emergency situations because of the positive 5. Welker B: Nutritional myodegeneration. In Howard JL, editor:
effect such fluids have on vascular volume. Polyionic, pH- Current veterinary therapy, ed 3, Philadelphia, 1993, WB Saunders.
balanced fluids are the most useful. Continued therapy 6. Maas J et al: Nutritional myodegeneration. In Smith BP, editor:
depends on the animal’s response to the initial bolus. Oral Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
7. Reef VB, McGuirk SM: Valvular heart disease. In Smith BP,
and subcutaneous fluids are unlikely to restore adequate
editor: Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
cardiovascular function in animals in shock. Vasoactive
8. Fowler ME: Cardiotoxic plants. In Howard JL, editor: Current
drugs may be helpful to increase blood pressure, but these veterinary therapy, ed 3, Philadelphia, 1993, WB Saunders.
should be used in conjunction with fluids if possible. Cor- 9. Galey FD: Glycosides. In Smith BP, editor: Large animal internal
ticosteroids may be beneficial for nonseptic shock because medicine, ed 2, St Louis, 1996, Mosby.
of their antiinflammatory and membrane-stabilizing ef- 10. McCoy CP: Ionophores: monensin, lasalocid, salinomycin, and
fects. Because most shock in small ruminants has an in- narasin. In Howard JL, editor: Current veterinary therapy, ed 3,
fectious origin, the usefulness of these drugs is limited. Philadelphia, 1993, WB Saunders.
Other treatments for primary disease processes, including 11. Commission on Foreign Animal Diseases: African trypanosomiasis.
antimicrobial drugs, antitoxins, and antiinflammatory In Commission on Foreign Animal Diseases, editor: Foreign animal
drugs, may be indicated in specific cases. diseases, Richmond, VA, 1984, US Animal Health Association.
 Chapter 16

Anesthetic Management
HUI-CHU LIN AND D.G. PUGH

Sheep and goats are similar in many ways to cattle species, that should be anticipated and addressed with the proper
both anatomically and physiologically. Although some of precautions. When possible, adult animals should be
these animals may cost as much as purebred companion fasted for 12 to 24 hours and water withheld for 8 to 12
animals, often the small ruminant clinician is faced with hours before induction of anesthesia. The fasting of
the same economic issues and limited approved drugs for neonates is not recommended because of the potential for
use in surgical procedures requiring anesthesia as the clini- hypoglycemia.2 In emergency situations, fasting may not
cian in companion animal practice. Physical restraint and be possible and precautions should be taken to avoid aspi-
local anesthetic techniques are most commonly employed ration of gastric fluid and ingesta. This can be done effec-
to provide immobility and analgesia for small ruminants. tively by endotracheal intubation and positioning of the
These animals perceive pain no differently than other head so that the throat latch area is elevated relative to the
species, and therefore analgesia for prevention and easing mouth and thoracic inlet, which prevents pooling of saliva
of pain is just as important as it is for other companion and ruminal contents in the oral cavity.
animals. Occasionally general anesthesia is required for Venipuncture and catheterization of the jugular vein
surgical intervention. In these cases, balanced anesthetic are usually performed before anesthesia. A 16-gauge in-
technique should be employed to provide narcosis, analge- dwelling catheter is appropriate for adult sheep and goats
sia, and muscle relaxation and thereby minimize the stress and an 18-gauge catheter is suitable for younger animals.
response induced by surgery and anesthesia. The technique for catheterization in sheep and goats is
At the time of this writing, only one anesthetic drug similar to that used in calves (Figures 16-1 and 16-2).
had been approved for use in goats (ophthalmic propara- Intubation is more difficult to accomplish in sheep and
caine) and one for use in sheep (thiopental sodium). Table goats than in many other animals because the mouth does
16-1 summarizes meat and milk withdrawal intervals not open widely, the intermandibular space is narrow, and
recommended by the Food Animal Residual Avoidance the laryngeal opening is distant beyond the thick base of
Databank (FARAD) for some of the tranquilizers and the tongue.2 Intubation should be prompt and performed
injectable anesthetics used in an extra-label manner with the animal in sternal recumbency immediately after
for sheep and goats.1 Clinicians should consult with the induction of anesthesia. Intubation is best accom-
FARAD whenever using any unapproved drugs because plished if an assistant pulls the mouth open by placing a
withdrawal times are subject to change. loop of gauze around the upper jaw and a second loop
around the lower jaw and tongue (Figure 16-3). At the
same time the assistant should hyperextend the animal’s
PREANESTHETIC neck. If the larynx cannot be visualized, the neck should
be extended further.3 The clinician uses a long laryngo-
PREPARATION scope blade (250- to 350-mm) to suppress the tongue
Domestic ruminants have a multicompartmental stomach base and epiglottis and enable visualization of the larynx.
with a large rumen that does not empty completely2 and He or she then places the “guide tube” (preferably a 10
are therefore susceptible to complications associated with French, 22-inch-long polyethylene canine urethral cath-
recumbency and anesthesia. Tympany, bloat, regurgita- eter that is three times the length of the endotracheal
tion, and aspiration pneumonia are common problems tube), over which the endotracheal tube is slipped into
• 405 •
406 • Sheep and Goat Medicine
TABLE 16-1

THE FARAD RECOMMENDED WITHDRAWAL INTERVAL FOR SHEEP AND GOATS FOR SINGLE AND MULTIPLE
TREATMENTS OF ANESTHETIC DRUGS*
MEAT WITHDRAWAL MILK WITHDRAWAL
DRUG DOSE (mg/kg) INTERVAL (DAYS) INTERVAL (HOURS)

Acepromazine Up to 0.13, IV 7 48
Up to 0.44, IM
Detomidine Up to 0.08, IM, IV 3 72
Guaifenesin Up to 100, IV 3 48
Ketamine Up to 2, IV; 10, IM 3 48
Lidocaine with epinephrine Infiltration, epidural 1 24
Ultra–short-acting barbiturates Thiamylal, up to 5.5 1 24
Thiopental, up to 9.4
Xylazine 0.016 to 0.1, IV 10 120
0.05 to 0.3, IM
0.3 to 2.0, IM
Yohimbine Up to 0.3, IV 7 72
From Craigmill AL, Rangel-Lugo M, Riviere JE: Extralabel use of tranquilizers and general anesthetics, J Am Vet Med Assoc 211:302, 1997.
*Whenever using unapproved pharmacologics in animals intended for meat or milk production, the clinician should check with federal authorities
concerning proper withdrawal times.

animals the use of a tranquilizer or sedative may mini-

mize the stress caused by forceful restraint, ease the in-
duction process, and decrease the dose requirement of
anesthetic, thereby preventing the possibility of disastrous
hypotension (Table 16-2).

Phenothiazine Derivatives
Acepromazine maleate produces mild tranquilization
without analgesia. This drug has minimal effects on heart
rate and respiratory function. Its use may result in hy-
potension and increase the risk of regurgitation.4,5 When
administering acepromazine, the clinician should avoid
using the coccygeal vein for intravenous (IV) injection
Figure 16-1 Distention of the right jugular vein for intravenous because of the close proximity of the coccygeal artery.2
catheterization. In this case the goat is carefully restrained and the Prolapse of the penis with the potential for trauma after
head is turned 30° to 45° to the left on the long axis and tilted up the use of acepromazine sometimes occurs in horses and
15° to 20° from parallel to the ground. may occur in sheep and goats as well. Furthermore, the
use of acepromazine is contraindicated in debilitated or
hypovolemic animals.4
place. This method makes endotracheal intubation much
easier to achieve than with other methods (Figure 16-4).
A cuffed endotracheal tube should be used to prevent re-
a2 Agonists and Antagonists
gurgitation and aspiration of ruminal contents, and the a2 agonists. Xylazine hydrochloride is probably the
animal should be maintained in sternal recumbency until most popular a2 agonist in large animal practice today.
the cuff is inflated. Ruminants are very sensitive to xylazine, with goats ap-
pearing to be more sensitive than sheep.5 Xylazine is a
potent sedative, analgesic, and muscle relaxant that is fre-
PREANESTHETICS quently used as an preanesthetic or anesthetic adjunct in
Preanesthetic tranquilization or sedation is rarely needed ruminants. Xylazine alone produces dose-dependent
in small ruminants. However, in larger or more vigorous effects from standing sedation to recumbency, immobi-
 Chapter 16 Anesthetic Management • 407

Figure 16-2 Intravenous catheterization of the right jugular vein. The esophagus is on the left side of
the neck in most instances. Therefore many clinicians choose the right jugular furrow for catheter
placement.

Figure 16-3 Position of the head for endotracheal intubation.

lization, and complete anesthesia. Xylazine may cause existing cardiopulmonary disease or urinary tract ob-
bradycardia, hypotension, hypoxemia, hypercapnia, pul- struction. An up to six-fold increase in urine output is
monary edema, hyperglycemia, hypoinsulinemia, in- frequently observed after xylazine administration.8 Ad-
creased urine production, and an oxytocin-like effect.6 It ministration of xylazine to ruminants in the final
should be used with extreme caution in animals with pre- trimester of pregnancy may cause premature parturition
408 • Sheep and Goat Medicine

Figure 16-4 Endotracheal intubation with the aid of a guide tube and laryngoscope.

TABLE 16-2

DOSES OF PREANESTHETICS COMMONLY USED IN SHEEP AND GOATS

PREANESTHETICS DOSAGE FOR SHEEP (mg/kg) DOSAGE FOR GOATS (mg/kg)

Atropine 0.066, IV 0.066, IV

Glycopyrrolate 0.005 to 0.01, IM; 0.002 to 0.005, IV 0.005 to 0.01, IM; 0.002 to 0.005, IV
Acepromazine Less than 50 kg: 0.1 to 0.2, IV Less than 50 kg: 0.1 to 0.2, IV
More than 50 kg: 0.05 to 0.1, IV or IM More than 50 kg: 0.05 to 0.1, IV or IM
Xylazine 0.01 to 0.02, IV, standing sedation for 30 to 0.01 to 0.02, IV, standing sedation for 30
60 min; 0.1 to 0.2, IV, or 0.2 to 0.3, IM, to 60 min; 0.05 to 0.11, IV, or 0.11 to
recumbency for 60 min 0.22, IM, recumbency for 60 min
Detomidine 0.005 to 0.02, IV, or 0.01 to 0.04, IM, 0.005 to 0.02, IV, or 0.01 to 0.04, IM,
sedation for 45 to 60 min sedation for 45 to 60 min
Medetomidine 0.001 to 0.007, IV, sedation; 0.04, IM, 0.001 to 0.007, IV, sedation; 0.04, IM,
recumbency for 58 min recumbency for 58 min
Diazepam 0.25 to 0.5, IV, slowly 0.25 to 0.5, IV, slowly
Meperidine N/A 10, IM
Butorphanol 0.05 to 0.5, IM, sedation 0.4, IV, sedation 0.05 to 0.5, IM, sedation; 0.4, IV,
and ataxia sedation and ataxia
Xylazine and butorphanol X: 0.1 to 0.2, IV X: 0.1 to 0.2, IV
B: 0.01 to 0.02, IV B: 0.01 to 0.02, IV
Deep sedation to recumbency for 60 min Deep sedation to recumbency for 60 min
 Chapter 16 Anesthetic Management • 409

and retention of fetal membranes and should therefore be without risks: the death of a sheep after administration of
avoided.7 Lateral recumbency has been reported to a large dose of yohimbine (0.8 mg/kg IV) has been re-
induce a significant decrease in partial pressure of arterial ported.24 When administering an antagonist, slow injec-
oxygen (PaO2) in conscious sheep.9 This hypoxemia can tion is recommended to avoid sudden awareness of pain
occur even when the animal remains standing during and excitement on the part of the animal. Rapid injection
xylazine sedation.10,11 Severe hypoxemia and pulmonary of tolazoline has been reported to cause significant
edema have been implicated as the causes of death in cardiac stimulation, tachycardia, increased cardiac output,
sheep that die under xylazine anesthesia.12-14 Epidural vasodilation, coronary vasodilation, and gastrointestinal
administration of xylazine (0.07 to 0.1 mg/kg) with or distress.25 It has been hypothesized that ruminants are
without lidocaine into the sacrococcygeal space induces more sensitive to tolazoline than other species, and death
long-lasting good somatic analgesia for open castration has been reported in several animals after its use.26 Nev-
in rams (8 hours without lidocaine) and correction of ertheless, the undesirable effects of a2 antagonists are ex-
vaginal prolapse in ewes (24 hours with 0.5 mg/kg of li- tremely rare in healthy animals when the drugs are
docaine).15,16 However, visceral analgesia induced by administered by slow IV injection and at appropriate
xylazine alone may not be sufficient for ligation of the dosages.
spermatic cord.15
Detomidine hydrochloride, when administered at an
IV dose of 0.02 mg/kg, produces sedation comparable to
Benzodiazepines
that provided by 0.04 mg/kg of xylazine.17 Increasing the Diazepam is a minor tranquilizer. It produces mild seda-
dose to 0.03 mg/kg induces recumbency in sheep, which tion, hypnosis, decreased anxiety, and muscle relaxation.
is equivalent to xylazine at 0.15 mg/kg and medetomi- Diazepam is often used for its anxiolytic effect in high-
dine at 0.01 mg/kg.18 The pharmacologic effects of deto- risk animals because of its minimal cardiovascular and
midine are very similar to those of xylazine.18 Ruminants pulmonary effects at therapeutic doses. It also can be used
appear to be less sensitive to detomidine than they are to in combination with ketamine to improve muscle relax-
xylazine. Unlike xylazine, detomidine at IV doses smaller ation during anesthesia.27
than 0.04 mg/kg does not produce an oxytocin-like effect
on the uterus in gravid cattle. Even though detomidine
at doses higher than 0.04 mg/kg may increase the electri-
Opioid Analgesics
cal activity of the uterine muscles, it does not induce the Meperidine hydrochloride is a synthetic opioid that has
synchronization of the bursts of potentials that is charac- an analgesic potency of only 10% to 13% that of mor-
teristic of parturition. Detomidine is unlikely to induce phine. It produces mild sedation and analgesia. Its ad-
abortion in pregnant ruminants at therapeutic doses19,20 ministration can be associated with histamine release.28
and therefore may be safer for pregnant sheep and goats. In yearling goats, meperidine (10 mg/kg IM) can be used
Medetomidine hydrochloride in doses of 0.001 to as a premedicant 10 minutes before induction of anesthe-
0.007 mg/kg IV induces dose-dependent sedation and sia with thiopental. After intubation this combination
analgesia; 0.005 mg/kg appears to produce analgesia in provides 20 minutes of surgical anesthesia with complete
sheep comparable to that provided by 0.015 mg/kg of recovery in 90 minutes.29
fentanyl.21 At an intramuscular (IM) dose of 0.04 mg/kg, Butorphanol tartrate is an opioid agonist/antagonist
medetomidine induces recumbency for 58 minutes, as with an analgesic potency approximately five times higher
well as good analgesia and marked muscle relaxation for than that of morphine. Butorphanol has a unique “ceiling
30 to 45 minutes. Sheep usually recover within 1.5 to 2
hours after regaining the righting reflex.22 In sheep anes-
thetized with medetomidine (0.02 mg/kg IV) and keta-
mine (2 mg/kg IV) and breathing room air, PaO2, arterial TABLE 16-3
pH, and arterial oxygen (O2) saturation decrease and the
partial pressure of arterial carbon dioxide (PaCO2) in- DOSES OF a2 ANTAGONISTS COMMONLY
creases significantly. Supplementation of 100% O2 may USED IN SHEEP AND GOATS
improve PaO2 and hemoglobin saturation.23
DOSAGE FOR SHEEP DOSAGE FOR GOATS
a2 ANTAGONIST (mg/kg) (mg/kg)
a2 antagonists. The pharmacologic effects induced by
xylazine, detomidine, or medetomidine can be effectively Atipamezole 0.125 to 0.2, 0.125 to 0.2,
antagonized by an a2 antagonist such as yohimbine, tola- slow IV slow IV
zoline, or atipamezole (Table 16-3). These antagonists Tolazoline 2, slow IV 2, slow IV
can be used to shorten recovery time and prevent the sig- Yohimbine 0.125 to 0.22, 0.125 to 0.22
nificant adverse effects sometimes seen with agonists, es- slow IV slow IV
pecially accidental overdose. However, these drugs are not
410 • Sheep and Goat Medicine
effect”—that is, after effective action has been attained,
ANESTHETICS (Table 16-4)
further increases in dose do not increase or enhance the
Injectable Anesthetics
degree of desired pharmacologic effect.30 Butorphanol
may cause slight central nervous system (CNS) stimula- Thiopental sodium can be used to induce anesthesia in
tion, especially when used in animals that are not in pain. sheep and goats; the depth of anesthesia and muscle re-
Twitching of the facial muscles, lips, and head may laxation is sufficient for endotracheal intubation. Addi-
occur.31 Butorphanol can be given alone in sheep and tional incremental doses may be administered to prolong
goats to produce light sedation. No behavioral effects anesthesia.2 A guaifenesin- (GG-) thiopental mixture
were seen with butorphanol given at 0.05 mg/kg IV in can be administered to effect to induce and maintain
sheep, but ataxia was observed at 0.4 mg/kg IV, and ex- short-term anesthesia. The final concentration of the
citement occurred at 0.1 to 0.2 mg/kg IV.5,31,32 Butor- mixture is 5% (50 mg/ml) GG and 0.2% (2 mg/ml)
phanol is frequently used in combination with a sedative thiopental.33 Thiopental causes minimal cardiovascular
or tranquilizer to produce good standing sedation for depression. A moderate tachycardia, slight decrease in
minor surgery and diagnostic procedures. It also can be mean arterial blood pressure, and short period of respira-
administered postoperatively for pain relief. In sheep and tory depression usually occur immediately after rapid in-
goats, xylazine and butorphanol can be administered si- duction of anesthesia with thiopental. Transient apnea is
multaneously to produce deep sedation and recumbency not uncommon during induction with thiopental, and
for as long as 60 minutes.2 spontaneous breathing returns within several minutes. In

TABLE 16-4

DOSES OF GENERAL ANESTHETICS COMMONLY USED IN SHEEP AND GOATS

ANESTHETIC DOSAGE FOR SHEEP* DOSAGE FOR GOATS*

Thiopental 10 to 16, IV 10 to 16, IV

Guaifenesin (5%) and Induction: 2 ml/kg, IV, 50% to Induction: 2 ml/kg, IV,
thiopental (0.2%) 75% calculated dose first 50% to 75% calculated dose first
Maintenance: 2.2 ml/kg/hr or to Maintenance: 2.2 ml/kg/hr or
effect to effect
Guaifenesin (5%) and Induction: 2 ml/kg, 50% to 75% Induction: 2 ml/kg, 50% to 75%
ketamine (0.1%) calculated dose first calculated dose first
Maintenance: 2.2 ml/kg/hr or Maintenance: 2.2 ml/kg/hr or
to effect to effect
Acepromazine and ketamine A: 0.55, IV N/A
K: 2.2, IV
Xylazine and ketamine X: 0.22, IM, wait 10 min X: 0.22, IM, wait 10 min
K: 10 to 15, IM K: 11, IM
Guaifenesin (5%), xylazine Induction: 0.67 to 1.1 ml/kg Induction: 0.67 to 1.1 ml/kg
(0.01%), and ketamine Maintenance: 2.2 ml/kg/hr or Maintenance: 2.2 ml/kg/hr or
(0.1% to 0.2%) to effect to effect
Medetomidine and ketamine M: 0.02, IV M: 0.02, IV
K: 2, IV K: 2, IV
Diazepam and ketamine D: 0.11, IV D: 0.11, IV
K: 4.4, IV; or K: 4.4, IV
D: 0.25 to 0.5, IV
K: 4 to 7.5, IV
Propofol Induction: 3 to 4, IV; or Preanesthetic: detomidine, 0.01, IM
Induction: 4 to 8, IV; and butorphanol 0.1, IM
Maintenance: 18 to 40 mg/kg/hr Induction: 3 to 5, IV
of IV infusion or to effect Maintenance: 31 ml/kg/hr
Tiletamine and zolazepam 5.5, IV, anesthesia for 100 min 5.5, IV, anesthesia for 100 min
(Telazol) 5.5, IV with butorphanol 0.1, IV, 5.5, IV with butorphanol 0.1, IV,
anesthesia for 100 min anesthesia for 100 min
*Dose is in mg/kg unless stated otherwise.
 Chapter 16 Anesthetic Management • 411

case of prolonged apnea the animal should be intubated

Inhalation Anesthetics
and ventilated until spontaneous breathing resumes.34 Inhalation anesthetics require expensive and specialized
Recovery from thiopental anesthesia relies mainly on re- equipment for delivery to the patient. However, they
distribution of the drug from the brain to the peripheral allow veterinarians to perform complicated and pro-
tissues. Administration of a large dose or prolonged infu- longed surgery. Either halothane or isoflurane can be
sion may result in extremely prolonged recovery. There- used effectively and safely in sheep and goats. Mask
fore maintenance of anesthesia with thiopental is not rec- induction may not be a wise choice in healthy, adult
ommended if the surgery requires more than 1 hour.34 animals but can be used in smaller or debilitated animals.
Ketamine hydrochloride, a dissociative derivative, is A small animal anesthesia machine with a double carbon
probably the most commonly used injectable anesthetic dioxide (CO2) absorbent canister is usually adequate
in sheep and goats. Acepromazine, diazepam, xylazine, for most sheep and goats. The clinician should be aware
and medetomidine can be used in combination with ket- of a rare condition called halothane-induced hepatitis, an
amine to enhance the degree of analgesia and muscle re- acute, massive liver necrosis that sometimes occurs after
laxation during anesthesia. Unlike other conventional halothane anesthesia in healthy goats, especially after
anesthetics, ketamine does not depress cardiovascular prolonged exposure.42,43 Clinical signs, including depres-
function; instead, heart rate and arterial blood pressure sion, inappetence, salivation, teeth grinding, head press-
increase during ketamine anesthesia as a result of central ing, and icterus, usually occur within 24 hours. Serum
sympathetic stimulation. A mixture of ketamine (1 concentrations of aspartate transaminase, bilirubin, alka-
mg/ml) and GG can be used to maintain short-term line phosphatase, creatinine, and blood urea nitrogen are
anesthesia.35 A combination of GG (50 mg/ml), keta- significantly increased from normal ranges. Death usually
mine (1 to 2 mg/ml), and xylazine (0.1 mg/ml), often re- occurs within 4 days and necropsy reveals centrilobular
ferred to as GKX or Triple Drip, can be used both for in- necrosis. Necrosis of the proximal renal tubules, abomasal
duction and maintenance of anesthesia.36 ulceration, and hepatic encephalopathy have been ob-
Telazol (Fort Dodge Animal Health, Fort Dodge, served in some cases.42,43 Severe hypotension, hypox-
Iowa) is a proprietary combination of tiletamine (dis- emia, and hepatic hypoxia may encourage the reductive
sociative) and zolazepam (benzodiazepine) in a 11 metabolism of halothane, leading to the production of
(weightweight) ratio. Compared with ketamine, Telazol toxic free radicals.44 Therefore, maintaining adequate
anesthesia produces better muscle relaxation, more pro- cardiovascular function and oxygenation through careful
found analgesia, and longer lasting effects. In ruminants monitoring and supportive therapy are the keys to suc-
the induction of anesthesia after Telazol administration is cessful anesthesia.
rapid and smooth, and the recovery is usually gradual and
prolonged.14 Similar to ketamine, this drug causes cardio-
vascular stimulation rather than depression.35 Hypoventi-
Local Anesthetics
lation and hypothermia may occur during Telazol-induced Local anesthetics produce their effects by blocking the
anesthesia. Assisted or controlled ventilation with O2 sup- propagation of action potentials along nerve axons in a
plementation may be required in cases of severe hypoven- reversible manner. These anesthetics can be injected into
tilation and hypoxemia. Animals should be placed in the tissue at the surgical site to produce local anesthesia
sternal recumbency with support throughout the recovery or they can be administered in the perineural area of
period.14 major nerves to produce regional anesthesia (see Chapter
Propofol is a unique short-acting anesthetic. Struc- 6). In small ruminants, many surgical procedures are per-
turally, this drug does not relate to any of the injectable formed safely and painlessly under local or regional anes-
anesthetics currently available in veterinary practice. thesia. All local anesthetics have similar physical proper-
Propofol is only slightly water-soluble and comes as an ties and molecular structures. Most of them are weakly
emulsion containing 10 mg of propofol, 100 mg of basic tertiary amines with a hydrophilic end, a lipophilic
soybean oil, 22.5 mg of glycerol, and 12 mg of egg lecithin end, and an intermediate hydrocarbon chain. They are
per ml in sterile glass ampules. Because this emulsion con- generally available as acid solutions of the water-soluble
tains no preservative, after the ampule is opened, the con- salts. The acid salt is neutralized in the tissue, liberating
tents should be used or discarded within 8 hours.35 A the base, which then penetrates the cell membrane and
single dose of propofol (2 mg/kg) induces approximately interrupts the propagation of the action potential. This
10 minutes of anesthesia with complete recovery occurring mechanism of action means that a local anesthetic is less
in 20 to 30 minutes.2,37 Propofol is best used for induction effective in inflamed tissue with lower pH because less
before inhalation anesthesia; it also can be used as a con- liberation of the basic form of the drug occurs.45 Local
tinuous infusion to maintain short-term anesthesia.38-40 anesthetics are classed as ester-link or amide-link drugs
In goats a combination of detomidine, butorphanol, and depending on the intermediate chain structure. Inactiva-
propofol for induction and continuous IV infusion of tion of ester-link local anesthetics (e.g., procaine, tetra-
propofol for maintenance provides adequate anesthesia for caine) depends on hydrolysis by cholinesterase enzymes
castration or ovariectomy.41 in the plasma and to a lesser extent in the liver. Metabo-
412 • Sheep and Goat Medicine
lism of amide-link local anesthetics (e.g., lidocaine, bupi-
vacaine, mepivacaine) relies on microsomal enzymes TABLE 16-5
located primarily in the liver.45 Lidocaine is probably the NORMAL VITAL SIGNS AND VALUES
most popular local anesthetic used and may produce FOR ANESTHETIZED SHEEP AND GOATS
anesthesia for 0.75 to 2 hours. Because of its ability to
induce vasoconstriction in the tissue around the injected VALUES FOR SHEEP
area, epinephrine decreases systemic absorption of con- VITAL SIGN OR VALUE AND GOATS
currently administered local anesthetics. Therefore epi-
nephrine (1200,000 to 150,000) at concentrations of 5 Heart rate (beats/min) 80 to 150
to 20 mg/ml can be incorporated with or added to lido- Respiratory rate (breaths/min) 20 to 40
caine solution to prolong the duration of local anesthe- Systolic arterial pressure (mm Hg) 80 to 120
sia.46 Mepivacaine (which lasts for 1.5 to 3 hours) and Mean arterial pressure (mm Hg) 75 to 100
bupivacaine (which lasts for 4 to 8 hours) can be used for Diastolic arterial pressure (mm Hg) 60 to 80
procedures that require a longer duration of local anes- Partial pressure of arterial carbon 28 to 36
thesia.45 Administration of a large single dose or repeated dioxide (PaCO2) (mm Hg)
small doses of local anesthetics can result in toxicity in Partial pressure of arterial oxygen 72 to 90
sheep and goats, especially in neonatal and young pa- (PaO2) (mm Hg)
tients. Clinical signs of toxicity include nystagmus, Arterial pH 7.48 to 7.58
muscle fasciculation, CNS stimulation progressing to From Riebold TW, Geiser DR, Goble DO: Clinical techniques for
opisthotonos and convulsions, hypotension, respiratory food animal anesthesia. In Riebold TW, Geiser DR, Goble DO,
arrest, circulatory collapse, and death.45 The maximum editors: Large animal anesthesia: principles and techniques, ed 2, Ames,
calculated safe dose of lidocaine was reported to be 13 IA, 1995, Iowa State University Press; Alon E et al: Effects of
mg/kg in one study.47 In another study, accumulated IV propofol and thiopental on maternal and fetal cardiovascular and acid-
base variables in the pregnant ewe, Anesthesiology 78:562, 1993.
doses of 5.8 mg/kg, 18 mg/kg, and 42 mg/kg induced
signs of toxicity in adult, neonatal, and fetal sheep, re-
spectively.48 IV infusion of meperidine in sheep induced
convulsions at doses of 7.5 to 7.9 mg/kg and cardiovascu- Samples for measurement of end-tidal CO2 are collected
lar collapse at doses as high as 52 to 69 mg/kg.49 Bupiva- directly at the connecting point between the breathing
caine is approximately four times more potent than lido- system (Y piece) of the anesthesia machine and the end of
caine, and therefore a 0.5% solution produces the same the endotracheal tube; the partial pressure of CO2 is de-
degree of neuronal blockade as a 2% lidocaine solution.50 termined by infrared absorption. Normal end-tidal CO2
Ewing51 suggests using a maximum of 6 mg/kg of lido- should be closely related to alveolar CO2, assuming the
caine or mepivacaine and 2 mg/kg of bupivacaine in anesthetized patient is healthy and has no preexisting dif-
small ruminants. With this maximum safe dose in mind, fusion disturbance in the lung tissues. Arterial hemoglo-
the clinician should dilute lidocaine and mepivacaine so- bin O2 saturation is measured by pulse oximetry with the
lutions to 1% and 0.5%, respectively, to prevent over- sensor clip placed on the lingual artery in the tongue or
dosage when using these drugs in lambs and kids.51 Di- on the auricular artery in the ears. Normal arterial hemo-
azepam (0.1 mg/kg IV) or thiopental (5 mg/kg IV) globin O2 saturation should always be close to 98% to
should be administered if seizure activity or convulsions 100%. Indirect arterial blood pressures can be measured
caused by accidental overdose persist longer than 1 to 2 by a oscillometric blood pressure machine (Dinamap)
minutes.50,52 with an inflatable pressure cuff placed on the coccygeal or
dorsal metatarsal artery. Normal values for heart rate, re-
spiratory rate, arterial blood pressures and various arterial
PERIOPERATIVE blood gases are provided in Table 16-5. A balanced elec-
MANAGEMENT trolyte solution (5 to 10 ml/kg/hr) should be adminis-
AND RECOVERY tered IV for supportive hydration during anesthesia. Ad-
ministration of 5% dextrose solution is required to
prevent hypoglycemia in neonates and young animals. A
Monitoring During Anesthesia circulating warm water blanket can be used to maintain
Animals should be monitored continuously throughout body temperature during anesthesia and recovery.
anesthesia. Peripheral pulses should be palpable and an Sheep and goats usually recover from anesthesia grad-
electrocardiogram, if available, should be used at all times. ually and smoothly. Emergence delirium and premature
Recently, the use of capnograms to evaluate end-tidal attempts to stand seldom occur in these animals. They
CO2 and pulse oximeters to assess arterial O2 saturation should be placed in sternal recumbency with support, if
have became part of the routine monitoring accessories necessary, during the recovery period (Figure 16-5). If re-
used to ensure adequate ventilation and gas exchange. gurgitation occurred during anesthesia, the oral cavity
 Chapter 16 Anesthetic Management • 413

Figure 16-5 Sternal recumbency for postanesthetic recovery.

and pharynx should be lavaged to prevent aspiration of respiratory distress.Treatment of affected animals involves
ruminal materials and subsequent aspiration pneumonia. either draining or surgically removing the abscessed
The endotracheal tube should be left in place until the nodes. Depending on the size and invasiveness of the
animal regains its chewing and coughing reflexes. It abscess, general anesthesia is sometimes required to ensure
should be removed with the cuff inflated. immobilization so that vital tissues (e.g., carotid artery,
vagus nerve, esophagus) are not compromised during
Influences of Pathophysiologic Alterations dissection.55 Animals with respiratory embarrassment
should be handled with great caution and with as little
on Anesthesia stress as possible. Stress and excitement may worsen the
Obstructive urolithiasis is the inability to void urine nor- severity of respiratory embarrassment, resulting in severe
mally because of obstruction of the urinary outflow tract hypoxemia and death. Induction of anesthesia and intuba-
by calculi (see Chapter 10). It occurs most frequently in tion to maintain the airway should be performed rapidly.
young castrated goats. In cases of urethral obstruction Tracheal intubation may be difficult because the larynx
without ruptured bladder, perineal urethrostomy can be may be obscured by the swollen pharyngeal tissues.There-
performed under local infiltration or epidural analgesia. fore the skin over the upper third of the trachea should be
General anesthesia is induced for bladder repair, penile clipped and surgically prepared before the induction of
urethrostomy, and tube cystotomy.53,54 Xylazine, detomi- anesthesia. Tracheostomy can be performed to ensure a
dine, medetomidine, and other a2 agonists are con- patent airway should difficulty in endotracheal intubation
traindicated in obstructive urolithiasis because their occur. Tracheostomy and placement of a cuffed tra-
potent diuretic effects can result in bladder rupture before cheostomy tube also can be performed under local anes-
the obstruction can be relieved and the bladder emptied.6 thesia before the induction of general anesthesia. Anes-
Most of the routine anesthetic regimen can be safely used thesia can be induced with either IV injectable anesthetics
in cases of obstructive urolithiasis and ruptured bladder. or inhalation anesthetics through the tracheostomy tube.
However, anesthetic dosage adjustments may be neces- The tracheostomy tube should be left in place for 48 to 72
sary depending on the animal’s physical condition, partic- hours after surgery if possible. If removal of the tra-
ularly in animals with increased blood urea nitrogen and cheostomy tube is necessary after completion of the
creatinine levels and/or hypoproteinemia.53 surgery, the clinician should assess airway patency rostral
Caseous lymphadenitis in sheep and goats is a chronic to the tracheostomy tube by deflating the cuff and ensur-
contagious disease caused by Corynebacterium pseudo- ing good air flow before removing the tube.54
tuberculosis; it is discussed in various chapters in this text. Cesarean section is sometimes preformed as an elec-
Airway obstruction may result from occlusion of the tive surgery to save valuable fetuses and relieve dystocia in
pharynx by the enlarged pharyngeal lymph nodes. In some sheep and goats. The selection of suitable anesthetics and
cases, respiratory embarrassment is severe enough to cause techniques is vital for the survival of the dam and fetus.
414 • Sheep and Goat Medicine
Pregnancy induces several physiologic changes that can drugs decline slowly after absorption from the injection
affect the response to anesthesia. Because of hormonal site. They can accumulate in the fetus and cause fetal de-
changes, minute ventilation increases and the require- pression when large doses are administered.54
ment for inhalation anesthetics decreases (by 25% for Preanesthetic tranquilizers or sedatives are usually re-
halothane, 32% for methoxyflurane, and 40% for iso- served for excited or unruly animals. General anesthetics
flurane). Therefore induction of anesthesia is more rapid with low lipid solubility, short duration of action, and
than it is in nonpregnant patients.54 Heart rate and minimal cardiovascular depression are preferred. Low
cardiac output increase because of the increased cardiac doses of thiopental, a combination of xylazine and keta-
work required by pregnancy and at parturition. Conse- mine, or Triple Drip can be used for induction; anesthesia
quently, cardiac reserves decrease and pulmonary conges- is maintained with Triple Drip IV infusion to effect or in-
tion and heart failure may occur in animals that are ex- halation anesthesia (halothane or isoflurane). Tracheal in-
hausted or prone to shock because of prolonged and tubation should be performed in these animals even when
difficult delivery; animals with preexisting cardiovascular they are under injectable anesthesia for prevention of pos-
diseases also are at risk.54 Furthermore, venous engorge- sible aspiration pneumonia and administration of sup-
ment resulting from increased intraabdominal pressure plemental O2. Neonatal respiratory or CNS depression
from the enlarged uterus reduces the space available for caused by anesthetic effects can be antagonized by the ad-
local anesthetic administration by epidural injection, with ministration of doxapram or an a2 antagonist immedi-
resultant cranial migration of the anesthetics. This migra- ately after delivery.
tion may result in sympathetic blockade, profound mater-
nal hypotension, and reduction of uteroplacental perfu- PERIOPERATIVE ANESTHETIC
sion. Therefore the dose of local anesthetic administered
to produce adequate epidural anesthesia should be COMPLICATIONS
reduced to one third to one half that used in nonpregnant
animals.54 Drugs administered to induce or enhance Regurgitation and Aspiration Pneumonia
uterine contraction during parturition (e.g., oxytocin) Regurgitation can occur during both light (active regurgi-
cause peripheral vasodilation and hypotension when ad- tation) and deep (passive regurgitation) anesthesia in ru-
ministered in large or repeated doses and can result in de- minants in spite of preoperative fasting and withholding
creased uterine perfusion to the fetus and decreased fetal of water. Active regurgitation is a reflexive, protective
viability. Fluid with balanced electrolytes should be ad- mechanism of a body intent on rejecting unwanted mate-
ministered to animals with severe hypotension before in- rials from the pharynx, upper airway, and upper digestive
duction and during anesthesia.54 tract. Passive regurgitation occurs when the esophageal
Either general anesthesia or local anesthesia is suitable muscles and transluminal pressure gradients relax as a
for cesarean section. Selection of the anesthetic regimen result of the anesthetic effects. Aspiration of acidic
should be based on maternal and/or fetal safety. Most stomach or gastric contents may result in aspiration
anesthetics have physicochemical properties that allow pneumonia, which is characterized by reflex airway
them to cross the blood-brain barrier; these properties also closure, bronchospasm, dyspnea, hypoxemia, and cya-
permit them to cross the placenta, with resultant depres- nosis. Pulmonary hemorrhage and/or edema may result
sion of the fetal CNS. The only exceptions are neuromus- from destruction of type II alveolar cells and pulmonary
cular blocking agents such as succinylcholine, pancuro- capillary lining cells after aspiration of large amounts of
nium, and atracurium. These drugs cannot cross the particulate material or extremely acidic material. In severe
placenta as easily as other anesthetics because of their qua- cases, animals die before an endotracheal tube can be
ternary molecular structure. To ensure fetal viability, the placed to protect the airway. Therefore preoperative with-
intended incision site should be clipped and roughly pre- holding of feed and endotracheal intubation with the cuff
pared before induction, the period between induction of adequately inflated are recommended in all anesthetized
anesthesia and removal of the fetus should be as short as ruminants for prevention of aspiration pneumonia.56
possible, and the anesthetic concentration should be kept Placing a sandbag or some other rolled padding beneath
to a minimum. For these reasons, in addition to economic the animal’s neck to elevate the occiput and avoiding vig-
concerns, local anesthesia is often chosen for this proce- orous manipulation of the rumen and other internal ab-
dure. Local infiltration of anesthetic along the incision site dominal organs during surgery helps minimize the occur-
and lumbosacral epidural or subarachnoid anesthesia are rence of aspiration pneumonia. If regurgitation occurs
the two most commonly used techniques for cesarean before intubation can be completed, the clinician should
section in most food animals. Procaine and tetracaine, either quickly lower the animal’s head or place the endo-
which are esters of para-aminobenzoic acid, do not accu- tracheal tube in the esophagus and inflate the cuff to
mulate in the dam and fetus. Lidocaine, mepivacaine, allow ruminal contents to flow out of the mouth while
bupivacaine, and etidocaine are amide-link local anesthet- another tube is placed in the trachea.2 IV aminophylline
ics that depend on hepatic microsomal enzymes for inacti- (2 to 4 mg/kg over a 5-minute period or 11 mg/kg over a
vation of drug effects.45 Blood concentrations of these 20-minute period) or other bronchodilators along with
 Chapter 16 Anesthetic Management • 415

100% O2 can be administered to relieve bronchospasm at membranes, and bradycardia (heart rate less than 70 to 80
the time of aspiration. If the animal survives the initial beats/min) or tachycardia (heart rate greater than 150
insult, corticosteroids and broad-spectrum antibiotics are beats/min) can lead to cardiovascular collapse. Causes of
indicated for the treatment of pneumonia.2,33 this perioperative collapse include significant endotoxin-
induced peripheral vasodilation, severe hypovolemia re-
sulting from dehydration and/or blood loss, and deep
Ruminal Tympany anesthesia resulting in profound myocardial depression.
Ruminal tympany is sometimes observed during anesthe- Treatment of impending cardiovascular failure should
sia as a result of the accumulation of gas produced by fer- begin with correction of the causative disease status, rapid
mentation of ingesta and the animal’s inability to eructate administration of supportive fluid (90 ml/kg), and re-
(see Chapter 3). Pressure increases within the abdomen duction or even cessation of anesthesia.57 Additional
and on the diaphragm, resulting in reduced functional symptomatic treatment includes vasoactive drugs (e.g.,
residual capacity of the lungs and impeded ventilation. dopamine, phenylephrine, ephedrine) for hypotension, in-
Placing the animal in sternal recumbency immediately otropic drugs (e.g., dobutamine) for myocardial depres-
after anesthesia helps eliminate the accumulated gas in the sion, chronotropic drugs (e.g., atropine, glycopyrrolate)
rumen. However, decompression of the rumen may need for bradycardia, and antiarrhythmic drugs (e.g., lidocaine)
to be performed while the animal is still anesthetized and for ventricular arrhythmias such as ventricular tachycar-
the surgery is in progress. Passage of a stomach tube or in- dia or premature ventricular contractions. Dobutamine
sertion of a 12-gauge needle through the abdominal wall (1 to 5 mg/kg/min) is a b1 agonist that increases cardiac
allows outflow of the accumulated gas, reducing the pres- output and arterial blood pressure by increasing myocar-
sure in the abdomen and on the diaphragm and thereby dial contractility when administered at a low dosage.
improving ventilation. Most anesthetics, particularly a2 Dobutamine seldom increases heart rate, except in the
agonists and opioid agonists, decrease gastrointestinal presence of reduced total blood volume.58 Dopamine is a
motility; an antagonist can be administered to treat the re- dose-dependent, dopaminergic, b and a agonist. When
sultant ruminal tympany if necessary. Preoperative fasting administered at an IV infusion rate of 1 to 2 mg/kg/min,
reduces the amount of fermentable ingesta in the rumen dopamine increases renal perfusion by stimulating dopa-
and thereby decreases the chance for development of peri- minergic receptors. Increasing the infusion rate to 2 to 10
operative ruminal tympany.56 mg/kg/min causes stimulation of b1 receptors and a re-
sultant increased heart rate. Vasoconstriction and the
subsequent increase in arterial blood pressure mediated
Hypoventilation by stimulation of a1 receptors are not evident until the in-
In conscious sheep, lateral recumbency alone can induce fusion rate is greater than 10 mg/kg/min.58 Phenyl-
significant hypoxemia.9 During anesthesia, severe hy- ephrine (2 to 4 mg/kg IV bolus or 0.2 to 0.4 mg/kg/min
poventilation and hypoxemia (characterized by a signifi- via infusion) and ephedrine (22 to 66 mg/kg IV) have
cant increase in PaCO2 and decrease in PaO2) may result both been used to treat hypotension in anesthetized
from the abnormal surgical body position combined with animals.59 Ephedrine appears to have a longer dura-
the respiratory depressing effect of the anesthetic drugs. tion of action (30 to 60 minutes) than dobutamine or
Ventilation should be assisted or controlled by squeezing dopamine, which may be undesirable if tachycardia oc-
the rebreathing bag with a positive pressure of 20 to 25 curs after ephedrine administration.59
cm H2O if an inhalation anesthetic is used. Supplemental Prolonged untreated cardiovascular collapse may result
O2 also can be provided to sedated and recumbent in cardiac arrest and death. Cardiopulmonary resuscita-
animals through an orotracheal or endotracheal tube by tion (CPR) should follow the ABC technique. A entails
using an O2 demand valve, particularly if xylazine is part opening of the airway by endotracheal intubation, B is the
of the anesthetic regimen. Occasionally apnea may occur initiation of controlled breathing by squeezing an Ambu
and persist throughout anesthesia. The anesthetist should bag or using the rebreathing bag on the anesthesia
ensure that the animal is under an adequate plane of machine (12 to 20 breaths/min), and C is the establish-
anesthesia before instituting any drug treatment. A respi- ment of artificial circulation by cardiac compression (80 to
ratory stimulant (doxapram 0.1 to 0.5 mg/kg IV) can be 100 compressions/min). After CPR has been instituted,
administered to initiate respiration. If the depression per- an IV catheter should be placed if one is not already
sists, doxapram can be administered as a continuous IV present. If the attempts at IV catheterization is unsuccess-
infusion (5 to 10 mg/kg/min).57 ful, emergency drugs may be administered intratracheally
through the endotracheal tube at 2 to 2.5 times the IV
dose after dilution with sterile water or saline to a volume
Cardiovascular Collapse of 5 to 10 ml. Absorption of the drugs from the lung is
During anesthesia, prolonged decreases in pulse pressure, sometimes significant enough to be more effective than
hypotension (mean arterial pressure less than 60 to 75 IM, subcutaneous, or IV administration through a periph-
mm Hg), increases in capillary refill time, pale mucous eral vein.57 Emergency drugs and products frequently
416 • Sheep and Goat Medicine
used during CPR include 100% O2, balanced electrolyte space between the fifth sacral and first coccygeal verte-
solutions, atropine, lidocaine, and epinephrine. Depend- brae or between the first coccygeal and second coccygeal
ing on the animal’s condition, the vasoactive drugs men- vertebrae. The area over the site is clipped and aseptically
tioned previously can be used in conjunction with emer- prepared. The needle (18- to 20-gauge, 4-cm) is placed
gency drugs. Electrical defibrillation is the most effective into the correct interspace at a 90° angle to the skin. The
treatment for conversion of ventricular fibrillation, but it is needle (without an attached syringe) is pushed ventrally
not practical in field situations. Epinephrine (10 mg/kg through the interarcuate ligament toward the floor of the
IV) is usually the drug of choice for treatment of ventricu- neural canal.60 A sight vacuum should be noted on enter-
lar fibrillation. Epinephrine induces peripheral vasocon- ing the epidural space. If blood is visualized in the hub or
striction and increases arterial diastolic blood pressure, flows from the needle, the needle should be withdrawn
intracranial and coronary blood flow, coarseness of ven- because it has been inappropriately placed into a venous
tricular fibrillation, and positive inotropic effect by stimu- sinus. As a general rule, 1 ml of 2% lidocaine per 45 kg of
lating a and b adrenoceptors. Potential side effects of epi- body weight is adequate and therefore a total dose of 1 to
nephrine include increased myocardial and cerebral O2 2 ml is effective for most sheep and goats. The onset of
demand, post-resuscitation arrhythmia, and tachycardia. analgesia occurs within 1 to 5 minutes, and the duration
Lidocaine (0.5 to 2 mg/kg IV) may be used to treat the is about 1 hour.1 This technique also is described in
post-resuscitation ventricular arrhythmia.57 Chemical de- Chapters 3 and 6.
fibrillation with IV potassium chloride (1 mg/kg) and
acetylcholine (6 mg/kg) followed by administration of
10% calcium chloride (1 ml/10 kg) is recommended for
Lumbosacral Epidural Anesthesia
treatment of ventricular fibrillation. Although it is ineffec- If properly performed, a lumbosacral epidural provides
tive in defibrillation, this technique usually converts fibril- analgesia caudal to the diaphragm (abdominal wall
lation to asystole.57 A normal sinus rhythm is actually caudal to the umbilicus, inguinal region, flank, and per-
more easily initiated from asystole. ineal area).1 The site for injection can be palpated in
The best treatment for perioperative complications is some sheep and goats as a soft spot where the dorsal
prevention, which requires a devoted and vigilant anes- midline intersects an imaginary line drawn between the
thetist. Careful preanesthetic evaluation and preparation cranial borders of the two iliac wings2 (Figure 16-6). In
and proper use of anesthetic regimens can prevent most sheep and goats this lumbosacral space is located just
anesthetic-related complications; close monitoring allows caudal to the spinous process of the last lumbar vertebra.
the anesthetist to recognize potentially dangerous situations The skin over the space between the last lumbar vertebra
quickly and institute corrective measures at an early stage. and the first sacral vertebra is clipped and aseptically pre-
The clinician should keep in mind that “there is no safe pared. A needle (18- to 20-gauge, 4- to 9-cm) is ad-
anesthetic or anesthetic technique, only safe anesthetists.” vanced through the skin at a 90° angle. Occasionally a
slight cranial movement of the needle is required. If cere-
brospinal fluid or blood is encountered, the needle is in
SPECIFIC NERVE BLOCKS the subarachnoid space. In this case the needle should be
Many of the local anesthetic techniques for specific sur- withdrawn and the procedure should be attempted again.
geries are covered in the text as part of the surgical de- A slight vacuum should be noted on entering the
scription. However, three commonly used local and re- epidural space. If local anesthetic is injected into the sub-
gional anesthetic techniques are described in this chapter. arachnoid space, rear-limb paralysis occurs within 3 to 5
The authors of this chapter perform caudal epidural anes- minutes.60,61 After passing through the epidural space,
thesia routinely and lumbosacral epidural anesthesia oc- the needle “pops” through the interarcuate ligament.61
casionally, but rarely use local anesthetic techniques for The syringe can then be injected slowly without resis-
horn removal. When removing large horns from adult tance. A dosage of 0.3 to 0.5 ml of a 2% lidocaine hy-
goats or rams, the authors prefer to use general anesthesia. drochloride solution per 10 kg of body weight is adequate
However, on occasion local anesthesia for horn removal is for most surgeries.61 The onset of analgesia and rear-
warranted and therefore it is included here. limb paralysis occurs after 5 to 15 minutes and lasts 1 to
2 hours.60,61
Caudal Epidural
If properly performed, caudal epidural anesthesia de-
Horn Anesthesia
sensitizes the perineum, vulva, vagina, and rectum. To As dehorning in adult goats and rams is a very bloody
locate the injection site the clinician grasps the tail and surgical procedure, general anesthesia should probably be
locates the most cranial moveable intervertebral space. used; however, some clinicians prefer local anesthesia.
Location of this space is enhanced by “pumping” the tail. The administration of local anesthesia for dehorning
In sheep and goats the injection site is either in the inter- sheep (rams) is similar technically to that provided for
 Chapter 16 Anesthetic Management • 417

A B C
Figure 16-6 Lumbosacral anesthesia. The site is located on the dorsal midline, behind the most
caudal lumbar vertebra and midway between the dorsal aspect of the iliac wings. A, The clinician’s
thumbs are pressing on the iliac wings. B, The index finger indicates the site to be injected. C, The
clinician locates the site, places the needle about 90° to the skin, and injects the anesthetic agent without
resistance.

with a local anesthetic. In one of the authors’ experience

(Dr. Pugh) the ring block has yielded the most repro-
ducible results. Because of the potential for lidocaine tox-
icity, the 2% lidocaine should be mixed with an equal
volume of sterile saline.64
a b
In the goat the horn and immediately surrounding
skin can be anesthetized by “blocking” the corneal branch
of the lacrimal nerve. This nerve is anesthetized by inject-
ing a local anesthetic (1 to 2 ml of 2% lidocaine 1.5 to 2
cm deep) adjacent to the caudal ridge of the base of the
supraorbital process. The cornual branch of the intra-
trochlear nerve, which is located dorsomedial to the eye
and adjacent to the margin of the orbit (Figure 16-7), can
be palpated in some animals. Local anesthetic (1 to 2 ml
of 2% lidocaine) can be administered there about 1 cm
Figure 16-7 The location of the cornual branch of the deep. By anesthetizing both of these anesthetic sites,
intratrochlear nerve (a) and the cornual branch of the lacrimal nerve good horn analgesia is attained.63
(b). Local anesthetic can be infiltrated into these two areas to attain
good analgesia of the horn and surrounding skin.
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2. Riebold TW: Ruminants. In Thurmon JC, Tranquilli WJ, Benson
the zygomatic ridge toward the horn. Another protocol
GJ, editors: Lumb & Jones’ veterinary anesthesia, ed 3, Baltimore,
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5. Taylor PM: Anesthesia in sheep and goats, In Pract 13:31, 1991. 29. Singh B, Kumar A: Meperidine as preanesthetic to thiopentone
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xylazine, Proc Assoc Vet Anaesth Great Br Ire 6:30, 1976-1977. 33. Thurmon JC, Benson GJ: Anesthesia in ruminants and swine. In
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the respiratory blood gas changes in conscious sheep, Vet Rec Thurmon JC, Tranquilli WJ, Benson GJ, editors: Lumb & Jones’
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83:117, 1993. fol in sheep, Proceedings of the Fourth International Congress of Vet-
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16. Gessert ME, Scott PR: Combined xylazine and lidocaine caudal 39. Reid J, Nolan AM, Welsh E: Propofol as an induction agent in
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turient vaginal or cervico-vaginal prolapse, Agri-Pract 16:15, 1995. 1993.
17. Ruckebusch Y, Allal C: Depression of reticulo ruminal motor 40. Lin HC, Purohit RC, Powe TA: Anesthesia in sheep with propo-
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18. Celly CS et al:. Comparative cardiopulmonary effects of four a-2 41. Carroll GL et al: Detomidine-butorphanol-propofol for carotid
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19. Pyrörälä E et al: Detomidine to pregnant cows, Nord Vet Med Surg 27:75, 1998.
38:237, 1986. 42. Fetcher A: Liver diseases of sheep and goats, Vet Clin North Am:
20. Jedruch J, Gajewski Z: The effect of detomidine hydrochloride Large Anim Pract 5:525, 1983.
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Vet Scand 82:189, 1986. in goats, J Am Vet Med Assoc 189:1591, 1986.
21. Muge DK et al: Analgesic effects of medetomidine in sheep, Vet 44. Riebold TW, Geiser DR, Goble DO: Clinical techniques for food
Rec 135:43, 1994. animal anesthesia. In Riebold TW, Geiser DR, Goble DO,
22. Mohammad FK, Zangana IK, Abdul-Latif AR: Medetomidine editors: Large animal anesthesia: principles and techniques, ed 2,
sedation in sheep, J Vet Med A40:328, 1993. Ames, IA, 1995, Iowa State University Press.
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medetomidine-ketamine anaesthesia in sheep, with and without cology and physiology in anesthetic practice, Philadelphia, 1987, JB
100% oxygen and its reversal with atipamezole, J Vet Anaesth 22:9, Lippincott.
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24. Hsu WH, Schaffer DD, Hanson CE: Effects of tolazoline and Vet Clin North Am: Food Anim Pract 2:621, 1986.
yohimbine on xylazine-induced central nervous system depression, 47. Scarratt WK, Trout HF: Iatrogenic lidocaine toxicosis in ewes,
bradycardia, and tachycardia in sheep, J Am Vet Med Assoc 190:423, J Am Vet Med Assoc 188:184, 1986.
1987. 48. Morishima HO et al: Toxicity of lidocaine in adult, newborn, and
25. Yellin TO, Sperow JW, Buck SH: Antagonism of tolazoline by fetal sheep, Anesthesiology 55:57, 1981.
histamine H2-receptor blockers, Nature 253:561, 1975. 49. Santos AC et al: Does pregnancy alter the systemic toxicity of local
26. Read MR, Duke T, Toews AR: Suspected tolazoline toxicosis in a anesthetics?, Anesthesiology 70:991, 1989.
llama, J Am Vet Med Assoc 216:227, 2000. 50. Hall LW, Clarke KW: General principles of local analgesia. In
27. Gray PR, McDonell WN: Anesthesia in goats and sheep, Part II: Hall LW, Clarke KW, editors: Veterinary anaesthesia, ed 9,
general anesthesia, Cont Edu 8:S127, 1986. London, 1991, Bailliere Tindall.
28. Flacke JW et al: Histamine release by four narcotics: a double 51. Ewing KK: Anesthesia techniques in sheep and goats, Vet Clin
blind study in humans, Anesth Analg 66:723, 1987. North Am: Food Anim Pract 6:759, 1990.
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52. Alon E et al: Effects of propofol and thiopental on maternal and 59. Klein L: Anesthetic complications of equine anesthesia, Vet Clin
fetal cardiovascular and acid-base variables in the pregnant ewe, North Am: Equine Pract 6:665, 1990.
Anesthesiology 78:562, 1993. 60. Purohit RC: Anesthesia. In Wolfe DF, Moll HD, editors: Large
53. Smith MC, Sherman DM: Urinary system. In Smith MC, animal urogenital surgery, Baltimore, 1998, Williams & Wilkins.
Sherman DM, editors: Goat medicine, Philadelphia, 1994, Lea & 61. Hooper RN: General surgical techniques for small ruminants: Part
Febiger. II, Small Ruminants for the Mixed Animal Practitioner Western Vet-
54. Benson GJ: Anesthetic management of ruminants and swine with erinary Conference, 1998, Las Vegas, NV.
selected pathophysiologic alterations, Vet Clin North Am: Food 62. George AN: A note on the anatomy of the horns of sheep, Br Vet J
Anim Pract 2:677, 1986. 111:391, 1955.
55. Smith MC, Sherman DM: Subcutaneous swellings. In Smith 63. Greenough PR, Johnson L: The integumentary system: skin, hoof,
MC, Sherman DM, editors: Goat medicine, Philadelphia, 1994, claw, and appendages. In Oehme FW, Prier JE, editors: Textbook of
Lea & Febiger. large animal surgery, Baltimore, 1974, Williams & Wilkins.
56. Steffey EP: Some characteristics of ruminants and swine that 64. Hooper RN: General surgical techniques for small ruminants: Part
complicate management of general anesthesia, Vet Clin North Am: I, Small Ruminants for the Mixed Animal Practitioner Western Veteri-
Food Anim Pract 2:507, 1986. nary Conference, 1998, Las Vegas, NV.
57. Kruse-Elliott KT: Management and emergency intervention dur-
ing anesthesia, Vet Clin North Am: Food Anim Pract 12:563, 1996.
58. Riebold TW, Geiser DR, Goble DO: Anesthetic emergencies. In
Riebold TW, Geiser DR, Goble DO, editors: Large animal anes-
thesia: principles and techniques, ed 2, Ames, IA, 1995, Iowa State
University Press.
 Chapter 17

F lock Health
SEYEDMEHDI MOBINI, CINDY WOLF, AND D.G. PUGH

This chapter provides a brief overview of flock and herd

Dry Does and Does in Late Pregnancy
health care programs for sheep and goats. Treatment and The major disease problems in this group are pregnancy
prevention of specific diseases are addressed in other toxemia, abortion, and pseudopregnancy. Goats that are
chapters. In this chapter goat herd programs are covered over-conditioned during this period are at risk of preg-
first, followed by sheep flock programs. nancy toxemia, vaginal prolapse, and dystocia.1,3 The
primary objective for these animals is proper nutritional
management, avoidance of obesity in early gestation, and
GOATS provision of adequate nutrients to support the rapid
growth of the fetus in the final trimester.1 Supplement
Herd Health Management feeding where needed should commence at the beginning
Herd health management and preventive medicine pro- of the final trimester of pregnancy and be increased
grams are designed to minimize potential adverse effects steadily until parturition. Obesity, however, should be
of predictable problems and to protect against unexpected avoided. To protect pregnant does from infectious abor-
ones.1 The goal of a herd health program is to improve tion, no new animals should be introduced into the
the goat herd’s productivity through general husbandry, group.
nutritional management, parasite control, vaccination,
and environmental management.2 An understanding of Management Practices
various management practices and common disease prob- • Vaccinate for abortion diseases (if the herd has a
lems is helpful to accomplish this goal. history of abortion) 1 month before the start of
Because of their remarkable adaptability, goats are breeding.
maintained over a more diverse range of production • Perform pregnancy diagnosis on all bred does 45 to
systems than any other domestic livestock species. Goat 60 days after breeding.
production can be divided into dairy, fiber, meat, pet, and • Prevent over-conditioning and provide plenty of
show production. The largest body of information about exercise for parturient does.
goat herd health management and preventive medicine • Do not mix any new animals with pregnant does.
focuses on dairy and fiber-producing goats. Still, with the • In areas or on farms with a history of infectious
recent expansion of the meat goat industry in North abortion, consider adding ionophores and/or
America, development of herd health protocols in this tetracyclines to feeds or mineral mixtures.
area is desirable. Herd health management programs • Give yearly vaccination boosters of toxoids for
must be designed to fit an individual herd and vary ac- Clostridium perfringens type C and D and C. tetani
cording to the herd size, its purpose, and the owner’s pro- 30 days before kidding. This helps protect the doe
duction goals.2 In an attempt to organize information ap- and ensures high levels of antibodies to protect the
plicable to goat herd health into a simple, usable, and newborn kid.
easily remembered format, herd health management • Deworm 30 days before kidding and continue
practices are divided into groups of dry does and does deworming through the birthing season for meat
in late pregnancy, kidding does, kids and weanlings, and fiber goats. Pregnant does experience a
and bucks. preparturient nematode parasite egg rise and exhibit
• 421 •
422 • Sheep and Goat Medicine
increased shedding of parasite eggs around kidding. Management Practices
The authors of this chapter avoid levamisole and • Tape the teats of does that are CAEV-positive to
albendazole for the deworming of pregnant does. prevent accidental nursing of kids.
Monitor fecal egg count during this period. • Clean dams’ teats and strip milk from each teat to
• Infuse mammary glands of dairy goats with half a ensure the presence of colostrum.
tube of dry cow antibiotic products at the time of • In dairy goats, dry off kids and separate them from
dry off (40 to 60 days before parturition). their dams.
• Trim feet as needed. Avoid hoof disease late in • Dip the navel cord with tincture of iodine
gestation. immediately after birth.
• In deficient areas, administer vitamin E and • Ensure that kids receive colostrum within 4 hours
selenium to does 30 to 45 days before kidding. of birth. In dairy goats feed 60 ml of pasteurized
Ensure adequate selenium intake with a free-choice colostrum by bottle or stomach tube within 1 hour
mineral mixture. of birth. Continue colostrum feeding for 3 to 4
• Provide a clean, dry, draft-free area for maternity days.
pens, or a well-drained, clean pasture with shelter. • Examine kids for congenital defects.
• Assess body condition score of does. Scores of 2.5 • Ensure that does pass the placenta within 12 hours
to 3.5 (on a 5-point system) are desirable.1,4 of parturition.
• Periodically check pregnant does’ urine for ketones • In dairy breeds, disbud and castrate kids at 4 to 10
with urine sticks in herds experiencing pregnancy days. Meat goat owners may prefer to leave horns
toxemia. If an individual or a large percentage of the on their goats. In meat goats the age of marketing
animals examined have higher than normal ketone determines the need for castration. For pet or show
values, take steps to correct the problem (e.g., feed goats, castration should be delayed until after
niacin and/or ionophores, feed more grain, force puberty.
more exercise). • In deficient areas, inject kids with vitamin E and
selenium at 1 to 2 weeks.
• Properly identify kids (e.g., by ear tag or neck
Kidding Does collar).
Kidding should be a well-anticipated event and not an un- • Begin coccidiosis prevention at the second week of
expected surprise.1 Where possible the pregnant doe must life and parasite control at 1 month.
be given adequate exercise until the time for kidding. • Vaccinate kids at 1 to 2 months for C. perfringens
Kidding does should be moved to a clean pen or pasture as type C and D and administer C. tetani toxoids if the
parturition nears. The udders of dairy goats should be dams were vaccinated during the final month of
clipped 2 weeks before the due date. Being prepared for pregnancy. If the dams were not vaccinated, begin
routine processing of kids at birth, including navel dipping, kid vaccination at 1 week of age and repeat
colostrum feeding, and readiness to respond to emergen- vaccination in 3 or 4 weeks.
cies, reduces neonatal losses.5 A timed induction of parturi- • Expose kids to hay and grain early in life to
tion using prostaglandins (PGF2 2.5 to 20 mg IM) is one promote rumen development.
management option to ensure does are attended at birth.
Great emphasis should be placed on kid-rearing tech-
niques that reduce neonatal mortality and diseases that
Kids and Weanlings
inhibit the rapid, efficient growth of young kids. The Weaning may occur at 6 to 12 weeks in dairy goats or
major obstacles to newborn kids’ survival are hypother- orphaned kids, depending on the feeding and manage-
mia, hypoglycemia, and infectious diseases resulting from ment system. Meat goats are usually weaned at 4 to 6
delayed or inadequate colostral intake. Failure of passive months.1,4 Common diseases encountered during the
transfer of maternal antibodies to newborn kids leads to weaning period include pneumonia, coccidiosis, and gas-
an increased incidence of disease and death. Caprine trointestinal (GI) nematode parasites. In finishing pro-
arthritis-encephalitis virus (CAEV) infection is a major grams in which young bucks are fed high-concentrate
concern in dairy goats. Newborn dairy kids should be a feed, conditions such as bloat, urinary calculi, and entero-
focus of CAEV control programs because the virus is pri- toxemia are frequently encountered. The authors have di-
marily spread from infected does to susceptible kids by agnosed cases of urinary calculi in male Boer kids as
colostrum and milk. To help prevent the spread of young as 2 to 3 months. Providing a continuous supply of
CAEV, colostrum can be heat-treated at 56° C (133° F) clean, fresh water and increasing the concentration of salt
for 60 minutes before being fed. The mammary form of in the ration to a maximum of 4% are helpful manage-
CAEV infection often occurs at the onset of lactation. ment tools to prevent calculi. Prophylactic use of urinary
The udder appears normal but is firm, and hypogalactia acidifiers also has been advocated. The continuous ad-
or agalactia are usually present.1,6 ministration of ammonium chloride at a level of 1% to
 Chapter 17 Flock Health • 423

2% of the diet is recommended in castrated and intact • Monitor fecal egg counts and deworm as needed.
bucks. Polioencephalomalacia can occur under intensive Deworm 1 month before breeding season.
management conditions. Weaned meat goat kids con- • Apply petroleum jelly to any urine-scalded areas of
suming rations containing high levels of concentrates or the head and back of front legs.
grains are highly susceptible. Causes of polioencephalo- • Maintain a 21 ratio of dietary calcium to
malacia include thiamine deficiency, inhibition of thi- phosphorus and provide a high level of salt (up to
amine activity, and sulfate contamination of water or 4%) and 1% to 2% ammonium chloride in the diet
feed. Increasing the roughage and decreasing the grain to prevent urinary calculi. Ensure that drinking
portion of the diet, decreasing sulfate ingestion, and pos- water is clean, fresh, and readily available.
sibly including thiamine in the diet are all good therapeu-
tic tools.
Vaccination Protocol
Management Practices Enterotoxemia and tetanus. A minimal vaccination
• Separate doe kids from intact buck kids before 3 or program for goats includes vaccinations against C. per-
4 months to avoid unwanted breeding. fringens type C and D (enterotoxemia) and C. tetani.1,2,7-9
• Provide coccidiostats in feed or water and maintain Some multivalent clostridial vaccines, including those
good sanitary practices. against blackleg, malignant edema, and bacillary hemo-
• Monitor fecal egg counts (McMaster’s score higher globinuria, are used in goats. These are unusual diseases
than 100 eggs per gram) and deworm as needed. in goats, and vaccination to prevent them is usually not
• Provide free-choice hay when feeding concentrates. economically justified, but many vaccines contain seven
• Examine the external genitalia for abnormalities or eight bacterins in one shot. Vaccination site considera-
such as intersex. tions include the potential for development of blemishes,
• Maintain a 21 dietary calcium–to–phosphorus lameness, and site reactions that require trimming at
ratio and provide high levels of salt (up to 4% salt) slaughter or cause poor performance in the show ring.
and 1% to 2% ammonium chloride in the diets of Subcutaneous injection in the caudolateral neck region
bucks and wethers to prevent urinary calculi. Allow or behind the elbow is often preferred. Injection over
for sufficient trace mineral intake (e.g., selenium, the ribs is an alternative for adult animals.9 All the
zinc), particularly in deficient areas. Ensure that animals should be vaccinated initially with clostridial
drinking water is clean, fresh, and readily available. and tetanus toxoid products and receive a second vaccina-
tion in 3 to 4 weeks. Pregnant does should receive their
annual vaccination 1 month before parturition. Bucks,
Bucks yearlings, and other adults should receive annual boosters
Bucks are too often neglected and omitted from herd at the same time to streamline animal handling. Animals
health management practices. Urolithiasis is probably the that are fed large amounts of concentrate may need to
most important disease condition in bucks. Although they receive a booster vaccination every 6 months. This can
are more common in castrated males, urinary calculi also be accompanied by vaccination of does a month before
have been observed in intact males (especially meat goats); breeding.
they can result in the bucks’ destruction as breeding Kids from immunized dams should be vaccinated at 1
animals. Providing fresh water, increasing salt concentra- to 2 months and given a booster 3 to 4 weeks later. Kids
tion in the diet to 2% to 4%, and using urine acidifiers are from nonimmunized dams should be vaccinated at 1 to 3
as important in the herd health management of bucks as weeks and given a booster 3 to 4 weeks later. A C. perfrin-
they are in the management of kids and weanlings. gens type C and D antitoxin is available for treatment in
Bucks become very aggressive during the breeding case of failure of passive transfer of colostral antibodies
season and can injure workers and one another. They and for use in endemic areas. Similarly, C. tetani antitoxin
urinate on their faces and forelimb during breeding is available and should be used before surgeries (e.g., cas-
season, which can cause severe urine scald, secondary tration, dehorning) and parturition, if the previous vacci-
bacterial dermatitis, and stench. nation status of the animal is unclear. The dosage of the
tetanus antitoxin for young kids is 150 to 250 units and
Management Practices 400 to 750 units for adult goats.2,5 A basic vaccination
• Allow exercise. protocol for goats is shown in Box 17-1.
• Vaccinate the bucks at the same time as the does (C.
perfringens type C and D and C. tetani toxin). Contagious ecthyma. Goats should be vaccinated to
• Trim feet as needed. protect against contagious ecthyma only if the disease has
• Perform breeding soundness examination 1 to 2 been identified in the herd.2,7 Because the vaccine is a live
months before breeding. Determine body condition virus, herds not exposed to the disease should not be vac-
scores and maintain animals at a score of 3 to 3.5. cinated because the virus may survive in the environment
424 • Sheep and Goat Medicine
BOX 17-1 Caseous lymphadenitis. Caseous lymphadenitis is a
common disease of goats that causes abscesses at the
B V
ASIC ACCINATION P ROGRAM FOR G OATS
lymph nodes and results in poor production, weight loss,
and death. A vaccine is usually available singly or in com-
bination with C. perfringens type C and D and C. tetani
PREGNANT DOES
vaccines for sheep. The value of this vaccine in controlling
• Vaccinate does during last month of caseous lymphadenitis in goats has been questioned.1 The
pregnancy for Clostridium perfringens type C vaccine itself can cause severe local or systemic reactions
and D and C. tetani. in infected goats and may interfere with some forms of
KIDS serologic testing.5,9 However, either autogenous or com-
• Immunize kids from immunized dams at 1 to mercial vaccines may reduce the number and severity of
2 months of age for Clostridium perfringens lesions in individual animals (see Chapter 8).
type C and D and C. tetani; repeat
immunization in 3 to 4 weeks. Other vaccines. Vaccines for some diseases of goats are
• Immunize kids from non-immunized dams at commercially available only for sheep and cattle but may
1 to 3 weeks of age for Clostridium perfringens be beneficial on an as-needed basis. Vaccines against
type C and D and C. tetani; repeat abortion-causing diseases are not commonly adminis-
immunization twice at 3- to 4-week intervals. tered to goats. In the United States, Chlamydia and Toxo-
plasma are the most commonly identified infectious
BUCKS AND YEARLINGS
causes of abortion in goats. Campylobacter, which is one of
• Immunize bucks and yearlings at the same the most common causes of abortion in sheep, is rela-
time pregnant does are vaccinated, with tively uncommon in North American goats.10 Listeria
emphasis on Clostridium species. also should be considered a potential cause of abortion in
• In endemic areas, vaccines for rabies, and meat goats.11
leptospirosis may be of value. Sheep vaccines against chlamydiosis can be used in
BREEDING DOES goats if the disease is a problem in a particular herd. Ini-
• Vaccinate breeding does for Chlamydia and tially, all breeding adults and replacement yearlings
Campylobacter before breeding, and repeat in should be vaccinated 60 days and 30 days before the
mid-gestation. breeding season. In successive years, all adults should be
vaccinated 2 to 4 weeks before the start of the breeding
season. A combined vaccine against Chlamydia and
Campylobacter for sheep can be used in the rare event that
Campylobacter is a problem in a particular goat herd. The
for long periods and act as a source of herd infection. efficiency of these vaccines is questionable because several
After the environment becomes contaminated by the biotypes of these two diseases exist and vaccines against
vaccine-virus or through natural infection, vaccination is one biotype may not be cross-protective.
warranted. During outbreaks, disinfection of goat han- No vaccine against Toxoplasma is presently available
dling and working areas after the animals’ lesions have for use in sheep or goats and commercial vaccines against
cleared is recommended if the owner elects not to vacci- listeriosis are not available in the United States. Autoge-
nate. In a herd in which the showing or buying of goats is nous biologics may be prepared by the practitioner or a li-
a regular practice, vaccination of the original animals is censed facility and may be valuable tools in some man-
recommended 6 months before they are to be commin- agement systems. An autogenous bacterin developed
gled with animals from outside the herd. The initial vac- from six different isolates of a listeriosis outbreak in
cination for contagious ecthyma should include all Georgia reduced the incidence of abortion in a meat goat
animals in the herd. After the initial vaccination, only herd.11 Cattle leptospirosis vaccines can be used in goats
new kids and unvaccinated purchased animals should be that are kept near cattle or hogs or housed in an area
vaccinated.2,7 The preferred site for vaccination is inside where confirmed Leptospira abortion is a problem in
the ear pinna or beneath the tail.1 The skin is lightly scar- other species.7 Pinkeye in goats is usually caused by My-
ified, and the virus suspension is applied. Scabs appear at coplasma and Chlamydia and no vaccine is currently avail-
the vaccination site within 1 to 3 days and indicate suc- able to prevent this condition. Moraxella bovis, a causative
cessful immunization. Persons exposed to the vaccine can organism of pinkeye in cattle, can rarely cause keratocon-
become infected. Proper precautions such as wearing junctivitis in goats. Therefore cattle pinkeye vaccine is of
gloves during vaccine administration and properly dis- little benefit in goats. No rabies vaccine is approved for
posing of vaccine containers reduce human health risks. use in goats in the United States. Vaccination of valuable
Vaccines can cause severe lesions in humans if they are breeding stock or pets with a killed vaccine approved for
accidentally self-injected. sheep is advisable in endemic areas.1
 Chapter 17 Flock Health • 425

Some cattle respiratory vaccines are occasionally used from the first week of life to promote rumen develop-
by goat producers and veterinarians. The efficacy of these ment. Adult bucks and wethers should be fed a ration
vaccines and their value in reducing respiratory disease similar to one that is appropriate for nonpregnant, non-
complex for goats are questionable. Bovine K99 Esche- lactating does. Bucks should be on urinary calculi preven-
richia coli vaccine has been demonstrated to produce in- tion programs. Body condition scores can be used to
creased K99-specific antibodies in doe serum and colos- monitor the long-term energy intake of goats. Because of
trum. However, confirmation of K99 E. coli in outbreaks their curiosity and browsing habits, goats are exposed to
of kid diarrhea is currently limited.1 toxic plants but are not likely to eat fatal quantities of any
given plant. However, when feed supply is scarce, they are
at risk of toxicity. Also, confined goats may be at higher
Nutritional Management risk of consuming anything within their reach, including
Based on body size, goats have larger nutritional require- toxic plants.
ments than other ruminants. They have an almost unique
browsing and foraging ability and consume a wide variety
of grass, legume, weed, and browse species as food.12
Production Management
Goats seem to prefer about 50% browse, 20% grasses and In dairy goat operations the monitoring of milk and udder
legumes, and 20% forage in their diets. Good-quality health is an important aspect of production management.
grass forage and minimal grain feeding with a trace Complete animal records are important for both dairy and
mineral and salt supplement and fresh water is generally fiber-producing goat operations. Records can be kept on
sufficient to meet most nutritional requirements of goats, individual animals by a card file or computer system. Dairy
particularly those kept as pets.1 Dairy goats with high Herd Improvement Association (DHIA) records should
genetic potential for milk production benefit from rela- be kept for dairy goats, both for individual animals and the
tively high levels of grain feeding during early lactation. herd as a whole. Animal identification is imperative if in-
Does in late gestation and early lactation and breeding dividual animal records are to be kept. Dairy goats are
bucks also may benefit from the feeding of concen- usually identified by neck tags and/or ear tattoos. Plastic
trates, particularly if forage quality and quantity is poor. ear tags are more commonly used in meat goats.
However, excessive grain feeding can result in health
problems. The likely cost benefit of feeding grain to some
meat goats, with respect to feed-induced health prob-
Facilities
lems, is not sufficient to warrant this practice. The most important aspect of facility management for
Flushing, or increasing the feed intake of does 3 to 4 most types of goats is fencing. The two goals of a fence are
weeks before and during the breeding season, increases to keep goats in and predators out. Both of these goals are
the ovulation rate, particularly in animals of moderate very difficult. A 6- by 12-inch woven wire, 48-inch tall
body condition. Flushing can be accomplished by provid- fence is the most suitable perimeter fencing for horned
ing high-quality pasture free choice, supplement grain goats. Electric fencing also can be used for the perimeter
feeding, or creep grazing pasture. Pregnant does should or for cross-fences. Ease of handling requires the use of
receive supplemental feed 4 weeks before and after working pens. Furthermore, goats require some shelter
kidding. Over- or under-conditioning can predispose from inclement weather, especially at or around kidding or
females to pregnancy toxemia. Free access to legumes after shearing (especially for Angora goats). Shelters
should be limited during the final trimester of gestation provide shade in summer and protect animals from wind,
(particularly in dairy goats) to prevent excessive calcium rain, and snow in winter. Goats tolerate cold weather
intake, which can predispose to milk fever.1 Pregnant rather well as long as they are dry and can move out of the
animals in selenium-deficient areas should receive dietary wind.
supplementation or vitamin E and selenium injections Feeders are necessary for supplemental feeding of
during the final months of pregnancy. A complete, loose, grain or concentrates and for allowing free access to min-
trace mineralized salt containing selenium should be erals. They should be constructed in such a way that goats
offered free choice year-round to all goats. Salt and/or cannot lay or defecate in them. A feeder space of 1.5 to 2
mineral blocks designed for cattle may not be suitable for feet per adult goat will usually suffice. Goats prefer fresh,
goats, particularly in deficient areas or for growing or lac- clean water and should have access to a constant supply.
tating goats. Predator control should never be overlooked, particularly
Proper feeding of colostrum is crucial to the health for pastured meat or pet goats. Guard dogs (Great Pyre-
and survival of the kid. Properly treated, slow-pasteurized nees) are commonly used, but donkeys and llamas also
colostrum should be used in dairy herds for CAEV have predator control value. These other herbivores may
control. If goat colostrum is not available, heat-activated become goat companions (i.e., llamas, donkeys).
cattle colostrum can be used. A creep feeding starter Goats should be separated into groups based on pro-
ration and good-quality hay should be provided to kids duction status. Males should be separated from females,
426 • Sheep and Goat Medicine
and females of breeding age should be maintained North America. However, the peak breeding season of
separately from other animals. Meat goat kids should be October through December results in kidding in January
kept in a “grow-out” group. Stocking rates for meat goats through March. The transition periods are approximately
are around six to eight adults per adult cow/calf unit. As 2 months before and after the breeding season. The
many as 10 adult goats can be maintained on the same “deepest” anestrous period is April through May.13
land required to feed a cow and her calf, if the land is pre- Dairy goats are generally not expected to kid more
dominately browse. Although many space requirements than once per year because of selection for 10 months of
have been suggested, one of the authors (Dr. Pugh) rec- lactation. They frequently have numerous offspring and
ommends for 55- to 110-lb (25- to 100-kg) goats that a low neonatal mortality because of the intense rearing
minimum of 15 square feet (if kept alone) to 11.5 square practices under which they are kept.7 Selective hand-
feet (if kept in groups of five or more) should be made mating or artificial insemination is the usual breeding
available. Goats weighing less than 60 lb should be practice in dairy goats.
allowed a minimum of 10 square feet (if kept alone) or Goals for reproductive efficiency in meat goats include
7.5 square feet (if kept in groups of five or more), whereas high fertility (greater than 90%), optimal litter size (1.5 to
goats weighing more than 50 lb should have 20 square 2 kids), high survival to weaning (more than 90%), and
feet of space (if kept alone) or 15 square feet (if kept in kidding intervals of less than 12 months. Establishing the
groups of five or more). Overstocking predisposes the time of mating marks the commencement of the annual
herd to losses from parasites, poor pasture forage produc- production cycle. It can be calculated based on the desired
tion, and greater production costs. Pasture rotation is es- date of parturition in a given region to take advantage of
sential for the profitable farm. good spring pasture. The bucks should be left with does
Unproductive animals should be identified and culled. for 32 days (one and a half reproductive cycles), resulting
Does that fail to conceive, fail to carry their kids to birth, in kids being born within a month. This short kidding
or fail to raise kids to weaning and those that produce period should produce a uniform kid crop and streamline
kids with genetically undesirable traits should be culled. weaning and other herd health management practices.
Any buck that fails to aggressively seek out and breed After 32 days with the does, the bucks’ job is finished
females should be culled. Herd improvement can be ac- for the year. Pregnancy diagnosis 45 to 60 days after
complished by focusing on increasing kidding percentage buck removal is an important component of reproductive
and rate of growth. management.
Finally, biosecurity is at the heart of a herd health Controlled accelerated kidding programs (three kid
program. Denying disease-causing organisms access to crops every 2 years) require out-of-season breeding.
the herd is more economical than attempts at elimina- Proper nutrition, intense management, early weaning,
tion. Biosecurity can be achieved by buying goats from and some hormonal manipulation are required for such
herds free of contagious disease, performing pre-purchase programs to be successful. If enhanced production is the
examinations, testing for disease, instituting on-farm aim of the breeding program, at least 20% of the breeding
quarantine for a minimum of 30 days, retesting during females should be replaced annually. The kidding per-
quarantine, providing treatment with antibacterial agents centage can be increased by retaining female replace-
and anthelmintics to address subclinical carrier states, ments that are twins and the daughters of twins. Selec-
and immunizing incoming goats against certain diseases.2 tion of highly fertile males also contributes to the
Excellent immunity should be maintained in the nucleus attainment of this goal.
herd by routine vaccination, deworming, and proper
dietary intake in case of a breakdown in biosecurity.
Parasite Control
GI nematodes are the most serious problem affecting goat
Reproductive Management production worldwide.14,15 Economic losses caused by GI
Efficient reproductive management is essential to the nematodes are related to decreased production, costs for
profitability of a goat enterprise. Reproductive manage- treatment and prophylaxis, and animal death. Effective
ment of goats in the United States has focused primarily control of internal parasites of goats is one of the most dif-
on milk and fiber production systems. However, the intro- ficult challenges facing the veterinary practitioner. The
duction of exotic meat goat breeds (South African Boer, major GI nematode of fiber and meat goats is Haemonchus
New Zealand Kiko) is encouraging a greater emphasis on contortus (barber’s pole worm).7,16,17 In dairy goats, several
reproductive management to increase the number of off- other GI nematodes such as Ostertagia, Trichostrongylus,
spring born and weaned.13 The production of out-of- and Nematodirus species may significant in certain geo-
season kids and milk is desirable to take advantage of graphic areas.7,14 In addition to Haemonchus infestation,
market premiums. Goats are seasonally polyestrous, but coccidiosis can be a major problem in recently weaned
some degree of breed-specific variation does exist. The meat and dairy kids.17 GI nematodes have similar life
natural breeding season is August through March in cycles. Haemonchus thrives in warm, moist conditions. The
 Chapter 17 Flock Health • 427

survival time of the infective stage is short during hot BOX 17-2
summers (30 to 60 days) and prolonged during the winter
(4 to 8 months).17 The degree of infestation varies with the
management system employed. Goats kept in dry lots
AS R UMMARY ECOMMENDATION FOR
(e.g., dairy goats) may have minimal problems with GI
nematodes. Kids grazing on range land pastures seem to be
P C
ARASITE ONTROL*

less affected by coccidiosis, but in confined quarters they 1. Make certain that the anthelmintic or
are very susceptible to infestation. Meat goats grazing land combination of anthelmintics used on the farm
with adequate brush and tall weeds suffer little exposure to actually works (kills at least 90% of the variable
infective parasitic larvae. These browsing goats develop worms). Check for resistance with fecal egg
little immunity and are highly susceptible to infection if counts before and after deworming.
they then graze infested pastures. Parasite infestation may 2. Use strategic deworming. Deworm the flock
be insignificant in dry years and in certain range land while the parasites are in hypobiosis and are
areas. Parasites are a continual problem in moist, temper- being transmitted at low levels (i.e., the winter).
ate areas.7 Haemonchus has the ability to undergo hypobio- This reduces the frequency of exposure to
sis, or become metabolically inactive, within the host deworming products.
during adverse weather conditions.17 This dormancy 3. Employ pre- and post-birthing deworming
results in better parasite survival and increased transmis- starting 1 month before birthing at 2- to 4-week
sion from spring to fall. Implementation of a control intervals and ending 2 to 4 weeks after the final
program for GI parasites of goats requires a working lamb or kid is born.
knowledge of the important parts of their life cycle. 4. Tactical dewormings (based on increased levels
Prevention, rather than cure, is the philosophy used in of parasite eggs or 10 to 14 days after rainfall)
developing control programs against GI nematodes. It enhance the effectiveness of a parasite program.
must be assumed that “worms” cannot be eradicated but 5. Use clean or safe pastures when possible: the
may be limited to the point where they do not cause aftermath of crops, annual forage, and rotational
serious economic loss to the producer.16,17 A combina- grazing or co-grazing with cattle or horses.
tion of management and treatment is necessary to achieve Permanent Pastures Promote Parasites.
control. Feeding practices that decrease stocking rates 6. Deworm new animals and place them in a non-
and lessen pasture contamination help minimize parasite pasture environment such as a dry lot or barn
infestation. Drought, inclement weather, and lack of ade- after treatment for as long as 72 hours before
quate forage (or pasture) may increase animal concentra- moving them to a safe pasture.
tion and encourage parasitism. Therefore, when animals 7. Rotate anthelmintics yearly if effective drugs
are fed supplemental feeds, owners should take care to are available.
minimize the intake of nematode larvae. Feeders that 8. Do not under-dose animals. Dose for the
minimize fecal contamination of feedstuffs should be heaviest animal in a group.
used. Feed should never be placed on the ground.14 Goats 9. Identify and select individuals resistant to
flock together and tend to bed down in the same place internal parasites.
nightly. This allows a heavy parasite population to
develop in concentrated areas. Several approaches for the
*The reader is encouraged to review more in-depth recommendations
use of anthelmintics in control regimens are summarized in Chapter 4.
in Box 17-2.
Few dewormers are approved for goats in the United
States, but extra-label use of anthelmintics designed for used are effective. This can be accomplished by a fecal egg
cattle is not uncommon.18 Dewormers and coccidiostats count reduction test. Fecal samples are collected on the
used in goats are listed in Tables 17-1 and 17-2, respec- day of deworming and 10 to 14 days later. McMaster’s
tively. Anthelmintics should only be administered orally floatation (see Chapter 3) is performed on both samples,
to goats. Clinicians and owners should keep in mind that and the numbers of parasite eggs per gram (EPG) are
anthelmintics may be metabolized at different rates by compared. If the drop in EPG is less than 90%, an-
goats than by cattle or sheep. Unless a dose has been es- thelmintic resistance is present and the animals should be
tablished for goats, the animals should generally receive a switched to another class of dewormer.16 Assessment of
dose 1.5 times larger than that given to sheep.16 Effective fecal egg count is a valuable tool for parasite control pro-
anthelmintics should only be used for approximately 1 grams in goats. A McMaster’s EPG count of 500 to 1000
year before rotation to another class of dewormer. in the spring or early summer or more than 2000 in the
Because of the increasing resistance of parasites to ant- fall suggests serious infection. Regular egg counts help
helmintics, goats must be examined after deworming so the veterinarian determine when animals are to be de-
clinicians and owners can determine whether the drugs wormed. Perhaps the most overlooked component of a
428 • Sheep and Goat Medicine
BOX 17-3

G ENERIC M ANAGEMENT C ALENDAR FOR S PRING K IDDING AND L AMBING

January Evaluate range and forage conditions; monitor body condition of does and ewes and supplement
if necessary; ensure adequate intake of minerals, salt, and water; vaccinate during the final
month of gestation for clostridial disease and any other endemic diseases.
February Begin supplemental feeding of pregnant females and consider pre-birthing shearing; begin
birthing; check teats for milk and identify lambs and kids; ensure lambs and kids ingest
adequate colostrum; institute pre- and post- birthing strategic deworming; maintain an
ionophore in feed or mineral mixture before and after birthing to decrease Coccidia
contamination of pasture.
March Separate singles from twins; confine and feed females with their lambs and kids as needed; feed
does and ewes to maintain milk production; continue strategic deworming program.
April Continue to feed a supplement to lactating does and ewes; monitor for parasites.
May Wean small, stunted lambs and kids; discontinue supplemental feeding of does and ewes;
monitor internal parasites (with fecal samples and McMaster’s).
June Continue parasite control program.
July Monitor internal parasites; watch for signs of heat stress; wean lambs and kids.
August Continue parasite control program; continue weaning lambs and kids and supplement
replacement does, ewes, bucks, and rams; select replacement males and females; evaluate and
cull unsound and inferior animals; perform breeding soundness evaluation of males. Criteria
for culling include the following:
• Poor or slow growth
• Barren females (missed one season)
• Unsound teats or udders (too big or too small)
• Poor dentition
• Structural defects (feet, leg, or back abnormalities)
• Testicles that are small or soft or have other abnormalities (animal fails a breeding
soundness evaluation)
• Unthriftiness (caused by old age or chronic disease)
September Begin supplemental feeding of females and males on fresh green pasture with 1⁄2 lb
feed/head/day for 2 to 3 weeks before and after males are placed with females; continue
parasite control program.
October Begin breeding; maintain good male-to-female ratio, depending on pasture size and conditions;
continue supplemental feeding of females for 2 to 3 weeks after start of breeding season.
November Evaluate range and forage conditions; determine females’ body condition and plan winter
supplemental and feeding program; control internal and external parasites; remove some of
males’ feed to regain body condition; determine pregnancy status and number of fetuses.
December Watch body condition of does and supplement feed if needed; monitor internal and external
parasites.
 Chapter 17 Flock Health • 429

7. Bretzlaf K: Production medicine and health programs for goats. In

TABLE 17-1 Howard JL, editor: Current veterinary therapy in food animal prac-
tice, ed 3, Philadelphia, 1993, WB Saunders.
ANTHELMINTIC PRODUCTS AND DOSAGES* 8. East NE: Vaccination programs for sheep and goats. In Smith BP,
editor: Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
ACTIVE AGENT DOSAGE ROUTE
9. Council on Biologies and Therapeutic Agents: Vaccination guide-
lines for small ruminants, J Am Vet Med Assoc 205:539, 1994.
Albendazole 10 mg/kg PO
10. Mobini S: Infectious causes of abortion in the goat. In Youngquist
Doramectin 0.3 mg/kg PO
B, editor: Current therapy in large animal theriogenology, Philadel-
Eprinomectin 0.5 mg/kg PO phia, 1997, WB Saunders.
Fenbendazole 10 mg/kg PO 11. Wiedmann M et al: Molecular investigation of a listeriosis out-
Ivermectin 0.3 mg/kg PO break in goats caused by an unusual strain of Listeria monocyto-
Levamisole 8 mg/kg PO genes, J Am Vet Med Assoc 215:369, 1999.
Morantel tartrate 10 mg/kg PO 12. Terrill T: Grazing habits and diet selection of goats, Proceedings of
Moxidectin 0.5 mg/kg PO the Symposium on Meat Production from Goats in Georgia, 1998, Fort
Oxfendazole 10 mg/kg PO Valley, GA.
13. Mobini S: Reproductive management in goats, Proceedings of the
*See also Appendix I. North American Veterinary Conference, 2000, Orlando, FL.
14. Pugh DG, Mobini S, Hilton CD: Control programs for gastroin-
testinal parasites in sheep and goats, Comp Cont Ed Pract Vet,
TABLE 17-2 20(4):S112, 1998.
15. Miller JE: Parasites affecting goats in the Southeast, Proceedings of
COCCIDIOSTATS FOR USE IN GOATS the Conference on Goat Production Market Opportunity South, 1995,
FOR HERD PROBLEMS Baton Rouge, LA.
16. Craig TM: Control of gastrointestinal nematodes of sheep and
CHEMICAL NAME TRADE NAME DOSE goats in North America, Proceedings of the American Association of
Small Ruminant Practitioners Symposium on the Health and Disease
Amprolium* Corid 42 g/100 gallon water of Small Ruminants, 1996, Nashville, TN.
Monensin† Rumensin 15 to 20 g/ton of feed 17. Craig TM: Goats—condominiums for parasites: What should a
producer do?, Proceedings of the Fourteenth Annual Goat Field Day,
Lasalocid Bovatec 25 g/ton of feed
1999, Langston, OK.
Decoquinate† Decox 27 g/ton of feed
18. Mobini S: Practice tips related to medications in goats, Proceedings
*Do not use for more than 28 days. of the North American Veterinary Conference, 2000, Orlando, FL.
†Approved for use in goats in the United States.

well-managed parasite control program is the identifica-

SHEEP
tion and selection of parasite-resistant goats or at least Many of the herd health protocols and basic ideas dis-
animals that are apparently less susceptible. Individuals cussed in the section on goats are applicable for sheep
with the lowest EPG in a herd may have the most resis- flock health. Each chapter of this book also describes
tance.16 A generic herd health program is provided in health care practices that are applicable for sheep. There-
Box 17-3. fore the following section is an abbreviated discussion of
flock health. A generic herd and flock health program is

R EFERENCES
1. Smith MC, Sherman DM: Goat medicine, Philadelphia, 1994, Lea
provided in Box 17-3.

Definition of Flock Health

& Febiger.
2. Olcott BM: Production medicine and health problems in goats. In Flock health programs target the production groups and
Howard JL, Smith B, editors: Current veterinary therapy in food needs present in an operation throughout the year. Al-
animal practice, ed 4, Philadelphia, 1999, WB Saunders. though flock health programs focus on populations of
3. Mobini S: Herd health management practices for goats, Vet Tech J animals, the needs of individual sheep are not intentionally
16:238, 1995. ignored. Instead, they are better addressed through proac-
4. Pugh D: Small ruminant medicine and nutrition, Proceedings of the
tive approaches. Because the demands of various stages of
Southern Georgia Veterinary Medical Association, 1999, Fort Valley,
production are anticipated and addressed, the sheep are
GA.
5. Mobini S: Herd health management practices for meat goat pro-
better off than those in a flock that does not have a well-
duction, Proceedings of the Southeast Region Meat and Goat Produc- timed and well-thought-out health program in place. The
ers Symposium, 1996, Tallahassee, FL. aim of a flock health program is to improve the overall
6. Rings DM: Basic neonatology, Proceedings of the American Veteri- health and welfare of the flock, including decreasing
nary Medicine Association, 1999, New Orleans, LA. losses from disease. Successful programs increase both the
430 • Sheep and Goat Medicine
productivity and the profitability of the flock. The use and can review strategies to prevent disease such as vaccinating
analysis of production, health, and financial records are the against clostridial diseases 4 weeks before lambing and
best ways to gauge the success of the program. Flock providing a clean environment. The management plan at
health programs vary in their intensity because different lambing time, including the layout and use of facilities, also
breeds of sheep, production levels, and environments should be reviewed. This plan should include a component
dictate different approaches. Regardless of the approach to educate personnel to recognize when intervention is
used, flock health programs should include a written com- needed for lambing problems.
ponent that addresses the whole year at a time. Minimum standards and target production parameters
Flock health programs are developed for multiple uses. for morbidity, mortality, culling, and growth rates should
They may be used by an individual operation or incorpo- be set. Box 17-4 provides a list of target production pa-
rated into operations for the control and eradication of rameters. At this time a quality assurance program should
specific diseases either by voluntary or mandatory coop- be designed for the flock. To date, the sheep-packing in-
eration with state and federal animal health officials. Pro- dustry has not required producers to participate in flock
grams used by individual operators are generally planned quality assurance programs, but such programs exist and
annual approaches that address the following: will become more common in the future as a result of
consumer demand. Quality assurance programs educate
• Prevention of common disease conditions through
producers in good production practices. They encourage
the use of appropriate vaccination schedules
cooperation between practitioners and area producers for
• Management strategies that minimize risk factors
the betterment of the operation and the sheep.
for disease occurrence
• Provision of appropriate levels of nutrition for the
stage of production Biosecurity Aspects of Flock Health Programs
• Assessment of metabolic status and productivity
Biosecurity programs are geared to control infectious
In order to provide correct advice the veterinarian disease. They include management steps to reduce the
must have a sound knowledge base regarding the sheep likelihood of introduction of a new disease from an exter-
industry and the individual production system. The client nal source. Another benefit of a biosecurity program is
and veterinarian should work out the details of a record- that it reduces the spread of infectious disease already
keeping system. present in the flock. Scientifically sound approaches re-
Veterinary visits are usually timed to occur with garding the introduction of new sheep into a flock are re-
major production events (e.g., before breeding; in mid- quired to prevent the introduction of new diseases into
pregnancy; before, during, and after lambing; in mid- the resident sheep population. Practical biosecurity pro-
summer). During the first visit the veterinarian assigns a grams include purchasing animals directly from the farm
body condition score to the ewe flock. He or she then of origin, transporting them in clean and disinfected
makes nutritional and feeding management recommenda- transport vehicles, housing them in true isolation facili-
tions to optimize the ovulation rate at breeding. Evaluation ties while following practical isolation practices for 1
of the rams should include a physical and fertility examina- month, and regularly observing for conditions such as
tion (see Chapter 6). A written record should indicate the pruritus, lameness, external lumps, and unexplained
ram’s body condition score and weight, problems identified weight loss. In addition, isolated sheep should be started
on the physical examination, an action plan to address any
problems that are crucial to breeding, and whether the ram
passed or failed the fertility examination. The mid- BOX 17-4
pregnancy visit primarily focuses on ultrasound pregnancy
determination and fetal counting and aging. Based on
these results the veterinarian can develop a plan to feed the
P RODUCTION T ARGETS
ewes appropriately and economically based on fetal
numbers and stage of pregnancy.This visit can be crucial in Pregnancy
preventing metabolic disease in late pregnancy and assist- Ewes More than 95%
ing the farmer in making the operation profitable.The pre- Ewe lambs More than 75%
lambing visit entails a review of the nutrition of the late- Visible abortion Less than 5%
gestation ewe so that she can perform up to her genetic Lambing
potential at lambing. Properly fed ewes produce maximal Ewes More than 90%
amounts of colostrum and milk, give birth to thrifty lambs Ewe lambs More than 70%
without difficulty, and demonstrate excellent mothering Stillbirths Less than 2%
abilities. The final 2 months of pregnancy are crucial to Weaning More than 95%
successful lamb rearing. During this visit the veterinarian
 Chapter 17 Flock Health • 431

on the flock’s regular vaccination program, dewormed immunization program. A generic vaccination program
with an effective anthelmintic, and have their feet for sheep is provided in Box 17-5. It can be modified for
trimmed and visually inspected for footrot. Even before the individual farm.
performing a visual examination and obtaining the
history of the flock of origin, the producer or clinician
may wish to give them a foot bath for 15 minutes in a
Internal Parasite Control Programs
10% solution of zinc sulfate. During isolation the sheep Programs that control internal parasites must be tailored
may be serologically tested for diseases of concern to to the region of the country where the flock resides. The
the buyer. If the sheep were tested for various diseases program also must take into account whether the flock is
before purchase, the buyer should request the official test confined or pastured. The epidemiology of pathogenic
forms and results to check the results and test dates. sheep nematodes and protozoan species depends on the
Wherever practical, sheep should be thoroughly exam- climate of the region. Successful programs implement
ined for obvious clinical manifestations of contagious or regular monitoring of the efficacy of anthelmintics,
infectious diseases such as sore mouth, pinkeye, external sheep-friendly handling equipment for anthelmintic de-
parasites, caseous lymphadenitis, scrapie, footrot, straw- livery such as well-designed pens and chutes, and use of
berry footrot, and dermatophilosis. automatic syringes and/or drench guns. Other compo-
nents of a parasite control program include the use of
Vaccination Programs
Through regular and correct usage, vaccines are designed BOX 17-5
to reduce the incidence and/or severity of a specific
disease. Few vaccines can completely prevent disease.
However, when used properly, their beneficial effects
B V
ASIC ACCINATION P ROGRAM FOR S HEEP
far outweigh their drawbacks. Local veterinarians can
PREGNANT EWES
provide advice on prevalent diseases that are preventable
• In endemic areas, vaccinate ewe lambs or
by vaccination. Farms in different areas have different
needs. The local veterinarian should work with the pro- previously vaccinated animals against
ducer to design a farm-specific vaccination program for Campylobacter and Chlamydia abortion in mid-
ewes, young lambs, market or feedlot lambs, replacement gestation.
breeding stock, and rams. His or her knowledge of preva- • Vaccinate for Clostridium species (C.
lent diseases in the area and diagnostic laboratory data are perfringens type C and D, C. novyi, C. sordelli,
the best bases for developing a vaccination program. C. chauvoei, C. septicum, C. tetani) in the last
Vaccination should proceed according to label direc- month of pregnancy.
tions because the timing of doses is crucial to optimal • Repeat Chlamydia and Campylobacter
protection. vaccinations for previously unvaccinated
Clostridial diseases are the only universal group of animals and give yearly booster to other ewes
diseases that all sheep should be vaccinated against. Deci- 2 to 4 weeks after birth.
sions regarding the inclusion of other vaccines in an indi- LAMBS
vidual flock health program should be based on knowl- • Immunize lambs from immunized dams at 1
edge of prevalent diseases in the area and the needs of the to 2 months for Clostridium species (C.
particular flock. In areas where a disease is known to perfringens type C and D, C. novyi, C. sordelli,
occur but no vaccine is available, risk factors for that C. chauvoei, C. septicum, C. tetani); repeat
disease should be controlled with proper management. immunizations in 3 to 4 weeks.
Sheep that are frequently exhibited are at greater risk of • Immunize lambs from nonimmunized dams
contracting contagious and infectious diseases. For this at 1 to 3 weeks for Clostridium species (C.
reason they should be vaccinated against more diseases perfringens type C and D, C. novyi, C. sordelli,
than sheep in a closed flock. C. chauvoei, C. septicum, C. tetani); repeat
Other diseases that have a labeled sheep vaccine avail- immunizations twice at 3- to 4-week
able in the United States include some infectious causes intervals.
of abortion such as Campylobacter species and Chlamydia
psittaci; multisystemic diseases such as caseous lymph- Rams and yearlings can be vaccinated at the
adenitis, musculoskeletal diseases such as footrot, neuro- same time as ewes, with an emphasis on Clostridium
logic diseases such as rabies, and integumentary diseases species. Vaccines against rabies and leptospirosis
such as sore mouth. If past history indicates that the flock may be given in endemic areas.
is at risk of a disease, such vaccines can be included in an
432 • Sheep and Goat Medicine
multiple measures to minimize the buildup of nematode (see Chapter 2). If target scores are not achieved, the pro-
eggs on pasture; this can be achieved by deworming ewes ducer and veterinarian need to determine why and make
with larvicidal doses during winter housing, 4 weeks after appropriate management changes. If the correct changes
spring turn-out, and 3 weeks into lambing. Control also are implemented, future scores should reflect improved
is enhanced by the use of management practices that production.
reduce reliance on chemical anthelmintics such as grazing If mortality rates exceed targets, representative sheep
clean ground with weaned lambs, “vacuuming” nematode should be necropsied. Gross findings can be clarified
eggs by grazing the previous year’s sheep pastures with by ancillary laboratory-based tests, if necessary. Fortu-
cows or horses, and selecting for and breeding nematode- nately, common sheep diseases that affect production
resistant sheep (see Chapter 4). are often straightforward to diagnose based on gross
When circumstances dictate that the flock graze close necropsy findings.
to the ground and nutritional input is marginal, nema-
tode infestation may accelerate and clinical parasitism in
stressed sheep is likely. The veterinarian and producer
Culling Practices
should develop an annual calendar that details the entire Culling practices should be based on genetics, productiv-
flock health program. The producer should record details ity, poor fertility, substandard growth, parasite and disease
about any procedures performed on the production susceptibility, and disease (e.g., footrot, caseous lymph-
groups. Box 17-2 summarizes recommendations to adenitis, scrapie, ovine progressive pneumonia). Not all
improve parasite control. Tables 17-1 and 17-2 show sick or thin animals survive to the point of culling. Each
some commonly used anthelmintics and coccidiostats, operation must have a plan for carcass disposal. Carcass
respectively. disposal procedures should be legal in the area and state,
environmentally friendly for the size of the animal and
number of carcasses, and practical for the producer. Many
External Parasite Control Programs states legally permit sheep composting (Box 17-6). A
Keds and biting lice are the prevalent external parasites sheep of any size will turn into compost if the procedure
of sheep. Many sheep flocks have not introduced these is done correctly. Sheep composting fulfills the previously
parasites. In these flocks, all newly purchased sheep described criteria. Some diseased carcasses may by law
should be treated prophylactically while they are in isola- require incineration (e.g., scrapie, foot-and-mouth disease).
tion to prevent parasite introduction. In flocks where
either parasite is endemic, all sheep on the property
should be treated at the same time so that one group does
Neonatal Care
not serve as a reservoir for reintroduction. Treated sheep The phrase “sip, dip, strip, and clip” regarding manage-
should be kept out of any contaminated buildings for 2 ment of the newborn lamb is sound advice for beginning
weeks because buildings also can serve as reservoirs and advanced clinicians and owners alike. A practitioner
during this time. Further treatments should not be neces- should strip the wax plug from the teat so the lamb can
sary after the whole flock is properly treated. The flock sip colostrum, as well as clip and dip the umbilicus in 7%
should be monitored for ectoparasite infestation after iodine or another antiseptic or astringent (e.g., solutions
reintroduction from carrier sheep or improperly applied of chlorhexidine, povidone iodine). Owners and practi-
whole flock treatment. An external parasite control tioners should be able to recognize normal maternal and
program is described in Chapter 8. neonatal behavior as well as normal appearing and func-
tioning mammary glands. The recognition of normal
traits and conditions allows abnormal ones to be detected
Flock Health Monitoring and dealt with appropriately. Equipment and facilities
Program records should include a flock inventory divided should be prepared and organized before the start of
into production groups: lambing. Records to guide improvements in management
should be kept and used. Regardless of whether animals
• Ram-to-ewe ratios at breeding
are raised in confinement or on pasture, periparturient
• Pregnancy rates
ewes should be grouped together based on expected
• Lambing percentages
lambing dates and fetal numbers, if available. These
• Ewe and ram mortality numbers and reasons
groupings enable tailored levels of feeding, which are eco-
• Pre- and post-weaning lamb mortality rates and
nomically justifiable, minimize the occurrence of meta-
reasons
bolic disease, and prevent fetal under- or over-nutrition.
• Ram morbidity and treatment outcomes (especially
The result is the birth of more viable lambs. When lamb
those that pertain to breeding use)
losses occur, representative cases should be necropsied by
The average body condition score of the ewe flock the local veterinarian and management changes should be
should be recorded at breeding, lambing, and weaning based on the necropsy findings.
 Chapter 17 Flock Health • 433

BOX 17-6 sheep or those with abscesses or mastitis, foot trimming,

and deworming. All procedures need to be considerate of
S HEEP OR G COAT OMPOSTING
the sheep and the shearers. Freshly trimmed feet can lac-
erate a shearer if the sheep kicks. The owner should be
encouraged to be present at shearing, listen to the shear-
• A 5– to 10–square foot enclosure or container ers’ observations, and consider this information in con-
makes a good composter. The sides (e.g., junction with other professional opinions. Pre-lambing
corrugated wire, fine wire mesh) should have shearing of ewes may decrease the incidence of pregnancy
enough holes to allow for maximal airflow during toxemia, improve the desire of the ewe to seek shelter on
the composting process. cold days (with the resultant moving of lambs to warm,
• The composter should be placed separate from the dry environments), decrease the maintenance require-
flock but in an area where water is easily attainable ments of the ewe (because of less fleece weight), and
to keep the composted material moist. All runoff enhance the likelihood that newborns will nurse the
should be kept out of the flock’s water supply. udder instead of the ewes’ wool.
• The carcass, aborted material, or offal should be Most small flock facilities lack a permanent shearing
placed in the composter so 1 foot of sawdust set-up. Therefore many shearers shear on sheets of
separates it from the ground and the sides. The plywood or pieces of indoor/outdoor carpet that they
carcass should then be covered with 1 to 1.5 feet carry in their trucks and use every day on numerous
of sawdust. Approximately 1 cubic foot of farms. Owners should provide their own shearing sur-
sawdust is required for every 10 lb of carcass faces instead of using surfaces that have been on many
weight. Green or freshly cut sawdust is superior farms and can transmit bacteria, fungi, and even viruses.
for composting.
• Water should be added to attain a water-to–dry
matter ratio between 50:50 and 60:40. During Foot Care
very rainy seasons, the composter should be Part of the annual care of sheep should include assessment
covered to prevent excessive water accumulation. of the condition and length of their hooves. Depending on
• A 2- to 4-foot-long thermometer should be the terrain and rainfall in the area, some flocks do not
placed into the stack and the temperature require annual foot trimming, but most flocks in the Mid-
monitored. The temperature should be maintained western and eastern regions of the United States do. The
at 130° F for 1 week to destroy most pathogenic timing of this procedure is not important as long as the
bacteria. If the composter’s temperature drops feet are not allowed to grow long and predispose the
below 100° F, water should be added and the animals to other foot problems such as toe abscesses and
material aerated (i.e., stirred, forked). footrot. Many farm flocks trim the ewes’ feet around
• The material can be safely placed on the pasture lambing time while they are in confinement and being
after 21 to 30 weeks. However, in the case of handled regularly. Many range flocks only require foot
animals dying of scrapie, the owner should notify trimming of a few individual animals. Many sheep wear
local, state, or federal authorities and follow their their feet down adequately on dry, rough terrain, and some
guidelines (e.g., incineration). breeds are predisposed to slower foot growth. Rams should
have their feet trimmed 4 to 8 weeks before breeding.
Adapted from Estienne MJ: Disposing of dead goats, Practical Goat Their feet should definitely not be trimmed in the week
Farming Seminar, 1998, Salisbury, MD (http://www.sheepandgoat. before the start of breeding in case overzealous trimming
com/compost.html).
causes temporary lameness. A generic footrot prevention
program is provided in Box 9-1.
Shearing Management
Shearing is the most stressful experience for a sheep. The
Facility Design and Function
handling set-up should be designed so that handling stress Sheep housing should be designed and constructed for
is minimized. Many preventive health procedures are proper ventilation and efficient manure handling.
often performed at shearing. These include pre-lambing
vaccination against clostridial diseases, especially C. per-
fringens type C and D and C. tetani. Ewes should be vac-
Water Availability and Design
cinated against colibacillosis (where used) approximately Water is an essential nutrient of all ages of sheep. It
30 days before lambing on farms where previous neonatal should be palatable and readily available. Cleanliness,
lamb diarrhea cases are known or suspected to be caused taste, impurities, and temperature all affect palatability.
by pathogenic E. coli. Other procedures frequently per- Key times during which the quality of the water supply
formed at shearing include sorting out noncompetitive has a direct influence on the productivity or health of the
434 • Sheep and Goat Medicine
sheep include the lambing and finishing phase, late preg-
Specific Diseases Introduced by Carrier Sheep
nancy, and lactation (see Chapter 2). Sheep can carry and introduce into a flock a number of
diseases that are not visible to the naked eye. These
disease conditions include footrot, chlamydia, campy-
Role of Management in Maintaining Health lobacteriosis, and anthelmintic-resistant nematode infes-
The level of management determines the success and tation. In general, tests for these diseases do not exist or
sustainability of a farming operation. Excellent man- are not financially feasible for whole flocks. Therefore all
agers make most decisions correctly relative to the care animals introduced into the flock should undergo a com-
of their flock. Accordingly, the flock responds by meeting plete physical examination and be quarantined from the
target production goals. In today’s economic envi- rest of the flock for 21 to 30 days to minimize the intro-
ronment, sound management decisions are based on duction of new diseases.
a combination of records and observational subjective
findings.
 Appendix I

Cin ommonly Used Drugs

Sheep and Goats:
Suggested Dosages*
VIRGINIA R. FAJT AND D.G. PUGH

DRUG SHEEP GOATS

Acepromazine maleate 0.03 to 0.05 mg/kg IV1 0.03 to 0.1 mg/kg IV1,2
(see Chapter 16, Tables 16-1 0.05 to 0.10 mg/kg IM1 0.05 to 0.1 mg/kg IM1
and 16-2 0.2 mg/kg IM for tetany2
Acetic acid (5% solution) 0.5 to 1.0 L/head PO for ammonia
toxicosis3
Albendazole 5 mg/kg PO for nematodes and 7.5 mg/kg PO6
tapeworms4
7.5 mg/kg PO for flukes4
10 mg/kg PO for cestodes5
Ammonium chloride 0.5% of diet for prevention of urinary
calculi7
100 to 200 mg/kg PO BID to prevent
urolithiasis8
Ammonium molybdate 100 mg/head/day PO to prevent copper
toxicity9
20 mg/L in sole source of drinking
water to prevent copper toxicity9
100 mg/head/day PO for copper
toxicity10
Ammonium 3.4 mg/kg SC for 5 days to treat copper
tetrathiomolybdate toxicity9
50 to 100 mg/head PO twice weekly10
*Some of the drugs and uses listed in this appendix may be illegal, unavailable, or extra-label in the United States or other countries. It is the
responsibility of attending veterinarians to be familiar with the laws governing drugs in their practice areas. The clinician should be cognizant of
and take steps to reduce drug residues in food animals.
SC, subcutaneously; IM, intramuscularly; IV, intravenously; IP, intraperitoneally; PO, per os (orally); IU, international units; BID, twice a day; TID,
three times a day.
When no dosage was available for sheep or goats, a general “ruminant dose” was provided if available. If a dose is provided only for sheep and not
for goats, unless the drug appears to be contraindicated or toxic to goats, one of the authors (Dr. Pugh) usually extrapolates the sheep dose for use in
goats, or vice versa. Some of the anesthetic dosages listed here are the same as seen in Chapter 16 and are referenced as such. For anesthetics that
have different dosages, the clinician may choose to review the dosages listed in Chapter 16 and compare the two.
Continued

• 435 •
436 • Sheep and Goat Medicine
DRUG SHEEP GOATS

Amoxicillin–clavulanic acid 20 mg/kg IM or IV TID4 20 mg/kg IM or IV TID4

Amoxicillin trihydrate 10 mg/kg IM TID11 10 mg/kg IM TID11
Ampicillin sodium 10 to 20 mg/kg IV or IM BID11 10 to 20 mg/kg IV or IM BID11
Ampicillin-sulbactam 10 mg/kg IM every 12 to 24 hrs11 10 mg/kg IM every 12 to 24 hrs11
Amprolium 10 to 60 mg/kg orally in water or feed 25 to 40 mg/kg PO daily for 5 days for
once a day for 14 to 21 days to treat treatment; 5 mg/kg daily PO for 21
coccidiosis in lambs12 days for prevention14
100 to 200 ppm or 10 mg/kg/day in
water for 5 days for coccidiosis13
25 to 40 mg/kg PO daily for 5 days for
treatment; 5 mg/kg daily PO for 21
days for prevention14
Antivenin polyvalent 10 to 200 ml IV15
Aspirin 100 mg/kg PO BID2
Atipamezole (see Chapter 16, 0.125 to 0.2 mg/kg IV slowly 0.125 to 0.2 mg/kg IV slowly
Table 16-3)
Atropine 0.06 to 0.10 mg/kg IV to prevent 0.02 to 0.1 mg/kg IV to prevent
(see Chapter 16, Table 16-2) bradycardia during anesthesia16 bradycardia during anesthesia2,16
0.25 to 0.50 mg/kg (one fourth IV, then 0.25 to 0.50 mg/kg (one fourth IV, then
rest IM or SC) for organophosphate rest IM or SC) for organophosphate
poisoning17 poisoning17
Boldenone undecylenate 50 to 100 mg IM once (or repeat 50 to 100 mg IM once (or repeat
treatment in 3 weeks) for adjunctive treatment in 3 weeks) for adjunctive
therapy of anemia18 therapy of anemia18
Buprenorphine 6 mg/kg IV for 4 to 8 hours of pain
relief1
Butorphanol 0.05 to 0.50 mg/kg IM for sedation and 0.05 to 0.50 mg/kg IM for sedation and
analgesia16 analgesia16
Calcium borogluconate 50 ml of 20 mg calcium/ml solution IV, 60 to 100 ml of 20% to 25% solution for
50 ml SC to treat hypocalcemia19 hypocalcemia2
100 ml of 20% solution IV to treat
acute oxalate poisoning9
Calcium gluconate 1 g calcium ions/45 kg (50 to 100 ml of
10% to 23% calcium ion solution) IV
for hypocalcemia20
Carprofen 4 mg/kg SC for postoperative analgesia1
Ceftiofur sodium 1.0 to 2.2 mg/kg IM every 24 hours11 1.0 to 2.2 mg/kg IM every 24 hours11
21
Charcoal (activated) 0.5 kg PO for plant poisoning
2 to 9 g/kg PO15
Chloral hydrate No specific dosage for sheep or goats is
reported but 50 to 70 mg/kg IV is
reported for ruminants22
Chlorpromazine 0.55 to 4.4 mg/kg IV24 2.0 to 3.5 mg/kg IV24
24
2.2 to 6.6 mg/kg IM
Chlortetracycline 80 mg/head/day to reduce the incidence
of abortion caused by Campylobacter
fetus23
Cloprostenol 125 to 150 mg at 9- to 11-day interval for 125 mg for luteolysis and estrus
estrus synchronization25 synchronization26
150 mg IM for pregnancy termination27
2
Clorsulon 7 mg/kg PO for flukes 7 mg/kg PO for flukes2
 Appendix I Commonly Used Drugs in Sheep and Goats: Suggested Dosages • 437

DRUG SHEEP GOATS

Closantel 10 mg/kg PO for flukes and Oestrus

ovis4
Decoquinate 2 mg/kg orally throughout gestation to 0.5 mg/kg in feed for at least 28 days for
prevent abortion caused by Toxoplasma coccidiosis13
gondii28
100 ppm in complete feed for coccidiosis
control in lambs12
2 mg/kg PO during pregnancy to reduce
lamb mortality from toxoplasmosis29
0.5 mg/kg in feed for at least 28 days for
coccidiosis13
Detomidine 0.005 to 0.02 mg/kg IV for standing 0.005 to 0.02 mg/kg IV
(see Chapter 16, Tables 16-1 sedation16
and 16-2) 0.03 mg/kg IV for recumbency16 0.01 to 0.04 mg/kg IM
Dexamethasone 15 to 20 mg IV or IM to induce 20 to 25 mg IM after 141 days for
parturition19,12 or to terminate pregnancy termination27
pregnancy27 0.44 mg/kg IM once as an antiinflam-
0.1 to 1 mg/kg IV or IM for matory2
inflammation22
Dexamethasone sodium 1 to 2 mg/kg IV as a mediator inhibitor 1 to 2 mg/kg IV as a mediator inhibitor
phosphate in circulatory shock therapy30 in circulatory shock therapy30
Dextrose (glucose) 60 to 100 ml of 50% solution IV for 1 g every 4 hours IV until recovery
treatment of pregnancy toxemia19 (ketosis)20
5 to 7 g IV for pregnancy toxemia31
10 ml/kg of 20% solution
intraperitoneally for weak lambs2
Diazepam 0.5 to 2.0 mg/kg1 0.5 to 1.0 mg/kg IV or 2 mg/kg IM for
(see Chapter 16, Tables 16-2 0.25 to 0.50 mg/kg IV for sedation premedication before ketamine
and 16-4) without analgesia16 anesthesia2
0.25 to 0.50 mg/kg IV in combination 0.04 mg/kg IV to stimulate appetite2
with ketamine for induction16 0.25 to 0.50 mg/kg IV for sedation
without analgesia16
0.5 to 1.5 mg/kg IV for tetany2
Digoxin In ewes, 0.025 mg/kg IV every 8 hours
three times for loading dose, 0.005 to
0.015 mg/kg every 12 hours for
maintenance18
In lambs, 0.04 mg/kg IV every 8 hours
three times for loading dose, 0.008 to
0.025 mg/kg every 12 hours for
maintenance18
Dinoprost (prostaglandin F2a) 15 mg IM twice at 9- to 11-day interval 2.5 to 20 mg IM for induction of
for estrus synchronization25 parturition32
5 to 10 mg IM to terminate pregnancy 5 mg IM or SC for retained placenta33
between days 5 and 5027 5 to 10 mg IM for luteolysis and estrus
synchronization6
Dopamine 2 to 10 mg/kg/min IV drip as inotrope, 2 to 10 mg/kg/min IV drip as inotrope,
5 to 10 mg/kg/min IV drip as 5 to 10 mg/kg/min IV drip as
vasopressor30 vasopressor30

Continued
438 • Sheep and Goat Medicine
DRUG SHEEP GOATS

Doramectin 200 mg/kg SC for lungworms, Cooperia, 200 mg/kg6

and gastrointestinal parasites, 300 (Anecdotal reports suggest this dosage
mg/kg SC for Nematodirus and may not be clinically effective against
psoroptic mites4 some nematode parasites in sheep and
goats and the clinician may need to
increase this dosage by 1.5 to 2 times)
EDTA (calcium EDTA) 75 mg/kg IV slowly every 24 hours (may
be given for the first 48 hours as
divided doses every few hours) for lead
poisoning9
55 to 90 mg/kg slowly IV or IM BID
for 3 to 5 days for lead poisoning34
Enrofloxacin 5 mg/kg IV or IM every 24 hours11
Epinephrine (1:1000 sol) A dosage of 0.02 to 0.03 mg/kg SC, IM,
or IV for use in ruminants has been
reported22
Eprinomectin 0.5 mg/kg PO 0.5 mg/kg PO
Erythromycin 3 to 5 mg/kg IM every 8 to 12 hrs11 3 to 5 mg/kg IM every 8 to 12 hrs11
4 mg/kg IM for treatment of virulent
footrot caused by Dichelobacter
nodosus35
Estradiol cypionate 1 to 2 mg IM weekly for pseudoestrus 1 to 2 mg IM weekly
in females; used to tease male for
semen collection
Febantel 5 mg/kg PO4 5 mg/kg PO2
Fenbendazole 5 mg/kg PO4 5 mg/kg PO6
(Anecdotal reports suggest that this
dosage may not be clinically effective
and 10 to 20 mg/kg PO may be
required to control nematode parasites
in sheep and goats)
Fenprostalene 500 mg IM for pregnancy termination27
11
Florfenicol 20 mg/kg IM every 48 hours 20 mg/kg IM every 48 hours11
Flunixin meglumine 1.1 to 2.0 mg/kg IV or IM1 1 mg/kg IV or IM every 24 hours for
0.3 to 1.0 mg/kg IV as a mediator pain relief 2
inhibitor in circulatory shock30 0.3 to 1.0 mg/kg IV as a mediator
inhibitor in circulatory shock30
Follicle-stimulating hormone Six doses at 12-hour intervals beginning Decreasing doses BID for 2 to 4 days
(see Chapter 6) 2 days before progestin removal, with before progestin removal for a total
the last dose given 12 hours after dose of 18 to 20 mg (e.g., 5, 4, 4, 3, 2,
progestin removal, for a total dose of and 2 mg)37 or 3 mg BID for 3 days
18 to 22 mg for superovulation36 before progestin removal for
superovulation37
Furosemide 2 to 5 mg/kg PO or 1 to 2 mg/kg IV or 2 to 5 mg/kg PO or 1 to 2 mg/kg IV or
IM every 12 to 24 hours for heart IM every 12 to 24 hours for heart
failure18 failure18
5 to 10 mg/kg IV for anuria8 5 to 10 mg/kg IV for anuria8
Glycerol monoacetate 0.55 ml/kg IM every half hour for
(Monoacetin) several hours as an antidote to
fluoracetate poisoning
 Appendix I Commonly Used Drugs in Sheep and Goats: Suggested Dosages • 439

DRUG SHEEP GOATS

Griseofulvin 7.5 to 60 mg/kg PO for 7 to 20 days for

dermatophytosis38
Guaifenesin-ketamine-xylazine 0.5 to 1.0 mg/kg IV for induction,
(see Chapter 16, Tables 16-1 2 ml/kg/hr for maintenance
and 16-4) (concentrations in the solution are
50 mg/ml guaifenesin, 1 to 2 mg/ml
ketamine, and 0.1 mg/ml xylazine)16
Hypertonic saline (7%) 4 ml/kg IV over 5 to 10 minutes30 4 ml/kg IV over 5 to 10 minutes30
Insulin 20 to 40 units IM of repository insulin
for pregnancy toxemia31
Iron (ferrous sulfate) 0.5 to 2.0 g/day PO for up to 2 weeks18 0.5 to 2.0 g/day PO for up to 2 weeks18
Ivermectin 200 mg/kg PO or SC4 200 mg/kg6
200 mg/kg SC, two doses at a 7-day (Anecdotal reports suggest that this
interval for psoroptic mites4 dosage may be clinically ineffective in
sheep and goats, and more than 300
mg/kg may be needed for nematode
parasite control)
Ketamine 5 to 15 mg/kg IM for induction in 11 mg/kg IV or IM2
(see Chapter 16, Tables 16-1 combination with xylazine16 5 to 15 mg/kg IM for induction in
and 16-3) 4.0 to 7.5 mg/kg IV in combination combination with xylazine16
with diazepam16
2 to 10 mg/kg IV or IM1
Ketoprofen 3 mg/kg IV or IM every 24 hours39 3 mg/kg IV or IM every 24 hours39
Lasalocid 30 ppm in complete feed for coccidiosis 0.5 to 1.0 mg/kg/day11
control in lambs12
1 mg/kg/day, 20 to 30 g/ton PO for
coccidiosis13
Levamisole 8 mg/kg PO40 8 mg/kg PO40
(Anecdotal reports suggest that this
dosage may be clinically ineffective for
nematode parasite control in sheep and
goats, and 12 mg/kg PO may be
needed)
Lidocaine (2%) 1 to 2 mg/kg IV over 60 seconds for 2 to 4 ml for caudal epidural anesthesia2
(see Chapter 16, Table 16-1) ventricular arrhythmias18 (see Chapter 16 for possible toxicity of
0.3 to 0.4 mg/kg/minute IV infusion for this drug)
15 minutes, followed by 0.1 to
0.2 mg/kg/minute for 45 minutes for
arrhythmias18
Lincomycin hydrochloride 10 to 20 mg/kg IM every 12 to 24 hrs11 10 to 20 mg/kg IM every 12 to 24 hrs11
Lincomycin/spectinomycin 5 mg/kg lincomycin and 10 mg/kg
spectinomycin for treatment of virulent
footrot caused by Dichelobacter
nodosus35
Magnesium 50 to 100 ml IV of solutions containing
1.5 to 4 g of magnesium boroglyconate,
chloride, or gluconate for treatment of
hypomagnesemic tetany41

Continued
440 • Sheep and Goat Medicine
DRUG SHEEP GOATS

Mannitol 0.25 to 1.5 g/kg IV over 5 minutes for 0.25 to 1.5 g/kg IV over 5 minutes for
diuresis8` diuresis8
Mebendazole 15 mg/kg PO4
Medetomidine 0.001 to 0.007 mg/kg IV 0.001 to 0.007 mg/kg IV
(see Chapter 16, Tables 16-2 0.04 mg/kg IM for recumbency 0.015 to 0.04 mg/kg IM for recumbency
and 16-4)
Melengesterol acetate 0.125 mg BID for 8 to 14 days for estrus
synchronization25
Methocarbamol 22 mg/kg IV for tetany2
1
Methohexitone (methohexital) 4 mg/kg IV for anesthesia
Methylene blue 10 mg/kg IV for treatment of nitrate
toxicity9
Metoclopramide 0.1 mg/kg IM or IV BID42
Midazolam 4 mg/kg IM or IV1
Mineral oil 0.5 to 1.0 L PO for treatment of bloat43
Monensin sodium 15 mg/head/day orally throughout 1 mg/kg/day PO, 10 to 30 g/ton for
gestation to prevent abortion caused by coccidiosis13
Toxoplasma gondii12
11 to 22 ppm in complete feed for
coccidiosis control in lambs12
Morantel tartrate 10 mg/kg PO44 10 mg/kg PO6
Moxidectin 200 to 500 mg/kg PO or SC for 500 mg/kg PO22
nematodes4,22
200 mg/kg SC for psoroptic mites4
Nandrolone phenproprionate 50 to 100 mg IM every 7 to 10 days for 50 to 100 mg IM every 7 to 10 days for
adjunctive therapy of anemia18 adjunctive therapy of anemia18
Neomycin soluble powder 12 mg/kg BID PO in water for treat- 12 mg/kg BID PO in water for
ment and control of colibacillosis treatment and control of colibacillosis
caused by Escherichia coli susceptible to caused by E. coli susceptible to
neomycin45 neomycin45
Neostigmine methylsulfate 0.01 to 0.02 mg/kg SC24 0.01 to 0.02 mg/kg SC24
Netobimin 7.5 mg/kg PO for adult nematodes and
developing larvae, 20 mg/kg PO for
arrested larvae and flukes4
Niacin 1 to 2 g/head/day PO for 1 to 2 weeks
prepartum and 10 to 12 weeks
postpartum for prevention of ketosis20
Nitroxynil 10 mg/kg SC for flukes and
nonhematogenous nematodes4
Norgestomet 6 mg implant One half implant (3 mg) for estrus One half (3 mg) or full implant (6 mg)
synchronization25 for estrus synchronization26
Oxfendazole 5 mg/kg PO4 5 mg/kg PO6
4.5 mg/kg PO for cestodes5 (Anecdotal reports suggest that this dose
may be clinically ineffective and
10 mg/kg PO may be more effective in
gastrointestinal nematode control of
sheep and goats)
Oxyclozanide 15 mg/kg PO for flukes and tapeworms4
 Appendix I Commonly Used Drugs in Sheep and Goats: Suggested Dosages • 441

DRUG SHEEP GOATS

Oxytetracycline hydrochloride 10 mg/kg IV or IM BID for at least 7 10 mg/kg IV or IM every 12 to 24 hrs11

days for listeriosis46
10 mg/kg IV or IM every 12 to 24 hrs11
Oxytetracycline (in feed) 250 to 300 mg/head/day orally to 400 to 500 mg/head/day PO for 2 weeks
prevent abortion caused by orally for control of abortion caused by
Campylobacter species and Chlamydia Chlamydia and Campylobacter48
psittaci28
200 to 400 mg/head/day orally to
prevent abortions caused by Leptospira
interrogans28
10 mg/lb/day PO for treatment of
bacterial enteritis caused by Escherichia
coli and bacterial pneumonia caused by
Pasteurella multocida susceptible to
oxytetracycline47
Oxytetracycline (long-acting) 20 mg/kg IM every 48 to 72 hours11 20 mg/kg IM every 48 to 72 hours11
20 mg/kg IM twice a week in the last
4 to 6 weeks of gestation to prevent
abortion caused by Chlamydia and
Campylobacter49
Oxytocin 30 to 50 IU IV, IM, or SC for obstetric 10 to 20 IU IM every 2 hours for
use49 retained placenta33
10 to 20 IU IM for uterine inertia or to
stimulate uterine contractions after
dystocia50
Penicillamine 50 mg/kg/day PO to increase fecal
elimination of copper9
52 mg/kg/day PO for 6 days10
Penicillin G, potassium or 20,000 to 40,000 IU/kg IV every 6 20,000 to 40,000 IU/kg IV every 6
sodium hours11 hours4
Penicillin G procaine 20,000 to 45,000 IU/kg IM every 24 20,000 to 45,000 IU/kg IM very
hrs11 24 hrs11
70,000 IU/kg for virulent footrot caused
by Dichelobacter nodosus35
44,000 IU/kg IM or SC BID for 7 to
14 days, followed by 7 to 14 days of
22,000 IU/kg BID for listeriosis46
50,000 IU/kg IM for clostridial
infections15
Pentobarbital (pentobarbitone) 10 to 30 mg/kg IV or IP to control
seizures9
24 to 33 mg/kg IV (to effect) for
anesthesia1
Phenylbutazone 10 mg/kg PO every 24 hours for pain
relief 2
Poloxaline 2 g/head/day in feed or molasses blocks
or 10 g/45 kg to prevent or treat
bloat43
Praziquantel 10 to 15 mg/kg PO for tapeworms24 10 to 15 mg/kg PO for tapeworms24
Continued
442 • Sheep and Goat Medicine
DRUG SHEEP GOATS

Pregnant mare serum 250 to 400 IV and up to 500 IU for out- 200 to 600 IU for estrus
gonadotropin (equine of-season breeding synchronization26
chorionic gonadotropin, eCG, 1000 to 1500 IU 48 to 72 hours before 500 to 1500 IU 24 to 48 hours before
or PMSG) progestin removal for superovulation36 progestin removal37
300 to 500 IU at the time of progestin
removal before artificial insemination51
150 to 250 IU simultaneously with first
dose of follicle-stimulating hormone to
improve consistency of
superovulation36
Propofol 4.0 to 6.0 mg/kg IV for induction16 4.0 to 6.0 mg/kg IV for induction16
(see Chapter 16, Table 16-4) 3 to 4 mg/kg IV1
Propylene glycol 60 ml of 600 mg/ml solution orally for 1 to 2 oz PO for treatment of ketosis20
mild signs of pregnancy toxemia
(noncomatose)19
100 to 200 ml PO 2 to 4 times/day for
pregnancy toxemia31
Pyrantel pamoate 25 mg/kg PO16 25 mg/kg PO6
Salinomycin 200 ppm in complete feed for coccidiosis 11 to 16 g/ton in feed for period of
control in lambs12 risk11
11 to 16 g/ton in feed for period of risk11
Selenium 0.75 mg/head SC at birth in selenium-
deficient areas if ewes have not been
supplemented12
0.1 to 0.3 mg/kg of total ration dry
matter to supplement ewes in
selenium-deficient areas12
3 mg/45 kg every 14 days for a
maximum of four doses in the last
trimester of pregnancy in selenium-
deficient areas12
Sodium bicarbonate 2 L of isotonic (1.3%) solution IV for 25 g/doe/day PO after parturition for
treatment of pregnancy toxemia acidosis prevention20
(70-kg ewe)19
Sodium iodide 1 g/14 kg IV, repeated at 3- to 7-day
intervals for dermatophytosis38
70 mg/kg IV every 7 to 10 days52
Sodium nitrate 10 to 20 mg/kg IV for hydrocyanic
(prussic) acid poisoning9
Sodium sulfate (anhydrous) 1 g/head/day PO for copper toxicity in
combination with ammonium
molybdate10
Sodium thiosulfate 0.5 mg/kg IV for hydrocyanic (prussic)
acid poisoning9
Stanozolol 25 to 50 mg IM weekly up to four doses 25 to 50 mg IM weekly up to four doses
for adjunctive therapy of anemia18 for adjunctive therapy of anemia18
Sulfamethazine 110 mg/kg PO daily for 5 days for 110 mg/kg PO daily for 5 days for
treatment of coccidiosis14 treatment of coccidiosis14
Sulfaquinoxaline 8 to 70 mg/kg PO for 5 days for 8 to 70 mg/kg PO for 5 days for
treatment of coccidiosis14 treatment of coccidiosis14
 Appendix I Commonly Used Drugs in Sheep and Goats: Suggested Dosages • 443

DRUG SHEEP GOATS

Sulfonamides 50 mg/kg (100 mg/kg loading dose) PO 50 mg/kg (100 mg/kg loading dose) PO
or in water every 24 hours11 or in water every 24 hours11
Testosterone proportionate 25 mg IM three times a week for 25 mg IM three times a week for
adjunctive therapy of anemia18 adjunctive therapy of anemia18
Thiabendazole 44 mg/kg PO53 44 mg/kg PO6
(Anecdotal reports suggest that this
drug may only rarely be clinically
effective for sheep and goats)
Thiamine 2 mg/kg IM BID for up to 13 days to 10 to 20 mg/kg IM or SC (or IV in
reduce clinical signs of lead dextrose or other isotonic fluid) TID
poisoning34 for at least 3 days54
10 to 20 mg/kg IM or SC (or IV in 50 to 60 mg/head/day in feed53
dextrose or other isotonic fluid) TID
for at least 3 days54
Thiopental sodium 10 to 16 mg/kg IV for anesthesia1 10 to 20 mg/kg IV for induction of
(see Chapter 16, Tables 16-1 anesthesia2
and 16-4)
Thiophanate 100 mg/kg PO for lungworms and
Nematodirus, 50 mg/kg PO for
gastrointestinal nematodes4
Tiletamine-zolazepam 2.0 to 4.0 mg/kg IV for induction; 5.5 mg/kg IV for general anesthesia2
(Telazol) administer additional as needed to
(see Chapter 16, Table 16-4) prolong anesthesia16
Tilmicosin 10 mg/kg SC11 (Anecdotal reports suggest that the use
of this drug may result in death in
some goats)
Tolazoline 2 to 4 mg/kg slow IV, titrate to effect24 1.5 to 2 mg/kg IV to reverse xylazine2
(see Chapter 16, Table 16-3) 2.1 mg/kg IV to reverse xylazine-
ketamine anesthesia2
Triclabendazole 10 mg/kg PO for flukes4 5 to 15 mg/kg PO for flukes2
Trimethoprim-sulfonamide 24 to 30 mg/kg IM every 12 to 24 24 to 30 mg/kg IM every 12 to 24
hours11 hours11
Tylosin 20 mg/kg IM every 12 hours11 20 mg/kg IM every 12 hours11
Vitamin B12 (cyanocobalamin) 1000 mg/head IM for deficiency18 1000 mg/head IM for deficiency18
Vitamin K1 (phylloquinone) 0.5 to 2.5 mg/kg IM for poisoning by 0.5 to 2.5 mg/kg IM for poisoning by
warfarin and related compounds24 warfarin and related compounds24
Xylazine 0.05 to 0.2 mg/kg IV or IM1 0.03 to 0.04 mg/kg IV for brief
(see Chapter 16, Tables 16-1, 0.1 to 0.2 mg/kg IV or 0.2 to 0.3 mg/kg procedures2
16- 2, and 16-4) IM for light planes of general 0.05 mg/kg IV or 0.10 mg/kg IM for
anesthesia and for induction16 painful procedures2
0.22 mg/kg IM followed 10 minutes
later by 11 mg/kg ketamine IM for
general anesthesia2
0.05 mg/kg IV or 0.1 mg/kg IM for
light planes of general anesthesia and
for induction16
Yohimbine 0.125 to 0.22 mg/kg slow IV 0.125 mg/kg IV to reverse xylazine2
(see Chapter 16, Table 16-3)
444 • Sheep and Goat Medicine
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Large animal internal medicine, ed 2, St Louis, 1996, Mosby. 36. Buckrell BC, Pollard J: Embryo transfer in sheep. In Youngquist
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GJ, editors: Lumb and Jones’ veterinary anesthesia, Baltimore, 1996, ogy, Philadelphia, 1997, WB Saunders.
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19. Menzies PI, Bailey D: Diseases of the periparturient ewe. In 40. Corwin RM: Anthelmintic therapy. In Howard JL, Smith RA,
Youngquist RS, editor: Current therapy in large animal theriogenol- editors: Current veterinary therapy 4: food animal practice, Philadel-
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20. East NE. Metabolic diseases of the puerperal period. In 41. Goff JP: Ruminant hypomagnesemic tetanies. In Howard JL,
Youngquist RS, editor: Current therapy in large animal theriogenol- Smith RA, editors: Current veterinary therapy 4: food animal prac-
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 Appendix I Commonly Used Drugs in Sheep and Goats: Suggested Dosages • 445

42. Rings DM: Abomasal emptying defect in sheep. In Howard JL, 49. Arrioja-Dechert A: Anthony Products Co. Oxytocin injection. In
Smith RA, editors: Current veterinary therapy 4: food animal prac- Arrioja-Dechert A, editor: Compendium of veterinary products, Port
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43. Gumbrell RC: Other enteric conditions. In Martin WB, Aitken 50. Braun W, Jr: Parturition and dystocia in the goat. In Youngquist
ID, editors: Diseases of sheep, ed 3, Oxford, UK, 2000, Blackwell RS, editor: Current therapy in large animal theriogenology, Philadel-
Science. phia, 1997, WB Saunders.
44. Kimberling CV: Jensen and Swift’s diseases of sheep, ed 3, Philadel- 51. Mylne MJA, Hunton JR, Buckrell BC: Artificial insemination in
phia, 1988, Lea & Febiger. sheep. In Youngquist RS, editor: Current therapy in large animal
45. Arrioja-Dechert A: Pharmacia & Upjohn, Neomix 325 soluble theriogenology, Philadelphia, 1997, WB Saunders.
powder. In Arrioja-Dechert A, editor: Compendium of veterinary 52. Smith BP: Actinomycosis (lumpy jaw). In Smith BP, editor: Large
products, Port Huron, MI, 1999, North American Compendiums. animal internal medicine, ed 2, St Louis, 1996, Mosby.
46. Finley MR, Dennis SM: Listeriosis (circling disease, silage sick- 53. Herd RP, Zajac AM: Nematode infections in cattle, sheep, goats,
ness). In Howard JL, Smith RA, editors: Current veterinary therapy and swine. In Howard JL, Smith RA, editors: Current veterinary
4: food animal practice, Philadelphia, 1999, WB Saunders. therapy 4: food animal practice, Philadelphia, 1999, WB Saunders.
47. Arrioja-Dechert A: Pfizer Animal Health, Terramycin type A 54. George LW: Polioencephalomalacia (polio, cerebrocortical necro-
medicated article. In Arrioja-Dechert A, editor: Compendium of sis). In Smith BP, editor: Large animal internal medicine, ed 2, St
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48. Mobini S: Infectious causes of abortion. In Youngquist RS, editor:
Current therapy in large animal theriogenology, Philadelphia, 1997,
WB Saunders.
 Appendix II

Practical Fluid Therapy

CHRISTINE B. NAVARRE

1. ESTIMATING PERCENT (%) thing but dehydration. However, elevated protein can
DEHYDRATION occur with severe, chronic inflammation. Also, an animal
with anemia and hypoproteinemia in conjunction with
PERCENT (%)
dehydration can have a normal PCV/TP. Therefore
DEHYDRATION* CLINICAL SIGNS PCV/TP is most useful in monitoring the progress of
fluid therapy.
5% Minimal depression, skin tent only a
few seconds, minimal enophthal- 3. CALCULATING A FLUID
mos, mucous membranes still moist,
capillary refill slightly greater than 2 DEFICIT FROM DEHYDRATION
seconds % dehydration  body weight in kg  fluid deficit in liters
8% Obvious depression, skin tent 2 to 4
seconds, obvious enophthalmos, For example, a 50-kg animal with 8% dehydration needs
mucous membranes have a purple 4 liters of fluid.
tint and are tacky, capillary refill 3 to For neonates the calculated fluid deficit in liters
4 seconds (usually less than 1) should be converted to milliliters. For
10% Severe depression, weakness, possible example, a 5-kg lamb with 10% dehydration needs 0.5
recumbency, skin tent remains for liters, or 500 milliliters.
several seconds, severe enophthal-
mos, mucous membranes dark and 4. CALCULATION OF
dry, capillary refill more than 4
seconds, cold extremities MAINTENANCE NEEDS
After treating deficits and dehydration, maintenance
*These are estimates only. Other factors may change the physical
examination parameters and mimic dehydration. For example, severe
needs should be met if the animal is not taking in fluids
weight loss can cause enophthalmos, and chronic debilitation makes on its own.
the skin less elastic and causes prolonged tenting. Also, certain
Maintenance for adults and neonates  approximately 1 ml/lb/hr
diseases cause excess salivation, which keeps the mucous membranes
moist, even during dehydration. A 10-lb kid needs 10 ml/hour

If the animal has diarrhea, the clinician should give

two times maintenance and assess rate daily with physical
2. USE OF PACKED CELL examination and PCV/TP, adjusting rate as needed. For
VOLUME AND TOTAL PROTEIN diuresis with renal disease, the clinician can give two
times maintenance and assess daily with physical exami-
(PCV/TP) nation, PCV/TP, and creatinine concentrations, adjusting
The PCV and TP can be used as tools to assess dehydra- rate as needed.
tion but should not replace an estimation from physical CAUTION: Small ruminants on continuous fluid
examination. An elevated PCV is rarely caused by any- therapy are inclined to become hypoproteinemic quickly.
• 447 •
448 • Sheep and Goat Medicine
Diligent assessment of total protein is needed to 6. HELPFUL CONVERSIONS
prevent this. AND TIPS*
5. CALCULATION OF 1 level teaspoon of most salts (e.g., NaCl, NaHCO3)
is approximately 5 g.
BICARBONATE NEEDS Isotonic NaHCO3: 13 g/L, or 1.3%, or 156 mEq/L of
To correct metabolic acidosis, a total carbon dioxide HCO3 (312 mEq/L total for both Na and HCO3).
(CO2) measurement from a chemistry panel or blood gas Approximately 3 teaspoons of baking soda/L water
or an evaluation of base deficits from blood gas assess- is isotonic sodium bicarbonate.
ments are needed. Isotonic saline: 9 g/L noniodized table salt.
Rule of thumb. The clinician should correct half of Approximately 2 teaspoons of NaCl/L water is
the calculated deficit if the acidosis results from dehydra- isotonic saline.
tion only. The entire deficit may be corrected if the dehy- Supplemental potassium: 10 to 20 mEq/L, or 1 g/L
dration is from neonatal diarrhea (not adults) or rumen (14 mEq/L). Supplemental potassium can be
acidosis. provided by 1⁄2 teaspoon lite salt/L of water (lite
salt is half sodium chloride and half potassium
Adults: Body weight in kg  0.3 
chloride).
base deficit  bicarbonate deficit in mEq
Supplemental glucose can be provided with a 1% to
Neonates: Body weight in kg  0.5 
2% dextrose solution (20 ml of 50% dextrose/L for
base deficit  bicarbonate deficit in mEq
each 1% of dextrose needed).
Base deficit can be substituted with (normal total CO2  Calcium borogluconate can be supplemented at 25
measured total CO2). The normal range for total CO2 is ml/L.
usually 20 to 30, so the clinician can use 20 to 25 mmol/L
to be conservative. Commercial bottles of sodium bicar-
bonate define the mEq of bicarbonate/ml of fluid, EASY IV FORMULA FOR
making the calculation of the total ml of this solution NONDIARRHEIC DEHYDRATED
easy. Solutions of 5% sodium bicarbonate can be given
without dilution if dehydration needs are corrected at the
ANIMALS
same time. Alternatively, 1.3% isotonic bicarbonate can Balanced isotonic electrolyte solution for base fluid
be given. (e.g., lactated Ringer’s, Ringer’s, plasmalyte)
Add 1 g/L KCl (14 mEq/L)
A 100-kg ewe with a base deficit of 8:
Add 15 g dextrose/L (30 ml of 50%/L)  1.5%
100 kg  0.3  8  240 mEq bicarbonate needed
dextrose
1.3% sodium bicarbonate has 0.156 mEq/L,
Add 25 ml/L calcium borogluconate for adults only
so 240/0.156  approximately 1.5 liters
5% sodium bicarbonate has 0.6 mEq/ml, so 240/0.6  400 milliliters
8% sodium bicarbonate has 1 mEq/ml, so 240/1  240 milliliters EASY IV FORMULA FOR
If no total CO2 or base deficit is available. If the NEONATAL DIARRHEA
animal is only 5% to 8% dehydrated, correcting the fluid Calculate fluid deficit and give three quarters of the
deficit and the primary problem are usually sufficient. If previous fluid and one quarter as isotonic sodium
the animal is 10% dehydrated, some supplementation is bicarbonate.
needed:
If no neonatal diarrhea or rumen acidosis is present, EASY PO FORMULA FOR
the clinician can give 2.5 mEq/kg body weight of bicar-
bonate. If neonatal diarrhea or rumen acidosis is present, NEONATAL DIARRHEA
5 mEq/kg body weight of bicarbonate can be given. 2 teaspoons noniodized table salt
1 teaspoon lite salt
50 ml 50% dextrose
Add to 1 qt or L of water

*CAUTION: The use of commercially prepared products for IV and oral use is
strongly recommended. These tips for using table salts and baking soda are
approximations of commercial products and should be given only in
emergency situations and only one time. If fluid therapy continues,
commercial products should be used. The IV use of nonsterilized salts and
water is strongly discouraged because bacteremia and endotoxemia from
pyrogens may lead to infection or adverse reactions.
 Appendix II Practical F luid T herapy • 449
EASY PO FORMULA
ml/kg body weight rapid IV push of a 7% solution. If
FOR ADULTS hemorrhage has occurred, it may be exacerbated when
8 teaspoons noniodized table salt blood pressure increases after administration of HSS. The
2 teaspoons lite salt clinician should consider blood transfusion after adminis-
100 ml calcium solution tering HSS for hemorrhage. If dehydration is present,
Add to 1 gal or 4 L of water HSS should be followed with IV isotonic or oral fluids in
both neonates and adults. HSS often increases the
HYPERTONIC SALINE animal’s drive for water intake, so many adult animals will
consume oral fluids or water and not need to have fluids
SOLUTION (HSS) administered to them.
HSS can be used in severe hypovolemic shock situations—
either from severe hemorrhage or dehydration. It tem-
porarily improves cardiac output. The clinician can give 4
 Appendix III

NConversions
ormal Values and

D.G. PUGH

TABLE A

ERYTHROCYTE PARAMETERS

Sheep Goats

PARAMETER RANGE MEAN RANGE MEAN

Hematocrit (packed cell volume [PCV]) % 27 to 45 35 22 to 38 28

Hemoglobin (Hb) g/dl 9 to 151,2 11.51 8 to 121,2 101
Erythrocytes (red blood cells [RBCs]) 106/ml 9 to 151,2 121 8 to 181,2 131
Mean corpuscular volume (MCV) fl 28 to 401,2 341 16 to 251,2 19.51
Mean corpuscular hemoglobin (MCH) pg 8 to 121,2 101 5.2 to 81,2 6.51
Mean corpuscular hemoglobin concentration (MCHC) g/dl 31 to 341,2 32.51 30 to 361,2 331
Platelet count, N  103/l 205 to 7052 5001 300 to 6001,2 4501
800 to 11001
RBC diameter (mm) 3.2 to 6.01 4.5 2.5 to 3.9 3.2
RBC life (days) 125 140 to 150
Myeloid:erythroid ratio (M/E) 0.71 0.77 to 1.71
0.8 to 1.72 0.7 to 12

TABLE B

LEUKOCYTE PARAMETERS, PLASMA PROTEIN, AND FIBRINOGEN

Sheep Goats

PARAMETER PERCENTAGE RANGE MEAN PERCENTAGE RANGE MEAN

White blood cell count (WBC) n/ml 4000 to 12,0002 4000 to 13,0002
2
Segmented neutrophils (seg) (%) n/ml 10 to 50 700 to 60001,2 2400 1
30 to 48 1
1200 to 72001,2 32501
Banded neutrophils (band) (%) n/ml 0 0
Lymphocytes (lymph) (%) n/ml 40 to 752 2000 to 90001,2 50001 50 to 701 2000 to 90001,2 50001
Monocytes (mono) (%) n/ml 6 to 62 0 to 7501,2 2001 0 to 41 0 to 5501,2 2501
Eosinophils (eos) (%) n/ml 0 to 102 0 to 10002 4001 1 to 81 50 to 6501,2 4501
Basophils (baso) (%) n/ml 0 to 32 0 to 3001,2 501 0 to 11 0 to 1201,2 501
Plasma protein (PP) g/dl 6 to 7.51,2 6.0 to 7.51,2
Fibrinogen (mg/dl) 100 to 5001,2 100 to 4001,2

• 451 •
452 • Sheep and Goat Medicine
TABLE C

SERUM BIOCHEMICAL VALUES

VALUE SHEEP GOATS

Acetone mmol/l 0 to 1.723

Acetylcholinesterase U/l 6403 2703
Albumin, g/dl 2.4 to 3.02,3 2.7 to 3.92,3
Alkaline phosphatase (ALP) U/l 68 to 3872,3 93 to 3872,3
Arginase (ARG) U/l 0 to 143
Aspartate aminotransferase (AST, SGOT) U/l 60 to 2802,3 167 to 5132,3
b-hydroxybutyrate (b-OHB) mmol/l normal: 0 to 7
moderate: 0.8 to 1.6
severe underfeeding: 1.7 to 3.0
pregnancy toxemia: 6.5
Bicarbonate (HCO3 ) mmol/l 20 to 253
Bilirubin, total mg/dl 0.1 to 0.52,3 0.10 to 1.713
Bilirubin, unconjugated (UCB) mg/dl 0 to 0.123
Bilirubin, conjugated (direct) mg/dl 0 to 0.272,3
Cholesterol mg/dl 52 to 761 80 to 1301
Carbon dioxide, total (TCO2) mmol/l 21 to 283 25.6 to 29.63
Creatinine phosphokinase (CPK) U/l 8 to 133 0.8 to 92,3
Creatinine mg/dl 1.2 to 1.93 1 to 1.822,3
Gamma-glutamyl transferase (GGT) U/l 44  112 20 to 563
20 to 523
Globulin g/l, g/dl 3.5 to 5.73 2.7 to 4.13
Glucose mg/dl 50 to 802,3 50 to 752,3
Glutamate dehydrogenase (GD) U/l 203
Hemoglobin mg/dl 90 to 1403 80 to 1203
Icterus index 2 to 53 2 to 53
Isocitrate dehydrogenase (ICD) U/l 0.4 to 8.03
Lactate dehydrogenase (LDH) U/l 238 to 4402 123 to 3922,3
88 to 487
Lactate mmol/l 1 to 1.333
Protein, total serum g/dl 6 to 7.93 6.4 to 72,3
Sorbitol dehydrogenase U/l 5.8 to 27.93 14 to 23.63
Blood urea nitrogen (BUN) mg/dl 8 to 202,3 10 to 202,3

TABLE D

SERUM ELECTROLYTE AND MINERAL CONCENTRATIONS

PARAMETER SHEEP GOATS

Calcium mg/dl 11.5 to 12.81 8.9 to 11.71

Phosphate mg/dl 5.0 to 7.31 4.2 to 9.11
Magnesium mg/dl 2.2 to 2.81 2.8 to 3.61
Sodium mEq/l 139 to 1521 142 to 1551
Chloride mEq/l 95 to 1031 99 to 110.31
Potassium mEq/l 3.9 to 5.41 3.5 to 6.71
Bicarbonate (HCO3) mEq/l 20 to 251
Iron mmol/l 29.7 to 39.73
mg/dl 162 to 2223
Copper mmol/l 9.13 to 25.23
Lead mmol/l 0.24 to 1.213 0.24 to 1.213
mg/dl 5 to 253 5 to 253
 Appendix III Normal Values and C onversions • 453

TABLE E

VITAMINS AND MINERALS IN SERUM AND LIVER (SHEEP)

MEASURED ELEMENT DEFICIENT ADEQUATE TOXIC

Vitamin A (serum) ng/ml7 Newborn 20 30 to 100

Yearling 150 225 to 500
Adult 150 225 to 500
Vitamin A (liver) mg/g dry weight7 Newborn 20 50 to 100
Yearling 40 100 to 500
Adult 40 300 to 1100
Vitamin E (liver) mg/dl dry weight7 Newborn 3 7 to 35
Yearling 10 20 to 40
Adult 10 20 to 40
Selenium (serum) ng/ml7 Newborn 20 50 to 90
Yearling 50 80 to 120
Adult 50 110 to 160
Zinc (serum) ppm 0.22 to 0.458 0.8 to 27.8 30 to 50
Zinc (liver) mg/kg (dry weight) 105 to 250 400
Copper (serum) mg/kg 0.6 0.7 to 2.07,8 3.3 to 20
Copper (liver) mg/kg (dry weight) 0.5 to 4.0 88 to 3507 250 to 400
Iron (serum) mg/kg (as soluble element) 1.6 to 2.27
Iron (liver) mg/kg (dry weight) 105 to 1050
Manganese 7 to 15
Molybdenum 1.5 to 6

TABLE F TABLE G

CEREBROSPINAL FLUID3 URINALYSIS

PARAMETER SHEEP GOATS TEST NORMAL RESULTS

White blood cells 0 to 5 0 to 4 Color Pale yellow

number/ml Glucose Negative
Erythrocytes number/ml Ketones Negative
Calcium mg/dl 5.1 to 5.5 4.6 Protein Negative to trace
Magnesium mg/dl 2.2 to 2.8 2.3 Specific gravity 1.015 to 1.045
Chloride mg/dl 128 to 148 116 to 130 Bilirubin Negative
Phosphorus mg/dl 1.2 to 2 Turbidity Clear
Potassium mg/dl 3.0 to 3.3 3.0 Crystals Rare
Sodium mg/dl 145 to 157 131 Casts Occasional hyaline
Hydrogen ion (pH) 7.3 to 7.4 Epithelial cells Occasional
Glucose mg/dl 52 to 85 70 Gamma-glutamyl transferase 40 U/l
Total protein mg/dl 29 to 42 12 (GGT)
Red blood cells (RBC) 5
White blood cells (WBC) 5
454 • Sheep and Goat Medicine
TABLE H

PARACENTESIS4,5

CHARACTERISTIC NORMAL VALUE

Odor None
Color Colorless to yellow
Turbidity Clear to slightly turbid
Total protein g/dl 3
Neutrophils 10,000
Specific gravity 1.018

TABLE I

SYNOVIAL FLUID6

CHARACTERISTIC NORMAL INFLAMMATION OR LOW-GRADE INFECTION SEPTIC DEGENERATIVE JOINT DISEASE

Color Clear Yellow to red Yellow to red Yellow

Clarity Transparent Translucent Cloudy Transparent
Leukocytes/ml 200 2000 to 10,000 30,000 to 100,000 200 to 2000
Neutrophils % 25 75 75 25
Viscosity Very viscous Poor Poor Variable

TABLE J TABLE K

CONVERSIONS9 MISCELLANEOUS CONVERSIONS9

PREFIX VALUE CONVERSION MULTIPLY BY

Milli- 1/1000 grain to milligrams 64.799

Centi- 1/100 ounces to grams 28.35
Deci- 1/10 pounds to grams 453.6
Deca- 10 pounds to kilograms 0.4536
Necto- 100 tons to metric tons 0.9
Kilo- 1000 grams to ounces 0.035
kilograms to pounds 2.205
metric tons to tons 1.102
mg/lb to g/ton 2
g/lb to g/ton 2000
lb/ton to g/ton 453.6
mg/g to mg/lb 453.6
mg/kg to mg/lb 0.4536
mcg/kg to g/lb 0.4536
ppm to mg/lb 0.4536
mg/lb to ppm 2.2046
ppm to g/ton 0.907
g/ton to g/lb 0.0005
g/ton to lb/ton 0.0022
g/ton to % 0.00011
% to g/ton 9072.2
g/ton to ppm 1.1
% to ppm Divide by 10,000
ppm to % 10,000
 Appendix III Normal Values and C onversions • 455

TABLE L BOX A

ENGLISH TO METRIC AND METRIC TO

ENGLISH CONVERSION
C ENTIGRADE TO F AHRENHEIT AND F AHRENHEIT

VALUE CONVERTED EQUIVALENT

TO C ENTIGRADE

To change centigrade to Fahrenheit, multiply the

1 oz 28.5 g
1 lb 16 oz
degrees in centigrade by 1.8, then add 32 to the
1 kg 1000 g
number.
1 ton 2000 lb Example: 40° C
1.07 kg (1.8) (40)  32  104° F
1 metric ton 1000 kg To change Fahrenheit to centigrade, subtract 32
2205 lb from the degrees in Fahrenheit, then multiply that
1.102 ton number by 0.556.
1 mg/kg 1 ppm
Example: 104° F
(104  32) (0.556)  40° C

TABLE M

EQUIVALENT VALUES FOR CAPACITY OR VOLUME9

VALUE EQUIVALENT
R EFERENCES
1. Kramer JW: Normal hematology of cattle, sheep, and goats. In
Feldman BF, Zinkl JG, Jain NC, editors: Schlam’s veterinary hema-
a cubic cm 1 milliliter tology, ed 5, Philadelphia, 2000, Williams & Wilkins.
1 US pint 28.875 cubic inches 2. Duncan JR, Prasse KW: Veterinary laboratory medicine—clinical
0.5 quarts pathology, ed 2, Ames, IA, 1986, Iowa State University Press.
0.47316 liter 3. Kaneko JJ, Harvey JW, Bruss ML: Clinical biochemistry of domestic
1 US quart 57.75 cubic inches animals, ed 5, San Diego, CA, 1997, Academic Press.
2 US pints 4. Belknap EB, Navarre CB: Differentiation of gastrointestinal dis-
0.9463 liter eases in adult cattle, Vet Clin North Am: Food Anim Pract 16(1):63,
1 US gallon 231 cubic inches 2000.
5. Kopcha M, Schultze AE: Peritoneal fluid. Part II. Abdominocente-
8 US pints
sis in cattle and interpretation of non neoplastic samples, Comp Cont
4 US quarts
Ed Pract Vet 13(4):703, 1999.
3.7853 liters 6. Orsini JA: Septic arthritis (infectious arthritis). In Smith BP, editor:
1 liter 2.1134 US pints Large animal internal medicine, ed 2, St Louis, 1996, Mosby.
1.057 US quarts 7. Braselton WE: Animal Health Diagnostic Laboratory, personal
0.2642 US gallon communication, Michigan State University.
1 bushel 2150.42 cubic inches 8. D’Andrea G, Robert S: Veterinary Diagnostic Laboratory, personal
1.244 cubic feet communication, Auburn University.
9.309 US gallons 9. Ensminger ME, Oldfield JE, Heinemann WW: Feeds and nutrition,
ed 2, Clovis, CA, 1990, Ensminger Publishing.
 Index *

A Amputation(s)
of urethral process for urolithiasis, 268
Abdomen, of goat, examination of, 16 therapeutic, 231-232
Abdominocentesis, 71-72 udder, 347-349
Abducent nerve (VI) in neurological evaluation, 280 Amyloidosis, 263-264
Abomasitis, 78 Anagen defluxion, 218
Abomasum Anagen phase of hair growth, 198
diseases of, 78-79 Analgesics, opioid, 409-410
emptying defect of, 79 Anaplasma ovis in blood and tissue, 381-382
hemorrhage of, 78-79 Anemia
impaction of, 79 causes of, 361-362
Abortion, 175-185 treatment of, 362
Akabane viral, 176-177 Anesthesia
associated with deformities, 176-178 management of, 405-417
bluetongue and, 176 agents in, 410-412
border disease virus and, 177 monitoring in, 412-413
brucellosis and, 181-182 nerve blocks in, 416-417
Cache Valley virus and, 177 pathophysiologic alterations in, 413-414
Campylobacter, 178-179 perioperative, 412-416
Chlamydia, 179-180 complications in, 414-416
leptospirosis and, 182 preanesthetic preparation in, 405-406
listeriosis and, 184 preanesthetics in, 406-410
mycoplasmosis and, 184-185 retrobulbar, for enucleation, 339
noninfectious causes of, 185 Anesthetics, 410-412
prevention program for, 176b inhalation, 411
Q fever and, 180-181 injectable, 410-411
salmonellosis and, 182-183 local, 411-412
toxoplasmosis and, 183-184 Angora goats
Abscess(es) abortion in, 185, 192
bacteria forming, 379-380 feeding of, for fiber production, 55
brain, 300 Anterior chamber, evaluation of, 324
foot, in sheep, 8 Anthelmintic agents in deworming, 89, 90-92
kidney, 264 Antibiotic sensitivity testing of milk, 342
liver, 97 Antibiotics
pharyngeal, 65 dietary, 28
retropharyngeal, 111-112 toxicity of, 259-260
soft tissue, 207 Antidiuretic hormone (ADH), 188
spinal, 311-312 Antivenin polyvalent, dosages for, 436t
tooth root, 64 Anus, atresia of, 94
Accessory nerve (XI) in neurological evaluation, 283 Apocrine glands, 197
Acepromazine maleate Arcanobacterium pyogenes, sepsis from, 374
as anesthetic, doses of, 410t Artery, hyaloid, persistence of, 335
as preanesthetic, 406 Arthritis
doses of, 408t CAE virus, respiratory signs of, 126
dosages for, 435t septic, 236-238
Acetic acid, dosages for, 435t Arthritis-encephalitis, caprine, 239-241, 296
Acholeplasma oculi conjunctivitis, 332 Arthrogryposis, 229
Acid detergent fiber (ADF), 29, 32 Artificial insemination, 154-157
Acidosis, rumen, 75-77 cervical, 154-156
Acorn toxicity, 261 laparoscopic, 156-157
Actinobacillosis, 65, 206 vaginal, 154
Actinobacillus seminis, sepsis from, 374 Aspirates, bone marrow, 360
Actinomycosis, oral, 65 Aspiration pneumonia, 124
Adenocarcinomas, nasal, 110, 110f complicating anesthesia, 414-415
Adenomas Aspirin, dosages for, 436t
nasal, 110 Ataxia, 285
pituitary, 194 enzootic, 25, 311
Adenomatosis, sheep pulmonary, 118 Atipamezole as preanesthetic, 409
Adenopapillomas, nasal, 110 Atresia, intestinal, 94
Adenovirus Atrial septal defects, 396
renal disorders from, 262 Atropine
respiratory disease from, 114 as preanesthetic, doses of, 408t
Adnexa, anatomy of, 317-318 dosages for, 436t
Adrenal glands, 192 Auditory meatus, external, bactericidal solutions used to flush, 303t
Adult sepsis, 373-374 Auriculopalpebral nerve block in ophthalmic examination, 325
African trypanosomiasis, 402-403 Auscultation in respiratory system evaluation, 107
Agalactia, 349 Auscultation of heart, 393
Age, permanent tooth eruption and, 62t Autoimmune diseases, of skin, 213-214
Akabane virus Azalea toxicity, 79
abortion from, 176-177 Azotemia, neonatal, 368
hydrocephalus/hydranencephaly from, 312-313
Alfalfa, nutrient composition of, 30t B
Alopecia in skin diseases, 199 Babesia species in blood and tissue, 381-382
a2 agonists as preanesthetics, 406-409 Bacillus anthracis, sepsis from, 374
a2 antagonists as preanesthetics, 409
Bacteria
Ammonia toxicity, 309
abscess-forming, 379-380
Ammonium chloride, dosages for, 435t
blepharitis from, 327
Ammonium chloride/sulfate as feed additive, 28
meningitis from, 297-298
Ammonium molybdate, dosages for, 435t
sepsis from, 374
Ammonium tetrathiomolybdate, dosages for, 435t
skin diseases from, 205-208
Amoxicillin, dosages for, 436t
Bahia grass, nutrient composition of, 30t
Amprolium, dosages for, 436t
Bakery, nutrient composition of, 30t

*The letter t following the page number indicates a table; f indicates a figure; b indicates a box.

• 456 •
 Index • 457

Barley, nutrient composition of, 30t Butorphanol

Beet, sugar, nutrient composition of, 30t as preanesthetic, 409-410
Benzimidazole dewormers, resistance to, 90-91 doses of, 408t
Benzodiazepines as preanesthetics, 409 dosages for, 436t
Bermuda grass, nutrient composition of, 30t C
Biceps reflex test in neurologic lesion localization, 288
Bifid teats, 343-344 Cache Valley virus (CVV)
Bighead, 206, 371 abortion and, 177
Biochemistry profile in urinary tract evaluation, 258 hydrocephalus/hydranencephaly from, 313
Biopsy(ies) Calcium
core, 360 calculating, in ration balancing, 39-40
liver, 73 hoof condition and, 225
lung, 109 in feeding/nutrition, 23
mammary gland, 342 Calcium borogluconate, dosages for, 436t
renal, 256 Calcium gluconate, dosages for, 436t
skin, in skin disease diagnosis, 202-203 Calculi, urinary, 267-271
Black disease, 371-372 California mastitis test, 343
Black liver disease, 102 Callus formation, 217
Blackleg, 242-243, 372-373 Campylobacter abortion, 178-179
Bladder, ruptured, 272 Candidiasis, 209
Blepharitis, 327-328 Canola, nutrient composition of, 30t
Blindness, 337 Caprine arthritis-encephalitis (CAE), 239-241, 296, 388
bright, 336 hematologic/lymphatic manifestations of, 388
central, 337 respiratory signs of, 126
wool, 4 Caprine cloisonné lesions, 264-265
Bloat Caprine herpesvirus, 275
clinical signs of, 74 respiratory disease from, 115
diagnosis of, 74 Carcass disposal, 432
in sheep, 5 Carcinoma
pathogenesis of, 74 ovine pulmonary, 118
prevention of, 74-75 squamous cell, of skin, 220
treatment of, 74 Cardiotoxicity, plant, 399-400
Blood Cardiovascular system
cultures of, 360 collapse of, complicating anesthesia, 415-416
parasites infesting, 381-382 examination of, 393-396
viral diseases of, 384-387 blood gases in, 394
Blood gas analysis, 394 echocardiography in, 395-396
in respiratory system evaluation, 108 electrocardiogram in, 394-395
Blood vessels heart auscultation in, 393
diseases of, 402-404 mucous membranes in, 394
of eye, 319 peripheral pulses in, 393
Bluebag, 350-351 pressures in, 394
Bluetongue virus, 66, 205 pulses in, 394
abortion associated with, 176 thoracic radiographs in, 396
hematologic/lymphatic diseases from, 384 venous filling in, 393-394
hydrocephalus/hydranencephaly from, 313 in head and neck, of goats, examination of, 15
retinal disorders from, 336 of goats
Body condition scoring, 40-43 abdominal, examination of, 16
Boldenone undecylenate, dosages for, 436t in thorax and forelimbs, examination of, 15
Bone marrow aspirates and core biopsies, 360 pelvic and hindlimb, examination of, 16
Border disease, 219 of sheep, examination of, 5
abortion and, 177 Carprofen, dosages for, 436t
hematologic/lymphatic manifestations of, 389-391 Carpus, fractures of, 231
hydranencephaly in, 313 Caseous lymphadenitis, 207-208
Boreis burgdorferi, sepsis from, 374 anesthesia and, 413
Bottle feeding of lamb or kid, 50-51 control program for, 209b
Botulism, 306-307 respiratory signs of, 126-127
Bovine viral diarrhea, 389-391 vaccination for, in goats, 424
Bracken fern, retinal degeneration from, 336 Castration, 140-141
Brain Casts for fractures, 232-233, 234f
abscesses of, 300 Cataracts, 334-335
lesions of, signs of, 290t-291t Caudal epidural nerve block, 416
Branhamella ovis conjunctivitis, 332 Cecal volvulus, 94
Braxy, 372 Ceftiofur sodium, dosages for, 436t
Breath sounds, evaluation of, 107 Central blindness, 337
Breech presentation, 164-165 Central nervous system
Breeding depression of, plants associated with, 314t
artificial insemination for, 154-157 stimulation of, plants associated with, 314t
feeding females during, 46 Cereal grains, for energy supplementation, 21
Breeding programs, alternative Cerebellum, lesions of, signs of, 290t-291t
for goats, 153 Cerebral cortex
for sheep, 152-153 lesions of, signs of, 290t-291t
Breeding soundness examination necrosis of, 309-310
of buck, 135-136 Cerebrospinal nematodiasis, 303-305
of female, 149 Cervical insemination, 154-156
of ram, 132-135 Cesarean section, 165-166
Breeding systems, natural, 153-154 anesthesia for, 413-414
Bright blindness, 336 Cestode infestation, 92
Broken mouth, 5 Charcoal, activated, dosages for, 436t
Bronchitis, parasites causing, 123-124 Chlamydia psittaci
Broomweed, reproductive dysfunction from, 172 abortion from, 179-180
Browse in diet, 19 conjunctivitis from, 331
Brucella melitensis, infection from, 374 infection from, 374
Brucellosis, abortion in, 181-182 pneumonia from, 118
Buck(s) Chlamydial polyarthritis, 238
breeding soundness examination in, 135-136 Chloral hydrate, dosages for, 436t
in herd management, 423 Chlorine, in feeding/nutrition, 23-24
puberty in, 130 Chlorpromazine, dosages for, 436t
recommended male-to-female ratios for, 153t Chlortetracycline
seasonal breeding activity of, 130 dietary, 28
selection and management of, 131-132 dosages for, 436t
Buck effect in estrus cycle control, 150 “Choke,” 67-68
Buffers as feed additives, 29 Chondritis, laryngeal, 112
Bulbus oculi, 319 Chondrodysplasia, hereditary, 228-229
Buprenorphine, dosages for, 436t Chorioptic mange, 211-212
Burdizzo emasculatome for castration, 141 Choroid, anatomy of, 321-322
Burns, 217-218 Ciliary body, anatomy of, 321
Circling, 285
Citrus, nutrient composition of, 30t
458 • Index
Cloprostenol Crustiness, in hair sheep breeds, 4
dosages for, 436t Crusts in skin diseases, 199
in pregnancy termination, 163 Cryptosporidiosis, 82-83
Clorsulon, dosages for, 436t Culling of sheep, 432
Closantel, dosages for, 437t Culture(s)
Clostridia blood, 360
infections from microbial, in skin disease diagnosis, 202
enteric, 369-371 milk, 342
non-enteric, 371-373 somatic cell of milk, 342-343
noninvasive, 373 yeast, as feed additive, 28
tissue-invading, 368-373 Cyclopia, 338
Clostridial myonecrosis, 242-243 Cystic ovarian disease, reproductive dysfunction from, 174
Clostridium botulinum, 306-307 Cysticercosis, 100
Clostridium chauvoei, blackleg from, 372-373 Cystitis, 272-273
Clostridium haemolyticum, red water disease from, 373 Cystotomy for urolithiasis, 268-270
Clostridium novyi infections, 371-372 Cysts, salivary, 65
Clostridium perfringens
D
diarrhea from, 84
enteric infections from, 369-371 Dandruff, in hair sheep breeds, 4
Clostridium septicum infections, 372 Dandy-Walker syndrome, 312
Clostridium tetani, 305-306 Decoquinate
Clover, nutrient composition of, 30t as feed additive, 28
Club lamb fungus, 208-209 dosages for, 437t
Cobalt Deformities, abortion associated with, 176-178
deficiency of, white liver disease and, 99 Degenerative joint disease, 244-245
in feeding/nutrition, 25-26 Dehorning, anesthesia for, 416-417
Coccidioidomycosis, respiratory signs of, 127 Demodectic mange, 212
Coccidiosis Dental anatomy, normal, 61-63; see also Tooth (teeth)
diarrhea in, 84-85 Depression
feed additives to control, 28 in neonates, causes of, 367-368
Coccidiostats, 85, 86t plants associated with, 314t
Cochliomyia hominivorax, 212 Dermatitis
Colesiota conjunctivae, conjunctivitis from, 331 contagious pustular, 66-67
Coliform mastitis, 350 staphylococcal, 206-207
Collagen tissue dysplasia, 219 Dermatome, 283-284
Colon, atresia of, 94 Dermatophilosis, 205-206
Colostrum Dermatophilus congolensis, 205-206
feeding of, to kids, 425 Dermatophytosis, 208-209, 327-328
for orphaned newborn, 50 Dermatosis, ulcerative, 204, 274
in diarrhea prevention, 87 Dermis, anatomy of, 197
inadequate ingestion of, passive transfer failure and, 363-364 Descenting, 22
Complete blood count (CBC), in respiratory system evaluation, 107-108 Detomidine hydrochloride
Composting, sheep or goat, 432b as preanesthetic, 409
Cones, 322 doses of, 408t
Confinement feeding, 44-45 dosages for, 437t
Congenital defects, of urinary tract, 273 Deworming
Congenital pathologies of skin, 219 opportunistic, 90
Conjunctiva salvage, 90
anatomy of, 318 strategic, 89-90
examination of, 324 suppressive, 90-92
pathology of, 329-333 tactical, 90
scrapings of, diagnostic, 325-326 Dexamethasone, dosages for, 437t
trauma to, 329 Dextrose, dosages for, 437t
Conjunctivitis Diabetes mellitus, 192-193
Acholeplasma oculi, 332 Diaphragmatic hernia, respiratory signs of, 127
Branhamella ovis, 332 Diarrhea, 80-88
Chlamydia psittaci, 331 bovine viral, 389-391
Colesiota conjunctivae, 331 Clostridium perfringens–induced, 84
infectious, 329 from enterotoxigenic Escherichia coli, 80-82
Listeria monocytogenes, 332 from rotavirus, 82
Mycoplasma, 329-331 Giardia-induced, 83
prevention of, 333 in adult sheep and goats, 88
therapy of, 332-333 in coccidiosis, 84-85
Consciousness, levels of, 278t in cryptosporidiosis, 82-83
Contagious caprine pleuropneumonia, 117-118 in neonatal lambs and kids, 80
Contagious ecthyma, 66-67, 203-204 in newborn lambs and kids, 80-84
vaccination for, in goats, 423-424 in older lambs and kids, 84-85
Copper in sheep, 5
deficiency of, 24-25 infectious
abortion associated with, 178 control measures for, 87
skin manifestations of, 214 differentiation of, 81t
hoof condition and, 225 miscellaneous causes of, 86
toxicity of, 25 neonatal, uncomplicated, 365-367
kidneys in, 265 nutritional, 83-84
toxicosis from, 100-101 Salmonella-induced, 83
Corn treatment of, 86-87
for energy supplementation, 21 Diazepam
nutrient composition of, 30t-31t as anesthetic, doses of, 410t
Cornea as preanesthetic, 409
anatomy of, 319-320 doses of, 408t
examination of, 324 dosages for, 437t
scrapings of, diagnostic, 325-326 Dichelobacter nodosus, infectious footrot from, 225-226
trauma to, 329 Dictyocaulus filaria, lung infection from, 123
Corynebacterium (Actinomyces) pseudotuberculosis Diencephalon, lesions of, signs of, 290t-291t
caseous lymphadenitis from, 126-127, 207-208 Digestive system
lymph node infection from, in sheep, 8 of goats, in head and neck, examination of, 14
Corynebacterium pseudotuberculosis, abscess formation by, 379 of sheep, examination of, 5
Cotton, nutrient composition of, 31t Digoxin, dosages for, 437t
Counterirritants, injection of, in rectal prolapse correction, 96 Dinoprost, dosages for, 437t
Cowdriosis, 397-398 Disbudding, 221-222
Coxiella burnetii Dishorning, 222
abortion from, 180-181 Doe(s)
infection from, 374-375 dry, 421-422
Crackles, evaluation of, 107 estrus cycle of, 148
Cranial nerves in neurological evaluation, 278-283 gestation in, 148
Cranial tibial reflex test in neurologic lesion localization, 287-288 in late pregnancy, 421-422
Creep feeding, of lambs and kids, 51 induction of kidding in, 164
Cretinism, 189-190 kidding, 422
Crimson clover, nutrient composition of, 30t periparturient care of, 170-171
Crossed extensor reflex in neurologic lesion localization, 288 pregnant, management of, 162-163
 Index • 459

Doe(s)—cont’d Estrus cycle

puberty in, 147-148 control of, 149-152
reproductive system of, physiology of, 147 manipulation of, methods of, 150b
Donor for embryo transfer, management of, 157 of doe, 148
Dopamine, dosages for, 437t of ewe, 147
Doramectin, dosages for, 438t Ethylene glycol toxicity, renal disorders from, 260-261
Down, 198 Ewe(s)
Drug(s) estrus cycle of, 147
abortion from, 185 gestation in, 147
administration of, in goats, restraint for, 10-11 induction of lambing in, 163-164
anesthetic, withdrawal intervals for, 406t pregnant, management of, 162-163
dosages of, 435-443t reproductive system of
residues of anatomy of, 146
in goat meat and milk, avoiding, 12-13 physiology of, 146
in milk, avoidance of, 357 Excretory program in urinary tract evaluation, 255-256
skin manifestations of, 220 Exophthalmos, 338
Dry lot feeding, 45 Exploratory laparotomy, 72-73
Dublin-Johnson syndrome, 102 Extensor carpi radialis reflex test in neurologic lesion localization, 288
Dyscoria, 324-325 Extraocular muscles, anatomy of, 317-318
Dysentery, lamb, 370 Eye(s), 317-339
Dysmetria, 285 anatomy of, 317-323
Dystocia management, 164 diseases of, diagnostic tests for, 325-326
examination of, 323-325
E
of sheep, examination of, 4-5
Echocardiography in cardiovascular examination, 395-396 removal of, 339
Ecthyma, contagious, 203-204 vascular supply of, 319
vaccination for, in goats, 423-424 Eyelids
Ectropion, 327 anatomy of, 318
Ecythma, contagious, 66-67 evaluation of, 324
Edema pathology of, 326-328
malignant, 206, 372 F
udder, 345
EDTA, dosages for, 438t Facial nerve (VII)
Eggs, nematode, in feces, quantitation of, 71b in neurological evaluation, 281
Ehlers-Danlos syndrome, 219 paralysis of, 328
Ehrlichia infections, 382 Fascia, orbital, 317
Elaeophora schneideri infection, retinal disease from, 335-336 Fat
Elaeophoriasis, 328 for energy supplementation, 21-22
Elaeophorosis, 212-213 orbital, 317
Elastrator castration, 141 Fatty liver syndrome, 97-99
Electrocardiogram, evaluation of, 394-395 Febantel, dosages for, 438t
Electroejaculators, 133, 133f Fecal examination, 70
Emasculatome, Burdizzo, for castration, 141 Feces, nematode eggs in, quantitation of, 71b
Embryo transfer, 157-159 Feed(s)
Emphysema, subcutaneous, 217 analysis of, 29, 30t-32t, 32-33
Encephalitis, CAE virus, respiratory signs of, 126 for goats, 12
Encephalopathies, transmissible spongiform, 293 pelleted, 29
Endocarditis, vegetative, 398-399 Feed additives, 28-29
Endocrine system, 187-195 Feeding/nutrition, 19-60
pituitary gland in, 187-189 balancing ration in, 33, 34t-37t, 38-40
Endometritis, 168 body condition scoring in, 40-43
Endoscopy confinement feeding in, 44-45
of esophagus, 61 disorders of, 48-50
of pharynx, 61 energy in, 21-22
Endotracheal intubation, preanesthetic, 405-406, 407f-408f feed additives in, 28-29
Energy feed analysis in, 29, 30t-32t, 32-33
deficiencies in, abortion from, 185 fiber in, 29
in feeding/nutrition, 21-22 for adult male, 45-46
Enrofloxacin, dosages for, 438t for female, 46-48
Enteric infections, clostridial, 369-371 for fiber production, 54-55
Enterotoxemia, 261-262 hoof condition and, 224-225
hemorrhagic, 370 in urolithiasis prevention, 271
vaccination for, in goats, 423 minerals in, 23-27
Enterotoxigenic Escherichia coli, 80-82 feeding of, 27-28
Entropion, 326-327 of geriatric animals, 55-56
Enucleation, 339 of lamb or kid, 50-53
Environment, of sheep, examination of, 8 bottle feeding in, 50-51
Environmental pathologies, skin manifestations of, 217-219 creep feeding in, 51
Enzootic ataxia, 25, 311 finishing in, 52-53
Enzootic hematuria, 273 weaning in, 51-52
Enzootic nasal tumor, 110 of show animals, 54
Enzootic pneumonia, 115-116 of yearlings, 53-54
Eperythrozoon ovis in blood and tissue, 381-382 parenteral nutrition in, 56-60
Epidermolysis bullosa, 219 pastures in, 43-44
Epididymectomy, 142 pelleted feeds in, 29
Epididymitis programs for, 43-45
in older males, 137 protein in, 22-23
in younger males, 137-138 range in, 44
Epidural anesthesia, 416 vitamins in, 27
Epinephrine, dosages for, 438t water in, 19-20
Epiphysitis, 250 Femoral fractures, 231
Epitheliogenesis imperfecta, 219 Femoral nerve paralysis, 292
Eprinomectin, dosages for, 438t Fenbendazole, dosages for, 438t
Equine chorionic gonadotropin, dosages for, 442t Fenprostalene, dosages for, 438t
Ergot, reproductive dysfunction from, 172 Fern, bracken, retinal degeneration from, 336
Ergot alkaloids, reproductive dysfunction from, 172 Fertilization, in vitro, 159-160
Ergot toxicosis, musculoskeletal manifestations of, 251 Fescue, tall, nutrient composition of, 31t
Erysipelothrix polyarthritis, 237 Fescue hay, analysis of, 33b
Erythema in skin diseases, 199 Fescue toxicity, skin manifestations of, 214
Erythromycin, dosages for, 438t Fetal hydrops, 166
Escherichia coli, enterotoxigenic, 80-82 Fetal membranes, retained, 167-168
Esophagus Fetotomy, 166
diseases of, 67-68 Fiber
diagnostic procedures for, 61 in feed analysis, 29, 32
obstruction of, 67-68 in feeding/nutrition, 29
Estradiol cypionate, dosages for, 438t production of, anatomy related to, 198
Estrogen-reproducing plants, reproductive dysfunction from, 173 Fibromas, interdigital, 227-228
Estrone sulfate in pregnancy determination, 162 Fibropapillomatosis, 219-220
460 • Index
Fibrous tunic, 319-320 Gastrointestinal system, 69-105
Finishing diseases of
of goats, 53 diagnostic procedures for, 69-73
of lambs, 52 abdominocentesis as, 71-72
Fish, menhaden, nutrient composition of, 31t clinicopathologic data in, 69
Fistula, teat, 347 exploratory laparotomy as, 72-73
Fixation, external, of fractures, 233-235 fecal examination as, 70
Fleece rot, 206 laparoscopy as, 72
Flexor withdrawal reflex test in neurologic lesion localization, 288 liver biopsy as, 73
Floating of teeth, 63 radiography as, 72
Flock health rumen fluid analysis as, 69-70
definition of, 429-430 ultrasonography as, 72
for goats, 421-428 of abomasum, 78-79
bucks in, 423 of forestomachs, 74-77; see also Forestomachs, diseases of
does in late pregnancy in, 421-422 of intestines, 80-97; see also Intestines
dry does in, 421-422 of reticulorumen, 77-78
facilities in, 425-426 in head and neck, of goats, examination of, 14
herd health management and, 421 Genital system, of sheep, examination of, 7
kidding does in, 422 Geriatric animals, feeding of, 55-56
kids in, 422-423 Gestation
nutritional management in, 425 feeding/nutrition during, 46-47
parasite management in, 426-428 in doe, 148
production management in, 425 in ewe, 147
vaccination protocol in, 423-425 Giardia-induced diarrhea, 83
weanlings in, 422-423 Gilbert’s syndrome, 102-103
for sheep, 429-433 Gland(s)
biosecurity aspects of, 430 adrenal, 192
culling practices in, 432 lacrimal, anatomy of, 318
diseases introduced by carrier sheep in, 433 mammary, 341-357; see also Mammary gland(s)
facility design and function in, 433 of Zeiss, 318
foot care in, 433 parathyroid, 191-192
management in, in maintaining health, 433 pituitary
monitoring in, 432 anterior, 187-188
neonatal care in, 432-433 posterior, 188-189
parasite control programs in tumors of, 189
external, 431-432 scent, removal of, 222
internal, 431 sebaceous scent, anatomy of, 197
shearing management in, 433 sweat, 197
vaccination programs in, 430-431 thyroid, enlargement of, 189-191
Floppy kid syndrome, 368 Globe, 319
Florfenicol, dosages for, 438t Glomerulonephritis, 263
Fluids, in diarrhea management, 86 mesangiocapillary, 262-263
Flukes, liver, 99-100 Glossopharyngeal nerve (IX) in neurological evaluation, 283
Flunixin meglumine, dosages for, 438t Glycerol monoacetate, dosages for, 438t
Fluorine poisoning, musculoskeletal manifestations of, 252 Glycopyrrolate as preanesthetic, doses of, 408t
Fluorosis, musculoskeletal manifestations of, 252 Goat(s)
Flushing, 46 Angora, abortion in, 185
in goats, 425 behavior patterns of, 3t
Fly strike, 212 body condition scoring for, 40, 42b, 43f
Follicle-stimulating hormone, dosages for, 438t daily nutrient requirements of, 38t
Foot drug dosages for, 435-443t
abscess of, in sheep, 8 drug residues in meat and milk of, avoiding, 12-13
diseases of, 225-228 energy requirements for, calculation of, 57b
Foot-and-mouth disease, 236, 386-387 facilities for, 11-13
Footrot feed for, 12
in sheep, 8 feeding of, 19-60
infectious, 225-227 for fiber production, 55
prevention program for, 227b for show, 54
strawberry, 205-206 geriatric, 55-56
Forage fencing for, 11-12
management of, 43-44 flock health for, 421-428; see also Flock health for goats
samples of, for copper and trace mineral analysis, 25 hard udder of, 356
Foreign body(ies) health considerations for, 9
in skin, 217 hematologic parameters for, normal, 361t
intestinal obstruction by, 94 housing for, 12
Forelimbs, of goats, examination of, 15 metal toxicity in, 259
Forestomachs, diseases of, 74-77 new, introduction of, to herd, 13
bloat as, 74-75 nutrition for, 19-60
parakeratosis as, 77 physical examination of, 13-17
reticulitis as, 77 abdomen in, 16
rumen acidosis as, 75-77 forelimbs in, 15
rumenitis as, 77 head in, 13-14
simple indigestion as, 75 hindlimbs in, 16-17
Forked teat, 343-344 neck in, 13-14
Fracture(s), 230-236 pelvis in, 16-17
casts for, 232-233, 234f thorax in, 15
external fixation of, 233-235 physiologic parameters of, 7t
mandibular, 65 Pygmy, spastic paresis in, 229-230
maxillary, 65 restraint of, 9-13
splints for, 235-236 for head, 10
Francisella tularensis, infection from, 375 for hoof trimming, 11
Free gas bloat, 74-75 for medication administration, 10-11
Frontal lobe, lesions of, signs of, 290t-291t for physical examination, 9-10
Frostbite, 218 safety considerations for, 9
in hair sheep breeds, 4 sick or injured, facilities for, 13
Frothy bloat, 74-75 water for, 12
Fundus, evaluation of, 325 Goat pox, 205, 387
Fungus(i) Goiter, 189, 190
blepharitis from, 327-328 Grains, cereal, for energy supplementation, 21
diseases of skin from, 208-210 Gram-negative sepsis, 378-379
mastitis from, 356 Granulomas, sperm, 138
Furosemide, dosages for, 438t Granulosa cell tumor, 194-195
Furstenberg’s venous ring, 341 Grass tetany, 24, 49-50
Fused teats, 343-344 Grasses
Fusibacterium infections, 376 causing staggers, 315t
nutrient composition of, 30t-32t
G
Griseofulvin, dosages for, 439t
Gait in neurologic lesion localization, 284-285 Growth hormone (GH), 187
Galactorrhea, 193-195 Guaifenesin as anesthetic, doses of, 410t
Gastrocnemius reflex test in neurologic lesion localization, 288 Guaifenesin-ketamine-xylazine, dosages for, 439t
 Index • 461

Guard hairs, 198 I

Gynecomastia, 345
Ileus, intestinal, 94-95
H Impaction
abomasal, 79
Habitual abortion syndrome in Angora goats, 185, 192
rumen, 77
Hair
Impression smear in skin disease diagnosis, 202
in hair sheep breeds, 4
In vitro fertilization, 159-160
loss of, in hair sheep breeds, 4
Inappropriate lactation syndrome, 193-195
Hair follicles, 197-198
Incontinence, urinary, 272
Hair sheep breeds, hair and skin in, 4
Indigestion, simple, 75
Hairy heel wart, 227
Infection(s)
Hairy shaker disease
ovine lentivirus, 118-120
abortion and, 177
umbilical, 104-105
of lambs, 219
zoonotic, 374-376
Halothane as anesthetic, 411
Infectious conjunctivitis, 329
“Hard milker,” 345-346
Infectious footrot, 225-227
Hay, fescue, analysis of, 33b
Inflammation
Head
mammary gland, 349; see also Mastitis
fetal, malposition or lateral deviation of, 165
pericardial, 401-402
of goat
Inherited retinal degeneration, 336
examination of, 13-15
Injection(s)
restraint of, 10
of counterirritants in rectal prolapse correction, 96
of sheep, examination of, 4-5
restraint of goat for, 10-11
swelled, 206
Insemination, artificial, 154-157
Heart
Insulin, dosages for, 439t
auscultation of, 393
Integumentary system, 197-222; see also Hair; Skin
diseases of, 396-401
Interdigital fibromas, 227-228
acquired, 397-401
Intermammary groove, 341
congenital, 396-397
Interstitial nephritis, 264
of goats, examination of, 15
Intertrigo, 217
Heartwater disease, 397-398
Intestines, 80-97
Heat stress, reproductive dysfunction from, 173-174
Hemangioma, 220 atresia of, 94
diseases of, diarrhea in, 80-88; see also Diarrhea
Hematology, basic, 359-360
ileus of, 94-95
Hematoma, 217
obstruction of, 94-97
Hematuria, enzootic, 273
parasitism in, 88-93; see also Parasitism, intestinal
Hemicastration, 141
Intramuscular injection, restraint of goat for, 10, 11f
Hemogram, changes in, 361-362
Intraocular pressure, evaluation of, 325
Hemolymphatic system, of goats
Intubation, preanesthetic, 405-406, 407f-408f
abdominal, examination of, 16
Intussusception, 94
in head and neck, examination of, 15
Iodine deficiency, 26
in thorax and forelimbs, examination of, 15
abortion associated with, 177
pelvic and hindlimb, examination of, 16
skin manifestations of, 214
Hemolysis, causes of, 361
Ionophores
Hemorrhage, abomasal, 78-79
as feed additives, 28
Hemorrhagic enterotoxemia, 370
toxicity of, myocardial damage from, 400-401
Hepatitis
Iridocorneal angle, 321
halothane-induced, 411
Iris
toxic, 101-102
anatomy of, 320-321
Hepatogenous photosensitization, 219
examination of, 324-325
Herd management, 421-433; see also Flock health
Iron, dosages for, 439t
Hereditary chondrodysplasia, 228-229
Isoflurane as anesthetic, 411
Hernia
Ivermectin
diaphragmatic, respiratory signs of, 127
dosages for, 439t
umbilical, 104
for Oestrus ovis infestation, 110-111
Herpesvirus
caprine, 275 J
respiratory disease from, 115
Hindlimbs, of goats, examination of, 16-17 Jaagsiekte, 118
Holangiotic, definition of, 322 Jaw, lumpy, 65
Holocrine glands, anatomy of, 197 Johne’s disease, 92-93
Hoof Johnson grass, nutrient composition of, 31t
care of, general, 223-225 Joint(s)
trimming of, in goats, restraint for, 11 bacterial infections of, 236-238
Hormone(s) disease of, degenerative, 244-245
antidiuretic, 188 Juvenile sepsis, 373-374
assays of, in pregnancy determination, 162 K
growth, 187
parathyroid, 191-192 Kemp, 198
thyroid-stimulating, 187 Keratitis
thyrotrophin-releasing, 187 mycotic, 332
Horn anesthesia, 416-417 parasitic, 332
Horner’s syndrome, 292 Keratoconjunctivitis
Horns, removal of, 221-222 mycoplasmal, 376
Horse flies, elaeophorosis and, 212 viral, 332
Humeral fractures, 231 Ketamine hydrochloride
Hyaloid artery, persistence of, 335 as anesthetic, 411
Hydranencephaly, 229, 312-313 doses of, 410t
Hydrocephalus, 312 dosages for, 439t
Hydrogen cyanide toxicity, respiratory problems from, 125 Ketoprofen, dosages for, 439t
Hyperbilirubinemia, congenital, 102 Kid(s)
Hyperkeratosis in skin diseases, 199 feeding of, 50-53
Hyperparathyroidism, nutritional secondary, 191-192 bottle, 50-51
Hyperthermia, neonatal, 367-368, 368 creep, 51
Hypertonic saline, dosages for, 439t finishing in, 52-53
Hypocalcemia, 48-49 weaning in, 51-52
in pregnancy, 169 finisher diets for, 53t
Hypoglossal nerve (XII) in neurological evaluation, 283 floppy, 368
Hypoglycemia, neonatal, 368 management of, 422-423
Hypomagnesemia, 49-50 weaning of, 422-423
Hypospadias, 273 Kidding, generic management calendar for, 428b
Hypothalamus, ventral, lesions of, signs of, 290t,-291t Kidding does, 422
Hypothermia, neonatal, 367, 368 Kidney(s)
Hypothyroidism, neonatal, 189-190 biopsy of, 256
Hypotrichosis, 199 disease of
congenital, 219 chronic, 262-265
Hypoventilation complicating anesthesia, 415 pulpy, 261-262
Hypoxemia, neonatal, 368 failure of, acute, 259
neoplasms of, 273
462 • Index
Kidney(s)—cont’d Lymphatic system—cont’d
plants toxic to, 257t of sheep, examination of, 8
polycystic, 273 viral diseases of, 384-387
Lymphosarcoma, 363
L
Lysosomal storage diseases, inherited, 316t
Lacerations, teat, 346-347 M
Lacrimal gland, anatomy of, 318
Lacrimal system, anatomy of, 318-319 Macrolides, resistance to, 90
Lactation Maedi, 118-120
aberrant, 193-195 Magnesium
feeding/nutrition during, 47-48 dosages for, 439t
water intake and, 20 in feeding/nutrition, 24
Lactoliths, 346 Maize, nutrient composition of, 30t-31t
Ladino clover, nutrient composition of, 30t Male pseudohermaphrodites, 139
Lamb(s) Malignant contagious ecthyma, 204
dysentery in, 370 Malignant edema, 206, 372
feeding of, 50-53 Mammary gland(s), 341-357; see also Milk; Teat(s); Udder(s)
bottle, 50-51 anatomy of, 341
creep, 51 biopsy of, 342
finishing in, 52-53 “blind,” 345
for show, 54 diseases of, 343-345
weaning in, 51-52 “hard milker,” 345-346
finisher diets for, 53t inflammation of, 349; see also Mastitis
hairy shaker disease of, 219 neoplasia of, 357
Lambing of sheep, examination of, 7-8
generic management calendar for, 428b poor suspensory ligament support for, 344
management of, 169-170 ultrasound of, 342
Laminitis, 227 zoonotic pathogens affecting, 355-356
Laparoscopic insemination, 156-157 Mandibular fractures, 65, 231
Laparoscopy, of abdomen, 72 Manganese deficiency, abortion associated with, 178
Laparotomy, exploratory, 72-73 Mange
Laryngeal chondritis, 112 chorioptic, 211-212
Laryngitis, necrotic, 112 demodectic, 212
Lasalocid psoroptic, 211
as feed additive, 28 sarcoptic, 211
dosages for, 439t Mange mites, 211
Lateral geniculate, lesions of, signs of, 290t-291t Mannitol, dosages for, 440t
Laurel toxicity, 79 Mastectomy for inappropriate lactation, 195
Lead toxicity, 308 Mastitis, 349
Leg, front, fetal, malposition of, 165 acute, 349-350
Leiomyoma, 273 bacterial, 351
Lens treatment and prevention of, 353-354
anatomy of, 320 chronic indurative, of sheep, 356
evaluation of, 325 coliform, 350
Leptospira interrogans, 375 fungal, 356
Leptospirosis, 375 Mycoplasma, 354-355
abortion and, 182 prevention of, 356, 357t
renal manifestations of, 262 subclinical, 351-353
Leukogram, changes in, 362 viral, 356-357
Levamisole, dosages for, 439t Mastitis test, California, 343
Libido serving capacity Maxilla, fractures of, 65
of buck, testing of, 132 McMaster’s quantitative technique for nematode egg quantitation in feces, 71b
of ram, testing of, 131 Meat, goat, drug residues in, avoiding, 12-13
Lice, 210-211 Mebendazole, dosages for, 440t
Lidocaine Medetomidine hydrochloride
as local anesthetic, 412 as anesthetic, doses of, 410t
dosages for, 439t as preanesthetic, doses of, 408t
Limb posture in neurologic lesion localization, 286 dosages for, 440t
Limbic system, lesions of, signs of, 290t-291t Medications; see also Drug(s)
Lincomycin hydrochloride, dosages for, 439t administration of, in goats, restraint for, 10-11
Lincomycin/spectinomycin, dosages for, 439t Melanoma, 220
Lip and leg ulceration, 274 Melengesterol acetate, dosages for, 440t
Listeria monocytogenes, 375-376 Melophagus ovinus, 211
Listeria monocytogenes conjunctivitis, 332 Menace test, 324
Listeriosis, 298-299, 375-376 Menhaden fish, nutrient composition of, 31t
abortion and, 184 Meningitis, bacterial, 297-298
Liver Mental status in neurological evaluation, 278
abscesses of, 97 Meperidine hydrochloride as preanesthetic, 409
biopsy of, 73 doses of, 408t
diseases of, 97-103 Mesaesophagus, 68
Liver flukes, 99-100 Mesangiocapillary glomerulonephritis, 262-263
Locomotor system Mesencephalon, lesions of, signs of, 290t-291t
in sheep, examination of, 8 Mesentery, root of, torsion of, 94
of sheep, examination of, 8 Metabolic acidosis, neonatal, 368
Locoweed Metabolic conditions of musculoskeletal system, 246-250
reproductive dysfunction from, 172 Metacarpal bones, fractures of, 230-231
retinal disorders from, 336 Metal toxicity in goats, 259
Louping ill, 385 Metatarsal bones, fractures of, 230-231
Lower motor neuron (LMN), lesions of Metencephalon, lesions of, signs of, 290t-291t
localization chart for, 289t Methocarbamol, dosages for, 440t
signs of, 289t Methohexital, dosages for, 440t
Lower motor neuron (LMN) reflexes in neurologic lesion localization, 286-288 Methohexitone, dosages for, 440t
Lumbosacral epidural anesthesia, 416 Methylene blue, dosages for, 440t
Lumpy jaw, 65 Metoclopramide, dosages for, 440t
Lumpy wool, 208-209 Metritis, 168
Lumpy wool disease, 205-206 Microbial culture in skin disease diagnosis, 202
Lungs Microphthalmia, congenital, 338
biopsy of, 109 Midazolam, dosages for, 440t
of goats, examination of, 15 Milk
Lyme disease, 242 drug residue avoidance in, 357
Lymphadenitis, caseous, 207-208 goat
anesthesia and, 413 drug residues in, avoiding, 12-13
control program for, 209b mastitis, pathogens isolated from, 352b
respiratory signs of, 126-127 in diarrhea management, 86-87
vaccination for, in goats, 424 sheep/goat
Lymphatic system antibiotic sensitivity testing of, 342
assessment of, 362-363 California mastitis test for, 343
diseases of, 363-371 composition of, as percentage of dry matter, 50b
in sheep, examination of, 8 culture of, 342
 Index • 463

Milk—cont’d Nematodiasis, cerebrospinal, 303-305

sheep/goat—cont’d Neomycin soluble powder, dosages for, 440t
flow of, obstruction of, 345-355 Neonate
production of, 342 care of, 169-170
somatic cell culture on, 342-343 depression in, causes of, 367-368
tests on, interpretation of, 353t diarrhea in, uncomplicated, 365-367
zoonotic pathogens contaminating, 355-356 hypothyroidism in, 189-190
Milk replacer(s) sepsis in, 364-365
for orphaned newborn, 50 weakness in, causes of, 367-368
in diarrhea management, 86-87 Neoplasia
Milk stones, 346 eyelid, 328
Milo, nutrient composition of, 32t mammary gland, 357
Mineral oil, dosages for, 440t musculoskeletal, 253
Minerals renal, 273
feeding of, 27-28 respiratory, 127
hoof condition and, 225 skin, 219
in feeding/nutrition, 23-27 urinary tract, 273
supplemental Neospora caninum infections, 383
for parenteral nutrition, guidelines on, 59b Nephritis, interstitial, 264
in pasture feeding, 44 Nerve(s)
Mint, Perilla, atypical interstitial pneumonia from, 124-125 cranial, in neurological evaluation, 278-283
Mites optic, 323
mange, 211 peripheral, damage to, effects of, 285t
sheep itch, 211 Nerve block(s), 416-417
Molasses, nutrient composition of, 31t auriculopalpebral, in ophthalmic examination, 325
Monensin sodium Nervous system
as feed additive, 28 in sheep, examination of, 8
dosages for, 440t of sheep, examination of, 8
Morantel tartrate Netobimin, dosages for, 440t
as feed additive, 28 Neural tunic, anatomy of, 322-323
dosages for, 440t Neurohypophysis, 188-189
Mouth; see also Oral cavity Neurologic system, 277-316
broken, 5 ancillary tests of, 293
sore, 66-67 diseases of, 293-316
wave, 63 bacterial meningitis as, 297-298
Moxidectin, dosages for, 440t botulism as, 306-307
Mucous membranes, assessment of, 394 brain abscesses as, 300
Muellerius capillaris, lung infection from, 123f, 124, 124f caprine arthritis-encephalitis as, 296
Murmur, washing machine, 401 cerebrospinal nematodiasis as, 303-305
Muscles, extraocular, anatomy of, 317-318 enzootic ataxia as, 311
Muscular dystrophy, nutritional, 246-248 hydranencephaly as, 312-313, 315
Musculoskeletal system, 223-254 hydrocephalus as, 312, 315
anatomy of, 223 lead toxicity as, 308
congenital conditions of, 228-230 listeriosis as, 298-299
examination of, 223 organophosphate toxicosis as, 307-308
hoof care in, 223-225 otitis externa as, 300-301
metabolic conditions affecting, 246-250 otitis interna as, 300-302
neoplasia of, 253 otitis media as, 300-302
nutritional conditions affecting, 246-250 plants associated with, 314t
of goats polioencephalomalacia as, 309-310
abdominal, examination of, 16 pseudorabies as, 297
head and neck, examination of, 13-14 rabies as, 296-297
pelvic and hindlimb, examination of, 16 scrapie as, 293-295
thoracic and forelimb, examination of, 15 sodium toxicosis as, 308-309
toxic conditions affecting, 250-252 spinal trauma/abscesses/tumors as, 311-312
traumatic conditions affecting, 230-245 tetanus as, 305-306
fractures as, 230-236; see also Fracture(s) tick paralysis as, 307
infectious conditions and, 236-245 urea toxicity as, 309
predator attack as, 230 water deprivation as, 308-309
Mycetoma, 209 examination of, 277-283
Mycobacteria, infection by, 380-381 history in, 277
Mycoplasma observations in, 278-283
conjunctivitis from, 329-331 signalment in, 277
diseases from, 376 in head and neck, of goats, examination of, 15
Mycoplasma mastitis, 354-355 lesions of, localization of, 283-289, 289t-291t, 292
Mycoplasma mycoides cluster, 116 gait in, 284-285
Mycoplasma pneumonia posture/postural reactions in, 286
of goats, 116-117 sensorium in, 283-284
of sheep, 115-116 spinal reflexes in, 286-288
Mycoplasmal polyarthritis, 238-239 of goats, in thorax and forelimbs, examination of, 15
Mycoplasmosis, abortion and, 184-185 Neuropathies, peripheral, 292
Mycotic keratitis, 332 Neutral detergent fiber (NDF), 29, 32
Mycotoxins, skin manifestations of, 215-217 Neutralizing agents as feed additives, 29
Myelencephalon, lesions of, signs of, 290t-291t Niacin, dosages for, 440t
Myodegeneration, nutritional, 398 Nictitating membrane, 318
Myonecrosis, clostridial, 242-243 abnormalities of, 328
Myotonia, 285 Nitrate nitrogen in water, dangerous concentrations of, 20t
Myotonia congenita, 228 Nitrate-nitrite toxicity
abortion from, 185
N
hoof condition and, 225
Nandrolone phenproprionate, dosages for, 440t respiratory problems from, 125
Nasal bot Nitrogen
in sheep, 5 nitrate, in water, dangerous concentrations of, 20t
nasolacrimal infection from, 328 non-protein, in feeding/nutrition, 22
Nasal swab in respiratory system evaluation, 108 Nitroxynil, dosages for, 440t
Nasal tumor, enzootic, 110 Nodules, skin, in hair sheep breeds, 4
Nasolacrimal system Non-protein nitrogen (NPN), in feeding/nutrition, 22
anatomy of, 318-319 Non-steroidal antiinflammatory drugs (NSAIDs), in diarrhea management, 87
disease of, 328 Norgestomet implant, dosages for, 440t
evaluation of, 324 Nose, tumor of, enzootic, 110
Neck, of goat, examination of, 13-15 Nutrition, 19-60; see also Feeding/nutrition
Necrotic laryngitis, 112 abnormalities of, reproductive dysfunction from, 173
Nematode eggs in feces, quantitation of, 71b deficiencies in
Nematode infestation, 88-92 abortion from, 185
clinical signs of, 89 hydranencephaly from, 313
control program for, 89-92 in flock health management, in goats, 425
diagnosis of, 89 parenteral, 56-60
etiology of, 88-89 Nutritional diarrhea, 83-84
pathogenesis of, 88-89
treatment of, 89-92
464 • Index
Nutritional diseases Paralysis—cont’d
of musculoskeletal system, 246-250 radial nerve, 292
of skin, 214-215 sciatic nerve, 292
Nutritional muscular dystrophy, 246-248 tick, 307
Nutritional myodegeneration, 398 Paraphimosis, 139, 140
Nutritional secondary hyperparathyroidism, 191-192 Parasite-resistant sheep and goats, selection of, 91
Nyctalopia, 336-337 Parasites
Nystagmus, positional, 280 blepharitis from, 328
O blood and tissue, 381-382
causing bronchitis, 123-124
Oak toxicity, 261 in flock health management
Oat cells in pasteurellosis, 113 for sheep, 431-432
Oats, nutrient composition of, 31t in goats, 426-428
Obstructive urolithiasis, anesthesia and, 413 intestinal, 88-93
Obturator nerve paralysis, 292 cestode infestation as, 92
Oculomotor nerve (III) in neurological evaluation, 279-280 Johne’s disease from, 92-93
Oestrus ovis, nasolacrimal infection from, 328 nematode infestation as, 88-92; see also Nematode infestation
Oestrus ovis infestation, 110f, 110-111 keratitis from, 332
Olfactory nerve (I) in neurological evaluation, 278-279 otitis from, 301
Omphalophlebitis, in sheep, 5 renal disorders from, 264
Onchocerca species infestation, 213 skin diseases from, 210-213
Ophthalmic examination, 323-325 Parathyroid gland, 191-192
Ophthalmoscopy, indirect, 325 Paratuberculosis, 92-93
Opioid analgesics, 409-410 Parenteral nutrition (PN), 56-60
OPP; see Ovine progressive pneumonia problems with, serum chemistry changes indicating, 57t
Opportunistic deworming, 90 solutions for, recipes for, 58t
Optic nerve (II), 323 Paresis, 285
in neurological evaluation, 279 spastic, 229-230
Oral cavity Parturition, 163
diseases of, 61-67 induction of, 163-164
actinobacillosis as, 65 Passive transfer failure, 363-364
actinomycosis as, 65 Pasteurella haemolytica
bluetongue as, 66 bluebag from, 350-351
contagious ecthmya as, 66-67 infection from, 377
periodontitis as, 63-64 Pasteurella multocida infections, 377
pharyngeal abscess as, 65 Pasteurella trehalosi infections, 377
salivary cysts as, 65 Pasteurellosis, 112-114, 377
tooth root abscesses as, 64 Pastures
fractures of, 65 in feeding program, 43-44
Orbit safe, in deworming programs, 89-90
anatomy of, 317 Patella luxation, 229
evaluation of, 324 Patellar reflex in neurologic lesion localization, 287
pathology of, 338 Patent ductus arteriosus (PDA), 396-397
Orchard grass, nutrient composition of, 31t Peanut, nutrient composition of, 31t
Orchitis, 138 Pearson square in balancing ration, 39
Organophosphate toxicosis, 307-308 Pediculosis, 210-211
Orphans, feeding of, 50-51 Pelleted feeds, 29
Orthokertosis in skin diseases, 199 Pellets in semen storage, 144
Osteochondrosis, 250 Pelvis, of goats, examination of, 16-17
Osteodystrophia fibrosa, 249-250 Pemphigus foliaceus, 213-214
Osteomalacia, 248-249 Penicillamine, dosages for, 441t
Osteomyelitis, 239 Penicillin G, dosages for, 441t
Otitis externa, 300-301 Penis
clinical signs of, 301 abnormalities of, 139-140
pathogenesis of, 301 anatomy and physiology of, 129
treatment of, 302-303 translocation of, 142-143
Otitis interna, 300-302 Penning for umbilical hernia, 104
clinical signs of, 302 Pentobarbital, dosages for, 441t
diagnosis of, 302 Pericardial disease, 401-402
pathogenesis of, 301-302 Pericarditis, 401-402
treatment of, 303 Perilla mint, atypical interstitial pneumonia from, 124-125
Otitis media, 300-302 Perineal reflex in neurologic lesion localization, 288
clinical signs of, 302 Periodontitis, 63-64
diagnosis of, 302 Peripheral nerves, damage to, effects of, 285t
pathogenesis of, 301-302 Peripheral neuropathies, 292
treatment of, 303 Peripheral pulses, assessment of, 393
Ovariectomy, 174-175 Peritonitis, 95
Ovary(ies) Peroneal nerve injury, 292
disease of, cystic, reproductive dysfunction from, 174 Peste des petits ruminants, 384-385
tumors of, reproductive dysfunction from, 174 Pestivirus, hydrocephalus/hydranencephaly from, 313
Ovine herpesvirus, respiratory disease from, 115 Pharyngitis, 111
Ovine lentivirus (OvLV) infection, 118-120 Pharynx
Ovine progressive pneumonia (OPP), 118-120 abscess of, 65
hematologic/lymphatic manifestations of, 388-389 inflammation of, 111
mammary glands in, 7-8 Phenothiazine derivatives as preanesthetics, 406
musculoskeletal manifestations of, 241-242 Phenylbutazone, dosages for, 441t
Ovine venereal disease, 274-275 Pheochromocytomas, 192
Oxalate toxicity, renal disorders from, 260 Phimosis, 139
Oxfendazole, dosages for, 440t Phosphorus
Oxyclozanide, dosages for, 440t calculating, in ration balancing, 39-40
Oxytetracycline hydrochloride in feeding/nutrition, 23
dietary, 28 Photoreceptors, 322
for pasteurellosis, 113 Photosensitization, 215
Oxytetracycline hydrochloride, dosages for, 441t causes of, 216t
Oxytocin, 188-189 hepatogenous, 219
dosages for, 441t in hair sheep breeds, 4
Physical examination
P
of goats, 13-17; see also Goats, physical examination of
Palpebral reflex test, 324 of sheep, 1-9; see also Sheep, physical examination of
Pancreas, 192-193 Pithomycotoxicosis, 215-216
Papillomas, 219-220 Pituitary adenomas, 194
Papules in skin diseases, 199 Pituitary gland
Parainfluenza type 3, respiratory disease from, 114 anterior, 187-188
Parakeratosis, 77 posterior, 188-189
in skin diseases, 199 tumors of, 189
Paralysis Pizzle rot, 274
facial nerve, 328 Plant cardiotoxicity, 399-400
femoral nerve, 292 Plants
obturator nerve, 292 causing gastrointestinal or hepatic disease, 102t-103t
plants associated with, 314t nephrotoxic, 257t
 Index • 465

Plants—cont’d Psoroptic mange, 211

neurologic diseases associated with, 314t Ptosis, oculomotor nerve dysfunction and, 279
toxicities of Ptyalism, in sheep, 5
abortion associated with, 177 Puberty
musculoskeletal manifestations of, 252 in buck, 130
pneumonias from, 124-125 in doe, 147-148
renal disorders from, 260 in ram, 130
reproductive dysfunction from, 171-173 Pulpy kidney disease, 261-262
retinal disorders from, 336 Pulses
with high oxalate content, 260t assessment of, 394
Pleuritis, 128 peripheral, assessment of, 393
Pleuropneumonia, contagious caprine, 117-118 Purse-string suture in rectal prolapse correction, 95-96
Pneumocystis carinii pneumonia, 127 Pustules in skin diseases, 199
Pneumonia(s) Pyelonephritis, 263
aspiration, 124 Pygmy goats, spastic paresis in, 229-230
atypical, 115-116, 123-124 Pyometra, 168
atypical interstitial, from plant toxicities, 124-125 Pyrantel pamoate, dosages for, 442t
Chlamydia, 118 Q
chronic nonprogressive, 115-116
complicating anesthesia, 414-415 Q fever, abortion and, 180-181
enzootic, 115-116 Queensland fever, abortion and, 180-181
herpesvirus, 115 Query fever, abortion and, 180-181
in sheep, 5
R
Mycoplasma
in goats, 116-117 Rabies, 296-297
in sheep, 115-116 in sheep, 8
ovine progressive, 118-120 Radial fractures, 231
mammary glans in, 7-8 Radial nerve paralysis, 292
musculoskeletal manifestations of, 241-242 Radiography
Pasteurella, 112-114 contrast, in urinary tract evaluation, 255-256
Pneumocystis carinii, 127 in pregnancy determination, 162
respiratory syncytial virus, 114-115 in respiratory system evaluation, 108
typical, 112-114 of abdomen, 72
verminous, 123-124 of head and neck, 61
Pneumothorax, 127-128 thoracic, in cardiovascular examination, 396
Poisoning, fluorine, musculoskeletal manifestations of, 252 Rain scald, 205-206
Polioencephalomalacia (PEM), 309-310 Ram(s)
Poloxaline, dosages for, 441t breeding soundness examination in, 132-135
Polyarthritis breeding soundness prediction in, 134-135
chlamydial, 238 physical examination in, 132
Erysipelothrix, 237 scrotal circumference in, 132-133, 133t
mycoplasmal, 238-239 semen evaluation in, 133-134
Polycystic kidneys, 273 serologic screening in, 135
Polydactyly, 229 testicular biopsies in, 135
Positional nystagmus, 280 ultrasonography in, 135
Posthitis, ulcerative, 274 puberty in, 130
Postural reactions in neurologic lesion localization, 286 recommended male-to-female ratios for, 153t
Posture in neurologic lesion localization, 286 seasonal breeding activity of, 130
Potassium, in feeding/nutrition, 24 selection and management of, 131
Pox, sheep and goat, 205, 387 Ram effect in estrus cycle control, 150
Praziquantel, dosages for, 441t Range feeding, 44
Preanesthetic preparation, 405-406 Ration
Preanesthetics, 406-410 balancing, 33, 34t-37t, 38-40
a2 agonists as, 406-409 calculating phosphorus and calcium supplementation in, 39-40
benzodiazepines as, 409 fixed ingredients in, 33, 38-39
opioid analgesics as, 409-410 Pearson square in, 39
phenothiazine derivatives as, 406 substitution method of, 33
Precocious udder, 193, 344-345 for sheep, examination of, 9
Pregnancy Recipients for embryo transfer, management of, 157-158
anesthesia and, 414 Rectum
determination of, 160-162 atresia of, 94
termination of, 163-164 prolapse of, 95-97
water intake and, 20 Red water disease, 373
Pregnancy toxemia, 97-99, 168-169 Reflexes, spinal, in neurologic lesion localization, 286-288
Preparturient disease, 166-169 Regurgitation, complicating anesthesia, 414-415
Prepubic tendon, rupture of, 166 Relative feed value (RFV), 33
Pressures, venous, assessment of, 394 Renal biopsy, 256
Production management, in goats, 425 Reproduction; see also Breeding
Progesterone, in pregnancy determination, 162 dysfunction of, 171-175; see also Abortion
Progestins in estrus cycle control, 151 failure of, 171
Prolactin (PRL), 187 female, 146-185
Prolapse ring in rectal prolapse correction, 96 breeding management in, 149-152
Propofol breeding soundness examination for, 149
as anesthetic, 411 female management in, 162-163
doses of, 410t male, 129-145
dosages for, 442t anatomy and physiology in, 129-130
Propylene glycol, dosages for, 442t diseases affecting, 137-140
Prostaglandins epididymitis as, 137-138
in estrus cycle control, 150-151 intersex as, 139
in pregnancy termination, 163 orchitis as, 138
Protein penile abnormalities as, 139-140
crude, in feed analysis, 32 sperm granulomas as, 138
deficiencies in, abortion from, 185 testicular hypoplasia and degeneration as, 138-139
in feeding/nutrition, 22-23 varicoceles as, 137
Protein B, pregnancy-specific, in pregnancy determination, 162 puberty and, 130
Protostrongylus rufescens, lung infection from, 123-124 seasonality and, 130
Pruritus special procedures related to, 140-143
in hair sheep breeds, 4 Reproductive system, of goats, examination of, 16-17
in skin diseases, 199 Respiratory syncytial virus (RSV), respiratory disease from, 114-115
Pseudohermaphrodites, male, 139 Respiratory system
Pseudorinderpest, 344-345 diseases of, 107-128
Pseudomonas, mastitis from, 351 evaluation of, 107-109
Pseudopregnancy, 174 in head and neck, of goats, examination of, 14
inappropriate lactation in, 193-194 of goats
Pseudorabies, 297 abdominal, examination of, 16
in sheep, 8 in thorax and forelimbs, examination of, 15
Psorergates ovis, 211 of sheep, examination of, 5
Psoroptes cuniculi infestation, 211 upper, diseases of, 110-112
of ear, 301 viral diseases of, acute, 114-120
466 • Index
Restraint, of goats, 9-13 Sheep—cont’d
Retained fetal membranes, 167-168 feeding of—cont’d
Reticular activating system, lesions of, signs of, 290t-291t for wool production, 54-55
Reticulitis, 77 geriatric, 55-56
Reticuloperitonitis, traumatic, 77 flock health for, 429-433; see also Flock health for sheep
Reticulorumen, diseases of, 77-78 hematologic parameters for, normal, 361t
Retina nutrition for, 19-60
degeneration of, inherited, 336 physical examination of, 1-9
pathology of, 335-337 body systems in, 3-4, 5, 7-8
plant toxicity affecting, 336 cardiovascular system in, 5
sensory, 322 digestive system in, 5
Retrobulbar anesthesia, for enucleation, 339 environmental, 8
Retropharyngeal abscesses, 111-112 external, 3
Rhododendron toxicity, 79 genital system in, 7
Rice, nutrient composition of, 31t handling before and during, 1-2
Rickets, 248-249 head in, 4-5
Ringwomb, 165 locomotor system in, 8
Ringworm, 208-209 lymphatic system in, 8
Rods, 322 mammary glands in, 7-8
Rostral cerebellum, lesions of, signs of, 290t-291t necropsy findings in, 9
Rotavirus, diarrhea from, 82 nervous system in, 8
Rumen, impaction of, 77 “over the fence,” 2-3
Rumen acidosis, 75-77 ration in, 9
Rumen fluid respiratory system in, 5
analysis of, 69-70 urinary system in, 5, 7
characteristics of, normal, 71t physiologic parameters of, 7t
for transfaunation, collection, handling, and storage of, 76b Sheep itch mite, 211
Rumenitis, 77 Sheep ked, 211
Rumenotomy, 77-78 Sheep pox, 205, 387
Ruminal tympany complicating anesthesia, 415 Sheep scab, common, 211
Rupture of prepubic tendon, 166 Shock, 403-404
Rye, nutrient composition of, 31t Show animals, feeding of, 54
Ryegrass, nutrient composition of, 32t Silage in dry lot feeding, 45
Sinus centesis in respiratory system evaluation, 108
S
Sinusitis, 111
Salinomycin, dosages for, 442t Skin
Salivary cysts, 65 anatomy of, 197
Salmonellosis, 83 biopsy of, in skin disease diagnosis, 202-203
abortion and, 182-183 diseases of
Salt-mineral supplementation, 27-28 autoimmune, 213-214
Salvage deworming, 89-90 bacterial, 205-208
Sarcocystis species, infections from, 383 by breed, 198t
Sarcocystosis, 243-244 congenital, 219
Sarcoptic mange, 211 diagnostic approach to, 198-203
Scent glands, removal of, 222 diagnostic tests for, 199, 202t, 202-203
Schroeder-Thomas splint, 235-236 environmental pathologies causing, 217-219
Sciatic nerve paralysis, 292 fungal, 208-210
Sclera, anatomy of, 320 lesion distribution of, typical, 200t-201t
Scrapie, 205, 293-295 mycotoxins causing, 215-217
blindness from, 336 neoplastic, 219
clinical signs of, 294-295 nutritional, 214-215
diagnosis of, 295 parasitic, 210-213
hematologic/lymphatic manifestations of, 390 viral, 203-205
in sheep, 8 drug residue issues involving, 220
pathogenesis of, 294 foreign bodies in, 217
prevention of, 295 melanoma of, 220
treatment of, 295 of goats
Scrapie-associated fibril, 293 abdominal, examination of, 16
Screw-worm, 212 head and neck, examination of, 13-14
Scrotal circumference (SC), in breeding soundness examination pelvic and hindlimb, examination of, 16
in buck, 135-136 thoracic and forelimb, examination of, 15
in ram, 132-133, 133t of sheep
Seasonal manipulation of estrus cycle, 151-152 disease of, in physical examination, 4
Sebaceous scent glands, anatomy of, 197 in hair sheep breeds, 4
Seizures, plants associated with, 314t nodules of, in hair sheep breeds, 4
Selenium papillomas of, 219-220
dosages for, 442t scraping and cytology of, 199, 202
in feeding/nutrition, 26-27 squamous cell carcinomas of, 220
toxicity of, musculoskeletal manifestations of, 250-251 ulceration of, 217
Self-feeder for orphaned newborn, 51 Sodium, in feeding/nutrition, 23-24
Semen Sodium bicarbonate, dosages for, 442t
frozen, handling of, 145 Sodium iodide, dosages for, 442t
of buck Sodium nitrate, dosages for, 442t
collection and storage of, 144 Sodium sulfate, dosages for, 442t
collection of, 136 Sodium thiosulfate, dosages for, 442t
evaluation of, 136 Sodium toxicosis, 308-309
of ram Somatic cell culture of milk, 342-343
collection and storage of, 143-144 Sore mouth, 66-67
cooled, 144 Sorehead, 212-213, 328
evaluation of, 133-134 Sorghum, nutrient composition of, 32t
Sensoruim in neurologic lesion localization, 283-284 Soybean, nutrient composition of, 32t
Sensory retina, 322 Soybean hulls, for energy supplementation, 21
Sepsis Spastic paresis, 229-230
adult, 373-374 Spasticity, 285
bacterial causes of, 374 Sperm granulomas, 138
gram-negative, 378-379 Spider lamb syndrome, 228-229
juvenile, 373-374 Spinal reflexes in neurologic lesion localization, 286-288
neonatal, 364-365 Spinal trauma/abscesses/tumors, 311-312
treatment for, 379 Splints for fractures, 235-236
Septic arthritis, 236-238 Spoon splint, 235
Sheath rot, 274 Squamous cell carcinomas of skin, 220
Shedding, in hair sheep breeds, 4 Stachybotryotoxicosis, 217
Sheep Staggers, grass, 315t
behavior patterns of, 3t Stanozolol, dosages for, 442t
body condition scoring for, 40, 41f-42f, 43f Staphylococcal dermatitis, 206-207
daily nutrient requirements of, 34t-37t Staphylococcus aureus
drug dosages for, 435-443t arthritis from, 236-237
energy requirements for, calculation of, 57b bluebag from, 350-351
feeding of, 19-60 STAR management program, 152
for show, 54 Stiffness, 285
 Index • 467

Stomatitis, vesicular, 205, 386-387 Torsion of root of mesentery, 94

Stones, milk, 346 Total digestable nutrients (TDN), 21
Strabismus, oculomotor nerve dysfunction and, 279 equation for, 32
Strategic deworming, 89-90 Total parenteral nutrition (TPN), 56-60
Strawberry footrot, 205-206 Toxemia, pregnancy, 97-99, 168-169
Straws in semen storage, 143-144 Toxic conditions, affecting musculoskeletal system, 250-252
Streptococcus dysgalactiae arthritis, 237 Toxic hepatitis, 101-102
Streptotricosis, 205-206 Toxicity(ies)
Stress ammonia, 309
abortion and, 185 antibiotic, 259-260
heat, reproductive dysfunction from, 173-174 ethylene glycol, renal disorders from, 260-261
Subcutaneous emphysema, 217 lead, 308
Subcutaneous injections, restraint of goat for, 11 metal, in goats, 259
Submucosal resection in rectal prolapse correction, 96 oak (acorn), 261
Sugar beet, nutrient composition of, 30t plant; see Plant(s), toxicities of
Sulfamethazine, dosages for, 442t urea, 309
Sulfaquinoxaline, dosages for, 442t Toxicosis
Sulfonamides, dosages for, 443t copper, 100-101
Sulfur, in feeding/nutrition, 24 ergot, musculoskeletal manifestations of, 251
Sunburn, 218 organophosphate, 307-308
in hair sheep breeds, 4 sodium, 308-309
Supernumerary teats, 343 Toxoplasma gondii infections, 383
Superovulation for embryo transfer, 158 Toxoplasmosis, abortion and, 183-184, 383
Suppressive deworming, 90-92 Trachea, collapse of, 112
Suture(s), purse-string, in rectal prolapse correction, 95-96 Tracheal sampling in respiratory system evaluation, 108
Swayback, 311 Transcervical insemination, 155-156
Sweat glands, 197 Transfaunation for rumen acidosis, 76
Swelled head, 206 Transmissible spongiform encephalopathies, 293
Synchronization of embryo transfer, 158 Trauma
conjunctival, 329
T
corneal, 329
Tactical deworming, 90 spinal, 311-312
Tail docking, 253-254 Traumatic conditions, affecting musculoskeletal system, 230-245
Tapeworms, 92 Traumatic reticuloperitonitis, 77
Tarsus, fractures of, 231 Triceps reflex test in neurologic lesion localization, 288
Teaser preparation, 141-142 Triclabendazole, dosages for, 443t
Teat(s) Trigeminal nerve (V) in neurological evaluation, 280-281
accessory, 343 Trimethoprim-sulfonamide, dosages for, 443t
anatomy of, 341 Triticale, nutrient composition of, 32t
bifid, 343-344 Trochlear nerve (IV) in neurological evaluation, 280
fistula of, 347 Trunk posture in neurologic lesion localization, 286
lacerations of, 346-347 Trypanosomiasis, African, 402-403
supernumerary, 343 Tsetse flies, African trypanosomiasis and, 402
web, 344 Tube cystotomy for urolithiasis, 268-270
weeping, 344 Tuberculosis, 126, 380-381
Teat “spider,” 346 Tubular necrosis, acute, 259
Telazol as anesthetic, 411 antibiotics causing, 259-260
Telogen defluxion, 218 Tumor(s)
Tendon, prepubic, rupture of, 166 granulosa cell, 194-195
Testicles nasal, enzootic, 110
anatomy and physiology of, 129 ovarian, reproductive dysfunction from, 174
biopsy of, in breeding soundness examination, of ram, 135 pituitary gland, 189
examination of, in buck, 135 skin, 219
hypoplasia and degeneration of, 138-139 spinal, 311-312
Testosterone proportionate, dosages for, 443t Tunica albuginea, 129
Tetanus, 305-306 Twinning rates, increasing, 152
in sheep, 8 Tylosin, dosages for, 443t
vaccination for, in goats, 423 Tympany, ruminal, complicating anesthesia, 415
Tetany, grass, 24, 49-50 U
Tetrahydropyrimidines, resistance to, 90
Tetralogy of Fallot, 396 Udder(s)
Thalamus, lesions of, signs of, 290t-291t amputation of, 347-349
Theriogenology, 129-195; see also Reproduction asymmetric, 344, 345f
Thiabendazole, dosages for, 443t edema of, 345
Thiamine, dosages for, 443t hard, of goats, 356
Thiopental sodium in sheep, examination of, 8
as anesthetic, 410-412 precocious, 193-195, 344-345
dosages for, 443t uneven, 344, 345f
Thiophanate, dosages for, 443t Ulceration
Third eyelid flaps for ulcerative keratitis, 333 cutaneous, 217
Thoracentesis, in respiratory system evaluation, 108 lip and leg, 274
Thorax, of goats, examination of, 15 Ulcerative dermatosis, 204, 274-275
Thyroid gland enlargement, 189-191 Ulcerative posthitis, 274
Thyroid-stimulating hormone (TSH), 187 Ultrasonography
Thyrotrophin-releasing hormone (TRH), 187 in breeding soundness examination, of ram, 135
Tibial fractures, 231 in pregnancy determination, 160-162
Tick paralysis, 307 in respiratory system evaluation, 108, 109f
Ticks, in heartwater disease transmission, 397-398 in urinary tract evaluation, 255, 256f
Tiletamine as anesthetic, doses of, 410t of abdomen, 72
Tiletamine-zolazepam, dosages for, 443t of mammary glands, 342
Tilmicosin, dosages for, 443t Umbilical hernia, 104
Tissue-invading Clostridia, 368-373 Umbilicus, pathology of, 104-105
Tissues, parasites infesting, 381-382 Upper motor neuron (UMN), lesions of, signs of, 289t
Tolazoline Urea as protein source, 22
as preanesthetic, 409 Urea toxicity, 309
dosages for, 443t Urethra, problems involving, 272-273
Tooth (teeth) Urinalysis, 256-258
abnormalities of, 64-65 Urinary incontinence, 272
attrition of, 63 Urinary tract, 255-275
floating of, 63 congenital defects of, 273
general care of, 63 diagnostics for, 255-258
normal, 61-63 evaluation of, 255
of goats infectious diseases of, 261-262
examination of, 14 lower, problems of, 267-275
permanent, age of eruption of, 62t neoplastic conditions of, 273
of sheep of sheep, examination of, 5, 7
examination of, 5, 6f upper, problems of, 259-261
permanent, age of eruption of, 62t Urogenital system, of goats, examination of, 16-17
root abscess in, 64
468 • Index
Urolithiasis, 267-271 W
clinical signs of, 267-268
diagnosis of, 267-268 Warts, 219-220
in sheep, 5, 7 hairy heel, 227
obstructive, anesthesia and, 413 Washing machine murmur, 401
pathogenesis of, 267 Water
prevention of, 270-271 deprivation of, 308-309
treatment of dissolved solids in, recommendations for, 20t
medical, 268 for goats, 12, 19-20
surgical, 268-270 for sheep, 19-20
Uterine prolapse, 167 in urolithiasis prevention, 270-271
Uveal tract, pathology of, 334 nitrate nitrogen in, dangerous concentrations of, 20t
Uveitis, 334 toxic contaminants of, recommended upper limits for, 21t
Wattles, 197
V removal of, 221
Vaccination Wave mouth, 63
in pasteurellosis prevention, 113-114 Weakness
protocol for in neonates, causes of, 367-368
for goats, 423-425 plants associated with, 314t
for sheep, 430-431 Weaning, 51-52
Vaginal insemination, 154 Weanlings, management of, 422-423
Vaginal prolapse Web teat, 344
in sheep, 7 Weeping teats, 344
preparturient, 166-167 Wheat, nutrient composition of, 32t
Vaginitis, reproductive dysfunction from, 174 Wheat middlings, for energy supplementation, 21
Vagus nerve (X) in neurological evaluation, 283 Wheezes, evaluation of, 107
Varicoceles, 137 Whey, nutrient composition of, 32t
Vascular diseases, 402-404 White blood cell count in urinary tract evaluation, 258
Vascular tunic, anatomy of, 320-322 White liver disease, 99
Vasectomy, 142 White muscle disease, 246-248, 398
Vegetative endocarditis, 398-399 Wool
Venereal disease, ovine, 274-275 changes in, in physical examination, 4
Venous filling, assessment of, 393-394 loss of, in physical examination, 4
Venous pressures, assessment of, 394 lumpy, 208-209
Ventricular septal defect (VSD), 396 production of
Veratrum californicum, reproductive dysfunction from, 171-172 anatomy related to, 198
Verminous pneumonia, 123-1247 feeding for, 54-55
Vesicles in skin diseases, 199 Wool blindness, 4
Vesicular stomatitis, 205, 386-387 Wool break, 218-219
Vestibular disease, signs of, 282t Wool break in skin diseases, 199
Vestibulocochlear nerve (VIII) in neurological evaluation, 281-283 Wool slip, 218-219
Virus(es) X
Akabane
abortion associated with, 176-177 Xylazine hydrochloride
hydrocephalus/hydranencephaly from, 312-313 as anesthetic, doses of, 410t
blepharitis from, 327 as preanesthetic, 406-407, 409
bluetongue, 66 as preanesthetic, doses of, 408t
abortion associated with, 176 dosages for, 443t
retinal disorders from, 336 Y
border disease, abortion associated with, 177
Cache Valley, abortion associated with, 177 Yearlings, feeding of, 53-54
foot and mouth disease, 236 Yeast culture as feed additive, 28
hematologic/lymphatic diseases from, acute, 384-387 Yersiniosis, 377-378
hematologic/lymphatic diseases of, chronic, 388-391 Yohimbine
herpes, caprine, 275 as preanesthetic, 409
keratoconjunctivitis from, 332 dosages for, 443t
mastitis from, 356-357 Z
respiratory, acute, 114-120
skin diseases from, 203-205 Zeiss, glands of, 318
Vision, evaluation of, 323-325 Zinc
Vitamin A deficiency deficiency of, 26
retinal manifestations of, 336-337 skin manifestations of, 214-215
skin manifestations of, 215 hoof condition and, 225
Vitamin B12, dosages for, 443t toxicity of, in goats, 259
Vitamin K1, dosages for, 443t Zolazepam as anesthetic, doses of, 410t
Vitamins Zoonotic infections, 374-376
hoof condition and, 225 Zoonotic pathogens contaminating milk, 355-356
in feeding/nutrition, 27
Vitreous
anatomy of, 320
evaluation of, 325
Volvulus, cecal, 94