Illustrated veterinary pathology (General & systemic pathology)

Illustrated
Veterinary Pathology
(General & Systemic
Pathology)
Prof. R.S. Chauhan
MVSc., PhD. (Path.), FNAVS, FSIIP,
FIAVP
International Book Distributing Co.

ILLUSTRATED
VETERINARY PATHOLOGY
(General & Systemic Pathology)
A widely preferred text book of Veterinary Pathology for second year
BVSc & AH students under Veterinary Council of India (VCI) Syllabus
Prof. R.S. Chauhan
MVSc., PhD. (Path.), FNAVS, FSIIP, FIAVP
Joint Director (CADRAD)
Centre for Animal Disease Research and Diagnosis
Indian Veterinary Research Institute
Izatnagar - 243 122 Bareilly, U.P. India
E-mail: rs_chauhan123@rediffmail.com
International Book Distributing Company
(Publishing Division)

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First Edition 2002
Second Revised and Enlarged Edition 2007
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FOREWORD TO THE FIRST EDITION
The past few decades have seen a tremendous change in concepts of livestock
and poultry diseases, many new diseases being added up. The large quantity of
information unearthed, most coming in small analytical bits, undigested and unrelated,
needed to be properly categorized, and incorporated in books in updated form.
The book, "Illustrated Veterinary Pathology" written by Dr. R.S. Chauhan,
NatIonal FellowlProfes~or, Department ofPathology, College ofVeterinary Sciences,
G.B. Pant University of Agriculture and Technology, Pantnagar, is an appropriate
attempt to fill the gap in the study ofVeterinary Pathology. The syllabi ofVeterinary
Sciences has been changed as per modem requirements and has been in vogue in
almost all the Veterinary Colleges of the country. The book prepared as per the
requirement of the new syllabus of Veterinary Council of India, has been divided
into two sections.
The General Pathology section covers topics including introductory part,
historical milestones, general concepts ofpathology such as degenerative and vascular
changes, healing, concretions, calcification, growth disturbances and inflammation
and their etiological factors. Each pathological condition has been described with rel-
evant photographs and diagrams to make it more understandable. Similarly, section
two has been divided in ten chapters covering systemic pathology of animals and
poultry. Pathology of each organ and system has been nicely presented with
macroscopic and microscopic features supported by photographs and diagrams. The
practical aspect has been covered in appendices containing post-mortem techniques,
VIscera examination, collection and preservation ofmaterial, necropsy of veterolegal
cases and dispatch of material to forensic laboratory for diagnosis. Steps of post-
mortem examination are suitably' presented with photographs and diagrams. In the
end of each chapter, model questions are given for self assessment of the students
and is one of the unique feature of the book.
I am sure the book will prove of immense value to the students, teachers and
veterinarians for better understanding ofVeterinary Pathology and disease processes.
N.P. Singb
Former Prof. Path. and Dean
Faculty of Veterinary Sciences, Pantnagar
International Consultant I1CA,
Fed. Mini. Agri. (Nigeria)/World Bank

"This page is Intentionally Left Blank"

PREFACE TO THE SECOND EDITION
Since the first edition ofthis book "Illustrated Veterinary Pathology" exhausted,
I received messages in the form of letters, phones, SMSs, etc. from the students of
BVSc&AH, from different parts of the country to bring out its second edition and
make it available to the students. During last 4 years various suggestions and appre-
ciations were also received about the book. Illustrated Veterinary Pathology book has
been revised as per the need of its readers. Differential features ofvarious Pathologi-
cal conditions are given to present in an easily understandable form. Various chapters
are updated with some new photographs. The latest classification ofviruses has been
incorporated in the chapter 'Etiology'. Students ofVeterinary Pathology will find it suit-
able for their study and to prepare for competitive examinations like ICAR, NET,
ASRB, etc. Feedback received from the readers is given due care while preparing
second edition of the book and most of the suggestions are incorporated.
In my opinion, it will become were useful to not only the students but also to the
teachers, field veterinarians and diagnosticians. I must extend thanks to all those who
helped me in this meticulous task.
Centre for Animal Disease Research and Diagnosis (CADRAD),
Indian Veterinary Research Institute, Izatnagar-243 122, Bareilly (UP) India
Email: rs_chauhan123@rediffmail.com
RS Chauhan

PREFACE TO THE FIRST EDITION
Ever since the VCI course curriculum was implemented, need ofsuitable literature
for students was felt at many fora. In the busy curriculum of veterinary sciences, the
subject ofpathology forms a vital link between basic subjects ofanatomy, biochemistry
and physiology on one hand, and the clinical subjects of surgery, gynaecology and
medicine, on the other. The students face difficulty in understanding pathology since
they are confronted with the dilemma ofchoosing between exhaustive and voluminous
books ofVeterinary Pathology, most ofthem without photographs/illustrations. Majority
of available textbooks on Veterinary Pathology are written by western authors and
English being a foreign language in this country, most of our students find it hard to
understand and reproduce the highly technical subject from these books. Most of the
available textbooks were written a decade or more than that back,and are out dated
in present scenario. Needless to say that some ofthe books written by Indian authors
are also too exhaustive and without illustrations, thu!>, creating confusion in the mind
of students.
In preparing this textbook, I have kept these problems in mind and recalled the
difficulties I faced as a student. How far have I succeeded in my endeavour is for the
students and my professional colleagues to judge.
The very purpose of the Illustrated Veterinary Pathology is to provide the
undergraduate Veterinary students a textbook with diagrams and photographs to make
the text comprehensive. To broaden the scope further, laboratory methods, including
post-mortem examination, histopathological procedures and clinicopathological
procedures are also included in the appendices.
Physically, the book is of the standard textboo~ size, each chapter being well
illustrated and provided with salient features of macroscopic and microscopic
observations. The book is divided into two sections ofGeneral Pathology and Systemic
Pathology. The text provides a complete, uptodate and concise coverage of the
traditionally difficult subject in simple, lucid and clear language. Wherever new
terms/unfamiliar words appear in the text, they are first defined and explained. The
material has been organized meticulously in such a way that the student can easily
understand, retain and reproduce it. Various levels of headings, sub-headings, bold
type set and italics given in the text are meant to aid the student for quick revision of
the subject. Another major point ofthis book is inclusion oforiginal and high standard
questions including fill in the gaps, true/false, definitions, short notes and multiple
choice questions (MCQ), which are not only helpful in their self-assessment but also

in preparation for competitive examinations like ICARjunior research fellowship (JRF)
etc.
In a work of this magnitude, it is natural for the sole author of a book to solicit
help and cooperation from others. The most overwhelming enthusiasm, good will,
love and affection have generously come from my students for which I shall remain
always indebted to them. I wish to express gratitude to the Vice-Chancellor, Dr. J.B.
Chowdhary, who always encouraged me to produce such a useful textbook for
undergraduate students. The SUppOlt and encouragement from Dr. Harpal Singh, Dean,
PGS & former Dean, V.Sc., Dr. Amresh Kumar, Dean, V.Sc. and Dr. S.P. Singh,
Head, Pathology in accomplishing this academic work is thankfully acknowledged. I
wish to thank my colleagues who helped me a lot during preparation ofthe text book,
including Dr. G.K. Singh, Prof. & Head, Anatomy, Dr. D.K. Agrawal, Assoc. Prof.,
Pathology and Dr. Avadhesh Kumar, SMS. The valuable suggestions and criticism
from Dr. Lokesh Kumar, Dr. B.P. Singh, Dr. Rajesh Kumar and Dr. Sumeet Bagga is
thankfully acknowledged. My teacher, Dr. Nagendra P. Singh, Ex-professor Pathology
and Dean, Veterinary Sciences, has been a source of constant inspiration and
encouragement to me for successful completion ofthis work. Some ofthe illustrations
provided by Dr. Ramesh Somvanshi, IVRI, Dr. Arup Das, Dr. Stayendra Kumar, Dr.
Avadhesh Kumar, Dr. R. Sharma, Dr. G.K. Singh and others are duly acknowledged.
I am thankful to Agricultural Research Service, United States, Department of
Agriculture (ARS/USDA) for the photographs of various unusual and rare disease
conditions and consent to produce them in this text book for the benefit of students.
The meticulous type setting and photograph setting by Sri. Navin Joshi and Tasabber
Khan are thankfully acknowledged.
Finally, I would be failing in my duties, if I fail to mention the contributions of
my family. The cooperation and help provided by my wife, Mrs. Vandana, and the
children, Ms. Mahima and Master Yatishwar cannot be overlooked because it was
their time that I used to spend in preparation of this book.
Lastly, in spite of my best efforts at perfection, element ofhuman error is still
likely to creep in which the readers are welcome to point out since that would help
me in improving the text book further.
College of Veterinary Sciences
G.B. Pant University of Agri. & Tech.
Pantnagar- 263145. Uttaranchal, INDIA
E-mail: rs_chauhan123@rediffmail.com
August, 2001
R.S. CHAUHAN
M.V.Sc. Ph.D. FNAVS
National Fellow
Department of Pathology

CONTENTS
Part A: General Veterinary Pathology
1. Introduction ............................................................................................ 1
2. Etiology ................................................................................................ 13
3. Genetic disorders developmental anomalies and monsters ....................... 35
4. Disturbances in growth .,........................................................................ 43
5. Disturbancesincirculation ..................................................................... 49
6. Disturbances incell metabolism .............................................................. 58
7. Necrosis, gangrene and post-mortem changes ........................................ 65
8. Disturbances incalcificationandpigment metabolism .............................. 76
9. Inflammationandhealing ........................................................................ 84
10. Concretions........................................................................................ 113
11. ImmunityandImmunopathology .......................................................... 118
Part B: ,Systemic Pathology
12. Pathologyofcutaneous system ............................................................ 137
13. Pathologyofmusculoskeletal system .................................................... 147
14. Pathologyofcardiovascularsystem ...................................................... 156
15. Pathologyofrespiratorysystem ........................................................... 168
16. Pathologyofdigestive system .......................................................,...... 183
17. Pathologyofhemopoietic and immune system ....................................... 204
18. Pathologyofurinarysystem ................................................................. 215
19. Pathologyofgenital system .................................................................. 226
20. Pathologyofnervous system ................................................................ 237
21. Pathologyofendocrine system, eyes and ear........................................ 244
22. Appendix ............................................................................................ 251
23. Index .................................................................................................. 294

Part A
General Veterinary Pathology

1
INTRODUCTION
• Definitions
• Historical Milestones
• Model Questions

DEFINITIONS
Pathology
Pathology is the study of the anatomical, chemical
and physiological alterations from normal as a
result of disease in animals. It is a key subject
because it forms a vital bridge between preclinical
sciences (Anatomy, Physioiogy, Biochemistry) and
clinical branches of medicine and surgery.
Pathology is derived from the Greek word pathos
= disease, logos = study. It has many branches,
which are defmed as under:
General Pathology
General Pathology concerns with basic alterations
of tissues as a result of disease. e.g. fatty changes,
thrombosis, amyloidosis, embolism, necrosis (Fig.
1.1 ).
Systemic Pathology
Systemic Pathology deals with alterations in
tissues/organs of a particular system. e.g.
respiratory system, genital system etc. (Fig. 1.2).
Specific Pathology
Specific Pathology is the application of the basic
alterations learned in general pathology to various
specific diseases. It involves whole body or a part
ofbody. e.g. tuberculosis, rinderpest.
Experimental Pathology
Experimental Pathology concerns with the
production of lesion through experimental methods.
e.g. Rotavirus 7 calves 7 enteritis/ diarrhoea in
calves (Fig. 1.3).
Clinical Pathology
Clinical Pathology includes certain laboratory
methods which help in making the diagnosis using
animal excretions/secretions/blood/skin scrapingsl
biopsy etc. e.g. urine examination, blood
examination (Fig. 1.4).
Post-mortem Pathology
Post-mortem Pathology is examination of an
animal after death. Also known as Necropsy or
Autopsy. It forms the base for study of pathology
(Fig. 1.5).
2
Microscopic Pathology
Microscopic Pathology deals with examination of
cells/tissues/organs using microscope. It is also
known as histopathology/cellular pathology. e.g.
microscopy, electronmicroscopy (Figs. 1.6 & 1.7).
Humoral Pathology
Humoral Pathology is the study of alterations in
fluids like antibodies in serum (Fig. 1.8).
Chemical Pathology
Chemical Pathology ·is the study of chemical
alterations of body fluids/tissues. e.g. enzymes in
tissue.
Physiological Pathology
Physiological Pathology deals with alteration in the
functions of organ/system. It is also known as
Pathophysiology. e.g. indigestion, diarrhoea,
miscarriage (Fig. 1.9).
Nutritional Pathology
Nutritional Pathology is the study of diseases due
to deficiency or excess of nutrients. e.g. Vit.-A
deficiency induced nutritional roup, rickets due to
calcium deficiency (Fig. 1.10).
Comparative Pathology
Comparative Pathology is the study of diseases of
animals with a comparative study in human beings
and other animals. e.g. zoonotic diseases such as
tuberculosis (Fig. 1.11).
Oncology
Oncology is the study of cancer/tumor/neoplasms.
Immunopathology
Immunopathology deals with the study of diseases
mediated by immune reactions. It includes
Immunodeficiency diseases, autoinununity and
hypersensitivity reactions (Fig. 1.12).
Cytopathology
Cytopathology is the study of cells shed off from
the lesions for diagnosis.

/Iltroductioll
Fig. 1.1 Necrosis in liver
Fig. 1.2. Female genital system ofpoulay
Fig. 1.3. ExperimentalPathology
Fig. 1.4. Examination ofblood for protozoan parasites
3
Fig. 1.5. Post-mortem examination ofpoulay
Fig. 1.6. Histopathological examination ofsldn section
showinj? inclusions ofpoxvirus infection.
Fig. 1.7. Electronmicrophotograph showing
poxvirus in cytoplasm ofa cell
Fig. I.B. Detection ofantibodies in serum
usinj? EL/SA

Health
Health is a state of an individual Iiving in complete
harmony with his environment/surroundings (Fig.
1.13). .
Disease
Disease is a condition in which an individual shows
an anatomical, chemical or physiological deviation
from the normal. (Discomfort with environment &
body) (Fig. 1.14).
Illness
Illness is the reaction of an individual to disease in
the form of illness.
Forensic Pathology
Forensic Pathology includes careful examination
and recording of pathological lesions in case of
veterolegal cases.
Homeostasis
Homeostasis is the mechanism by which body
keeps equilibrium between health and disease. e.g.
Adaptation to an altered environment.
Toxopathology
Toxopathology or Toxic Pathology deals with the
study of tissue/organ alterations due to
toxins/poisons (Fig.I.15).
Etiology
Etiology is the study of causation of disease (Fig.
1.16).
Diagnosis
Diagnosis is an art of precisely knowing the cause
of a particular disease (Dia= thorough, gnosis=
knowledge) (Fig 1.17).
Symptoms
Any subjective evidence of disease of animal
characterized by an indication of altered bodily or
mental state as told by owner (complaints of the
patients).
Signs
Indication of the existence of something, any
objective evidence of disease, perceptible to
4
veterinarian (observations ofthe clinicians).
Syndrome
A combination of symptoms caused by altered
physiological process.
Lesion
Lesion is a pathological alteration in structure/
function that can be detectable (Fig. 1.18).
Pathogenesis
Pathogenesis is the progressive development of a
disease process. It starts with the entry of causal
agent in body and ends either with recovery or
death. It is the mechanism by which the lesions are
produced in body.
Incubation period
Incubation period is the time that elapses between
the action of a cause and manifestation ofdisease.
Course of disease
Course of disease is the duration for which the
disease process remains till fate either in the form
ofrecovery or death.
Prognosis
Prognosis is an estimate by a clinician of probable
severity/outcome of disease.
Morbidity rate
Morbidity rate is the percentage/proportion of
affected animals out of total population in a
particular disease outbreak. e.g. out of 100 animals
20 are suffering from diarrhoea, the morbidity rate
of diarrhoea will be 20%.
Mortality rate
Mortality rate is the percentage/proportion of
animals out of total population died due to disease
in a particular disease outbreak. e.g. if in a
population of 100 animals, 20 fall sick and 5 died,
the mortality rate will be 5%.
Case fatality rate
Case fatality rate is the percentage/proportions of

Fig.1.9. A calfshowing diarrhoea
Fig. 1.10. Calcium deficiency causing rickets
in calf
Fig. 1.11. Transmission ofdisease from
animals to man.
FIg. J.12. Lamb showing DTH reaction on neck
Introduction
Fig. 1.13. A healthy calf
Fig. 1.14. Lamb suffering from pneumonia
Fig. 1.16. Rotavirus - A cause ofdiarrhoea
5

Fig. 1.17. Diagnosis ofdiseases in animals.
animals died among the affected animals. If in a
population of 100 animals, 20 fall sick and 5 die,.
the case fatality rate will be 25%.
Biopsy
Biopsy is the examination of tissues received from
living animals.
Infection
Infection is the invasion of the tissues of the body
by pathogenic organisms resulting in the
development of a disease process.
Fig. 1.lB. Haemorrhagic lesion in heart
Infestation
Infestation is the superficial attack of any
parasite/organism on the surface ofbody.
Pathogenicity
Pathogenicity is the capability of an organism for
producing a disease.
Virulence
Virulence is the degree of invasiveness of
pathogenic organism.
HISTORICAL MILESTONES
2500·1500 BC
2100 BC
Shalihotra
(Indian)
Muni Palkapya
(Indian)
Hammurabi
• First known veterinarian ofthe world
• Wrote Haya Ayurvedl Ashwa- Ayurved in Sanskrit, 8
volumes on equine medicine with diagnosis, treatment,
effect of planetary forces and evils on health
• Wrote a treatise on elephants - Gaj Ayurved
Conduct of Veterinary Practitioners, "Laws of Hammurabi"
6

1000 BC
800 BC
500 BC
460-375 BC
384-323 BC
300 BC
53 BC-37 AD
131-206 AD
450-500 AD
600 AD
Krishna
(Indian)
Nakul (4th
Pandav)
(Indian)
Sahdev
(5th
Pandav)
(Indian)
Charak
(Indian)
leevak (Indian)
Hippocrates
(Greece)
Aristotle
(Greece)
Chandra Gupta
Maurya period
Sarnrat Ashok
Cornelius Celsus
(Rome)
Claudius Galen
(Rome)
Renatus Vegetius
(Rome)
Madhav
Introduction
• Mathura is known for best cattle production/milk
production
• Wrote Ashwa- Chikitsa, a book on equine medicine.
• He is considered as an expert of equine management
• Expert in cattle rearing and disease management.
• Wrote Charak Sanhita with details of cause of diseases
and impact ofenvironment.
• Described the pathology ofbrain.
• Physician, studied malaria, pneumonia , also known as
"Father of Medicine"
• Humoral theory of disease
• Father ofZoology
• Originator ofModern Anatomy & Physiology
• In Kautilya, Arthshashtra description on "Animal
Husbandry and Veterinary Sciences", rules on animal
ethics and jurisprudence
• First Veterinary Hospital established for treatment of
animal diseases
• Prevention of cruelity on animals advertised through
writings on walls.
• Wrote 8 volumes ofpathology (IsI special pathology)
Cardinal signs of inflammation (redness, swelling, heat
and pain)
• Meat inspection
• 5
th
cardinal sign of inflammation "Loss of function"
• Father ofVeterinary Medicine
• Disregard divine pleasure
• Disease of animals' influence on man
• Described pathology ofdiarrhoea, dysentery, icterus,
tuberculosis and various toxic conditions.
7

980-1037 AD
1497 AD-1558 AD
1564 AD-1642 AD
1578-1657 AD
1617 AD-1619 AD
1617-1680 AD
1632 AD-1723 AD
1682-1771 AD
1712-1779 AD
1728- 1793 AD
1753-1793 AD
1762 AD
1771-1802 AD
1801-1858 AD
1804-1878 AD
1818-1865 AD
Avicenna
Jean Femel
Galileo Galilei
William Harvey
Drebbel
Solleysel
(French)
Antony van
Leeuwen-hoek
G.B. Morgagni
(Italian)
Bourgelat, C
(French)
John Hunter
(English)
Saint Bel
(French)
Bourgelat, C
(French)
Bichat
(French)
Mueller. J.
(German)
Carl Rokitan-
Skey (German)
Semmelwiss
(Hungarian)
• Cause of disease are minute organism
• Spreads through air, food, water.
• Compiled the information ofhis time First to attempt to
codify the knowledge ofPathology.
• Developed single microscope
• Blood vascular system and its impact on pathology
• Developed double lens microscope
• Book on Le Parfact Marechal
• Saw microbes fIrst
• Book - Little animals
• Conducted 700 autopsies
• Began modem pathology
• Book The seats and causes ofdisease
• New knowledge of equine medicine
• First experimental pathologist
• Teacher at Alfort established Vet School in England 1791
and in 1793 died due to glanders.
• 1st Veterinary school established - Ecole Veterinaire
Nationale'd Alfort
• Father ofpathological anatomy
• Foundation for the study of histology
• Father of histology
• Cellular pathologist, known for his work "The fIne
structure and form ofmorbid tumors"
• Supreme descriptive pathologist
• Surgery/autopsy
• Started hospital sanitation
8

1821-1902 AD
1822-1895 AD
1839-1884 AD
1843-1890 AD
1850-1934 AD
1869 AD
1883-1962 AD
1884 AD
1884-1955 AD
1885-1979 AD
1889 AD
1905-1993 AD
1913 AD
1924 AD
1926 AD
1931 AD
R. Virchow
(German)
Louis Pasteur
(French)
J. Colmheim
(German)
R. Koch
(German)
W.H. Welch
(U.S.A)
Bruck Muller
(USA)
G.N. Papanicolaou
E. Metchnikoff
Robert Feulgen
(German)
WilliamBo.Yci
(Canadian)
L. Ackerman
(American)
India
India
E. Joest
India
Introduction
• Journal Virchow's Archives
• Great work on cellular pathology, "Father of modern
Pathology"
• Bacteria cause of disease
• Originator of modern experimental pathology
• Detected 1eucocytes at the site of inflammation
• His work forms the basis for the pathology of
inflammation
• Introduced frozen sections
• Koch's postulates
• Identified Tuberculosis, Staphylococcus and Vibrio as
cause of disease
• Professor Pathology
• Started pathology in USA.
• Textbook ofpathological anatomy of domestic and zoo
animals.
• Father of exfoliative cytology
• Phagocytosis (microphages/macrophages)
• Founder ofHistochemistry
.• ' Aftthot ofTextbook ofPathology
• Establishment of Imperial Bacteriological Laboratory at
Mukteshwar (Now IVRI)
• Authority on interpretation of frozen sections.
• Imperial Bacteriological Laboratory (now IVRI)
established at new campus at Izatnagar- Bareilly
• The Publication of Indian Veterinary Journal started
• Wrote 5 volumes of Veterinary Pathology
• The publication ofIndian Journal of Veterinary Sciences
and Animal Husbandry (Presently Indian Journal of
Animal Sciences) started
9

1933 AD
1936 AD
1938 AD
1953 AD
1968 AD
1973 AD
1976 AD
1983 AD
1989 AD
1998 AD
Ruska and Lorries • First developed electronrnicroscope.
Bittner • Milk transmission ofcancer
R.A. Runnels • Wrote book on "Animal Pathology".
Watson and Crick • Structure of DNA
G.A. Sastry (India) • Author of Veterinary Pathology textbook.
• The Publication ofIndian Veterinary Medical Journal
started from Lucknow
• The publication ofIndian Journal ofVeterinary Pathology
started from Izatnagar
• Indian Association ofVeterinary Pathologist established.
• Veterinary Council ofIndia established
• Dr. C.M. Singh became 1st President ofVCI
• 1st
Veterinary and Animal Sciences University established
in Madras (now Chennai).
• Establishment of" Society for Immunology and
Immunopathology" at Pantnagar.
• Publication of "Journal ofImmunology and
Immunopathology" started from Pantnagar
From left to right: Dr. Ramesh Kumar, Professor. Microbiology, AIIMS;
Dr. N.K. Ganguly, Director General Indian Council of Medical Research;
Dr. C.M. Singh, Former Director, IVRI and President VCI; Dr. R.S. Chauhan, NatIonal Fellow,
at inaugural function of Society for Immunology and Immunopathology.
10

Introduction
MODEL QUESTIONS
Q.1. In a dairy farm a total of 1000 cows are kept for milk purpose. On 3.1.2001,80 animals were found
sick and were suffering from nasal discharge, fever and diarrhoea. Out of these 30 animals died till
18.1.2001 and rest recovered. The blood and serum samples were collected from affected animals
for laboratory examination. The dead animals were necropsied and their tissue samples were also
collected for microscopic examination. Based on this describe the followings:
1. Morbidity rate
2. Mortality rate
3. Case fatality rate
4. Course ofdisease
5. State the branch ofpathology under which following activity falls:
(a) Examination ofblood .................... .
(b) Examination ofdead animals .................... .
(c) Examination of serum for Ca, P, enzymes .................... .
(d) Microscopic examination oftissues .................... .
(e) Examination of serum for antibodies .................... .
(t) Examination of urine and faeces of affected animals..................... .
Q. 2. Fill in the blanks with suitable word(s).
Q.3.
1. ..........is the father of Veterinary Medicine.
2. .. ........gave 4 cardinal signs of inflammation which included ............., ...................,
............. and .......... while the fifth cardinal sign ............... was given by .............. .
3. .........deals with study ofdiseases ofanimals and man.
4. Immunopathology deals with the study ofdiseases mediated by ...... and it includes .........,
................ and ...........
5. Symptoms are any ............... evidence of disease of animals while signs are the existence
of any ................ evidence that is the observations of the clinicians.
6. .. ................is the progressive development of a disease process; it starts with the
............. of causal agent in body and ends either with ................ or .............. .
7. ............. is the examination oftissues received from living animals.
Define thefollowing.
1. Health
2. Disease
3. Experimental Pathology
4. Oncology
5. Homeostasis
6. Diagnosis
7. Syndrome
8. Prognosis
9. Lesion
10. Infection
Q. 4. Justify the statement "Pathology is a key subject in Veterinary Sciences, which is quite helpful
in prevention and control ofdiseases in animals".
Q. 5. Select most appropriate word(s) from thefour options given with each question.
1. The process of phagocytosis by macrophages was first described by.............. .
(a) B. Muller (b) E. Metchnikoff (c) Bittner (d) Bichat
11

2. First Veterinary School was established in the year ..........
(a) 1762 (b) 1884 (c) 1889 (d) 1773
3. The originator ofmodem Experimental Pathology is .............. .
(a) R. Koch (b) J. Cohnheim (c) John Hunter (d) R. Virchow
4. Study oftumors is known as ...........
(a) Cytopathology (b) Clinical Pathology (c) Chemical Pathology (d) Oncology
5. Study of zoonotic diseases fall under the branch of ............. Pathology.
(a) Nutritional (b) Comparative (c) Experimental (d) Systemic
6. Humoral Pathology is the study of alterations in.............. .in animals.
(a) Antibodies (b) Fibrin (c) Urine (d) Faeces
7. Immunodeficiency disorders of animals fall under the branch of ...........
(a) Cytopathology (b) Humoral Pathology (c) Microscopic Pathology
(d) Immunopathology
8. General Pathology does not include one ofthe following activity
(a) Fatty changes (b) Embolism (c) Inflammation (d) Digestive system
disorders.
9. Examination of dead animals is known as .................
(a) Necropsy (b) Autopsy (c) Lethopsy (d) Microscopy
10. Nutritional roup is an example of ...............Pathology
(a) Chemical (b) Nutritional (c) Humoral (d) Post-mortem
12

•
•
•
2
ETIOLOGY
Intrinsic Causes
Extrinsic Causes
• Physical Causes
• Biological Causes
• Chemical Causes
• Nutritional Causes
Model Questions

ETIOLOGY
Etiology is the study of cause of disease. It gives
precise causal diagnosis of any disease. Broadly,
the cause ofdiseases can be divided into two:
a. Intrinsic causes.
b. Extrinsic causes.
INTRINSIC CAUSES
Those causes which determine the type of disease
present within an individual over which he has no
control. These causes are further divided into
following subgroups:
Genus
Specific diseases occur in a particular genus or
species ofanimals. e.g. Hog cholera in pigs, Canine
distemper in dogs
Breed/Race
Diseases do occur in particular breed of animals
such as: dairy cattle are more prone for mastitis.
Brain tumors are common in Bull dog/ Boxer.
Family
Genetic relationship plays a role in occurrence of
diseases in animals. e.g. some chickens have
resistance to leucosis; hernia in pigs due to weak
abdominal wall.
Age
Age of animal may also influence the occurrence of
diseases such as:
• At young age diarrhoea/pneumonia (Fig. 2.1).
• Old age tumor
• Canine distemper - Young dogs
• Strangles - Young horse
• Prostatic hyperplasia - Old dogs
• Coccidiosis - Young chickens
Sex
Reproductive disorders are more common in
females
• Milk fever, mastitis and metritis in females.
14
• Nephritis is more common in male dogs than
female, but Bovine nephritis is more common
in females.
Colour
Colour may also play role in occurrence of
diseases. e.g. squamous cell carcinoma in white
coat colour cattle, melanosarcoma in grey and
white horses
Idiosyncracy
An unusual reaction of body to some substances
such as:
• Drug reaction: Small dose of drug may
produce reaction.
• Individual variations.
EXTRINSIC CAUSES
Some etiological factors which are present in the
outside environment may cause/influence the
occurrence of disease. These are also known as
exciting cause/acquired cause. Majority of causes
of diseases fall under this group which are further
classified as physical, chemical, biological and
nutritional causes.
PHYSICAL CAUSES
TRAUMA
Traumatic injury occurs due to any force or energy
applied on body of animal e.g. during control /
restraining, shipping or transport ofanimal.
ContusionslBruises
Contusions or bruises arise from rupture of blood
vessel with disintegration of extravassated blood
(Fig. 2.2).
Abrasions
Abrasions are circumscribed areas where
epithelium has been removed by injury and it may
indicate the direction offorce (Fig. 2.3).
Erosions
Partial loss of surface epithelium on skin or
mucosal surface is termed as erosion (Fig. 2.4).

Etiology
,rsl--V.,~.b.ll.'·f:III....~II~~;
, . ,
t ,}
'"'-- - --- - - - -----
Fig. 2.5. Diagram showing incised wound
Fig. 2.1. Rotaviral diarrhoea in young calf
Fig. 2.6. Diagram showing laceration
Fig. 2.2. Diagram showing contusion
Fig. 2.7. Photomicrograph ofthIrd degree bum in skin
Fig. 2.3. Diagram showing abrasion
Fig. 2.4. Diagram showing erosion Fig. 2.B. Electronmicrophotograph ofpoxvirus in CAM
15

Incised wounds/cuts
Incised wounds are produced by sharp-edged
instrument. They are longer than deep (Fig. 2.5).
Stab wound
Stab wounds are deeper than longer produced by
sharp edged instrument.
Laceration
Severance of tissue by excessive stretching and is
common over bony surfaces or are produced by cut
through a dull instrument (Fig. 2.6).
Compression
Compression injury is produced as a result of force
applied slowly e.g. during parturition.
Blast injury
Force of compression waves against surfaces
followed by a wave of reduced pressure. It can
rupture muscles/viscera.
Bullet wound
Hitting at 90° by flrearms to produce uniform
margins of abrasion. Exit wounds are irregular and
lacerated.
ELECTRICAL INJURY
High voltage current induces tetanic spasms of
respiratory muscles and hits the respiratory centre
of brain. It also produces flash burns. Lightning
causes cyanotic carcass, post-mortem bloat,
congestion of viscera, tiny haemorrhage and skin
damage.
TEMPERATURE
Burns
I degree burns
There is only congestion and injury to the
superflcial layers of epidermis e.g. sun burn on
hairless parts or white skinned animal.
11 degree burns
Epidermis is destroyed; hair follicles remain intact
and provide a nidus for healing ofepithelium.
16
III degree burns
Epidermis and dermis both are destroyed leading to
fluid loss, local tissue destruction, laryngeal and
pulmonary oedema, renal failure, shock and sepsis.
Till 20 hrs of burn, the burn surface remains sterile
then bacterial contamination occurs. After 72 hrs
millions of bacteria enter in the affected tissue.
Bacteria such as Staphylococci, Streptococci and
Pseudomonas aeruginosa invade the deeper layers
of skin and cause sepsis. There is a state of
immunosuppression in severe burns leading to
impaired phagocytosis by neutrophils (Fig. 2.7).
Hyperthermia
Hyperthermia means increased body temperature
due to high environmental temperature e.g. pets in
hot environment without water. Hyperthermia leads
to increased respiration (hyperpnoea), rapid heart
beat (tachycardia), and degeneration in
myocardium, renal tubules and brain.
Hypothermia
Hypothermia means decreased body temperature
and includes freeze induced necrosis of tissues at
extremities
RADIATION INJURY
Radiation as a result ofexposure to X-rays, Gamma
rays or ultra violet (UV) rays leads to cell swelling,
vacuolation of endoplasmic reticulum, swelling of
mitochondria, nuclear swelling and chromosomal
damage resulting in mutation. The impact of
radiation is more on dividing cells of ovary, sperm,
lymphocytes, bone marrow tissue and intestinal
epithelium. It is characterized by vomiting,
leucopenia, bone marrow atrophy, anemia, oedema,
lymphoid tissue and epithelial necrosis.
BIOLOGICAL CAUSES
Virus
Viruses are smallest organisms, which have only
one type of nucleic acid DNA or RNA in their core
covered by protein capsid.

Fig. 2.9. Electron microphotograph of
reovirus in CAM
Fig. 2 10. Electronmicrophotograph ofrotaVIruS
Fig. 2.11. Diagram ofLeptospira.
-., A
'::1, .........:
•••••• •
" "."••
.... ~(; C
..... --, ,
I, - ......."
",.:-
B
.....,.......•......"" It"
#,' .t
.~. ...
Fig. 2.12. Diagram ofbacteria (a) Staphylococci,
(b) Streptococci (c) Bacilli
Etiology
17
Fig. 2.13. Photomicrograph ofTrichophyton sp. a
cause ofringworm
~i~ 2.14. Photomic;ograph ofAspergillusflavus
.'~I ~ ••'J"'", "~tA • 11
• g' ' . --t!.i', '!f,.~ l''.cv .' .,1-'.,' ..,~.~ &. .1' -_ .1
Fig. 2.15. Photomicrograph ofTrypanosoma
evanSl infectIOn
A
11
ri'.~~I ':I' ;
:! 'I
" .;.!/
Fig. 2.16. Diagram ofEchinococcus and Taenia spp.

Viruses of Veterinary Importance with their classification
(International Committee on taxonomy ofviruses, 2005)
DNA Viruses (Fig. 2.8)
S.No. Family Genus Virus species Disease
Group I - ds DNA viruses ( Double stranded DNA virus)
I. Adenoviridae Aviadenovirus Fowl adenovirus IBH, EDS, HPS in birds
Atadenovirus Ovine adenovirus A Pneumonia in Sheep
Mastadenovirus Canine adenovirus I ICH in Dog
2. Herpesviridae Alphaherpes virus Herpes suis Pseudorabies in pigs
Bovine herpes virus - I (BHV-I) IBR, IPV in cattle
Equine herpes virus - I (EHV-I ) Equine viral abortion
Equine herpes virus - 4 (EHV-4) Rhinopneumonitis in equines
Equine herpes virus - 3 (EHV-3) Coital exanthema
Avian herpes virus type-I (AHV- ILT in birds
I)
Betaherpes virus Porcine cytomegalo virus Inclusion body rhinitis in pigs
Gammaherpes Malignant catarrhal fever virus MCF in cattle
virus
Marek's disease virus Marek's disease in birds
3. Papillomaviridae Papillomavirus Bovine papillomavirus Cutaneous papilloma in cattle
Oral papilloma in dogs
Canine oral papillomavirus Cutaneous papilloma in
Rabbit papillomavirus rabbits
4. Poxviridae Orthopox virus Vaccinia virus, Cowpox virus, Pox in animals
Buffalopox virus, Monkeypox
virus, Rabbitpox virus
Camelpox virus
Avipox virus Fowlpox virus, Pigeonpox virus, Fowl pox, Pigeon pox,
Turkeypox virus, Canarypox virus Turkeypox, Canarypox
Capripox virus Sheeppox virus, Goatpox virus Sheep pox, Goat pox
Leporipox virus Myxoma virus Myxomatosis in Rabbits
Suipox virus Swinepox virus Swine pox
Parapox virus Orfpox virus Orfin sheep
Group II - ss DNA viruses (Single stranded DNA virus)
I. Circoviridae Circovirus Porcine circovirus -
Gyrovirus Chicken anemia virus Chicken infectious anemia
2. Parvoviridae Parvovirus Murine minute virus
Bocavirus Bovine parvovirus Diarrhoea in cattle
Canine parvovirus Enteritis, myocarditis in dogs
Porcine parvovirus Infertility, fetal death in pigs
18

Etiology
RNAV'Iruses (F' 29 & 2 IQ)IgS.
Group 111- ds RNA virus ( Double stranded RNA virus)
1. Birnaviridae Avibimavirus IBD virus IBD in birds
Aquabimavirus Infectious pancreatic Infectious pancreatic
necrotic virus necrosis
2. Reoviridae Orthoreovirus Mammalian orthoreo virus Pneumoenteritis in calves
Orbivirus Blue tongue virus Blue tongue in sheep
Rotavirus Rotavirus Diarrhoea in neonates
Group IV - (+ve) ss RNA virus (Positive single stranded RNA or M RNA Iike~
1. Arteriviridae Arterivirus Equine arteritis virus Equine viral arteritis
2. Coronaviridae Coronavirus Infectious bronchitis virus Infectious bronchitis in
birds
Bovine coronavirus Diarrhoea in calves
3. Astroviridae Avastrovirus Turkey astrovirus -
4. Calciviridae Vesivirus Swine vesicular exanthema Vesicular exanthema in
virus pigs
Lagovirus Rabbit haemorrhagic Haemmorhagic disease in
disease virus rabbit
Norovirus Norwalk virus -
5. Flaviviridae Flavirus Yellow fever virus Yellow fever in man
Hepacivirus Hepatitis C virus Hepatitis in man
Pestivirus BVD virus, CSF virus BVD, CSF
6. Picomaviridae Enterovirus Poliovirus Polio in man
Rhinovirus Rhinovirus Rhinitis
Hepatovirus Hepatitis A virus Hepatitis
Cardiovirus Encephalomyocarditis Encephalomyocarditis
virus
Aphthovirus FMD virus FMD
Erbovirus Equine rhinitis B virus Respiratory disease in
equines
7. Togaviridae Alphavirus Equine Encephalomyelitis Equine encephalomyelitis
virus
Rubivirus Rubellavirus
Group V - (-ve) ss RNA virus (Negative single stranded RNA)
I. Paramyxoviridae Paramyxovirus Parainfluenza virus 1 (PI- Respiratory diseases in
1)- Pigs, pigs
Parainfluenza virus 2 (PI- Kennel cough in dogs
2)- Dogs,
Parainfluenza virus 3 (PI- Respiratory disease in
3)- Cattle cattle
Avulavirus Ranikhet disease virus Ranikhet disease in birds
Morbillivirus Canine Distemper virus CD in dogs
Rinderpest virus RP- in animals
PPR virus PPR - sheep, goat
19

2. Bomaviridae Boma disease virus Boma disease virus Boma disease in sheep
3. Filoviridae Ebolavirus - -
Filovirus - -
4. Rhabdoviridae Vesiculovirus Vesicular stomatitis virus Vesicular stomatitis in
bovines
Lyssavirus Rabies virus Rabies
Ephemerovirus Ephemeral fever virus Ephemeral fever in
animals
5. Bunyaviridae Hantavirus Hantaanvirus Hantavirus pulmonary
syndrome, Korean
haemorragic fever
Phlebovirus Nairobi sheep disease Nairobi Sheep disease,
virus, Rift valley fever RVF
virus, Akabana disease Akabana disease
virus
6. Orthomyxoviridae Influenza virus A Influenza virus A Influenza in animals
Influenza virus B Influenza virus B
Influenza virus C Influenza virus C
Group VI ss RNA-RT virus (Single stranded RNA virus with reverse transcriptase)
1. Retroviridae Alpharetrovirus Avian leucosis virus ALC in birds
Betaretrovirus Mouse mammary tumour Cancer in mice
virus
Gammaretrovirus Murine leukemia virus Leukemia in mice
Feline leukemia virus Leukemia in cats
Deltaretrovirus Bovine leukemia virus Bovine leukemia
Lentivirus Bovine immunodeficiency Bovine
virus immunodeficiency
syndrome
Feline immunodeficiency Feline immunodeficiency
virus syndrome
Group VII ds DNA-RT virus (Double stranded DNA virus with reverse transcriptase)
1. Hepadnaviridae Orthohepadnavirus Hepatitis B virus Hepatitis
Avihepadna virus Duck hepatitis B virus Duck hepatitis
20

Eti%gy
Subviral agents
• Prion proteins are infectious proteins without
any nucleic acid. e.g. Bovine spongiform
encephalopathy.
• Viroids have only nucleic acid without
proteins. They do not cause any disease in
animals. However, They are associated with
plant diseases.
Rickettsia
Coxiella burnetti causes Q-fever
Mycoplasma
Mycoplasma mycoides is responsible for
pneumonia, joint ailments and genital disorders
Chlamydia
Chlamydia trachomatis, C. psittaci cause abortions,
pneumonia, and eye ailments.
Spirochaete
Leptospira sp. causes abortion, icterus.
Borrelia ansernia causes fowl spirochetosis lD
chickens (Fig. 2.11).
Bacteria
Bacteria are classified as Gram positive and Gram
negative on the basis of Gram's staining. Gram
posItive bacteria include Staphylococci,
Streptococci, Corynebacterium, Listeria, Bacillus
Clostridia. Gram negative bacteria are Escherichia
coli, Salmonella, Proteus, Klebsiella, Pasteurella,
Pseudomonas, Brucella, Yersinia, Campylobactor
etc. Besides, there are certain organisms stained
with Zeihl Neelson stain and are known as acid fast
bacilli e.g.Mycobacterium tuberculosis and M.
paratuberculosis (Fig. 2.12).
Fungi
Fungi pathogenic for animals mostly belong to
fungi imperfecti. e.g. Histoplasmosis.
21
Fungi cause three type of disease - Mycosis e.g.
Actinomycosis; Allergic disease e.g. Ringworm;
Mycotoxicosis e.g. Aflatoxicosis (Figs. 2.13, 2.14).
Parasites
Parasites are classified mainly in 3 groups:
Protozoan parasites
Trypanosoma evansi, Theileria annulata, Babesia
bigemina, Toxoplasma gondii, Eimeria Spp. (Fig.
2.15).
Helminths
Nematodes - Roundworms e.g. Ascaris.
Trematod - Flat worms e.g. Liverfluke.
Cestodes - Tapeworms e.g Taenia spp. (Fig. 2.16).
Arthropods
Ticks, Mites, Flies, Lice (Figs. 2.17, 2.18, 2.19,
2.20).
TRANSMISSION
Biological agents are transmitted from one animal
to another through horizontal or vertical
transmission.
Horizontal Transmission
Horizontal transmission ofbiological causes occurs
through direct contact or indirectly via animal or
inanimate (fomites) objects. It is also known as
lateral transmission as it occurs in a population
from one to another. Various methods of horizontal
transmission are as under:

I Fig. 2.21. Photograph ofcalves with strychnine poisoning
Fig. 2.17. Diagram ofa tick
Fig. 2.22. Photograph ofcalves with strychnine poisoning
Fig. 2.18 Photograph ofbullock with tick infestation
Fig. 2.19. Diagram ofa Mite
Fig. 2.23. Pesticide spray in crops
Fig. 2.20. Photomicrograph ofSarcoptes scabei Fig. 2.24. Pesticide cycle in environment
22

Etiology
Ingestion
Food, water, faecal-oral route e.g. Salmonellosis,
Johne's disease, Rotavirus infection.
Inhalation
Air-borne infections, droplet infection e.g. R.P.,
FMD, Tuberculosis.
Contact
Fungal infection, Bacterial dermatitis, Flu,
Brucellosis, Rabies through bite.
Inoculation
Introduction of infection in body through puncture
either mechanically through needles or by
arthropods such as by ticks. Ticks transmit diseases
through transovarian (one generation to next
generation) or transstadial (through developmental
stages) transmission.
Iatrogenic
Transmission of infection during surgical
procedures or caused by doctor, through dirty
instrument and contaminated preparations.
Coitus
Through sexual contact of animals, biological
agents spread from one to another animals. e.g.
Campylobacteriosis, Trichomonosis.
Vertical Transmission
Vertical transmission occurs from one generation to
another generation in ova/in utero or through milk.
These include:
Hereditary
Infection/disease carried in the genome of either
parent e.g. Retrovirus
Congenital
Diseases acquired either in utero/in ova
• Infection in ovary/ ovum (Germinative
transmission) e.g. ALC in chickens, lymphoid
leukemia in mice, Salmonellosis in poultry.
• Infection through placenta. e.g. Feline
panleukopenia virus (Transmission to embryo)
23
• Ascending infection from lower genital canal
to amnion / placenta e.g. Staphylococci.
• Infection at parturition: Infection from lower
genital tract during birth. e.g. Herpex simplex
virus.
MAINTENANCE OF INFECTION
Biological agents face difficulty of survival at both
places - in environment and in host. Two types of
hazards which create problem to agent are:
Internal hazards e.g. Host's immune system
External hazards e.g. Desiccation, DV light
Agents try to maintain themselves by adopting
following maintenance strategies:
• Avoidance of a stage in the external
environment.
• Resistant forms e.g. Anthrax spores.
• Rapidly in-rapidly out strategy e.g. Viruses of
respiratory tract.
• Persistence within the host e.g. Mycobacterium
tuberculosis, Slow viral diseases.
• Extension of host range.
• Infection in .more than one host e.g. Foot and
mouth disease.
CHEMICAL CAUSES
Biological Toxins
Snake venom
Snake venom has phospholipase A2 which causes
lytic action on membranes of RBC and platelets.
The presence of hyaluronidase, phosphodiesterase
and peptidase in snake venom are responsible for
oedema, erythema, haemolytic anemia, swelling of
facial/laryngeal tissues, haemoglobinurea, cardiac
irregularities, fall in blood pressure, shock and
neurotoxicity.
Microbial toxins
Microbial toxins are those toxins/poisons that are
produced by microbial agents particularly by
bacteria and fungi.
Bacterial toxins
Bacterial toxins include structural proteins
(endotoxins) and soluble peptides/ secretary toxins
(exotoxins). Endotoxins are present in cell wall of

Gram-negative bacteria and are found to be
responsible for septicemia and shock. Exotoxins
are secreted by bacteria outside their cell wall and
are responsible for protein lysis and damage to cell
membrane. e.g. Clostridium toxins suppress
metabolism of cell. Most potent clostridial toxins
are botulinum and tetanus, which are the cause of
hemolysis and are powerful neurotoxin. Besides,
Clostridium chauvei toxins are responsible for
black leg disease in cattle.
Fungal Toxins (Mycotoxins)
There are several fungi known for production of
toxins. Such toxins are known as mycotoxins and
they are mostly found in food! feed items, which
cause disease in animals through ingestion.
Aflatoxins
Aflatoxins are produced by several species of fungi
including mainly Aspergillus flavus, A. parasiticus
and Penicillium puberlum. These aflatoxins are
classified as Bh B2, Gh G2, Mh M2, B2a, G2a and
aspertoxin. Aflatoxins are produced in moist
environment in grounded animaVpoultry feed on
optimum temperature and are more common in
tropical countries where storage conditions are poor
and provide suitable environment for the growth of
fungi. These toxins are known to cause
immunosuppression, formation of malignant
neoplasms and hepatopathy.
Ergot
Ergot is produced by Claviceps purpura in grains
which causes blackish discoloration. It produces
gangrene by chronic vasoconstriction, ischemia and
capillary endothelium degeneration. It is also
associated with summer syndrome in cattle
characterized by gangrene of extremities.
Fusarium toxins
Fusarium toxins are produced by Fusarium
tricinctum in paddy straw, which are found to cause
gangrene in extremities. Zearalenone toxin is the
cause ofovarian abnormality in sow.
24
Ochratoxins
Ochratoxins are produced by Aspergillus
ochraceous and A. viridicatum fungi in grounded
feed on optimum temperature and moisture and are
found to cause renal tubular necrosis in chickens
and pigs.
Plant toxins
Over 700 plants are known to produce toxin. e.g.
Braken fern which causes haematuria and
encephalomalacia. Strychnine from Strychnos
nuxvomica is highly toxic and causes death in
animals with nervous signs. It is used for dog
killing in public health operations to control rabies
(Figs. 2.21 & 2.22). HCN is found in sorghum
which is known to cause clonic convulsions and
death in animals characterized by haemorrhage in
mucous membranes.
Drug toxicity
• Antibiotics: Cause direct toxicity by destroying
gut microflora. Oxytetracyline, sulfonamides
are nephrotoxic. Neomycin and Lincomycin
cause Malabsorption diarrhoea and
immunosuppression.
• Anti-inflammatory drugs, like acetaminophen
causes hepatic necrosis, icterus and hemolytic
anemia.
• Anticoccidiostate drug: Monensin is
responsible for necrosis of cardiac and skeletal
muscles.
• Trace elements: There are various trace
elements, excess of which may cause
poisoning in animals. e.g. Selenium poisoning
"Blind staggers" or "Alkali Disease" in cattle
characterized by chronic debilitating disease. It
also causes encephalomalacia in pigs.
Environmentalpollutants
Environment is polluted due to presence of
unwanted materials in food, water, air and
surroundings of animals, particularly by
agrochemicals including pesticides and fertilizers.
The environmental pollutants exert their direct or
indirect effect on the animal health and production.
The main pollutants are:

Etiology
• Heavy metals such as mercury, lead, cadmium
are found in industrial waste, automobile and
generator smoke, soil, water and also as
contaminants ofpesticides and fertilizers. They
are responsible for damage in kidneys, immune
system and neuropathy. They are also
associated with immune complex mediated
glomerulonephritis.
• Sulphur dioxide is produced by automobiles,
industries and generators. It is responsible for
loss of cilia in bronchiolar epithelium.
• Hydrogen sulphide is produced by animal's
decay and in various industries. It inhibits
mitochondrial cytochrome oxidase leading to
death.
• Pesticides are agrochemicals used in various
agricultural, animal husbandry and public
health operations. They are classified as
insecticides, herbicides, weedicides and
rodenticides. Chemically, insecticides are
grouped mainly as organochlorine
organophosphates, carbamates and synthetic
pyrethroids. Acute poisoning of pesticides
causes death in animals after nervous clinical
signs of short duration. Chronic toxicity is
characterized by immunosuppression,
nephropathy, neuropathy, hypersensitivity and
autoimmunity in animals (Figs. 2.23 & 2.24).
NUTRITIONAL CAUSES
Malnutrition causes disease in animals either due to
deficiency or excess of nutrients. It is very difficult
to diagnose the nutritional causes and sometimes it
is not possible to fmd a precise cause as in case of
infectious disease because functions of one nutrient
can be compensated by another in cell metabolism.
Experimental production of nutritional deficiency
is not identical to natural disease. When tissue
concentration of nutrient falls down to the critical
level, it leads to abnormal metabolism and the
abnormal metabolites present in tissues can be
detected in urine and faeces. First changes of
nutritional deficiency are recorded in rapidly
metabolizing tissues e.g. skeletal muscle,
myocardium and brain. Immature animals are more
25
susceptible to nutritional disease. e.g. calves,
chicks, piglets etc.
Types of deficiency
• Acute/chronic e.g. thiamine deficiency in pigs.
• Multiple deficiencies: e.g. poor quality food.
• Nutritional imbalance: e.g. imbalance in
calcium: phosphorus (2:1) ratio.
• Protein malnutrition: e.g. malabsorption.
• Calorie deficiency: e.g. Loss of fat/ muscle
wasting.
Factors responsible for nutritional deficiency
• Interference with intake e.g. anorexia, G.!.
tract disorders.
• Interference with absorption e.g. intestinal
hypermotility, Insoluble complexes in food
(Fat/Calcium)
• Interference with storage e.g. hepatic disease
leads to deficiency of vit. A.
• Increased excretion e.g. polyuria, sweating and
lactation
• Increased requirement e.g. fever,
hyperthyroidism and pregnancy
• Natural inhibitors e.g. presence of thiaminases
in feed, leads to thiamine deficiency.
Calorie deficiency
Calorie deficiency in animals occurs due to food
deprivation or starvation.
Food deprivation
Dietary deficiency of food in terms of
quantity/quality leads to emaciation, loss of
musculature, atrophy of fat, subcutaneous oedema,
cardiac muscle degeneration and atrophy of viscera
including liver and pancreas. The volume of
hepatocytes reduced by 50% and mitochondrial
total volume also reduced by 50%.
Starvation
Starvation is the long continued deprivation of
food. It is characterized by fatty degeneration of
liver, anemia and skin diseases. Young and very
old animals are more susceptible to starvation
while in pregnant animals it causes retarded growth

of foetus. In animals, following changes can be
seen due to starvation.
Intestinal involution
Absorptive surface is reduced with shrunken cells
and pyknotic nuclei. Villi become shorter and show
atrophy.
Atrophy ofmuscles
There is decrease in muscle mass.
Lipolysis
Increased cortisol leads to increased lipolysis
resulting in formation of fatty acids in liver which
in turn converts into ketones used by brain.
Gluconeogenesis
In early fasting blood glucose level drops down.
The insulin level becomes low while glucagon goes
high in starvation. The glucose comes from skeletal
muscle, adipose tissue and lymphoid tissue during
starvation. Twenty-four hours of food deprivation
causes reduction in liver glycogen and blood
glucose. Fatty acid from adipose tissue forms
glucose and in mitochondria after oxidation it
forms acetoacetate, hydroxybutyrate and acetone.
These are also known as ketone bodies and are
present in blood stream during starvatibn. This state
is also known as ketosis e.g. ketosis/acetonemia in
bovines. Lack of glucose in blood leads to
oxidation of fatty acids which form ketone bodies
as an alternate source of energy. They are normal!
physiological at certain level but may become
pathological when their level is high.
Clinically it is characterized by anorexia,
depression, coma, sweet smell in urine.
Concentration of acetone increases in milk, blood
and urine along with hyperlipimia and acidosis. A
similar condition also occurs in sheep known as
pregnancy toxaemia which is characterized by
depression, coma and paralysis. This situation
occurs when many foetus are present in uterus.
There are fatty changes in liver, kidneys, and heart,
with subepicardial petechiae or echymosis.
26
Protein deficiency
Generally, protein deficiency does not occur.
However, the deficiency of essential amino acids
has been reported in animals when certain
ingredients are deficient in certain amino acids. e.g.
maize is deficient in lysine and tryptophan that
leads to slow growth; peanuts and soybean are
deficient in methioine. Protein deficiency is
characterized by hypoproteinemia, anemia, poor
growth, delayed healing, decreased or cesation of
cell proliferation, failure of collagen formation,
atrophy of testicles and ovary, atrophy of thymus
and lymphoid tissue.
Deficiency ofLipids
Generally, there is no deficiency of fat in animals.
However, essential fatty acids, including linolenic
acid, linoleic acid and arachdonic acid, deficiency
may occur which causes dermatoses in animals. Fat
has high calorie value and it is required in body
because there are certain vitamins soluble in fat
only.
Deficiency of Water
Deficiency of water may lead to dehydration and
slight wrinkling in skin. Deficiency may occur due
to fever, vomiting, diarrhoea, haemorrhage and
polyuria, which can be corrected through adequate
oral water supply or through intravenous fluid
therapy.
Deficiency of Vitamins
Vitamin deficiency may occur due to starvation.
There are two types of vitamins viz., fat soluble
and water soluble. Fat soluble vitamins are vit. A,
D, E and K and water soluble are vit B complex
andC.
Vitamin A
It is also known as retinol. It is derived from its
precursor carotene. It is found in abndance in plants
having yellow pigment, animal fat, liver, cod liver
oil, shark liver oil. ~-carotene is cleaved in gut
mucosa into two molecules of retinol (Vit. A
aldehyde) which, after absorption, is stored in liver.
Bile salts and pancreatic juice are responsible for

Etiology
absorption of vit. A from gut. Deficiency of vit. A
occurs due to damage in liver.
Vit. A deficiency may lead to following disease
conditions:
Squamous metaplasia of epithelial surfaces in
esophagus, pancreas, bladder and parotid duct,
which is considered pathognomonic in calves.
Destruction of epithelium! goblet cell in respiratory
mucosa is generally replaced by keratin
synthesizing squamous cells in vit. A deficient
animals. There are abnormal teeth in animals due
to hypoplasia of enamel and its poor
mineralization. Vitamin A deficiency is also
associated with still birth and miscarriages in pigs.
It causes night blindness (Nyctalopia) in animals.
Due to deficiency of Vit. A there are recurrent
episodes of conjunctivitis/ keratitis: In poultry,
there is distention of mucous glands, which opens
in pharynx and esophagus because of metaplasia of
duct epithelium leading to enlargement of
esophageal glands due to accumulation of its
secretions. The glands become spherical, 1-2 mm
dia. over mucosa. It is considered pathognomonic
for hypovitaminosis A. and is known as Nutritional
roup (Fig. 2.25a&b). Inflammation of upper
respiratory tract lead to coryza. Urinary tract of
cattle, sheep and goat suffers due to formation of
calculi, which may cause obstruction in sigmoid
flexure of urethra in males. Such calculi are made
up of desquamated epithelial cells and salts and the
condition is known as urolithiasis. Deficiency of
vit. A may also lead to in abnormal growth of
cranial bones and there may be failure of foramen
ovale to grow leading to constriction of optic
nerves which results in blindness in calves,
increased CSF pressure, blindness at birth and
foetal malformations. In sows, piglets are born
without eyes (Anophthalmos) or with smaller eyes-
(Microphthalmos).
Vitamin D
Vitamin D occurs in three forms viz. vitamin D2 or
calciferol, Vit. D3 or cholecaliciferol and Vit D, or
impure mixture of sterols. About 80% Vit. D is
synthesized in body skin through UV rays on 7-
hydrocholesterol. In diet containing egg, butter, it is
27
found in abundant quantity in milk, plants, grains
etc. Active forms of vit. Dare 25-hydroxy vit. D
and 1,25 dihydroxy vit D. (Calcitriol) which is 5 to
10 times more potent than former. Vit D is stored
in adipose tissue in body. The main functions of vit
D are absorption of Ca and P from intestines and
kidneys, mineralization of bones, maintenance of
blood levels of Ca and P and immune regulation as
it activates lymphocytes and macrophages.
• The deficiency of vitamin D is associated with
rickets in young animals (Fig. 2.26),
osteomalacia in adult animals and
hypocalcemic tetany.
• Excess of vitamin D leads to the formation of
renal calculi, metastatic calcification and
osteoporosis in animals.
Vitamin E (a- tocopherol)
Source of vitamin E is grains, oils, nuts, vegetables,
and in body it is stored in adipose tissue, liver and
muscles. It has antioxidant activity and prevents
oxidative degradation of cell membrane.
• Deficiency of vit E causes degeneration of
neurons in peripheral nerves. There is
denervation of muscles leading to muscle
dystrophy e.g. White muscle disease in cattle
and Stiff lamb disease in sheep and
Myoglobinuria in horses. Deficiency of vit. E
causes degeneration of pigments in retina and
reduces life span of RBC, leading to anemia
and sterility in animals. Crazy chick disease
(Encephalomalacia) is also caused by vit E
deficiency; the chicks become sleepy with
twisting of head and neck. There is muscular
dystrophy in chickens due to vit. E deficiency
(Fig. 2.27).
VitaminK
Vit. K occurs in two forms namely vit. K, or
phylloquinone found in green leaf and vegetables
and Vit- K2 or menadione which is produced by gut
microflora. Its main function is coagulation of
blood. Deficiency of vit K may leads to
hypoprothrombinemia and haemorrhages.

(a)
(b)
Fig. 2.25.(a) Diagram of squamous metaplasia in esophageal
glands due to vitamin A deficiency (b) Photograph of
eosophagus ofpoultry showing nutritional roup.
Fig. 2.26. Photograph ofa calf showing rickets
28
Fig 2.27. Muscular dystrophy due to vitamin E
deficiency
Fig. 2.28. Curled toe paralysis in a chick due to
Riboflavin deficiency
Fig. 2.29. Silpped tendon or perosis In chicks

Etiology
Vitamin B
Vitamin B is a water soluble vitamin which has at
least 9 sub types including B or thiamine, B2 or
riboflavin, B6 or pyridoxine, B2 or
cyanocobalamin, niacin or nicotinic acid, folate or
folic acid, choline, biotine and pantothenic acid.
Thiamine
In ruminants, synthesis of thiamine occurs in
rumen. Sources of vit. B are pea, beans, pulses,
green vegetables, roots, fruits, rice, wheat bran etc.
Strong tea, coffee have antithiamine action. It is
stored in muscles, liver, heart, kidneys and bones of
animals. Thiamine plays active role in carbohydrate
metabolism
• Deficiency of thiamine may lead to Beriberi
disease characterized by Ataxia and
neuraVlesions. Chastek paralysis in cats, fox
and mink and stargazing attitude of chicks due
to thiaminase (thiamine deficiency) in meal
may be observed. Bracken fern poisoning in
cattle and horses may cause deficiency of
thiamine due to presence of thiaminase
enzyme in bracken fern. Toxicity of thiamine
splitting drugs like amprolium, a coccidiostate,
may cause polioencephalomalcia in cattle and
sheep. Cardiac dialation in pigs has also been
observed due to vit. B deficiency.
Riboflavin
Riboflavin is a component of several enzymes and
is found in plants, meat, eggs and vegetables.
• Deficiency of riboflavin may cause Curled
Toe Paralysis in chicks and swelling of sciatic
and brachial nerves (Fig. 2.28).
Niacin
Role of niacin (NADINADP, nicotinamide adenine
dinucleotide) is in electron transport in
mitochondria of cells. It is found in grains, cereals,
meat, liver, kidneys, vegetables and plants.
• Deficiency of niacin is associated with skin
disorders in man Pellegra; anorexia, diarrhoea,
anemia in pigs and mucous hyperplasia,
haemorrhage in gastrointestinal tract and black
29
tongue in dogs which is also known as Canine
pellegra.
Pyridoxine
It is found in egg, green vegetables, meat, liver etc.
• Deficiency of pyridoxine causes uremia,
convulsions, dermatitis and glossitis
Pantothenic acid
• Pantothenic acid deficiency is associated with
stunted growth of chicks.
Folate
• Folic acid is required in formation of
erythrocytes and hence its deficiency leads to
anemia.
Cyanocobalamin
Deficiency of cyanocobalamin may also lead to
anemia, as it is also needed in RBC formation.
Biotin
Biotin deficiency causes paralysis of hind legs in
calves and perosis in chicks.
Choline
Choline deficiency is associated with fatty changes
in liver and perosis.
Vitamin C (Ascorbic acid)
It is found in green plants and citrus fruits.
Deficiency of vit. C may cause retardation of
fibroplasia, scurvy in G. pigs, haemorrhage,
swelling, ulcers and delayed wound healing in
animals.
MINERALS
Various minerals are also necessary for survival of
animals. Deficiency of anyone of them or in
combination may cause serious disease in animals.
Some ofthe important minerals are:
• Sodium chloride • Cobalt
• Calcium • Manganese
• Phosphorus • Potassium
• Magnesium • Fluorine
• Iodine • Sulphur
• Iron • Selenium
• Copper • Zinc

Sodium chloride
Sodium chloride is an essential salt which
maintains osmotic pressure in blood, interstitial
tissue and the cells because 65% of osmotic
pressure is due to sodium chloride. Chloride ions of
hydrochloric acid present in stomach also come
from sodium chloride.
• The excess of sodium chloride causes
gastroenteritis in cattle, gastroenteritis and
eosinophilic meningoencephalitis in pigs and
ascites in poultry.
• Deficiency of sodium chloride is characterized
by anorexia, constipation, loss of weight in
sows and pica, weight loss, decreased milk
production and polyurea in cattle. Deficiency
of salt occurs due to diarrhoea, dehydration
and vomiting.
Calcium
Normal range ofcalcium is 10-11 mg/lOO rnl blood
in body of animals. If it increases above 12 mg/IOO
rnl blood, metastatic calcification occurs, while its
level less than 8 mg/IOO rnl blood may show signs
ofdeficiency characterized by tetany.
Absorption of calcium from gut is facilitated by vit.
D. Paratharmone stimulates to raise blood Ca level
from bones while calcitonin from thyroid
stimulates its deposition in bones and thus reduces
blood Ca levels.
• In pregnant cows, calcium deficiency occurs
just after parturition. During gestation calcium
goes to foetus from skeleton ofcows, resulting
in weak skeleton of dam. If calcium is not
provided in diet, it may cause disease in dam
characterized by locomotor disturbances,
abnormal curvature of back, distortion of
pelvis, tetany, incoordination, muscle spasms,
unconsciousness and death. Such symptoms
occur in animals when their blood calcium
level falls below 6 mg/lOO ml of blood and if
it is less than 3 mg/lOOrnl blood, death occurs
instantly.
• Milk fever is a disease of cattle that occurs
due to deficiency of calcium just after
parturition. Cow suddenly becomes recumbent
and sits on sternum with head bending
30
towards flank and is unable of get up. No
gross/ microscopic lesion is reported in this
disorder. The calcium therapy recovers the
animal immediately.
• The excess of calcium may cause metastatic
calcification leading to its deposition in soft
tissue ofkidney, lungs and stomach.
Magnesium
It acts as activator of many enzymes e.g. alkaline
phosphatase. It is required for activation of
membrane transport synthesis of protein, fat and
nucleic acid and for generation! transmission of
nerve impulses. The normal blood levels are 2
mg/IOO rnl ofblood.
• Dietary deficiency leads to hypomagnesaemia
and a level below 0.7 mg/IOO rnl causes
symptoms in calves characterized by nervous
hyperirritability, tonic and clonic convulsions,
depression, coma and death.
• The post-mortem lesions of magnesium
deficiency includes haemorrhage in heart,
intestines, mesentery and congestion of
viscera.
• Microscopic lesions include calcification of
intimal layer~ of heart blood vessels
(metastatic) muscles and kidneys. Grass tetany
and Grass staggers occurs due to hypomagne-
saemia and are characterized by hyper-
irritability, abnormal gait, coma and death.
Phosphorus
Normal level of phosphorus is 4-8 mg/IOO rnl of
blood. In bones, it is in the form of calcium
phosphate. Deficiency of phosphorus qlay lead to
hypophosphatemia and is characterized by pica,
rheumatism and hemoglobinurea.
• Pica is licking/eating of objects other than
food. It mainly occurs in cattle, buffaloes and
camels, who eat bones, mud and other eartbern
materials. Such animals have heavy parasitic
load in their gut.
• Rheumatism like syndrome is characterized by
lameness in hind legs particularly in camels
and buffaloes.
• Hemoglobinurea is characterized by the
presence of coffee colour urine of animal due
to extensive intravascular hemolysis Hemo-

Etiology
globin urea is thus known as postparturient
hemoglobin urea.
Selenium
Deficiency of selenium causes hemolysis as it
protects cell membrane of RBC and thus its
deficiency leads to anemia. Blind Staggers occurs
due to excess of selenium.
Iron
Deficiency of iron leads to anemia, which is
hypochromic and microcytic but rarely occurs in
animals.
Copper
Deficiency of copper results in anemia and steel
wool disease in sheep, which is characterized by
loss of crimp in wool. Enzootic ataxia with
incoordination of posterior limb has been observed
in goats.
Cobalt
Vit. Bl2 is synthesized by ruminal bacteria from
cobalt in ruminants. Cobalt also stimulates
erythropoiesis. Its deficiency may cause wasting
disease, cachexia and emaciation in animals. The
pathological lesions are comprised of anemia,
hemosiderosis in liver, spleen and kidneys.
Manganese
Deficiency of manganese causes slipped tendon in
chicken or perosis characterized by shortening of
long bones in chickens. It occurs as the epiphyseal
cartilage fails to ossify at 12 week of age and
epiphysis becomes loose and thus gastrocnemious
tendon slips medially. This condition is known as
Slipped Tendon or Perosis (Fig. 2.29).
Zinc
Deficiency of zinc may cause parakeratosis in pigs
at 10-20 weeks' age. Calcium in diet with phytate
or phosphate forms a complex with zinc making it
unavailable for absorption leading to its deficiency,
which is characterized by rough skin of abdomen,
medial surface of thigh, which becomes homy. It
also causes fascial eczema in cattle, thymic
hypoplasia in calves and immunodeficiency in
animals.
Iodine
Deficiency of iodine causes goiter in newborn pigs
characterized by absence of hair on their skin.
Other signs ofiodine deficiencies include abnormal
spermatozoa, decreased spermatogenesis, loss of
libido, reduced fertility, suboestrus, anoestrus,
miscarriages, dystocia and hydrocephalus. Excess
ofiodine may lead to lacrimation and exfoliation of
dandruff like epidermal scales from skin.
Fluorine
Excess of fluorine causes mottling in teeth and
bones. The teeth become shorter, broader with
opaque areas.
MODEL QUESTIONS
Q. 1. Fill in the blanks with suitable word(s) to answer thefollowings.
1. .. .. .. .. .. .. ... in severe burns leads to impaired phagocytosis by .............. .
2. Radiation mainly affects the...............cells ofbody in........., ........., ......... and.........
3. Viruses are classified into two major groups viz................ and ............... on the basis of
presence of .............. .
4. Acid fast bacilli causing disease in animals are ..............., ............... and .............. .
5. The transmission ofinfection created by man / doctor is known as ........ .
6. Snake venom contains ............, ..............., ............... and ............ causing lysis of
erythrocytes and platelets leading to ................ and........... .
31

7. The gangrene on extremities produced by feeding of............... to the animals and is also
known as............... disease.
8. Fungal toxins like. .... ...... .... cause immunosuppression and hepatotoxicity while
............... causes renal damage in chickens.
9. Pesticides are classified into four major groups..............., ..............., ............. and,
............... of which a major group is .............. .
10. Heavy metals such as ..............., ............... and............... are immunotoxic as well as
nephrotoxic in animals.
11. The first changes of nutritional deficiency are recorded in rapidly metabolizing tissues such as
............, ............ and .......... ..
12............. animals are more susceptible to nutritional disorders.
13. Starvation is the ............ of food and is characterized by ............ , ............ and .......... ..
14. Ketone bodies are ............, ............ and .......... ..
15. Protein deficiency may lead to failure of collagen formation resulting in atrophy of
...............,.....................,........................and................. .
16. Maize is deficient in................... and ..............amino acids.
17. Essential fatty acids are ................., ..................... and...................
18. The deficiency ofVit. A is the cause ofrecurrent episodes of ......... and ......... in animals.
19. Encephalomalacia is caused by deficiency ofvitamin ....................
20. Perosis is caused by...................., ...................... and .................. deficiency in birds.
Q. 2. Write true orfalse against each statement and correct thefalse statement.
1. .........Hog cholera occurs only in pigs.
2. .. .......Beefcattle are more prone to mastitis.
3. .........Nephritis is more common in male in comparison to female bovines.
4. .........Canine distemper occurs in old dogs.
5. .........Burns and surgery may lead to immunosuppression.
6. .........Rabies is caused by lyssavirus which belongs to retroviridae family.
7. .........Pathogenic fungi belong to fungi imperfecti.
8. .........Trypanosomasis may be transmitted through inoculation.
9. .........Ochratoxin causes bile duct hyperplasia and hepatcarcinoma in birds.
10. .........Most ofthe antibiotics show their deleterious effect on gut microflora, which may
lead to gastrointestinal tract problems.
11. .........Newly born piglets are less prone to deficiency diseases.
12..........Starvation may cause stunted growth offoetus in pregnant animals.
13..........Presence of ketone bodies in blood should always be suspected for ketosis in cows.
14..........Soybean is deficient in lysine amino acid.
15. .........Vitamin B complex and Care water-soluble.
16..........Nyctalopia is caused by vitamin E deficiency.
17. .........Microphthalmos is defmed as newborn with smaller eyes.
18..........Vitamin D regulates the immune system of animals and activates the lymphocytes and
macrophages.
19..........Vitamin K2 is produced by gastrointestinal flora and is known as phylloquinone.
20..........Slipped tendon is caused by manganeese deficiency is birds.
32

Etiology
Q.3. Define thefollowings.
1. Multiple deficiency 11. Microphthalmos
2. Lipolysis 12. Parakeratosis
3. Dehydration 13. Perosis
4. Urolithiasis 14. Hemoglobinurea
5. Anophthalmos 15. Myoglobinurea
6. Idiosyncracy 16. Drug toxicity
7. Bums 17. Immunotoxicity of environmental pollutants
8. Mode of transmission 18. Microbial toxins
9. Maintenance of infection 19. Electrical injury
10. Aflatoxin 20. Radiation injury
Q.4. Write short notes on.
1. Erosions 11. Convulsions
2. Laceration 12. Neuropathy
3. Latency 13. Exotoxins
4. Septicemia 14. Hematuria
5. Blind staggers 15. Bacteriostate
6. Osteomalacia 16. Factors responsible for nutritional deficiency
7. Gluconeogenesis 17. Milk fever
8. Ketosis 18. Goiter
9. Pregnancytoxemia 19. White muscle disease
10. Nutritionalroup 20. Salt poisoning
Q. 5. Select one appropriate word from the four options provided with each question.
1. Hog cholera occurs in........................
(a) Pig (b) Dog (c) Horse (d) Cow
2. Partial loss ofepithelium on skin or mucous membrane is known as................
(a) Abrasion (b) Erosion (c) Laceration (d) Contusion
3. Bum area ofskin and tissues remains sterile till..........
(a) 12 hrs (b) 16 hrs (c) 20 hrs (d) 24 hrs
4. Epidermis and dermis are destroyed leading to shock in ...............bum.
(a) I degree (b) 11 degree (c) III degree (d) IV degree
5. Radiation affects the dividing cells of.......
(a) Ovary (b) Testes (c) Lymphocytes (d)All ofthe above
6. Leptospira is a......... which causes miscarriages in cattle.
(a) Bacteria (b) Virus (c) Chlamydia (d) Spirochaete
7. Coxiella burnetti is a...... which causes Q-fever in animals.
(a) Mycoplasma (b) Bacteria (c) Rickettsia (d) Chlamydia
8. Ringworm is caused by a.......
(a) Bacteria (b) Virus (c) Fungi (d) Parasite
9. Transmission ofdiseases from one generation to another is known as.......
(a) Vertical (b) Horizontal (c) Triangular (d)All of the above
10. Aflatoxins are produced by..........
(a) Aspergillusflavus (b) Asperfillus parasiticus (c) Penicillium puberlum (d)All of the above
33

11. Pesticide includes..... .
(a) Insecticide (b) Rodenticide (c) Weedicide (d)All ofthe above
12. Acetone, ~-hydroxybutyrate and acetoacetic acid are known as.......
(a) Ochratoxins (b) Ketone bodies (c) Heinze bodies (d)Pyknotic bodies
13. Prolonged starvation leads to................... ofmuscles
(a) Hypertrophy (b) Hyperplasia (c) Atrophy (d) Metaplasia
14. Deficiency ofvitamin A causes....................
(a) Nutritional roup (b) Nyctalopia (c) Calculi in urethra (d)All ofthe above
15. Vitamin D regulates the activity of......................
(a) Lymphocytes (b) Macrophages (c) All ofthe above (d) None ofthe above
16. Star grazing in chicks in caused by ....... deficiency
(a) Vitamin BJ (b) Vitamin B2 (c) Vitamin B6 (d) Vitamin BJ2
17. Curled toe paralysis is caused by ....... deficiency
(a) Thiamine (b) Riboflavin (c) Choline (d) Biotin
18. Crazy chick disease is caused by ....... deficiency
(a) Vitamin A (b) Vitamin C (c) Vitamin D (d) Vitamin E
19. Perosis is caused by ....... deficiency.
(a) Biotin (b) Choline (c) Manganese (d)All ofthe above
20. Rheumatism like syndrome is caused by deficiency of .......
(a) Calcium (b) Phosphorous (c) Copper (d) Zinc
34

3
GENETIC DISORDERS,
DEVELOPMENTAL
ANOMALIES AND MONSTERS
• Genetics
• Chromosomes
• Genetic disorders
• Aberrations in chromosomes
• Anomalies
• Monsters
• Model Questions

GENETICS
Genetics is the branch of science that deals with
study of genes, chromosomes and transmittance of
characters from one to generation another.
CHROMOSOMES
Chromosomes are thread-like structures present in
the form of short pieces in nucleus of a cell. They
are in pairs; of which one pair is sex chromosome
and others are autosomes.
Table 3.1 Number of chromosomes in different
species of animals
SI.
No.
1.
2.
3.
4.
5.
6.
7.
8.
•
•
•
•
Animal
Chromosomes
Male Female
Pairs Total
Cattle 30 60 XY XX
Sheep 27 54 XY XX
Goat 30 60 XY XX
Pig 19 38 XY XX
Dog 39 78 XY XX
Cat 19 38 XY XX
Horse 32 64 XY XX
Poultry 39 78 ZZ ZW
Each chromosome is composed of two
chromatids connected at centromere.
x__Chromathi
Fig. 3.1 Diagram o/Chromosomes
Chromosomes are grouped together on the
basis of their length, location of centromere
and this procedure is known as karyotyping.
The study of karyotyping is known as
cytogenetics.
Chromosomes are composed of 3 components:
• DNA-20%
• RNA -10%
• Nuclear proteins - 70%
36
Deoxyribo nucleic acid (DNA)
• Double helix structure of polynucleotide
chain.
• A nucleotide consists of phosphate, sugar and
base of either purine (Adenine, Guanine) or
pyrimidine (Thymine, Cytosine).
Fig. 3.2. Double helix DNA structure
• A sequence of 3 nucleotide determines the
synthesis of an amino acid and is known as
genetic code/codon.
• During cell division, one half of DNA
molecule acts as template for the synthesis of
other half by an enzyme DNA polymerase to
transmit the genetic information which may
also transit some disorders to next progeny.
Gene
• Sequence of nucleotides which controls the
synthesis of one specific protein is known as
gene. It is a unit of function. Study of genes is
termed as Genetics. In higher animals about
1.0 million genes are present.
• Genes located on X or Y chromosomes are
termed as sex linked and all other genes are
autosomal genes.
• When the genes at one locus are same from
both parents they are termed as homo(,Ygous
but when they are different at one locus they
are known as hetero(,Ygous.
• In heterozygous, characters of one gene are
manifested in phenotype and such gene is
known as dominant while unexpressed gene is
called as recessive.

Genetic Disorders, Developmental Anomalies and Monsters
Karyotyping
• Karyotyping is the study of chromosomes in
cell.
• Collection of blood, separation oflymphocytes
using Histopaque-l077 gradient.
• The lymphocytes are cultured with mitogen
concanavalin A (ConA) or phytohemagglutinin
- M (PHA-M) for 72 hrs.
• Colchicine is used after 72 hrs to arrest the cell
division at metaphase stage.
• Hypotonic solution is added to allow cells to
swell which causes separation of
chromosomes.
• Prepare glass slides and stain with Giemsa or
other special stain.
• Identify the chromosomes and photograph
them.
• Cut photographs having homologous chromo-
somes and make pairs.
GENETIC DISORDERS
ABERRATION IN CHROMOSOMES
• A large number of chromosomal aberrations
are removed due to death of gamete or zygote
which is termed as "species cleansing effect".
However, some aberrations persist and are
expressed in phenotype leading to illness.
1. Aberration in number
• Chromosomes are in pairs (2n). When number
of chromosomes are other than (n) or (2n). It
is known as heteroploidy.
(a) Heteroploidy
• The number of chromosomes are other than
(n) or (2n).
• When abnormal number is exact multiplies of
the haploid set due to errors in mitosis. The
polar body may fail to be extruded from ovum
leaving diplod set to be fertilized by sperm (n)
i.e. 2n + n = 3n (Triploid zygote).
• When abnormal number is not the exact
multiplies of haploid set. It may have specific
chromosome in triple number (trisomy) or in,
single number (monosomy).
37
(b) Duplication and deficiencies
• Duplication or deficiency may occur in a
section of chromosome and total number of
chromosomes remains same.
• Translocation is the rearrangement ofa part of
chromosome in two non-homologous
chromosomes. It may be reciprocal or non-
reciprocal. Absence of a piece of chromosome
is known as deletion.
(c) Mosaicism
• In mosaicism, there is more than one
population of cells in body; each population
differs in their chromosomes/ genes due to
error during development.
• May be due to chromosomal non-disjunction
there is, e.g. XXY in some cells, XY in other
cells.
(d) Chimerism
• In this, one type of cells are acquired in utero
from a twin e.g. Bovine twin, 1 male and 1
female, with~oint placenta. The blood cells of
male may go in female counterpart. Then the
female will have two types of cell population,
one of its own and another acquired from twin.
Similarly, male may also have XX leucocytes
in its blood. Such chimeric bulls are sterile.
2. Abnormalities in sex chromosomes
(a) Klinefelters syndrome
• Males have sex chromatin i.e. XXY = 47(2n)
in man.
• In some cells, different number of
chromosomes i.e. XX, XXY, XXXY, XXYY
• It is recognized in adolscence by small testes,
tall body, and low sexual characters, mostly
infertile.
• May occur in sheep, cattle and horse.
(b) Tortoiseshell male cat
• Male cat has small testes, lack of libido and
absence of spermatozoa in testes with 3n
chromosomes (XXY).

(c) Turner's syndrome
• Mare are with XO karyotype having gonadal
dysgenesis and such animals are sterile and do
not have sex chromatin.
• In mice XO karyotype is normal.
(d) Intersexes
• In this condition ambiguity occurs in genitalia
or the secondary sex characters are present for
both the sexes including male and female.
• Hermaphrodites have male and female
genitalia while pseudohermaphrodites hae
external genitalia of one sex and gonads of
opposite sex.
(e) Freemartinism
• In bovine twins, one male with (XY) and one
female (XX) karyotype but they share
placental circulation so cells of embryo
establish in other co-twin.
(j) Testicularjeminization
• The animal has female genitalia as external
and internal organs but in place of ovaries,
there are testes. It occurs due to single gene
defect and makes tissues unresponsive to
androgenic hormones.
3. Abnormalities in autosomal chromosomes
(a) Down's syndrome!Mongolism
• It occurs as a result of trisomy, number of a
particular chromosome increases leaving 2n, as
61 in bovines, 77 in dogs and 47 in man e.g.
bovine lymphosarcoma occurs in animals with
2n=61. Male dog with 2n= 77 are prone to
lymphoma.
(b) Sterility in hybrids
• Donkey has 2n=62 and horse has 2n=64. Their
cross mule has 2n=63.
• Cause of sterility in mules is not known, may
be due to uneven number ofchromosomes.
4. Abnormalities in genes
• Lethal genes are those genes which are
responsible for death ofzygote.
38
• Sublethal genes
• X-linked or sex linked: Diseases transmitted
by heterozygous carrier females only to male
offsprings who are homozygous for X-
chromosome.
ANOMALIES
Anomaly is a developmental abnormality that
occurs in any organ/tissue. It may be due to genetic
disorder and may affect the zygote itself within a
few days after fertilization or may occur during any
stage ofpregnancy. It may be classified as under:
1. Imperfect development
(a) Agenesis
Agenesis is incomplete development of an organ or
mostly it is associated with absence ofany organ.
• Acrania is absence ofcranium.
• Anencephalia is absence ofbrain.
• Hemicrania is absence ofhalf ofhead.
• Agnathia is absence oflower jaw.
• Anophthalmia is absence ofone or both eyes.
• Abrachia is absence offore limbs.
• Abrachiocephalia is absence of forelimbs and
head.
•
•
Adactylia is absence ofdigits.
Atresia is absence of normal opening e.g.
Atresia ani is absence ofanus opening.
(b) Fissures
Fissures are a cleft or narrow opening in an organ
on the median line ofhead, thorax and abdomen.
• Cranioschisis is a cleft in skull.
• Chelioschisis is a cleft in lips also known as
harelip.
• Palatoschisis is a cleft in palates; also known
as cleftpalate.
• Rachischisis is a cleft in spinal column.
• Schistothorax is a fissure in thorax.
• Schistosomus is a fissure in abdomen.
(c) Fusion
Fusion is joining ofpaired organs.
• Cyclopia is fusion ofeyes.

Genetic Disorders, DevelopmentalAnomalies and Monsters
• Renarcuatus is fusion of kidneys; also known
as horseshoe kidneys.
2. Excess of development
• Congenital hypertrophy ofany organ.
• Increase in the number of any organ or part
/tissue.
• Polyotia is increased number ofears.
• Polyodontia is increased number ofteeth.
• Polymelia is increased number oflimbs.
• Polydactylia is increased number of
digits.
• Polymastia is increased number of
mammary gland.
• Polythelia is increased number ofteats.
3. Displacement during development
(a) Displacement oforgan
• Dextrocardia is the transposition of heart into
right side instead of left side ofthoracic cavity.
• Ectopia cordis is the displacement of heart
into neck.
(b) Displacement oftissues
• Teratoma is a tumor ansmg due to some
embryonic defect and composed of two or
more types of tissues. In this at least two
tissues should be oforigin.
• Dermoid cyst is a mass containing skin, hair,
feathers or teeth depending on the species and
often arranged as cyst. It mostly occurs in the
subcutaneous tissues.
MONSTERS
Monster is a disturbance of development in several
organs and causes distortion of the foetus e.g.
Duplication of all or most of the organs (Fig. 3.3).
• Monsters develop from a single ovum; these
are the product of incomplete twinning.
• Monsters are classified as under:
1. Separate twins
One twin is well developed while another is
malformed and lacks the heart, lungs or trunk,
head, limbs.
39
Fig.3.3. Photograph showing monster calf.
2. United twins
These twins are united with symmetrical
development and are further classified as:
(a) Anterior twinning
Anterior portion of foetus is having double
structures while posterior remains as single.
• Pyopagus is a monster twin united in the
pelvic region with the bodies side by side.
• Ischiopagus is a monster twin united in the
pelvic region with the bodies at more than a
right angle.
• Dicephalus is a monster having two separate
heads, neck, thorax, and trunk.
• Diprosopus is a monster having double organs
in cephalic region without complete separation
of heads and with double face.
(b) Posterior twinning
When in monsters, the anterior portion remains
single and posterior parts become double.
• Craniopagus is a monster having separate
brain with separate bodies arranged at an acute
angle.
• Cephalothoracopagus is the monster having
united head and thorax.
• Dipygus is the monster having double
posterior extremities and posterior parts of
body.
(c) Almost complete twining
In some monster, twins have complete develop-
ment with joining in thorax and abdomen.

• Thoracopagus is a monsters united in thorax
region.
• Rachipagus is the monster in which thoracic
and lumber portion of vertebral column are
united in twin.• Prosopothoracopagus is the monster twin
united at thorax, head, neck and abdomen.
MODEL QUESTIONS
Q.1. Fill in the blanks with suitable word(s).
1. Chromosomes are grouped together on the basis of ................ and ................... and this
procedure is known as .....................
2. .. ................. is the rearrangement of a part of chromosome in two non-homologous
chromosomes and it may be ................... or ................... .
3. Acrania is absence of ................... while ................... is absence offorelimbs.
4. .. ........... is absence of normal opening; for example................ is absence ofanus opening.
S. .. ................, is a fissure in lips which is also known as ....................
6. Palatoschisis is a ................... in palates and is also known as...................
7. ................... is transposition ofheart into ................... ofthoracic cavity.
8. Monsters develop from ................... and are the products of ................... twinning.
9. ................... is a monstor united in the pelvic region with the bodies side by side.
10. .. ................. is fusion of kidneys and is also known as .................. ..
Q. 2. Write true orfalse against each statement. Correct the false statement.
Q.3.
1. ............Hemicrania is absence ofhead.
2. ............Polyotia is decreased number of ears.
3. ............Each chromosome contains about 70% DNA.
4. .. ..........Monsters develop from a single ovum.
5. .............Abrachiocephalia is a absence of forelimbs and head.
6. ............ Chromosomes are thread-like structures, composed to two chromatids connected
with a centromere.
7. ............Dipygus is a monster having double anterior extremities and other parts ofbody.
8. .. ...........Schistosomus is a fissure in spinal column.
9. .............Dicephalus is a monster having two separate head, neck, thorax and trunk.
10..............Prosopothoracopagus is a monster, which is not united at head.
Write short notes on the following.
1. Draw a diagram of DNA structure
2. Karyotyping
3. Freemartinism
4. Anomalies
5. Monsters
6. Dermoid cyst
7. Teratoma
8. Aberration in chromosomes
9. Testicular feminization
10. Mosaicism
Q. 4. Define the following with suitable examples.
1. Cytogenetics 11. Thoracopagus
2. Heteroploidy 12. Abrachia
3. Agnathia 13. Renarcuatus
40

Genetic Disorders, Developmental Anomalies and Monsters
4. Anophthalmia
5. Cyclopia
6. Polythelia
7. Ischiopagus
8. Ectopia cordis
9. Craniopagus
10. Polymelia
14. Pseudohermaphrodite
15. Rachischisis
16. Hemicrania
17. Chimerism
18. Rachipagus
19. Deletion
20. Cephalothoracopagus
Q. 5. Each question is provided with four options. Select most appropriate option to fill in or answer
the question.
1. Each chromosome contains the DNA content as...................
(a) 20% (b) 10% (c) 70% (d) 30%
2. The study ofkaryotyping of chromosomes falls under .............. .
(a) Immunogenetics (b) Cytogenetics (c) Moleculer genetics (d) Nuclear
genetics.
3. In heterozygous, one gene character is manifested in phenotype and such gene is known as...
(a) Autosomal (b) Recessive (c) Dominant (d) Sex linked
4. In karyotyping, colchicine is added in culture ofperipheral blood lymphocytes for arresting the
cell division in .......... ..
(a) Telophase (b) Meiosis (c) Anaphase (d) Metaphase
5. In heteroploidy, the chromosome number will be ...............in cells.
(a) n (b) 2n (c) 3n (d) All ofthem
6. Intersexes is the condition in animals which occurs due to ambiguity in..............
(a) Genitalia (b) Bones (c) Ears (d) Eyes
7. In Turner's syndrome, mare have karyotype as.................... .
(a) XX (b) XXX (c) XXXX (d) XO
8. Mules have chromosome number as...........
(a) 61 (b) 62 (c) 63 (d) 64
9. Bovine lymphosarcoma occurs in animals having chromosome number.......
(a) 60 (b) 61 (c) 62 (d) 64.
10. Dogs with chromosome number......... are more prone to lymphoma
(a) 76 (b) 78 (c) 77 (d) 75
11. Absence oflower jaw in foetus is known as.......... ..
(a) Acrania (b) Adactylia (c) Agnathia (d) Abrachia
12. Rachischisis is a cleft in .............. .
(a) Spinal column (b) Abdomen (c) Skull (d) Lips
13. Harelip is due to fissure in lips and is also known as.............
(a) Palatoschisis (b) Cranioschisis (c) Schistosomus (d) Chelioschisis
14. Fusion of eyes occurs in monsters and is known as................. .
(a) Renarcuatus (b) Columbia (c) Cyclopia (d) Anophthalmia
15. Increased number of limbs in monsters is known as .............. .
(a) Polythelia (b) Polymastia (c) Polymelia (d) Polydactylia
16. Dextrocardia is transposition ofheart in........... ..
(a) Right thorax (b) Left thorax (c) Neck (d) Abdomen
17. Tumor arising from embryonic defect and composed of more than two tissue.....
(a) Dermatoma (b) Hematoma (c) Papilloma (d) Teratoma
41

18. A monster having two separate brains with bodies separately arranged at an acute angle......
(a) Cephalothoracopagus (b) Dicephalus (c) Craniopagus (d) Cranioschisis
19. A monster united at thorax region and with complete development as twin is known as........ .
(a) Prosopothoracopagus (b) Thoracopagus (c) Dipygus (d) Cephalothoracopagus
20. A monster having thorax and lumber portion ofvertebral column united in twin is known as.....
(a) Rachipagus (b) Craniopagus (c) Thoracopagus (d) Dipygus
42

4
DISTURBANCES IN GROWTH
• Aplasia
• Hypoplasia
• Atrophy
• Hypertrophy
• Hyperplasia
• Metaplasia
• Anaplasia
• Dysplasia
• Model Questions

APLASIA/AGENESIS
Aplasia or agenesis is absence of any organ (Fig.
4.1).
HYPOPLASIA
Hypoplasia is failure of an organ!tissue to attain its
full size (Fig. 4.1).
Etiology
• Congenital anomalies e.g. hypoplasia of
kidneys in calves.
• Inadequate innervation.
• Inadequate blood supply.
• Malnutrition.
• Infections e.g. cerebral hypoplasia in bovine
viral diarrhoea.
Macroscopic features
• Organ size, weight, volume reduced
Microscopic features
• Reduced size of cells.
• Reduced number of cells.
• Connective tissue and fat is more.
ATROPHY
Atrophy is decrease in size of an organ that has
reached its full size (Figs. 4.2 & 4.3).
Etiology
• Physiological e.g. senile atrophy.
• Pressure atrophy.
• Disuse atrophy e.g. atrophy of immobilized
legs.
• Endocrine atrophy e.g. atrophy of testicles.
• Environmental pollution e.g. atrophy of
lymphoid organs.
• Inflammation! fibrosis.
• Size, weight, volume of organ decreased.
• Wrinkles in capsule of organ.
• Size of cell is smaller.
44
• Cell number is less.
• Fat and connective tissue cells are more.
HYPERTROPHY
Hypertrophy is increase in size of cells leading to
increase in size of organ! tissue without increase in
the number ofcells (Fig. 4.4).
Etiology
• Increase in metabolic activity e.g. myometrium
during pregnancy.
• Compensatory e.g. if one kidney is removed,
another becomes hypertrophied due to
compensatory effect.
• Organ becomes large in size.
• Organ weight increases.
• Size of cells increases.
HYPERPLASIA
JIyperplasia is increase in number of cells leading
to increase in size of organ!tissue (Fig. 4.5).
Etiology
• Prolonged lITltation e.g. fibrosis/nodules in
hands, pads.
• Nutritional disorders e.g. iodine deficiency
• Infections e.g. pox.
• Endocrine disorders e.g. prostate hyperplasia.
• Increase in size, weight of organ.
• Nodular enlargement of organ.
• Increased number of cells.
• Displacement ofadjacent tissue.
• Lumen ofducts/ tubules obstructed.
METAPLASIA
Metaplasia is defined as transformation of one type
ofcells to another type of cells (Fig. 4.6 & 4.7).

Disturbances in Growth
• +-- Aplasia
• +-- Hypoplasia
+- Normal
Fig. 4.1. Diagram showing Aplasia and
Hypoplasia
A B c
Fig. 4.2. Photograph ofspleen showing atrophy (c)
~ B
c
Fig. 4.3. Diagram showing atrophy (a) normal (b)
decrease in size and (c) decrease in number ofcells
A
Fig. 4.4. Diagram showing hypertrophy
(a) Normal (b) Hypertrophy
45
Fig. 4.5. Diagram showing hyperplasia
(a) Normal (b) hyperplasia
Fig. 4.6. Diagram showing Metaplasia
Fig. 4.7. Photograph showing Metaplasia
A
Fig. 4.8. Diagram showing anaplaslQ (a) Normal (b)
Anaplastic cells
A
Fig. 4.9. Diagram showing dysplasia
(a). Normal (b) Dysplasia

Etiology
• Prolonged rrntation e.g. gall stones cause
metaplasia of columnar cells to stratified
squamous epithelial cells in wall of gall
bladder.
• Endocrine disturbances e.g. in dog, columnar
epithelium of prostate changes into squamous
epithelium.
• Nutritional deficiency e.g. nutritional roup. In
poultry, cuboidal/columnar epithelium of
oesophageal glands change into stratified
squamous epithelium.
• Infections e.g. pulmonary adenomatosis
• Mucous membrane becomes dry in squamous
metaplasia.
• Presence of nodular glands on
mucous membrane due to
deficiency in chickens also
Nutritional roup.
oesophageal
vitamin A
known as
• Change of one type of cells to another type.
• In place of columnar cells, there are squamous
epithelial cells.
• In place of endothelial cells, cuboidal or
columnar cells in alveoli giving it glandular
shape. e.g. pulmonary adenomatosis.
ANAPLASIA
Anaplasia is defined as reversion of cells to a more
embryonic and less differentiated type. It is a
feature in neoplasia. Neoplasia is uncontrolled new
growth that serves no useful purpose, has no
46
orderly structural arrangement and is
undifferentiated or less differentiated in nature with
more embryonic characters of the cells (Fig. 4.8).
Etiology
• Chemicals.
• Radiation.
• Viruses e.g. oncogenic viruses.
• Enlargement oforgan! tissue.
• Nodular growth oftissue, hard to touch.
• Presence of pleomorphic cells and less or
undifferentiated cells.
• Hyperchromasia.
• Size of cells increases.
• Size ofnucleus and nucleolus increases.
• Presence of many mitotic figures.
• Seen in neoplastic conditions.
DYSPLASIA
Abnormal development of cells/tissues which are
improperly arranged. It is the malformation of
tissue during maturation (Fig. 4.9).
1. Spermatozoa head and tailpiece are structurally
abnormal or aligned in improper way.
2. Fibrous dysplasia in bones.
3. In gastrointestinal tract, disruption of cellular
orientation, variation in size and shape of cells,
increase in nuclear and cytoplasmic ratio and
increased mitotic activity.

Disturbances in Growth
MODEL QUESTIONS
1. Dysplasia is .......development ofcells which are ...............arranged during ............ .
2. In hypoplasia the size oforgan is ...............and it does not attain its ........... .
3. The number ofcells are ...............in atrophy.
4. In atrophied tissue the fat and connective tissues cells are .................... .
5. Papule in pox is an example of .................. growth disturbance.
6. Increase in size ofcells in known as..................which occurs as physiological reaction in
............ during pregnancy.
7. Metaplasia is defined as .................. ofone type ofcells to another type.
8. In anaplasia, the cells are more .................. and less ................. .
9. Hyperchromasia is a feature of ..................... growth disturbance.
10. Pulmonary adenomatosis is an example of .................. growth disturbance.
Q. 2. Write True or False against each statement. Correct thefalse statement.
1. .......Anaplasia is a feature of neoplasia.
2. .......Metaplasia is increase in size and shape of the cells.
3. .......Dysplasia is malformation in which the cells are arranged in an improper way.
4. .......Hyperplasia is increase in size ofcells..
5. .......Atrophy includes the reduction ofsize ofan organ! tissue.
6. .......Cerebral hypoplasia in calves is caused by an adenovirus.
7. ...... .In Hypertrophy, the weight oforgan does not affect much.
8. ...... Atrophy is reduction in size ofcells while hypoplasia is decrease in number ofcells.
9. ...... Wrinkles in capsule ofspleen are example ofatrophy.
10. ....... .Increased size of nucleus and nucleolus with increase in size ofcell occurs in anaplasia.
Q. 3. Define the followings.
1. Anaplasia
2. Metaplasia
3. Senile atrophy
4. Hyperplasia
5. Hypertrophy
Q. 4. Write short notes on.
1. Nutritional roup.
2. Pulmonary adenomatosis.
6. Dysplasia
7. Atrophy
8. Hyperchromasia
9. Neoplasia
10. Hypoplasia
Q. 5. Select most appropriate word(s) from thefour options given with each statement.
1. Cerebral hypoplasia in calves is caused by..............
(a) Adenovirus (b) Rotavirus (c) Bovine viral diarrhoea virus (d) Coronavirus
2. Increase in size ofcells leading to increase in size oforgan is known as........... .
(a) Atrophy (b) Hyperplasia (c) Hypertrophy (d) Metaplasia.
3. Fibrosis may lead to .................... .
(a) Atrophy (b) Hyperplasia (c) Dysplasia (d) Hypertrophy
47

4. Transformation ofone type ofcells to another cell type is known as ...........
(a) Hypoplasia (b) Dysplasia (c) Anaplasia (d) Metaplasia
5. Reversion ofcells towards embryonic type is known as........
(a) Anaplasia (b) Neoplasia (c) Metaplasia (d) Hypoplasia
6. Spermatozoa with defective head and tail piece is an example of ........ .
(a) Dysplasia (b) Anaplasia (c) Neoplasia (d) Metaplasia
7. Hyperehromasia in cells with their enlargement is known as ...........
(a) Hyperplasia (b) Hypertrophy (c) Metaplasia (d) Anaplasia
8. Increased number ofcells leading to increase in size and weight oforgan is known as........ .
(a) Hypertrophy (b) Anaplasia (c) Hyperplasia (d) Metaplasia
9. Environmental pollution may lead to ......... oflymphoid organs.
(a) Atrophy (b) Aplasia (c) Agenesis (d) Hypoplasia
10. Failure ofan organ to develop its full size is known as ..... .
(a) Hyperplasia (b) Aplasia (c) Neoplasia (d) Hypoplasia
48

•
•
•
•
•
•
•
•
•
•
5
DISTURBANCES IN
CIRCULATION
Congestion / Hyperemia
Haemorrhage
Thrombosis
Embolism
Ischemia
Infarction
Oedema
Shock
Sludged blood
Model Questions

CONGESTION/ HYPEREMIA
Hyperemia is increased amount of blood in
circulatory system. It is of two types, active and
passIve. In active hyperemia blood accumulates in
arteries while m passive hyperemia the amount of
blood increases in veins (Figs. 5.1. to 5.4).
Etiology
• As a result of inflammation.
• Obstruction ofblood vessels.
• Organ becomes dark red/cyanotic.
• Size of organ increases.
• Weight oforgan increases.
• Blood vessels become distended due to
accumulation ofblood.
• Increased amount ofblood in blood vessels.
• Veins/capillaries/arteries are distended due to
accumulation ofblood.
• Blood vessels become enlarged with blood and
their number increases.
HAEMORRHAGE
Escape of all the constituents of blood from blood
vessels. It may occur through two processes i.e.
rhexis- break in wall of blood vessel or through
diapedesis in which blood leaves through intact
wall of blood vessel. It occurs only in living
animals (Fig. 5.5).
Etiology
• Mechanical trauma.
• Necrosis ofthe wall ofblood vessels.
• Infections.
• Toxins.
• Neoplasm.
• Organ becomes pale due to escape ofblood
• As per size, the haemorrhage is classified as
under:
50
• Pinpoint haemorrhage of about one mm
diameter or pinhead size is known as
petechiae (Fig. 5.6).
• More than one to 10 mm diameter
haemorrhage are known as ecchymoses
(Fig. 5.6).
• Irregular, diffuse and flat areas of
haemorrhage on mucosal or serosal
surfaces are known as SUffusions.
• Haemorrhage appear in line in crests or
folds on mucous membrane are known as
linear haemorrhage (Figs. 5.7 & 5.8).
• Hematoma is the accumulation of blood
in spherical shaped mass (Fig.5.9).
• According to location, the haemorrhage is
classified as:
• Hemothorax: Blood in thoracic cavity.
• Hemopericardium: Blood in pericardial
sac. When there is increased amount of
blood in pericardial sac, it causes heart
failure and is known as cardiac
temponade (Fig. 5.10).
• Hemoperitonium: Blood in peritoneal
cavity.
• Hemoptysis: Blood in sputum.
• Hematuria: Blood in urine.
• Epistaxis: .Blood from nose.
• Metrorrhagia: Blood from uterus.
• Melena: Bleeding in faeces.
• Hematemesis: Blood in vomitus.
• Blood constituents .are seen outside the blood
vessels.
• Break in blood vessels.
• Presence of red blood cells in tissues outside
the blood vessels (Fig. 5.11).
THROMBOSIS
Formation ofclot ofblood in vascular system in the
wall of blood vessel. It occurs due to endothelial
injury leading to accumulation of thrombocytes,
fibrinogen, erythrocytes and leucocytes (Figs. 5.12
& 5.13).

Disturbances in Circulation
A VI
A..". V2
A
~V3
Fig. 5.1. Diagram showing congestion 1. Normal
blood vessel A-artertal and V-Venous end, 2. Active
congestIOn and 3. Passive congestion
Fig. 5.2. Photograph oftestes showing
congestion
Fig. 5.3. Photomicrograph oflung showing
congestion
51
Fig. 5.4. Photomicrograph of lymph node
showing congestion
Fig. 5.5. Diagram showing haemorrhage
through (A) diapedesis (8) rhexis
A
Fig. 5.6. Diagram showing (A) Petechial (8)
Ecchymotic haemorrhage

Etiology
• Injury in endothelium ofblood vessels.
• Alteration in blood flow.
• Alteration in composition ofblood.
• Blood clot in wall ofblood vessels.
• On removal ofclot, rough surface exposed.
• Clot may be pale, red or laminated.
• Occlusive thrombus totally occlude blood
vessels.
• Mural thrombus is on the wall ofheart.
• Valvular thrombus is on valves ofheart.
• Cardiac thrombus is in heart.
• Saddle thrombus is at the bifurcation of blood
vessel just like saddle on back ofhorse.
• Septic thrombus contains bacteria.
• Blood clot in blood vessel.
• Attached with wall ofblood vessel.
• Alternate, irregular, red and gray areas in
thrombi.
EMBOLISM
Presence of foreign body in circulatory system
which may cause obstruction in blood vessel (Fig.
5.14).
Etiology
• Thrombus, Fibrin.
• Bacteria.
• Neoplasm.
• Clumps ofnormal cells.
• Fat, Gas.
• Parasites.
• Emboli causing obstruction of blood vessels
lead to formation of infarct in the area.
• Organ! tissue becomes pale.
• Parasitic emboli e.g. Dirofilaria immitis
• Presence offoreign material in blood.
52
• Dependent area necrotic due to absence of
blood supply.
ISCHEMIA
Ischemia is deficiency of arterial blood in any part
ofan organ. It is also known as local anemia.
Etiology
• External pressure on artery.
• Narrowing/obliteration oflumen ofartery.
• Thrombi/emboli.
• Necrosis of dependent part.
• Occurrence of infarction.
• Dead tissue replaced by fibrous tissue.
• Lesions of infarction
INFARCTION
Local area of necrosis resulting from ischemia.
Ischemia is the deficiency of blood due to
obstruction in artery (Figs. 5.15 & 5.16).
Etiology
• Thrombi.
• Emboli.
• Poisons like Fusarium toxins.
• Necrosis in triangular area
• Red infarct is observed as red triangle bulky
surface.
• Pale infarct is grey in colour and seen as
triangle depressed surface.
• Necrosis in cone shaped area.
• Obstruction ofblood vessels.
OEDEMA
Accumulation of excessive fluid in intercellular
spaces and / or in body cavity (Figs. 5.17 to 5.20).

Fig. 5.7. Diagram oflinear haemorrhage
Fig. 5.B. Photograph ofLarge intestine showing
linear haemorrhage
Fig. 5.9. Diagram showing hematoma
Fig. 5.10. Diagram showing cardiac temponade
53
FIg. 5.11. Photomicrograph ofkidney showmg
haemorrhage
Fig. 5.12. Diagram ofthrombi formation in
wall ofblood vessel (A) Normal
(B) Thrombifonnation (e) Saddle thrombi

Etiology
• Deficiency ofprotein.
• Passive hyperemia.
• Increased permeability ofcapillaries.
• Obstruction of lyrnphatics.
• Swelling of tissue / organ / body.
• Weight and size of organ increased.
• Colour becomes light.
• Pitting impressions on pressure.
• Ascites is accumulation of fluid in peritoneum.
It is also known as hydroperitonium.
• Hydropericardium is fluid accumulation in
pericardial sa.;.
• Hydrocele is fluid accumulation in tunica
vaginalis ofthe testicles.
• Anasarca is generalized oedema ofbody.
• Hydrocephalus is accumulation of fluid in
brain.
• Hydrothorax is accumulation of fluid in
thoracic cavity.
• Intercellular spaces become enlarged.
• Serum/fluid deposits (pink in colour on H&E
staining) in intercellular spaces.
• Cells separated farther.
SHOCK
Shock is a circulatory disturbance characterized by
reduction in total blood volume, blood flow and by
haemconcentration.
Etiology
• Primary shock
• Occurs immediately after injury.
• Injury / extensive tissue destruction.
• Emotional crisis.
• Surgical manipulation.
• Secondary shock
• Crushing injury involving chest and
abdomen.
• Occurs after several hours of incubation.
54
•
•
•
•
Release of histamine and other substances
by injured tissue.
Extensive haemorrhage.
Bums.
Predisposing factors like cold, exhaustion,
depression.
• Acute general passive hyperemia.
• Dilatation ofcapillaries.
• Cyanosis.
• Numerous petechial haemorrhages.
• Oedema and loose connective tissue.
• Capillaries and small blood vessels are
distended due to accumulation ofblood.
• Number ofengorged blood vessels increased.
• Focal haemorrhage.
• Oedema, cells separated farther due to
accumulation of transudate in intercellular
spaces.
SLUDGED BLOOD
Sludged blood is agglutination of erythrocytes in
the vascular system of an animal.
Etiology
• Fluctuation in blood flow.
• Slow rate ofblood flow.
• Oedema.
• Emboli.
• Infarction.
• Necrosis.
• Clumping of erythrocytes in pulmonary
capillaries.
• Infarction, necrosis.
• Oedema.
• Erythrophagocytosis by reticuloendothelial
cells.

Fig. 5.13. Photomicrograph ofthrombi in
blood vessel oflung
Fig. 5.14. Diagram ofemboli in
blood vessel
FIg. 5.15. Diagram ofinfarction in kidney
Fig. 5.16. Photograph ofspleen showmg
infarctton
55
Fig. 5. 17. Photograph of('n elephant
showing oedema in sic region
Fig. 5.18. Dzagram showing Hydropericardium
Fig. 5. 19. Photograph ofpoultry showing
Hydropericardium
Fig. 520. Photograph ofbullock showing
oedema in mandibular region

MODEL QUESTIONS
1. Accumulation of increased amount ofblood in blood vessels in known as .................. .
2. Presence ofblood in urine, sputum and faeces is known as........., ...... and......, respectively.
3. .. ................haemorrhages in large intestine is example ofrinderpest in animals.
4. .. ................is generalized oedema of body while .................... .is accumulation of fluid
in tunica vaginalis.
5. ..................occurs in poultry due to accumulation of fluid in pericardial sac which is also
known as..............."..
6. Shock is circulatory disturbance characterized by decrease in........... , ......and by ........ .
7. Agglutination of erythrocytes in blood vessels is known as .................., which may act as
............and leads to .................., ........................and ...................... ..
8. Discharge of blood from uterus in known as ..................while the presence of blood in
vomitus is called as ............ ..
Q. 2. Write true orfalse against each statement. Correct thefalse statement.
1. .........Epistaxis is bleeding from mouth.
2. .........Cardiac temponade is failure ofheart due to excessive accumulation ofblood in
pericardial sac.
3. .........In arteries the increased amount ofblood as known passive hyperemia.
4. .........Hydrocephalus is accumulation ofblood in brain.
5. .........Melena is the presence ofblood in faeces.
6. .........Laminated thrombi alternatively have red and grey colour deposits.
7. .........Hematoma is the accumulation ofblood in spherical shaped mass.
8. .........Infarction is local area ofnecrosis as a result ofoedema.
9. .........Sludged blood is agglutination ofRBC after haemorrhage.
10..........Hydrothorax is accumulation of fluid in thoracic cavity.
1. Ischemia
2. Infarction
3. Primary shock
4. Oedema
5. Sludged blood
Q.4. Define the followings.
1. Hemoptysis 6. Acute general active hyperemia
2. Suffusions 7. Acute local passive hyperemia
3. Petechiae 8. Hydrocephalus
4. Hematoma 9. Valvular thrombi
5. Saddle thrombi 10. Hydropericardium
56

Q. 5. Select most appropriate word(s) from thefour options given against each statement.
1. Petechial haemorrhage are of .............. size.
(a) 1 mm (b) 2 mm (c) 5 mm (d) 10 mm
2. Parasitic emboli are formed in dogs due to .......................... ..
(a) Strongylus spp (b) Dirofilaria immitis (c) Coccidia spp. (d)Sarcoptes canis
3. Metrorrhagia is haemorrhage from .............. .
(a) Intestine (b) Stomach (c) Oviduct (d) Uterus
4. Septic thrombus must have......................... in it.
(a) Virus· (b) Parasite (c) Fungi (d) Bacteria
5. Presence offoreign material in blood vessels is known as .............. .
(a) Thrombus (b) Emboli (c) Ischemia (d) Infarction
6. Accumulation offluid in peritoneal cavity is known as..........
(a) Anasarca (b) Hydropericardium (c) Hydrothorax (d) Ascites
7. Shock is circulatory disturbance characterized by .............. .
(a) Reduced blood volume (b) Reduced blood flow (c) Hemoconcentration (d)All ofthe above
8. Active hyperemia is accumulation ofblood in ........ ..
(a) Veins (b) Lymphatics (c) Arteries (d) Intestines
9. Escape ofall blood constituents through intact blood vessel is known as..........
(a) Rhexis (b) Ecchymosis (c) Petechiae (d) Diapedesis
10. Erythrophagocytosis is a feature of ..........
(a) Congestion (b) Oedema (c) Sludged blood (d) Infarction
57

6
DISTURBANCES IN CELL
METABOLISM
• Cloudy Swelling
• Hydropic Degeneration
• Mucinous Degeneration
• Mucoid Degeneration
• Psuedomucin
• Amyloid Infiltration
• Hyaline Degeneration
• Fatty Changes
• Glycogen Infiltration
• Model Questions

Disturbances in Cell Metabolism
CLOUDY SWELLING
Swelling of cells occur with hazy appearance due
to a mild injury. The cells take more water due to
defect in sodium pump leading to swollen
mitochondria which gives granular cytoplasmic
appearance. It is the first reaction of cell to the
mildest injury. Cloudy swelling is a reversible
reaction (Figs. 6.1 & 6. 2).
Etiology
• Can be caused by even mildest injury.
• Any factor causing interference with
metabolism of the cell like bacterial toxins,
fever, diabetes, circulatory disturbances etc.
• Organ becomes enlarged and rounded.
• Weight of organ increases.
• Bulging on cut surfaces.
• Amount of fluid increases in organ.
• Swelling of cells, edges become rounded.
• Increased size ofcells.
• Cytoplasm of the cells becomes hazy/cloudy
due to increased granularity.
• Can be seen in liver, kidney and muscles.
HYDROPIC DEGENERATION
Cells swell due to intake of clear fluid. Such cells
may burst due to increased amount of fluid and
form vesicle. Hydropic degeneration can be seen in
epithelium of skin and for mucous membranes of
body (Figs. 6.3 & 6.4)
Etiology
• Mechanical injury.
• Bums.
• Chemical injury.
• Infections caused by virus like foot and mouth
disease virus, pox virus etc.
• Vesicle formation.
• Accumulation of fluid under superficial layer
ofskin/mucus membrane.
59
• Heals rapidly within 2-4 days.
• No scar formation.
• Pyogenic organisms may convert it into
pustule.
• Cell size increases due to accumulation of
clear fluid in cytoplasm.
• Droplets in cytoplasm as vacuoles.
• Cell bursts and epithelium protrudes leading to
blister.
• Mostly affects prickle cell layer (Stratum
spinosum) of skin.
MUCINOUS DEGENERATION
Excessive accumulation of mucin in degenerating
epithelial cells. Mucin is a glassy, viscid, stringy
and slimy is glycoprotein produced by columnar
epithelial cells on mucus membranes. Such cells
burst to release the mucin in lumen of organ and
are called as goblet cells. When mucin is mixed
with water, it is known as mucus (Figs. 6.5 & 6.6).
Etiology
• Any irritant to mucus membrane like
chemicals and infection.
• Bacteria e.g. E. coli.
• Virus e.g. Rotavirus.
• Parasite e.g. Ascaris.
• Over production of mucus in intestines which
covers intestinaoJ. contents/ stool.
• Over production of mucus in genital tract
during oestrus characterized by mucus
discharge from vulva.
• Nasal discharge during respiratory mucosa
involvement.
• Mucus is mucin mixed with water and slimy
and stringy in nature.
• Increased number ofgoblet cells.
• Goblet cells are elliptical columnar cells
containing mucus.

Fig. 6.1. Diagram showing cloudy swelling in liver
Fig. 6.2. Photomicrograph of liver showing cloudy swelling
-~ ;:...... ~'- ~"--- - "-~~,
Fig. 6.3. Diagram showing hydropic degeneratIOn
and vesicle in skm
Fig. 6.4. Photomicrograph ofhydropic degeneration in skin
60
Fig. 6.5. Photograph ofmtestine showing mucous
degeneration
mucous degeneration
Fig. 6.7. Photomicrograph ofspleen showing
amyloid infiltration
Fig 6.S. Photomicrograph showing hyalme
in muscles

• Mucin in lumen stains basophils through H &
E staining.
• Seen on mucous surfaces only.
MUCOID DEGENERATION
Mucoid degeneration is mucin-like glycoprotein
deposits in connective tissue.
Etiology
• In embryonic tissue e.g. umblical cord.
• In connective tissue tumors e.g. myxosarcoma.
• Myxedema due to thyroid deficiency.
• In cachexia due to starvation, parasitism or
chronic wasting diseases.
• Shrunken tissue giving translucent jelly-like
appearance.
• A watery, slimy and stringy material on cut
surface.
• Mucoid degeneration tissue stains blue
• Nuclei are hyperchromatic.
• Fibrous tissue is pale blue.
• Usually accompanied by fat necrosis.
PSEUDOMUCIN
Pseudomucin is secretion of ovaries and is
observed in cystadenomas. However, it is not a
disturbance of cell metabolism.
Etiology
• Cystadenoma, cystadenocarcinoma
• Paraovarian cysts.
• Transparent, slimy similar to mucin.
• It is not precipitated by acetic acid while
mucin is precipitated.
• Homogenous like plasma, stains pink with
H&E stain.
• Extracellular.
61
AMYLOID INFILTRATION
Deposition of amyloid between capillary
endothelium and adjacent cells. Amyloid is a starch
like substance which stains brownlbluelblack with
iodine and chemically it is protein polysaccharide
(Fig. 6.7).
Etiology
• Not exactly known.
• It is thought to be due to antigen-antibody
reaction/deposition of immune complexes ill
between capillary endothelium and adjacent
cells.
• Organ size increases with rounded edges, pits
on pressure, cyanotic/yellow in colour and
fragile.
• Sago spleen due to deposition of grey, waxy
sago-like material.
• Amyloid stains pink on H& E stain.
• It is a permanent effect in body and remains
the whole life without causing much adverse
effects.
HYALINE DEGENERATION
Glossy substance (glass-like) solid, dense,
smoothly homogenous deposits in tissues. Tissue
becomes inelastic. It is a permanent change.
Hyaline is very difficult to distinguish
macroscopically (Fig. 6.8).
Etiology
• Disturbance in protein metabolism.
• No specific cause.
Macroscopic and Microscopic features
Connective Tissue hyaline
• In old scars, due to lack of nutrients;
homogenous, strong acidophilic and pink in
colour. There are no nuclei and no fibrils.
Epithelial Hyaline
• Starch-like bodies in prostate, lungs, kidneys.

Fig 6 9 Photomicrograph ofkidney showing hyaline
Fig 6 10 PhotOlnlcrograph ofskin showing hyaline
(epithelial pearf)
• Microscopically characterized by round,
homogeneous, pink, within an alveolus of
lung.
• Homogenous, pink in kidney tubules/
glomeruli (Fig. 6.9).
Keratohyaline
• Occurs due to slow death of stratified
squamous epithelial cells because of lack of
nutrients. Keratinized epithelium is firm, hard
and colourless. Microscopically, it is seen in
epithelial pearls e.g. horn cancer, warts (Fig.
6.10).
FATTY CHANGES
Intracellular accumulation of fat in liver, kidneys
and heart. It is a reversible change.
62
Fig 6 11 Photomicrograph ofliver showingfatly changes
Fig 6 12 Photomicrograph ofliver showing glycogen
infiltratIOn
EtioIogy
• Increased release of fatty acids.
• Decreased oxidation of fatty acids.
• Lipotrope deficiency.
• In ketosis, diabetes, pregnancy toxaemia.
• Enlargement of organ.
• Cut surfaces are bulging and greasy.
• Organ colour becomes light.
• Intracellular deposition of fat droplets. (Fig.
6.11)
• In cytoplasm clear round/oval spaces with
eccentrically placed nucleus.
• Stains yellow orange with sudan Ill.

GLYCOGEN INFILTRATION Macroscopic features
(GLYCOGEN STORAGE DISEASE)
Glycogen accumulates when increased amount of
glycogen enters in the cells of kidneys, muscles and
liver (Fig. 6.12).
• Affected organ becomes enlarged.
• Intracellular deposits of glycogen in cells of
kidneys, liver and muscles.
Etiology
• Diabetes mellitus.
• Small clear vacuoles seen in distal portion of
proximal convoluted tubules, hepatocytes etc.
• Impaired carbohydrate metabolism due to
drugs e.g. corticosteroid therapy.
• It can be stained as bright red by Best's.
Carmine and PAS and reddish brown by
iodine.
MODEL QUESTIONS
1. Cells swell due to accumulation of clear fluid in ...............which occurs in ................
layers of epithelial cells or mucous membrane in case of .................. disease.
2. Pyogenic bacteria invades the vesicle and may convert it into .................
3. Cloudy swelling is a ........................ reaction against .................... injury/ irritant and it
is the ..................reaction ofbody.
4. Mucoid degeneration occurs due to ............. deficiency and in ................... due to
............. , ............ and ................. .
5. Pseudomucin appears in ............... and .............. and is characterized by appearance of
........... and ............material like mucin.
6. Amyloid is ................like substance which stains ...........with iodine and chemically it is
7. Connective tissue hyaline is seen in .............. due to lack of ...........and is characterized
by..................., ......................... and pink in colour.
8. Keratohyaline is ................. due to lack of nutrients and occurs in .............cancer.
Q. 2. Write True or False against each statement. Correct thefalse statements.
1. .........Vesicle formation occurs as a result ofbreaking ofcells due to cloudy swelling.
2. .........Amyloid is caused by antigen-antibody complexes.
3. .........Mucinous degeneration occurs in connective tissues with accumulation ofslimy and
stringy material.
4. .........Epithelial hyaline is characterized by the presence of epithelial pearls.
5. .........Diabetes mellitus may lead to glycogen storage disease.
6. .........Hydropic degeneration mostly occurs in prickle cell layer of skin or mucous membrane.
7. .........Cachexia due to starvation my lead to mucoid degeneration.
8. .........Cloudy swelling is characterized by hazy and cloudy cells due to swelling of
mitochondria.
9. .........Mucin is mucus mixed with water and stringy in nature.
10..........Glycogen is stained as redish brown by PAS.
63

1. Fatty changes
2. Keratohyaline
3. Glyocogen storage disease
4. Mucus
5. Cloudy swelling
Q. 4. Define thefollowing
1. Pseudomucin
2. Mucin
3. Hyaline
4, Amyloid
5. Vesicle
Q. 5. Differentiate the followings
1. Mucinous and mucoid degeneration.
2. V~sicle and Pustules.
3. Cloudy swelling and hydropic degeneration.
4. Hyaline and amyloid infiltration.
5. Fatty changes and glycogen infiltration.
6. Pustule
7. Goblet cells
8. Sago spleen
9. Epithelial pearl
10 Sodium pump
Q. 6. Select suitable word(s) from thefour options to correct thefollowing statements.
1. Hydropic degeneration leads to .............. formation in skin.
(a) Vesicle (b) Pustule (c) Scab (d) Papule
2. Cloudy swelling is characterized by hazy cytoplasm due to swollen ........ .
(a) Endoplasmic reticulum (b) Golgi bodies (c) Mitochondria (d) Nucleus
3. The mucous containing cells in mucous membranes are known as .......
(a) Epithelial cells (b) Pearl cells (c) Columnar cells (d) Goblet cells
4. Mucin stains ............ by H&E stain.
(a) Blue (b) Pink (c) Yellow (d) Black
5. Sago spleen is observed in .........
(a) Amyloid (b) Mucin (c) Hyaline (d) Pseudomucin
6. Epithelial pearl is an example of ..........
(a) Amyloid (b) Mucin (c) Hyaline (d) Cell Swelling
7. Ketosis in cow may cause.............. .
(a) Hyaline degeneration (b) Fatty change (c) Amyloid (d) Cell swelling
8. Mucous degeneration in intestine is caused by ..................
(a) Rotavirus (b) E. Coli (c) Ascaris (d)All ofthe above
9. Corticosteroid therapy may lead to ...............
(a) Fatty changes (b) Hyaline (c) Glycogen (d) Cell swelling
10. Amyloid occurs in body as a result of ..............
(a) Immune complexes (b) Antigen (c) Antibody (d) Starch
64

7
NECROSIS, GANGRENE AND
POST-MORTEM CHANGES
• Necrosis
• Coagulative Necrosis
• Caseative Necrosis
• Liquifactive Necrosis
• Fat Necrosis
• Apoptosis
• Gangrene
• Post-mortem Changes
• Autolysis
• Putrefaction
• Pseudomelanosis
• Rigor Mortis
• Algor Mortis
• Livor Mortis
• Hypostatic Congestion
• Post-mortem Emphysema
• Post-mortem Clot
• Displacement of Organs
• Imbibition of Bile
• Model Questions

NECROSIS
Local death of tissue /cells in living body is known
as necrosis, It is characterized by the followings.
• Pyknosis is condensation of chromatin
material, nuclei becomes dark, reduced in size
and deeply stained.
• Karyorrhexis is fragmentation ofnucleus.
• Karyolysis is dissolution of nucleus into small
fragments, basophilic granules/fragments.
• Chromatolysis is lysis ofchromatin material.
• Necrobiosis is physiological cell death after
completion of its function e.g. RBC after 140
days.
Necrosis is further classified into coagulative,
caseative, liquifactive and fat necrosis which are
different from apoptosis (Figs. 7.1 to 7.3).
COAGULATIVE NECROSIS
Local death of cells/tissue in living body
characterized by loss of cellular details, while
tissue architecture remains intact (Fig. 7.4).
Etiology
• Infections.
• Ischemia.
• Mild irritant e.g. toxins/chemical poisons.
• Heat, trauma.
• Organ becomes grey/white in colour, firm,
dense, depressed with surrounding tissue.
• Cellular outline present, which maintains the
architecture oftissue/ organ.
• Nucleus absent or pyknotic.
• Cytoplasm becomes acidophilic.
CASEATIVE NECROSIS
Local death of cells/tissue in living body; the dead
cells/tissues are characterized by presence of firm,
dry and cheesy consistency. It occurs due to
coagulation ofproteins and lipids (Fig. 7.5).
66
Etiology
• Chronic infections e.g. Mycobacterium
tuberculosis.
• Systemic fungal infections.
• Dead tissue looks like milk curd or cottage
cheese.
• Tissue dry, firm, agranular, white/grey/
yellowish in colour
• Disappearance of cells; no cell details/
architecture.
• Purplish granules on H&E staining, blue
granules from nucleus fragments, red granules
from cytoplasm fragments.
LIQUIFACTIVE NECROSIS
Local death of cells/tissues in living body
characterized by rapid enzyrnatic dissolution of
cells. The intracellular hydrolases and proteolytic
enzymes of leucocytes play role in dissolution of
cells (Fig. 7.6).
Etiology
• Pyogenic organisms.
• Liquifactive necrosed tissue present in a cavity
"Abscess".
• It contains small/large amount ofcloudy fluid,
which is creamy yellow (Pus).
• Areas ofliquifactive necrosis stains pink.
• Infiltration ofneutrophils.
• Sometimes empty spaces but infiltration of
neutrophils at periphery.
FAT NECROSIS
Local death ofadipose cells in living body.
Etiology
• Trauma.

Necrosis, Gangrene and Post-mortem Changes
B
c
E
Fig. 7.1. Diagram showing pathogenesis ofnecrosis
(A) Normal (B) Pyknosis (C) KaryorrhexIs
(D)Karyolysis (E) Chromatolysis,
(F) Apoptosis (G) Blebs and (H) Phagocytosis
..-~ ...... .::" ,,~~ F';
''': ~-~ ~"'·~'f: i;-".
Fig. 7.2. Diagram showing necrosIs (A) Normal
(B) Coagulative (C) Caseaative and (D)Liquifactive
67
B
Fig. 7.3. Photograph of(A) liver and (B) heart
showing necrosis
Fig. 7 4. PhotomIcrograph of(A) hver and
(B) Kidney showing coagulatIve necrosis

• Increased action of enzymes due to leakage of
pancreatic juice.
• Starvation
• Chalky whi.te mass deposits in organ.
• White opaque firm mass.
• Adipose cell without nucleus (Fig. 7.7).
• Macrophage giant cells contain fat droplets.
important role in the development and maintenance
of homeostasis and in the maturation of nervous
and immune systems. It is also a major defense
mechanism of the body, removing unwanted and
potentially dangerous cells such as self-reactive
lymphocytes, virus infected cells and tumor cells.
Most cells in animal have the ability of self-
destruction by activation of an intrinsic cellular
suicidal programme when they are no longer
needed or are seriously damaged. The dying cell
exhibits morphological alterations including
Table 7.1 Differential features of various types of Necrosis
Coagulative Liquifactive Caseative Fat
Macroscopic 1. Organ becomes 1. Llquifactive 1. Dead tissue 1. Chalky white
features gray/white in necrosed tissue looks like milk mass deposits in
colour, firm, dense, present in a cavity curd or cottage organ
depressed with "Abscess" cheese
2. White opaque
surrounding tissue
2. It contains small/ 2. Tissue dry, firm, firm mass
large amount of agranular,
cloudy fluid, which whlte/gray/
is creamy yellow yellowish in colour
(Pus)
Microscopic 1. Cellular out line 1. Areas of 1. Disappearance of 1. Adipose cell
features present, which liquifactive cells; no cell without nucleus
maintains the necrosis stains details/ architecture
2. Macrophages
architecture of pink.
tissue/ organ
2. Purplish granules giant cells contain
2. Infiltration of on H&E staining, fat droplets.
2. Nucleus absent neutrophils blue granules from
3. Presence of lime
or pyknotic
3. Sometimes
nucleus fragments,
salts in tissues.
3. Cytoplasm empty spaces but
red granules from
becomes infiltration of
cytoplasm
acidophilic neutrophils at
fragments.
• Presence of lime salts in tissues.
APOPTOSIS
Apoptosis is a finely tuned mechanism for the
control of cell number in animals; the process is
operative during foetal life, tumor regression and in
the control of immune response. Apoptosis plays an
shrinkage of cell, membrane blebbing, chromatin
condensation and fragmentation of nucleic acid.
Cells undergoing apoptosis often fragment into
membrane bound apoptotic bodies that are readily
phagocytosed by macrophages or neighbouring
cells without generating an inflammatory response.
68

These changes distinguish apoptosis from cell
death by necrosis. Necrosis refers to the
morphology most often seen when cells die from
severe and sudden injury such as ischemia,
sustained hyperthermia or physical and chemical
trauma. In necrosis, there are early changes in
mitochondrial shape and function; cell losses its
ability to regulate osmotic pressure, swells and
ruptures. The contents of the cell are spilled into
surrounding tissue, resulting in generation of a
local inflammatory response.
Necrosis is the consequence of a passive and
degenerative process while the apoptosis is a
consequence ofan active process.
Execution of apoptosis requires the coordinated
action of aspartate specific cysteine proteases
(caspases) which are responsible for cleavage of
key enzymes and structural proteins resulting in
death of cell. Apoptosis is triggered by a variety of
signals which activate the endogenous
endonucleases to initiate the process of
fragmentation of nuclear DNA into
oligonucleosomal size fragments. Initially, the
DNA fragments are large (50-300 Kb) but are later
digested to oligonucleosomal size (multimers of
180-200 bp). The formation of this distinct DNA
ladder is considered to be a biochemical hallmark
ofapoptosis.
There is rounding of nucleus with pyknosis and
rhexis, chromatin coalesces to form a crescent
along the nuclear membrane. Cell fragments to
form blebs, which may have one or more
organelles. Such changes occur in apoptotic cells
within 20 min duration.
Apoptosis is generally synonymously used with
"programmed cell death" but it differs from
programmed cell death as apoptosis cannot be
prevented by cycloheximide or actinomycin D,
rather these chemicals accelerate the process of
apoptosis while programmed cell death is
prevented by these chemicals.
69
GANGRENE
Necrosis of tissue is followed by invasion of
saprophytes. Gangrene is mainly divided into three
types: Dry, moist and gas gangrene.
DRY GANGRENE
Dry gangrene occurs at extremities like tail, tip of
ears, tip of scrotum, hoof etc. due to necrosis and
invasion of saprophytes. The evaporation of
moisture takes place resulting into dry lesions.
Etiology
• Mycotoxins from fungus Fusarium equiseti
found on paddy straw in low lying areas with
moisture (Degnala disease).
• Dry, fragmented crusts like lesions on tail,
scrotum, ear (Figs. 7.8 & 7.9).
• Hoof becomes detached due to necrosis and
gangrene, sloughing, exposing the red raw
surface (Figs. 7.10 & 7.11).
• Blackening ofthe affected area.
• Necrosis and invasion ofsaprophytes in skin of
tail, ear or scrotum.
MOIST GANGRENE
Moist gangrene mostly occurs in internal organs of
body like lungs, intestine, stomach etc. It occurs
due to necrosis and invasion of saprophytes leading
to dissolution ofthe tissues (Figs 7.12 & 7.13).
Etiology
• Drenching of milk, medicines etc. e.g.
Aspiration pneumonia! Drenching pneumonia.
• VolvoluslIntussusception or torsion in
intestine.
• Greenish or bluish discolouration of the
affected organ.
• Dissolution of affected part into fragments
• Presence of foreign material like milk, fibre,
oil, etc.

Fig. 75. Photomicrograph showing (([seatlve
necrOSIS
Fig. 7.6. Photomicrograph 5howll!g hqlllfactlCl'e
necrOSI
Fig 7.7. Photomicrograph o{fat shO'lIlg necrosIs
Fig. 7.S. Photograph ofbuffalo bull showing
dry gangrene in scrotum
70
Fig. 710 Photograph of huffala cah'es 5howl1lg
sloughing ofhoo/.I due to Degnala dllease
Fig. 711. Photograph o{huffalo caifsholl'l/lg
s!oughl1lR ofhoofs due ta Degnllla dl.lea le
Fig. 7.12. Diagram showmg mOist gangrene
1I1 mtestine

Fig. 7.13 Photograph showing mOist gangrene In
poultry
Fig 7. 14 Photograph showing gas
gangrene In heifer
Fig. 7./5 PhotOlmcrograph shol1'1Ilg
myositis/gas gangrene
71
• Necrosis and invasion of saprophytes
• Presence of foreign material like milk, fibres,
oil etc.
GAS GANGRENE
Gas gangrene occurs in muscles particularly of
thigh muscles of hind legs in heifers in case of
black leg (Black Quarter; B.Q.) (Figs. 7.14 &
7.15).
Etiology
• Clostridium chauvei
• Gram positive, rod, anaerobe.
• Produces toxins under anaefCIbic conditions
which cause disease.
• Stress, trauma, transportation predisposes
animals.
• Oedema of Muscles In affected part
particularly thigh region.
• Blackening of muscles due to production of
H2S by bacteria and its chemical reaction with
iron of free hemoglobin producing iron
sulphide.
• Presence of gas in the area giving crepitating
sound on palpation.
• Necrosis of muscles
• Presence of Gram positive rod shaped
Clostridia
• Dissolution of muscle fibers due to
saprophytes/ toxins ofthe organism.

Table 7.2 Differential features of various types of Gangrene
Dry Moist Gas
Macroscopic 1. Dry, fragmented crusts 1. Greenish or bluish 1. Oedema ofMuscles in
features like lesions on tail, discoloration ofthe affected part particularly
scrotum, ear affected organ. thigh region.
2. Hoofbecomes detached 2. Dissolution ofaffected 2. Blackening ofmuscles
due to necrosis and part into fragments due to production ofH2S
gangrene, sloughing,
3. Presence offoreign
by bacteria and its
exposing the red raw chemical reaction with iron
surface.
material like milk, fiber,
offree hemoglobin
oil, etc.
producing iron sulphide.
3. Blackening of the
affected area. 3. Presence ofgas in the
area giving crepitating
sound on palpation
Microscopic 1. Necrosis and invasion of 1. Necrosis and invasion of 1. Necrosis ofmuscles
features saprophytes in skin of tail, saproph)1eS
2. Presence ofGram
ear or scrotum
2. Presence offoreign positive rod shaped
material like milk, fibers, Clostridia
oil, etc.
POST-MORTEM CHANGES
Alterations in cells/tissues occur after death of
animal. The degree of such alterations and their
speed depends upon the environmental
temperature, size of animal, species of animal,
external insulation and nutritional state of the
animal. The postmortem changes occur rapidly in
high environmental temperature, large, and
fur/wool-bearing and fatty animals.
Autolysis
Autolysis is the digestion of tissue by its own
enzymes and is characterized by uniform
destruction of cells without any inflammatory
reaction. After death, a state of hypoxia occurs
leading to decreased ATP. The cell organe1les
degenerate and the membrane of lysosomes
dissolve releasing the lysosomal enzymes in the
cell responsible for digestion of cells/tissues. These
72
3. Dissolution of muscle
fibers due to saprophytes/
toxins ofthe organism
enzymes cause disintegration of cell components
into small granules in the cell. Microscopically,
autolysis is characterized by uniform dead cells
without any circulatory changes and inflammatory
reaction.
Putrefaction
Putrefaction is decomposition of tissue after death
by saprophytes leading to production of foul odour.
After autolysis the saprophytes invade from
external environment into the body, multiply and
eventually digest the tissues with their enzymes.
The tissue becomes fragile and produces foul
odour.
Pseudomelanosis
Pseudomelanosis is greenish or bluish
discolouration of tissues/organs after death.
Saprophytes causing putrefaction also produce
hydrogen sulfide which chemically reacts with iron

portion of hemoglobin to produce iron sulfide. Iron
sulfide is a black pigment and produces green, grey
or black shades on combination with other tissue
pigments.
Rigor mortis
Rigor mortis is the contraction and shortening of
muscles after death of animal leading to stiffening
and immobilization of body. It occurs 2-4 hours
after death and remains till putrefaction sets in.
Rigor mortis begins in cardiac muscles tirst and
then in skeletal muscles of head and neck with a
progression towards extremities. It is enhanced by
high temperature and increased metabolic activity
before death; while it is delayed by starvation, cold
and cachexia. Rigor appears quickly in case animal
has died due to strychnine poisoning as a result of
depletion of energy source ATP. Muscle fibres
shorten due to contraction and remain in
contraction in the absence of oxygen, ATP and
creatine phosphate. Rigor mortis remains till 20-30
hours of death, the duration depends on autolysis
and putrefaction. It disappears in same order as it
appeared from head, neck to extremities. It can be
used to detemrine the length of time after the death
ofanimal.
Algor mortis
Algor mortis is cooling of body. As after death
there is no circulation of blood, which maintains
the body temperature, body becomes cool.
However, it takes 2-4 hours, depending on the
species, environmental temperature and type of
animal.
Livor mortis
Livor mortis is the staining of tissues with
hemoglobin after death of animals. It gives pinkish
discolouration to the tissues.
73
Hypostatic congestion
Due to gravitational force, the blood is accumulated
in dependent ventral parts of body. It is helpful in
establishing of the state of the body at the time of
death.
Post-mortem emphysema
It occurs due to decomposition by gas producing
organisms including saprophytes. The gas is mainly
accumulated in gastrointestinal tract causing
rupture ofthe organ.
Post-mortem clot
It is clotting of blood after death of animal mainly
due to excessive release of thrombokinase from
dying leucocytes and endothelial cells. It is smooth
in consistency having glistening surface that is red
or yellow in colour. Post-mortem clot is uniform in
structure and it does not attach to the wall of blood
vessel as thrombus does. In anthrax, post-mortem
clot does not appear. Post-mortem clot is of two
types: Red or current jelly clot forms when the
components of blood are evenly .distributed
throughout the clot. It occurs due to rapid clotting
of blood. The yellow or chicken fat clot occurs
when the components of blood are not distributed
evenly. The dorsal position is red and upper
position in yellow due to WBC fibrin and serum. It
occurs due to prolonged coagulation time of blood
leading to sedimentation ofred blood cells.
Displacement of organs
Displacement of internal organs due to rolling of
dead animal. Mainly intestine/stomach and uterus
are affected with displacement which can be
differentiated from ante-mortem displacement by
absence ofpassive hyperemia.
Imbibition of bile
Cholebilirubin present in the gall bladder diffuses
to the surrounding tissues/organs and stains them
with yellow/ greenish pigmentation.

MODEL QUESTIONS
Q. 1. Fill in the blanks with suitable word(s) to answer the following.
1. ....... ... .... necrosis is caused by Mycobacterium tuberculosis and is characterized by
.............. material formed due to coagulation of .............. and ..............
2. Chromatolysis is the lysis of .............. material.
3. Necrosis is defined as death of cells/ tissue in ..... body and is characterized by ......, ....., and
4. Abscess is an example of.. ............ necrosis caused by .............. organisms.
5. Fat necrosis occurs by the action of enzymes of ........ and is characterized by ........ deposits
on organs.
6. Aspiration pneumonia in calves is an example of .............. gangrene.
7. Degnala disease is caused by ......... toxins found on paddy straw and is characterized by
........... gangrene.
8. Gas gangrene is caused by .............. in muscles of heifers and is characterized by
.............................. and .............. sound on palpation.
9. Autolysis is .............. oftissues by .............. enzymes.
10. Greenish discolouration of tissues after death is known as .............. as a result of ..............
action and production of .............. which combines with .............. ofhemoglobin.
Q. 2. Write true orfalse against each statement and correct the false statement.
1. ...........Autolysis is the local death of tissue in living body.
2. ...........Algor mortis is cooling ofbody after death.
3. ...........necrosis invaded by saprophytes leads to putrefaction.
4. ...........Hypostatic congestion may reveal the time of death of the animal.
5. ...........Diffusion of cholebilirubin present in gall bladder to surrounding tissues is known as
imbibition ofbile.
6. ...........Apoptosis is programmed cell death.
7. ...........Karyorrhexis is rounding of cells, which takes a deep stain.
8. ...........In coagulative necrosis, cellular details are maintained.
9. ...........Ischernia may lead to necrosis.
10. .........Fat necrosis is characterized by the presence of creamy yellow liquefied material.
1. Caseative Necrosis 4. Post-mortem changes
2. Abscess 5. Lysosomal enzymes
3. Gas gangrene
Q.4. Define thefollowing.
1. Pyknosis 6. Apoptosis
2. Karyolysis 7. Necrobiosis
3. Karyorrhexis 8. Necrosis
4. Chromatolysis 9. Autolysis
5. Gangrene 10. Livor mortis
74

Q. 5. Select appropriate word(s) from four options given against each statement.
1. In liquifactive necrosis.............. cells are present.
(a) Monocytes (b) Lymphocytes (c) Eosinophils (d) Neutrophils
2. Programmed cell death is known as .............. in living body.
(a) Apoptosis (b) Necrosis (c) Autolysis (d) None ofthe above
3. Chalky white deposits are observed in .............. necrosis.
(a) Coagulative (b) Liquifactive (c) Fat (d) Caseative
4. Gangrene in lungs is an example of .............. grangrene.
(a) Dry (b) Moist (c) Gas (d)All ofthe above
5. Degnala disease is an example of .............. gangrene.
(a) Dry (b) Moist (c) Gas (d) None ofthe above
6. Digestion ofcells/tissues by their own enzymes is known as ..............
(a) Necrosis (b) Autolysis (c) Gangrene (d) Putrefaction
7. Greenish discolouration oftissues after death is also known as ..............
(a) Pseudomelanosis (b) Melanosis (c) Necrosis (d) Imbibition ofbile
8. Algor mortis is the .............. ofbody.
(a) Staining with hemoglobin (b) Cooling (c) Hardening (d) Softening
9. Rigor mortis remains in body .............. hrs
(a) 12-15 hrs (b) 20-30 hrs (c) 35-48 hrs (d) 5-10 hrs
10. Lysis ofchromatin material is known as ..............
(a) Karyolysis (b) Karyorrhexis (c) Chromatolysis (d) Caseation
75

8
DISTURBANCES IN
CALCIFICATION AND
PIGMENT METABOLISM
• Calcification
• Dystrophic
• Metastatic
• Pigmentation
• Endogenous pigments
• Exogenous pigments
• Crystals
• Gout (Urates and uric acids)
• Model Questions

Disturbances in Calcification and Pigment Metabolism
CALCIFICATION
Calcification is the deposition of calcium
phosphates and calcium carbonates in soft tissues
other than bones and teeth. It may be classified as
dystrophic and metastatic calcification.
DYSTROPHIC CALCIFICATION
Dystrophic calcification is characterized by the
deposits of calcium salts in necrosed tissue of any
organ (Fig 8.1).
Etiology /Occurrence
• Necrosis.
• Parasitic infections.
• Tuberculous lesions.
• Organ becomes hard, nodular.
• Grey/white deposits in necrosed tissue looking
like honey comb.
• Gritty sound on cutting.
• Irregular deposits of calcium salts in necrosed
tissue.
• Calcium takes black/purplish colour on H & E
staining.
METASTATIC CALCIFICATION
Metastatic calcification is characterized by
deposition of calcium salts in soft tissue as a result
ofhypercalcemia (Fig. 8.2).
Etiology/ Occurrence
• Hyperparathyroidism.
• Renal failure.
• Excess of vitamin-D.
• Increased calcium intake.
• Organ becomes hard.
• Wall of arteries becomes hard due to calcium
deposits.
77
• Deposition of calcium in soft organs like
myocardium, arteries, muscles, etc.
• Purplishlblack colour calcium surrounded by
comparatively normal tissue.
MELANOSIS
Melanosis is the deposition of melanin, a brown!
black pigments in various tissues/ organs specially
in lung, blood vessels and brain (Figs. 8.3 to 8.5).
Etiology/Occurrence
• Hyperadrenalism.
• Melanosarcoma.
• Melanoma.
• Organ/tissue involved becomes black in
colour.
• Discolouration may be focal or diffused.
• Brownlblack colour pigment is seen in cells.
• The size, shape and amount ofpigment vary.
HEMOSIDEROSIS
Hemosiderosis is characterized by deposition of
hemosiderin pigment in spleen and other organs.
Hemosiderin is a blood pigment with a shiny
golden yellow colour and is usually found within
the macrophages (Fig. 8.6).
• Extensive lysis oferythrocytes.
• Haemorrhage.
• Hemolytic anemia.
• Colour oforgan becomes brownish.
• Brown induration oflungs.
• Presence of golden yellow/golden brown
pigment in red pulp of spleen, lungs, liver and
kidneys.

-
~,j,
Fig. 8 1 Photomicrograph oflung showmg dystrophIc
calcification In tuberculous granuloma
<~;'..... ,
Fig 8.2 Phou;mll rograph ofartene, ,howll1g metastatIc
calClficatlO1I
FIg 8.3. Photograph ,/wwlIIg melallo.II.1
Fig 8.';' Phofol1lu rngraph a/lA.Ul ')Iwl-J.,'mg 1ne/wlO<;l,
78
Fig. 8.5. P/lOtomlcrograph ofskin showing melanosis.
FIX. 8.6 Photonllcrograph ofspleen showmg
hemoslderosls
FIg 87 Photmnllrograph oflung ,howlIlg P"etln/OCOnlGSIS
FIg /i /i Photograph o/foot pad of" h,rd showing gout

•
FIg. 8.9. Photomicrograph o/kidney showmg
urates (gout)
Fig. 8.10. Photograph ofa bird showmg deposition
ofurates and uric acid in ureter (gout)
In most of the cases, the pigment is found
intracellularly in macrophages.
BILE PIGMENTS
Bile pigments are derived from the breakdown of
erythrocytes such as bilirubin and biliverdin. The
icterus is hyperbiIirubinemia as a result of either
excessive lysis of erythrocytes or due to damage in
liver or obstruction in the bile duct. The hemolysis
results in iron, globin and porphyin; the latter being
converted into biliverdin. Biliverdin is reduced to
produce bilirubin, an orange-yellow pigment bound
to albumin and transported by RE cells to liver. In
hepatic cells, it is separated from albumin and
conjugated with glucuronic acid and excreted in
bile as bilirubin diglucuronide. In intestine, it is
further reduced by bacteria to urobilinogen, which
is reabsorbed into circulation and carried to liver
for re-excretion in bile while a small amount enters
79
in circulation and is excreted through urine. The
unabsorbed urobilinogen is oxidized in lower
intestine to form urobilin and stercobilin, which
give normal pigment to faeces.
Hemolysis
/~~
Heme + Porphyrin + Globin
t
Kidney
tExcreted
in
urine
~
Biliverdin
1Bilirubin
Reduced by
Biliverdin reductase
1Albumin
Bilirubin + albumin
1RE cells
Liver
1
Conjugated with the
help of uridine
diphosphoglucose
glucuronyl transferase
Bilirubin diglucuronide
1Reduced by
Bacteria
Urobilinogen
It
Intestine
~
Urobilin and
stercobilin
(faeces)

ICTERUS
Icterus is increased amount of bile pigments in
blood and is often called as hyper- bilirubinemia or
jaundice. It is of three types hemolytic, toxic and
obstructive jaundice.
HEMOLYTIC JAUNDICE
Hemolytic jaundice occurs as a result of excessive
hemolysis in circulating blood. It is also known as
pre-hepatic jaundice.
Etiology/ Oc£urrence
• Piroplasmosis (Babesia bigemina).
• Anaplasmosis (Anaplasma marginale).
• Leptospirosis(Leptospira ictehaemmorrhagae).
• Equine infectious anemia virus.
• Anthrax (Bacillus anthracis).
• Clostriduum hemolyticum.
• ~- haemolytic streptococci.
TOXIC JAUNDICE
Toxic jaundice occurs as a result ofdamage in liver
leading to increased amount of unconjugated and
conjugated bilirubin in blood. It is also known as
hepaticjaundice.
Etiology
• ToxinIPoisons.
• Copper poisoning.
• Leptospirosis.
OBSTRUCTIVE JAUNDICE
Obstructive jaundice occurs as a result of
obstruction in bile duct causing hindrance in
normal flow of bile. It is also known as post-
hepaticjundice.
Etiology
• Blocking of bile canaliculi by swollen
hepatocytes.
Table 8.1 Differential features of varIOus types of Jaundice
Hemolytic (Prehepatic) Toxic (Hepatic) Obstructive (Post hepatic)
Etiology 1. Piroplasmosis 1. ToxinlPoisons 1. Blocking ofbile canaliculi by
(Babesia bigemina) 2. Copper swollen hepatocytes
2. Anaplasmosis poisoning 2. Obstruction in bile duct (Liver
(Anaplasma 3. Leptospirosis flukes, tapeworms and ascaris)
marginale) 3. Biliary cirrhosis, Cholangitis and
3. Leptospirosis Cholelithiasis
(Leptospira 4. Pressure on bile duct due to
ictehaemmorrhagae) abscess, neoplasm.
4. Equine infectious 5. Inflammation and swelling at duct
anemia virus opening in duodenum.
5. Anthrax (Bacillus
anthracis)
6. Clostriduum
hemolyticum
7. ~- haemolytic
streptococci
Vanden Berg's
reaction
Direct Negative Positive Positive
Indirect Positive Positive Negative
80

• Obstruction in bile duct (Liver flukes,
tapeworms and ascaris).
• Biliary cirrhosis, Cholangitis and
Cholelithiasis.
• Pressure on bile duct due to abscess, neoplasm
• Inflammation and swelling at duct opening in
duodenum.
• Mucous membrane yellow in colour.
• Omentum, mesentry, fat become yellow.
• Increased yellow colour in urine.
• Conjunctiva becomes yellow.
• Brownish pigment in tubules ofkidney.
• Bile pigments in spleen.
• Hemolysis, erythrophagocytosis.
• Hepatitis.
Diagnosis
• Van-den-Bergh reaction.
• Direct reaction detects bilirubin diglucuronide
(Obstructive jaundice).
• Indirect reaction detects hemobilirubin
(Hemolytic jaundice).
• Both reaction (Toxic jaundice).
T bI 82 V d Ba e . an en err s reaction
Type of Type of Type of
reaction jaundice pigment
l. Direct Obstmctive Cholibilimbin
reaction (+)
2. Indirect Hemolytic Hemobilirubin
reaction (+)
3. Biphasic Toxic/ Both present
reaction (+) Hepato-
cellular
PNEUMOCONIASIS
Pneumoconiasis is the deposition of dust/carbon
particles in lungs through air inhalation. It is also
81
known as anthracosis (carbon), silicosis (silica) or
asbestoses (asbestos) (Fig 8.7).
• Dusty air containing carbon/silicalasbestous
• Near factory/coal mines.
• Hard nodules in lungs.
• Nodules my have black !brown /grey colour
• Nodules may produce cracking sounds on cut.
• Presence of carbon/other exogenous pigment
in intercellular spaces or in cytoplasm of
alveolar cells and macrophages.
• Formation of granuloma around the foreign
particles including the infiltration of
macrophages, lymphocytes, giant cells and
fibrous tissue proliferation.
CRYSTALS
Deposition of different kinds of crystals in tissues
like uric acid, sulphonamides and oxalates etc. The
uric acid and urates when deposited in tissues are
known as gout.
GOUT (URATES & URIC ACIDS)
Gout is a disease condition in which urates and uric
acid are deposited in tissues and is characterized by
intense pain and acute inflammation (Figs. 8.8 to
8.10).
Etiology/Occurrence
• Common in poultry due to deficiency of
uricase enzyme.
• Deficiency ofvitamin A.
• Absence or inadequate amount ofuricase.
• White chalky mass ofurates and uric acid.
• Deposition of urates/uric acid on pericardium,
kidneys etc.
• Dialation of ureter due to excessive
accumulation of urates.

Microscopic features • Crystals are surrounded by inflammatory cells
including macrophages, giant cells and
lymphocytes.
• Presence of sharp crystals in tissue.
MODEL QUESTIONS
Q. 1. Fill in the blanks with suitable word(s}.
1. Metastatic calcification is characterized by deposition of calcium in soft tissues as a result of
............... which is caused by ............., ................, ................ and........ .. ......
2. Hemosiderosis is the deposition of pigment in spleen which is seen as ........... ,....... colour
and usually found in the ...................
3. Melanin is a ..........colour pigment usually gives colour to ............., ..........and .............
4. Bilirubin is a................... pigment and occurs in body due to ............, .............. and
..................., which is characterized by ................... colour of .................. ..
5. In liver bilirubin is conjugated with............ to give rise to............. which is excreted in bile
and reduced in intestine to.......... while unabsorbed portion is converted into............
and........... .
Q. 2. Write true orfalse against each statement and correct thefalse statements.
1. ......Bilirubin is produced as a result ofreduction ofbiliverdin.
2. ......Hyperadrenalism may lead to melanosis.
3. .. ....Stercobilin gives colour to urine
4. ......Hemolytic anernia may give rise to hemosiderosis.
5. .. ....The swollen hepatocytes may cause the appearance of both conjugated and unconjugated
biliruibin in blood.
6. ......Necrosed tissue is after some time calicified due to hypercalcernia.
7. ......Excessive hemolysis may cause jaundice.
8. ......Urobilin gives colour to urine and faeces.
9. ......Hemosiderin is green or red colour pigment.
10.......Anaplasmosis may cause post-hepatic jaundice.
1. Dystrophic calcification 6. Toxic icterus
2. Hemosiderosis 7. Van den Bergh reaction
3. Melanosis 8. Metastatic calcification
4. Hemolytic jaundice 9. Pneumoconiasis
5. Gout 10. Obstructive jaundice
Q.4. Define thefollowings.
1. Silicosis 6. Anthracosis
2. Urobilinogen 7. Uricase
3. Gout 8. Stercobilin
4. Urobilin 9. Hemosiderin
5. Asbestoses 10. Pneumoconiasis
82

Q. 5. Select appropriate word(s) from four options given against each statement.
1. Dystrophic calcification occurs in animals due to .............. .
(a) Tuberculosis (b) Parasitic infection (c) Necrosis (d)All of the above
2. Melanosis is the brownlblack discolouration of tissue/organ as a result of excessive
accumulation ofmelanin due to ...............
(a) Hyperadrenalism (b) Hyperthyroidism (c)Hyperparathyroidism (d)Hypermelanernia
3. Hemosiderin is...............colour pigment.
(a) Green (b) Red (c) Golden Yellow (d) Blue
4. Urobilinogen is the ...............form ofbilirubin.
(a) Unconjugated (b) Conjugated and reduced (c) Conjugated (d) Conjugated and oxidised
5. Hemolysis may give rise to............
(a) Pre-hepatic icterus (b) Post-hepatic icterus (c) Toxic icterus (d) None ofthe above
6. Obstructive jaundice occurs as a result of
(a) Hemolysis (b) Liver necrosis (c) Cholangitis (d) Prioplasmosis
7. Indirect Van den Bergh reaction is an indication of.............. .
(a) Obstructive icterus (b) Hemolytic icterus (c) Hepatic jaundice (d) None of the above
8. Deposition ofcarbon particles in lungs is known as........... .
(a) Silicosis (b) Asbestoses (c) Pneumoconiasis (d) Anthracosis
9. Gout is the deposition of............... in tissues.
(a) Uric acid crystals (b) Oxalate crystals (c) Hemosiderin (d) Urobilin
10. The absence of............... in poultry is the main cause of gout.
(a) Trypsin (b) Lymphnodes (c) Amylase (d) Uricase
83

•
•
•
•
•
•
•
9
INFLAMMATION AND
HEALING
Inflammation
Introduction and Terminology
Pathogenesis of Inflammation
• Vascular Changes
• Cellular Changes
• Chemical Changes
Phagocytosis
Types of Inflammation
Healing
Model Questions

Inflammation and Healing
INFLAMMATION
Inflammation is a complex process of vascular a,ud
cellular alterations that occur in body in response to
injury. The term inflammation has been derived
from the Latin word inflammare, means to set on
fIre. Inflammation is considered as an important
event in body that activates the existing defence
mechanisms in circulating blood to dilute,
naturalize or kill the irritant! causative agent. Thus,
it is said that immunity is the resistance of body,
while inflammation is the activation of that
immunity. It is benefIcial to body except when
chronic or immune origin. Inflammation stgrts with
sublethal injury and ends with healing.
Etiology
• Any irritant! injury.
• Bacteria, virus, parasite, fungus etc.
• Trauma.
• Physical or chemical injury.
• Inflammation is characterized by 5 cardinal
signs;
• Redness;
• Swelling (Fig. 9.1);
• Heat;
• Pain;
• Loss offunction
• Acute inflammation is characterized by more
intense vascular changes like congestion,
oedema, haemorrhages, leakage of fIbrinogen
and leucocytes (Fig. 9.2).
• Chronic inflammation is characterized by more
proliferative and/or regenerative changes such
as proliferation of fIbroblasts and regeneration
of epithelium along with inftltration of
leucocytes (Fig. 9.3).
INTRODUCTION AND TERMINOLOGY
Inflammation may occur in any organ/tissue
depending upon the type of injury and irritant. The
inflammed state of an organ is called most often
85
with a suffIx "itis" detailed nomenclature IS as
under for different organs/ tissues.
Abomasum Abomasitis
Artery Arteritis
Bileduct Cholangitis
Bone & bone marrow - Osteomyelitis
Bone Osteitis
Brain Encephalitis
Bronchi Bronchitis
Bursa Bursitis
Caecum Typhlitis
Cervix Cervicitis
Colon Colonitis
Conjunctiva Conjunctivitis
Connective tissue Cellulitis
Cornea Keratitis
Crop Ingluvitis
Durameter Leptomeningitis
Ear Otitis
Endocardium Endocarditis
Eosophagus Esophagitis
Epididymis Epididymitis
Eustachian tube Eustachitis
External ear Otitis externa
Eyelid Blepheritis
Eyes Ophthalmitis
Fascia Fascitis
Fat Steatitis
Gall bladder Cholecystitis
Glans penis Balanitis
Gums Gingivitis
Heart Carditis
Inner part ofuterus Endometritis
Internal ear Otitis interna
Intestine Enteritis
Iris Iritis
Joints Arthritis
Kidney & pelvis Pyelonephritis
Kidney Nephritis
Lacrimal gland Dacryadenitis
Larynx Laryngitis
Ligament Desmitis
Lip Cheilitis
Liver Hepatitis
Lungs PneumonitislPneumonia
Lymph nodes Lymphadenitis

Fig. 9.2. Photomicrograph ofacute inflammation
showing intense vascular changes
Fig. 9.3. PhotomIcrograph ofchronic inflammation
showing proliferative changes
Fig.9.4. Diagram ofa blood vessel showing (a)
Vasoconstriction and (b) Vasodilation.
86
A
B
c
D
'. ~.!VV _~.'-,
Fig. 9.5. Diagram ofblood vessel showing
altered bloodflow (a) Normal (b) Decreased
bloodflow (c) Pavementation and (d) increased
permeabIlity
Fig. 9.6. Diagram ofblood vessels showing (a) diapedesis and
(b) rhexis

Lymph vessels
Meninges
Middle ear
Mouth cavity
Muscle
Myocardium
Nails
Nasal passage
Nerve
Omasum
Ovary
Oviduct
Palates
Pancreas
Pericardium
Peritoneum
Pharynx
Piameter
Pleura
Prepuce
Rectum
Reticulm
Retina
Rumen
Salivary glands
Sinuses
Skin
Spermatic cord
Spinal cord
Spleen
Stomach
Synovial membrane -
ofjoints
Tendon
Testes
Tongue
Trachea
Ureter
Urethra
Urinary bladder
Uterus
Vagina
Vein
Vertebra
Vessel
Vulva
Lymphangitis
Meningitis
Otitis media
Stomatitis
Myositis
Myocarditis
Onychia
Rhinitis
Neuritis
Omasitis
Oophoritis
Salpingitis
Lampas I palatitis
Pancreatitis
Pericarditis
Peritonitis
Pharyngitis
Pachymeningitis
Pleuritis
Posthitis
Proctitis
Reticulitis
Retinitis
Rumenitis
Sialadenitis
Sinusitis
Dermatitis
Funiculitis
Myelitis
Spleenitis
Gastritis
Sinovitis
Tendinitis
Orchitis
Glossitis
Tracheitis
Ureteritis
Urethritis
Cystitis
Metritis
Vaginitis
Phlebitis
Spondylitis
Vasculitis
Vulvitis
87
PATHOGENESIS OF INFLAMMATION
Inflammation starts with sublethal injury and ends
with healing; in between there are many events that
take place which are described as under:
Transient vasoconstriction
The blood vessels of the affected part become
constricted for movement of blood as a result of
action ofirritant (Fig. 9.4A).
Vasodialation and Increase in permeability
The blood vessels become dilated. Endothelium
becomes more permeable and releases
procoagulant factors and prostaglandins. Fluid and
proteins come out due to leakage in endothelium.
Fluid contains water, immunoglobulins,
complement component, biochemical factors of
coagulation and mediators of inflammation (Fig.
9.4B).
Blood flow decrease
Due to stasis of blood in blood vessel, there is
increase in leakage of fluids Icells outside the blood
vessels. It gives rise to congestion! hyperernia.
There is margination of leucocytes also known as
pavementation (Figs. 9.)).
Cells in perivascular spaces
Due to pseudopodia movement, leucocytes come
out from the dilated blood vessels through intact
and swollen endothelium and this process is known
as "diapedesis". Cells also come out through break
in blood vessel and this process is called as
"rhexis" (Fig. 9.6).
Leucocytes degranulate in perivascular tissue
spaces
When Leucocytes reach tissue spaces, they release
chemical mediators of inflammation, antimicrobial
factors in tissues such as cationic proteins,
hydrogen peroxide, hydrolytic enzymes,
lysozymes, proteases, kinins, histamine, serotonin,
heparin, cytokines, and complement (Fig. 9.7).

Fig. 9.7. DIagram ofpolymorphonuclear cell showing
def!.ranulation
FIg 9.S. Photograph oftesticles showing congestion
Fig. 9.9. Photomicrograph of lung showing acute
inflammation
Fig. 9.10. Diagram ofan abscess
Fig. 9.11. Photomicrograph .howing
polymorphonuclear cells in fibrin network
88
CD,lf,lCD18
B
CD"
Fig. 9.12. A. Photomicrograph ofpolymorpho-
nuclear cell B. diagram ofpolymorphonuclear
cell showinl! different recevtors
A
CD"
CD 7 , CD ,sfCD2
MHC Molecule
TCR
CD,
CD, CD 3
./_. ~ _ . . CD"lIgG
, ,
CD,2,' 'ir CD 2,1 IgE
,
CD'24 ~ BCRJAg
CO 2,
Fig. 9.13. A. Photomicrograph of lymphocyte. B. Diagram
ofT-lymphocyte and C. B- lymphocyte showing different
recevtors.

Irritant is removed and damaged tissue healed
By the process of inflammation irritant is
neutralized/removed or killed. Fluids are absorbed
through lymphatics and debris is removed by
phagocytosis. Blood vessel becomes normal.
If the irritant is strong and not normally removed
by the inflammatory process, it remains at the site
and gets covered by inflammatory cells and after
some time by fibrous cells in order to localize the
irritant. e.g. granuloma.
VASCULAR CHANGES
In inflammation, there is transient vasoconstriction
followed by vasodilation increased capillary
permeability and decrease in blood flow.
Circulatory changes are more pronounced in acute
inflammation (Figs. 9.8 to 9.11).
Etiology
• Any irritant! injury causing inflammation.
• Congestion ofthe affected organ/tissue.
• Oedema.
• Haemorrhage.
• Congestion ofblood vessels.
• Oedema, presence offibrin net work.
• Infiltration of leucocytes such as neutrophils,
lymphocytes, macrophages, eosinophils etc.
CELLULAR CHANGES
In inflammation, there is infiltration of leucocytes
in the inflammed area in order to provide defense
to the body and to kill or neutralize the etiological
factors.
• Any irritant! injury causing inflammation.
• Formation of pus/ abscess if there is increased
number ofneutrophils in the inflammed area.
• Area becomes hard, painful, with swelling/
nodule.
89
• Presence of leucocytes ill the inflammation
area.
• Presence of the type of cell may also determine
the type of inflammation.
Cells of inflammation are polymorphonuclear cells,
lymphocytes, macrophages, eosinophils, mast cells,
plasma cells, giant cells, etc.
Polymorphonuclear cells
They are also known as neutrophils (mammals) and
heterophils (birds). Size of these cells vary from
10f.l to 20f.l. They are attracted by certain
chemotactic factors like bacterial proteins, C3a,
Csa, fibrinolysin and kinins. These cells are
produced in bone marrow and are short life of only
2-3 days. Mature cells have multilobed nucleus and
two types of granules. Primary granules are the
azurophilic granules present in lysosomes
containing acid hydrolases, myeloperoxidases and
neurarninidases. Secondary or specific granules
have lactoferin and lysozymes. These cells
degranulate through Fc receptor, binding with non-
specific immune complexes or opsonins (Fig.
9.12).
Lymphocytes
Lymphocytes are produced in primary lymphoid
organs like thymus, bursa of Fabricious and bone
marrow and their maturation takes place in
secondary lymphoid organs like spleen,
lymphnodes, tonsils, and mucosa associated
lymphoid tissue etc. These cells may survive for
years and in some cases for whole life of an animal.
There are two types of lymphocytes seen on light
rnicroscopy i.e. small and large. Smalllymphocytes
are mainly T-helper or T-cytotoxic cells having
nuclear cytoplasm ratio (N:C). The
larger lymphocytes have low N:C ratio and are
mainly B cells and NK cells. There are large
numbers of molecules present on cell surface of
lymphocytes which are used to distinguish the type
of cells. These are known as markers and are
identified by a set ofmonoclonal antibodies and are
termed as Cluster ofDifferentiation (CD system of

CD64 CDllb /CD 18
1
2
c
7 6
Fig. 9.14. A. Photomicrograph of macrophage/
monocyte B. Diagram of macrophage showing
different receptors and C. Diagram showing different
stages and types of phagocytic cells: 1. Stem cell 2.
Promonocyte 3. Monocyte 4. Microglia in brain 5.
Histiocyte in connectlve tissue 6. Kupffer cell in lzver
7. Alveolar macrophages and 8.00steoclasts In bone
Fig. 9.15. Photomicrograph ofeosinophil
Fig. 9.16. Photomicrograph ofbasophil
Fig. 9.17. Photomicrograph ofplasma cell
B-cell
Plasma cell
FIg. 9.18. Diagram of plasma cell
90

classification) e.g. CD4 T-helper cells, CDg T-
cytotoxic cell, CD2 and CDs Pan-cell marker and
CD? NK cells.
B-Iymphocytes are characterized on the basis of
presence of mature immunoglobulins (lgG, IgA,
IgM, IgE, IgD) on their surface. They comprise
only 5-15% of total peripheral blood lymphocytes.
The B-cells having IgM, IgG, IgD are present in
blood while IgA-bearing B-Iymphocytes are
present in large numbers on mucosal surfaces. The
B-Iymphocytes can be further divided into BI and
B2; BI are present predominantly in peritoneal
cavity and are predisposed for autoantibody
production while Brcells are conventional
antibody-producing cells (Fig. 9.13).
Natural Killer (N.K.) cells are also present in 10-
15% of total peripheral blood lymphocytes. These
are defmed as the lymphocytes which do not have
any conventional surface antigen receptor i.e. TCR
or immunoglobulin. In other words, they are
neither T nor B cells. The NK cells do not have
CD3 molecule but CDI6 and CDS6 are present on
their surface. These cells may kill tumor cells, virus
containing cells and targets coated by IgG non
specifically. They excrete gamma interferon
interleukin 1 and GM- CSF.
Macrophages
The mononuclear macrophages are the main
phagocytic and antigen presenting cells which
develop from bone marrow stem cells and may
survive in body till life. The professional
phagocytic cells destroy the particulate material
while antigen presenting cells (APC) present the
processed antigen to the lymphocytes. They have
horseshoe shaped nucleus and azurophilic granules.
They have a well developed Golgi apparatus and
many intracytoplasmic lysosomes which contain
peroxidases and hydrolases for intracellular killing
of microorganism. Macrophages have a tendency to
adhere to glass or plastic surface and are able to
phagocyte the bacteria and tumor cells through
specialized receptors. These cells also have CDI4
receptors for lipopolysaccharide (LPS) binding
protein normally present in serum and may coat on
Gram negative bacteria. There are CD64 receptor
91
for binding of Fc portion of IgG responsible for
opsonization, extracellular killing and
phagocytosis. Antigen presenting cells (APC) are
associated with immunostimulation, induction ofT-
helper cell activity and communication with other
leucocytes. Some endothelial and epithelial cells
may, under certain circumstances, also acquire the
properties of APC when stimulated by cytokines.
They are found in skin, lymphnodes, spleen and
thymus (Fig. 9.14).
Eosinophils
Eosinophils comprise 2-5% of total leucocyte count
in peripheral blood. They are responsible for killing
of large objects which carmot be phagocytosed
such as parasites. However, they may also act as
phagocytic cells for killing bacteria but it is not
their primary function. These cells have bilobed
nucleus and eosinophilic granules. The granules are
membrane-bound with crystalloid core. These
granules are rich in major basic protein which also
releases histaminase and aryl sulfatase and
leucocyte migration inhibition factor (Fig. 9.15).
Mast cells!Basophils
There are 0.2% basophils in peripheral blood which
have deep violet blue coloured granules. The tissue
basophils are known as mast cells. They are of two
types, mucosal mast cells and connective tissue
mast cells. Basophilic granules present in these
cells are rich in heparin, SRS-A and ECF-A. When
any antigen or allergen comes into contact with
cells, it crosses links with IgE bound on the surface
of mast cells and stimulates the cells to degranulate
and release histamine which plays an active role in
allergy (Fig. 9.16).
Platelets
Platelets are derived from bone marrow and contain
granules. These cells help in clotting of blood and
are involved in inflammation. When endothelial
surface gets damaged, platelets adhere
and aggregate on damaged endothelium and release

B
Fig. 9.19. Photomicrograph ofepithelioid cells
Fig. 9.20. PhotomIcrograph ofgiant cells
D
FIg. 9.21 Diagram of giant cells: A. foreign body B.
Langhan's C .Touton, and D. Tumor giant cell
92
Fig. 9.22. Photomicrograph showing proliferation of
jibroblasts
Fig. 9.23. Diagram ofA.jibroblasts and B.jibrocytes
Fig. 9.24. Diagram showing phagocytosIs. A.
Opsonization and Chemotaxis B - C. Engulfment
and D - E. Digestion.

substances to increase penneability, attract
leucocytes and activate complement.
Plasma cells
The plasma cells are modified B-Iymphocytes
meant for production of immunoglobulins. Plasma
cells have smooth spherical or elliptical shape with
increased cytoplasm and eccentrically placed cart
wheel-shaped nucleus. The cytoplasm stains
slightly basophilic and gives a magenta shade of
purplish red. In the cytoplasm, there is a distinct
hyaline homogenous mass called Russell body
which lies on the cisternae of the endoplasmic
reticulum. This is the accumulation of
immunoglobulin produced by these cells. Such
cells are present in almost all types of inflammation
(Figs. 9.17 & 9.18).
Epithelioid cells
They are the activated macrophages mostly present
in granuloma when macrophages become large and
foamy due to accumulation of phagocytosed
material (bacteria) and degenerated tissue debris.
These cells are considered as hallmark of
granulomatous inflammation. They are elongated
with marginal nucleus that looks like columnar
epithelial cell and hence the name "Epithelioid"
cells (Fig. 9.19).
Giant cells
The giant cells are multinucleated macrophages
fused together to kill the microorganisms. They are
fonned by the fusion of many macrophages to
phagocytose larger particles such as yeast, fungi
and mycobacteria. They have usually more than
one nucleus and abundant cytoplasm. Such cells are
fonned when macrophages fail to phagocytose the
particulate material. They are of several types as
listed blow (Figs. 9.20 & 9.21).
Foreign body giant cells: They have many nuclei,
upto 100, which are unifonn in size and shape and
resemble the macrophage nucleus. The nuclei are
scattered in the cytoplasm. Such cells are seen in
chronic infectious granulomas oftuberculosis.
93
Langhan's giant cells: They are horseshoe shaped
giant cells having many nuclei and are
characteristically present in tubercle. The nuclei
resemble that of macrophages and epithelioid cells.
The nuclei are mostly arranged at periphery giving
horseshoe shape.
Touton giant cells: They are multinucleated cells
having vacuolation in the cytoplasm due to
increased lipid content. They mostly occur in
xanthoma.
Tumor giant cells: These are larger, pleomorphic
and hyperchromatic cells having numerous nuclei
with different size and shape. Nuclei of such cells
do not resemble that of macrophages or epithelioid
~lls. They are not true giant cells and not fonned
from macrophages but are found in cancers as a
result of fast division of nuclei in comparison to
cytoplasm.
Fibroblasts
Fibroblast proliferates to replace its own tissue and
others which are not able to regenerate. The new
fibroblasts originate from fibrocyte as well as from
the fibroblasts through mitotic division. Collagen
fibres begin to appear on 6th
day as an amorphous
ground substance or matrix. They are characteristic
of chronic inflammation and repair. Fibroblasts are
elongated cells having long nuclei, sometimes
looking like the smooth muscle fibres. The
proliferation of fibroblasts is extremely active in
neonates and slow and delayed in old animals. The
fibroplasia can be enhanced by removal of
necrosed tissue debris and by fever (Fig. 9.22 &
9.23).
CHEMICAL CHANGES
There is a long list of chemical mediators
responsible for acute inflammation. These are
endogenous biochemical compounds, which can
increase the vascular penneability, vasodilation,
chemotaxis, fever, pain and cause tissue damage.
Such chemical mediators are released by cells,
plasma or damaged tissue and are broadly
classified as: cell and plasma derived chemical
meoiators ofinflammation.

CELL DERIVED MEDIATORS
Vasoactive amines
Histamine
Histamine -is found in basophilic granules of mast
cells or basophils and in platelets. It is released
through stimuli due to heat, cold, irradiation,
trauma, irritant, chemical and immunological
reactions and anaphylotoxins C3a, CSa and C4a.
Histamine is also released due to action of
histamine releasing factors from neutrophils,
monocytes and platelets. It acts on blood vessels
and causes vasodilation, increased vascular
permeability, itching and pain.
Serotonin (5-Hydroxy-tryptamine)
It is present in tissues of gastrointestinal tract,
spleen, nervous tissue, mast cells and platelets. It
also acts on blood vessels to cause vasodilation and
increased permeability but its action is mild in
comparison to histamine.
Arachidonic acid metabolites
Arachidonic acid is a fatty acid, which either comes
directly from the diet or through conversion of
linoleic acid to arachidonic acid. Arachidonic acid
is activated by CSa to form its metabolites through
either cyclo-oxygenase or lipo-oxygenase
pathways. Cyclo-oxygenase is a fatty acid enzyme
which acts on arachidonic acid to form
prostaglandin endoperoxidase (PGG) which is
further transformed into prostaglandins like PGD2,
PGE2• PGF2, thromboxane A2 (Tx A2) and
prostacyclin (PGI2). Prostaglandins act on blood
vessels to cause vasodilation, increased
permeability bronchodilation except PGF2u, which
is responsible for vasodilation and
bronchoconstriction. Thromboxane A2 is a
vasoconstrictor, bronchoconstrictor, and causes
aggregation of platelets leading of increased
function ofinflammatory cells. Prostacylin is found
to be responsible for vasodilation, bronchodilation
and inhibitory action on platelet aggregation.
Lipo-oxygnese acts on arachidonic acid to form
hydroperoxy eico-satetraenoic acid (SHPETE)
which is further converted into SHETE, a
chemotactic agent for neutrophils and leucotrienes
94
(LT) or slow reacting substance of anaphylaxis
(SRS-A). The leucotrienes include an unstable
form leucotriene A (LTA), which is soon converted
into leucotriene B (LTB), a chemotactic and
adherence factor for phagocytic cells, and
leucotriene C, D and E (LTC, LTD, LTE) causing
contraction of smooth muscles leading to
vasoconstriction, bronchoconstriction and increased
vascular permeability.
Lysosomal components
Lysosomal granules are released by neutrophils and
macrophages to cause degradation of bacterial and
extracellular components, chemotaxis and
increased vascular permeability. These lysosomal
granules are rich in acid proteases, collagenases,
elastases and plasminogen activator.
Platelet activating factor (PAF)
Platelet activating factor (PAF) is released from
IgE sensitized mast cells, endothelial cells and
platelets. It acts on platelets for their aggregation
and release, chemotaxis, bronchoconstriction,
adherance of leucocytes and increased vascular
permeability. In low amount PAF causes
vasodilation while in high concentration it leads to
vasoconstriction.
Cytokines
Cytokines are hormone-like substances produced
by activated lymphocytes (Lymphokines) and
monocytes (Monokines). These are glycoprotein in
nature with low molecular weight (8-7SKD) and
are composed of single chain. They differ from
hormones which are specifically produced by
endocrine glands to maintain homeostasis through
endocrine action as cytokines are produced by
many different cell types and act on different cells
of body with very high functional activity. They
cause autocrine, paracrine and endocrine action
leading to tissue repair and resistance to infection.
Cytokines are broadly classified as interleukins,
interferon, cytotoxins and growth factors.

Interleukins (IL)
Interleukins are cytokines required for cell to cell
interaction among immune cells. They are
numbered serially in order of their discovery;
however, their actions are different and not related
with each other.
Table 9.1 Interleukins
SI. Type of Size MW
Source Target I Action
No. interleukin (KD}
1. Interleukin-l 17 Macrophages, Langerhans T-cells, B-cells, Neutrophils,
(IL-l a, lL-lp cells, T-cells, B-cells, Eosinophils, Dendritic cells,
and IL-lRA) Vascular endothelium, Fibroblasts, Endothelial cells,
Fibroblasts, Keratinocytes. Hepatocytes, Macrophages.
2. Interleukin-2 15 T- helper-l cells (Th-l). T-cells, B-cells, NK cells.
(IL -2)
3. Interleukin-3 25 Activated T-cells, Th-l cells, Stimulates growth and maturation of
(IL-3) Th-2 cells, Eosinophils, Mast bone marrow stem cells,Eosinophilia,
cells. Neutrophilia monocytosis, Increases
phagocytosis, Promotes immuno-
globulin secretion by B-cells.
4. Interleukin-4 20 Activated Th-2 cells. B-cells, T-cells, Macrophages,
(IL-4) Endothelial cells, Fibroblasts, Mast
cells, IgE production in allergy,
Down regulate ILl, IL6, and TNF-a.
5. Interleukin-5 18 Th-2 cells, Mast cells, Eosinophils, Increases T-cell,
(IL-5) Eosinophils. cytotoxicity.
6. Interleukin-6 26 Macrophages, T-cells, B-cells, T-cells, B-cells, Hepatocytes, Bone
(IL-6) Bone marrow stromal cells, marrow stromal cells,
Vascular endothelial cells, Stimulates acute phase protein
Fibroblasts, Keratinocytes, synthesis, Acts as pyrogen.
Mesangial cells.
7. Interleukin-7 25 Bone marrow, Spleen cells, Thymocytes, T-cells, B-cells,
(IL-7) Thymic stromal cells. Monocytes, Lymphoid stem cells,
Generates cytotoxic T-cells.
8. Interleukin-8 8 Macrophages. T-cells, Neutrophils.
(IL-8)
9. Interleukin-9 39 Th-2 cells. Growth of Th-cells, Stimulates B-
(IL-9) cell, Thymocytes, Mast cells.
10. Interleukin-10 19 Th cells, B-cells,Macrophages, Th-1 cells, NK cells, Stimulates B-
(IL-lO) Keratinocytes, Th-2 cells. cells, Thymocytes, Mast cells.
11. Interleukin-ll 24 Bone marrow stromal cells, Growth ofB-cells, Megakaryocyte
(IL-l1) Fibroblasts. colony formation, Promotes the
production of acute phase proteins.
12. Interleukin-12 75 Activated macrophages. Th-l cells activity, T-cell
(IL-12) proliferation and cytotoxicity, NK
cell proliferation and cytotoxicity
Suppresses IgE production, Enhances
B-cell immunoglobulin production.
13. Interleukin- 13 10 Th-2 cells B-Cells, Macrophages, Neutrophils,
(IL-13) Inhibits macrophage activity,
95

General Veter;nary Pathology
Stimulates B-cell proliferation,
Stimulates neutrophils.
14. Interleukin 14 53 T-cells, Malignant B-cells Enhances B-cell proliferation,
(IL-14) Inhibits immunoglobulin secretion.
15. Interleukin- 15 15 Activated macrophages, T-cells, NK cells, Proliferation of
(IL-15) Epithelial cells, Fibroblasts. both cytotoxic and helper T-cells,
Generates LAK cells
16. Interleukin- 16 13 T-cells (CDs cells) T cells, CD4 cells, Chemotactic for
(IL-16) lymphocytes
17. Interleukin- 17 17 CD4 cells Promotes the production of
(IL-17) IL-6,IL-8.
18. Interleukin-18 Macrophage Induces y-interferon production
(IL-18)
19. Interleukin-19 Macrophage Inhibit inflammatory and immune
(IL-19) responses, suppress activities ofTb1
and Tb2 cells
20. Interleukin-20 Activated keratinocytes Proliferation ofkeratinocytes and
(IL-20) their differentiation, modulate skin
inflammation
21. Interleukin-21 Activated T-cells Regulation ofhaematopoiesis and
(IL-21) immune responses, promotes
production of T-cells, fast growth and
maturation ofNK cells and B-cells
population
22. Interleukin-22 Activated T-cells Induction of acute phase responses
(IL-22) and proinflammatory role
23. Interleukin-23 Monocytes, activated dendritic Induces y interferon production and
(IL-23) cells ThI lymphocyte differentiation
24. Interleukin-24 Tb2 cells Turnor suppression
(IL-24)
25. Interleukin-25 Tb2 cells Stimulates release ofIL-4, IL-5 and
(lL-18) IL-13 from non lymphoid accessory
cells
26. Interleukin-26 T- cells Proinflammatory role, cutaneous and
(IL-26) mucosal immunity
27. Interleukin-27 CD4 cells Rapid clonal expansion ofnaive T-
(IL-27) cells and CD4 cells, induces
proliferative response and cytokines
production by Ag specific effector/
memory Tb1 cells
28. Interleukin-28 Virus induced peripheral Immunity to viral infection (antiviral
(IL-28) blood mononuclear cells activity)
29. Interleukin-29 Virus induced peripheral Immunity to viral infection (antiviral
{IL-29} blood mononuclear cells activi!y}
Interjerons
Interferons are glycoproteins having antiviral
action and inhibit the virus replication in cells.
These are of'five types like alpha (Cl), beta (P),
gamma (y), omega (00), and tau (t).
96

Table 9.2. Interferons
SI.
No.
Interferon Source
1.
2.
Interferon alpha
(IFN- a)
Interferon beta
(IFN-~)
Interferon gamma
(IFN-y)
Lymphocytes,
Monocytes, Macrophages
Fibroblasts
3. Th-l cells, Cytotoxic T-
cells, NK cells,
Macrophages
4.
5.
Interferon Omega
(lFN-ro)
Interferon tau
Lymphocytes, Monocytes
Trophoblasts
Trophoblasts
(lFN-t)
Tumor necrosisfactor or cytotoxins
Tumor necrosis factor or cytotoxins are produced
by macrophages and T-cells and are associated
with apoptosis in tumors. Tumor necrosis factor
beta (TNF-~) is produced by T-helper I cells and
activates CDg+ T-cells, neutrophils, macrophages,
endothelial cells and B-Iymphocytes. Tumor
necrosis factor alpha (TFN-a) is produced by
macrophages, T- cells, B-cells and fibroblasts and
it activates macrophages and enhances immunity
and inflammatory reaction.
Chemokines
Chemokines are small proteins divided into two a
and ~ subfamilies. Alpha-chemokines include IL-8,
which is produced by fibroblasts, macrophages,
endothelial cells, lymphocytes, granulocytes,
hepatocytes and keratinocytes. It acts as
chemotactic agent for basophils, neutrophils and T-
cells. The neutrophils get activated and release their
granules and leucotrienes. There is increased
respiratory burst. Besides, it also acts on basophils
and lymphocytes. Macrophage inflammatory
protein MIP-I of ~-chemokines are produced by
macrophages, T and B-Iymphocytes, mast cells and
neutrophils. It acts on monocytes, eosinophils, B
and T-Iymphocytes. Beta-chemokines include
macrophage inflammatory protein (MIP-I),
monocyte chemoattractant protein (MCP) and
RANTES protein. The MCP is produced by
macrophages, T-cells, fibroblasts, keratinocytes
and endothelial cells and activates the monocytes,
97
Action
Inhibit viral growth, activates macrophages
Inhibit viral growth, activates macrophages
Stimulates B-cells, production,
enhances NK Cells activity
activates macrophages and phagocytosis.
Promotes antibody-dependent and cell-mediated
cytotoxicity.
Virus infected cells to check viral growth
Activate Macrophages
Virus growth, Immunity to faetus through
placenta.
stimulating them for respiratory burst and
lysosomal enzyme release. RANTES is released by
T-lymphocytes and macrophages and it acts as
chemotactic agent for monocytes, eosinophils,
basophils and some T-cells.
Growth factors
Many cytokines are also known as growth factors
which act on cells and stimulate them to proliferate.
Thus they play a very important role in
inflammation and healing. In nature these are
glycoprotein which controls the proliferation and
maturation of several blood cells. The growth
factors also include interleukin 3, 7, 11, and 15.
The granulocyte colony stimulating factor (G-CSF)
is produced by fibroblasts, endothelial cells and
macrophages. It acts on granulocyte progenitors
and regulate their maturation and production of
superoxide. Macrophage colony stimulating factors
(M-CSF) are the glycoproteins released by
lymphocytes, macrophages, fibroblasts, epithelial
cells and endothelial cells. They act on monocyte
progenitors for their proliferation and
differentiation and promote their killing activity.
Granulocyte macrophage colony stimulating factor
( GM-CSF) is released from macrophages, T-
lymphocytes, endothelial cells and fibroblasts and
facilitates phagocytosis, antibody dependent cell
cytotoxicity (ADCC) and superoxide production. It
activates eosinophils to enhance superoxide
production and macrophages for increased
phagocytosis and tumoricidal activity.
Transforming growth factor (TGF) are five related

proteins (TGF-Bt. B2, B3 in mammals; B4 and Bs in
poultry) released from neutrophils, macrophages,
T-and B-Iymphocytes and they inhibit the
proliferation of macrophages, T - and B-
lymphocytes and stimulates the proliferation of
fibroblasts.
PLASMA DERIVED MEDIATORS
Plasma derived mediators of inflammation are
kinins, clotting, fibrinolytic and complement
systems; each of them has initiators and
accelerators in plasma depending upon their need
through feedback mechanism. During inflammation
Hagman factor (Factor XII) is activated through
leakage in endothelial gaps in increased
permeability of blood vessels. The activated factor
XII acts on kinin, clotting and fibrinolytic systems
and end product of these systems activate
complement to generate C3a and C5a, which are
potent mediators of inflammation.
Kinin system
Through activation of factor XII, kinin system
generates the bradykinin which causes contraction
of smooth muscles. The activated factor XII (XIIa)
acts on prekallikrein activator which in turn
converts the plasma prekallikrein into kallikrein.
t
Kinin
System
tBradykinin
FactorXn
~ Contact
XII a
t
J
Clotting
System
tFibrin
Fibrin Split
Products
t
Fibrinolytic
System
tPlasmin
Lcompl~ment system
C3a, Csa
98
The bradykinin is formed from kininogen through
the action of kallikrein. The bradykinin acts on
smooth muscles leading to their contraction.
Bradykinin is also found to be responsible for
vasodilation, increased vascular permeability and
pain.
Clotting mechanism
The activated Hagman factor (XIIa) initiates the
cascade ofclotting system and factor XI
Clotting system
(a) Extrisic mechanism
111-.v Surface phenomenon
Activated factor XIIa lFactor XI _
t<~---'
MW:XI.JFactor IX
~ Ca++
Activated factor IXa I
Factor VIII ---..l
t~Ca++. phospholipid
Activated factor VIlla ]
Fact~X _
~ Ca++
Activated factor Xa
Factor V
~ Phospholipid
Facto~rit lFact~
ActivatJfactor Ha
FibrtOgen
tfi:----"c,-a+-+.....
Fibrin (soluble)
1Factor XII.
Ca++
Fibrin polymer (Insoluble)

(b) Intrisic mechanism
Factor
1
Tissue thromboplastin
Ca++, Factor VII
ACtiVated(facto, Xa IFactor V
~ Phospholipid
Fact~~ri;1
Fl~
Factor Ha
into Xla which along with factor VHa changes
factor X into Xa. Factor Xa along with factor Va
converts prothrombin into thrombin which acts on
fibrinogen to form fibrin responsible for clotting of
blood.
Fibrinolytic system
Plasminogen activator is released from endothelial
cells and leucocytes and acts on plasminogen
present as a component of plasma proteins to form
plasmin. The plasmin is responsible for breakdown
of fibrin into fibrinopeptides or fibrin split
products, conversion ofC3to C3a and stimulates the
kinin system to generate bradykinin.
Complement system
Complement is activated through classical and
alternate' pathways; the classical pathway includes
activation of complement through antigen-antibody
complexes while the alternate pathway gets
activated via non-immunologic agents such as
bacterial toxins. Complement system on activation
generates 3 anaphylotoxin through either of
pathway including C3a, C5a and C4a, which are
responsible for release of histamine from the mast
cells, increased vascular permeability and
chemotaxis for leucocytes. The complement
99
components are activated by antigen antibody
complex and form AAC1423 which causes
opsonization and enhances phagocytosis. C567 acts
as chemotactic factor for phagocytic cells. AAC 1.7
renders the cell susceptible for lymphocytotoxicity
by T-cell. The complement AAC 1-9 causes lysis of
erythrocytes and Gram negative bacteria. However,
Gram positive bacteria are resistant to complement
lysis.
Antigen- antibody complex (AA)
On cell surface
AAC14
I C2~ C2x
~ Kfnin-Iike product
AAC142
C3--7 C3a
Anaphylotoxin
l
Cl4~s --7 Csa
C6 Anaphylatoxin
AAC1423S6
1C7~ C567
Chemotacticfactor
AACI423S67
~ Cs
AAC1_s
1C
9
AAC 1-9
tCell lysis

PHAGOCYTOSIS
Phagocytosis is the process of engulfment and
digestion of particulate matter by certain cells of
body (phagocytes; phagocytic cells). Mainly there
are two types of the cells which perform the
phagocytosis including polymorphonuclear
neutrophils (PMN) or microphages and monocytes
or tissue mononuclear cells also known as
macrophages. The process of phagocytosis is
almost similar by these micro and macrophages and
involves 4 stages (Fig. 9.24):
I. Chemotaxis
The phagocytic cells, neutrophils and monocytes
are present in circulating blood while there are
several tissue macrophages found in inflammation.
Vasodilation and decreased blood flow leads to
disturbances in blood stream resulting in
margination of leucocytes. At that time endothelial
cells of blood vessels express certain proteins
known as selectins and integrins that bind with
neutrophils. Since they are attracted by certain
chemical mediators, these cells are directed to
migrate towards the chemical mediators. This
directed migration of phagocytic cells is known as
chemotaxis. Various chemotactic agents for
different phagocytic cells are as under:
Chemotactic agents
C3a• C Sa, CS67, Leucotriene B4,
Bacterial proteins, LPS.
C3a, C Sa, CS67, Bacterial
products
Neutrophilic cationic protein
Cytokines, Kinins
ECF-A, Parasitic proteins,
Complement C3., C Sa.
Phagocytic cells
Neutrophils
Macrophages/
monocytes
Eosinophils
The chemotactic agents diffuse at the site of tissue
damage to attract the phagocytic cells. However,
large dose of chemotactic molecules may make the
phagocytic cells insensitive to chemoattraction and
such non-responsive cells may migrate from the
damaged area after completion ofphagocytosis.
11. Adherence and opsonization
The phagocytic cells and foreign particle like
bacteria are suspended in body fluid with negative
charge that repel each other. The negative charge
on foreign particle is neutralized by coating of
positively charged protein and such proteins are
immunoglobulins (IgG) and C3b, the complement
component. Thus, the particle coated with IgG or
C3b reduces its surface charge and it is attracted
towards phagocytic cells. The molecules (IgG or
C3b) coatings on particulate matter to facilitate
phagocytosis are known as opsonins and this
process is termed as opsonization. The word
opsonin is derived from Greek language and means
sauce, implying that it makes the particles more
tastier to phagocytic cells. The phagocytic cells
have receptors for Fc portion of IgG and C3b
protein that facilitates the adherence of the particles
on the surface of the cells. Another mechanism is
trapping of particulate material through
pseudopodia movement ofthe phagocytic cells.
Ill. Ingestion
The phagocytic cell forms pseudopodia around the
particles to cover it from outside. The particle is
bound to the surface of cells through opsonization
and is drawn inside the cytoplasm through
engulfment. The phagocytic cell forms vacuole by
enveloping the particle which is known as
phagocytic vacuole. The plasma membrane
covering phagocytic vacuole breaks and the
ingested particle lies free in cytoplasm of
phagocytic cell. The lysosome present in cell
cytoplasm binds with phagocytic vacuoles to form
phagolysosome orphagosome.
100
There is degranulation on the particle and liberation
of hydrolytic enzymes and antibacterial substances
to kill the ingested particle.
IV. Digestion
The ingested particles are destroyed by the
phagocytic cells through two separate mechanisms,
the respiratory burst and by action of lysosomal
enzymes

Respiratory Burst
Soon after the ingestion of particulate material
phagocytic cell increases its oxygen consumption
nearly 100 fold and also activates the cell surface
enzyme NADPH-oxidase. This activated enzyme
converts NADPH to NADP+ with release of
electrons.
NADPH-Oxidase
NADPH +02 ) NADP++20'+H+
One molecule of oxygen accepts a single donated
electron, leading to the generation of one molecule
of superoxide anion. NADP+ increases the hexose
monophosphate shunt and converts sucrose to a
pentose, carbon dioxide and energy for utilization
of the cellular functions. Two molecules of
superoxide anions interact to generate one molecule
of hydrogen peroxide under the influence of
enzyme superoxide dismutase.
Superoxide dismutase
2(20-) + 2 H+ )1{z02 + O2
Superoxide anions do not accumulate in the cell
because under the influence of dismutase enzyme
they rapidly convert into hydrogen peroxide.
However, there is accumulation of hydrogen
peroxide in the cells which is also cOllVerted into
bactericidal compounds the hypohalids through the
action of myeloperoxidase.
Myeloperoxidase
) H20 2 + ocr
(Hypochloride)
Hypochloride kills bacteria by oxidizing their
proteins and enhancing the bactericidal activities of
the lysosomal enzymes.
Lysosomal en~mes
Once the phagolysosomes are formed, the
lysosomal enzymes are released in the particulate
matter that can kill the bacteria. Many Gram
positive and Gram negative bacteria are destroyed
by the lysosomal enzymes. However, there are
101
certain bacteria like Brucella, Listeria which are so
resistant that they even grow inside the cell and
may become fatal to the cell. Dying neutrophils
release elastases and collagenase which act as
chemotactic factors for macrophages. The
macrophages destroy the particulate material/
bacteria by both oxidative and non-oxidative
mechanisms. In cattle, macrophages, after
activation, synthesize the nitric oxide synthatase.
This enzyme acts on L-arginine by using oxygen
and NADPH to produce nitric oxide and citrulline.
Nitric oxide is not highly toxic but it reacts with
superoxide anions released during respiratory burst
to produce very toxic derivatives such as N02,N20 3
ONOO and N03 which can kill the ingested
bacteria and cause severe tissue damage.
Macrophages are also used by the body as
scavenger cells to remove the dead or dying cells.
When the foreign particulate material persists for
longer period, macrophages accumulate in large
number around it to kill and remove from the
system. The phagocytosed particles are so potent
that they kill the macrophages also. Then after
destruction of macrophages it is rephagocytosed.
This continuing destruction of macrophages leads
to excessive release of lysosomal enzymes and
reactive oxygen and nitric oxide metabolites
resulting in chronic tissue damage and chronic
inflammation. In such situation, macrophages
become elongated looking like epithelial cells and
such cells are termed as epithelioid cells. If these
cells are also unable to destroy the ingested
material then they combine/ fuse together to form
multinucleated giant cells.
TYPES OF INFLAMMATION
Inflammation is classified according to the duration
as of acute, subacute and chronic form. The acute
inflammation is characterized by the presence of
more vascular alterations while chronic
inflammation is identified on the basis of presence
of more proliferative changes, fibrosis and less
vascular alterations (Fig. 9.25-1 & 11).

Fig. 9.25-J. Photomicrograph showing A. acute and B. Chrome inflammation
TISSUE REACTION IN INFLAMMATION
CHRONIC
HEALING
PHASE
Fig. 9.25-II. Diagram showing tissue reaction in inflammation
102

Inflf!mmation and Healing
SI.
No.
1.
2.
Changes Acute
Vascular +++
changes
Proliferative +
changes
Subacute Chronic
++ +
++ +++
On the basis of the presence of exudate, the
inflammation is divided into catarrhal, serus,
fibrinous, suppurative, eosinophilic, lymphocytic,
haemorrhagic, granulomatous etc., described as
under:
CATARRHAL INFLAMMATION
Catarrhal inflammation occurs on mucus surfaces
and is characterized by the presence of increased
amount of mucin as principal constituent of
exudates e.g. catarrhal enteritis, catarrhal rhinitis
(Figs. 9.26 & 9.27).
Etiology
• Mild irritant on mucous membrane e.g.
Rotavirus infection in calves.
• Cold exposure causes excessive mucous
discharges from nasal mucosa.
• Congestion.
• Presence of increased amount of slimy, stringy
mucin along with stool.
• Mucus nasal discharge, if respiratory mucosa
is involved.
• Mucous vaginal discharges in uterine disorders
or as physiological phenomenon.
• Increased number of goblet cells on mucous
surface.
• Increased amount of mucin, which takes basic
stain.
• Hyperplasia of epithelial cells on mucous
surface.
• Infiltration of neutrophils, lymphocytes and
macrophages.
103
SERUS INFLAMMATION
Serus inflammation occurs due to any mild irritant
and is characterized by the presence of serum!
plasma as main constituent of the exudates (Figs.
9.28 & 9.29).
Etiology
• Mild irritants e.g. chemicals.
• Physical trauma.
• Infection:
• Virus e.g. Pox, FMD
• Bacteria e.g. Pasteurlla multocida
• Congestion.
• Watery exudate in cavity/vesicle/in
intercellular spaces.
• On rupture ofvesicle clear fluid comes out.
• Congestion.
• Presence of serus exudate-acidophilic in tissue.
• Infiltration of neutrophils/lymphocytes/
mononuclear cells.
FIBRlNOUS INFLAMMATION
Fibrinous inflammation is characterized by the
presence of fibrin as main constituent of the
exudates (Figs. 9.30 & 9.31).
Etiology
• Chemicals.
• Thermal injury.
• Bacteria e.g. Corynebacterium diphtheriae.
• Viruses e.g. Herpes virus, influenza virus.
• Organ becomes firm and tense.
• Surface oforgan loses its shine.
• Produces adhesions in between two layers or
two organs.
False membrane/crupous membrane present, which
can be removed easily e.g. fibrinous membrane
over heart and liver due to colisepticemia in birds.

Fig 9.26. Photograph ofintestine showing catarrhal
inflammation
Fig 9.27. Photomicrograph ofintestme showing catarrhal
inflammatIOn
Fig 9.28. Photograph oflung showing seras inflammation
Fig 9.29. PhotomlCrolvaph oflung ;howing seru5 mflammatlOn
104
Fig 9.30. Photograph of A. heart and B. Liver
showingfibrinous mflammation
Fig 9.3/. Photonllcrograph showing
fibnnous inflammation
----~------~.~
FIg 9.32. Diagram ofan abscess
(suppurative inflammation)
FIg 9.33. Photomicrograph showing
suppuratlve inflammation

• Congestion.
• Presence of fibrin network (thread-like) on the
surface or in the organ.
• Infiltration of inflammatory cells like
neutrophils, lymphocytes and macrophages.
SUPPURATIVE INFLAMMATION
Suppurative inflammation is characterized by the
presence of neutrophils (polymorphonuclear cells)
as principal constituent of the exudates (Figs. 9.32
& 9.33).
Etiology
• Bacterial infection e.g. Staphylococci.
• Chemicals e.g. turpentine.
• Presence ofpus in lesion
• Pus is white yellow/greenish, thin, watery or
viscid/material.
• When pus present in a cavity it is known as
abscess while the presence of pus diffusely
scattered throughout the subcutaneous tissue is
known as Phlegmon or cellulitis.
• Congestion.
• Presence of neutrophils as main constituent of
the exudate.
• Liquifactive necrosis ofthe cells / tissue.
HAEMORRHAGIC INFLAMMATION
Haemorrhagic inflammation is characterized by the
presence of erythrocyte as principal constituent of
the exudate (Figs. 9.34 & 9.35).
Etiology
• Extremely injurious chemicals e.g. phenol.
• Bacterial infection e.g. Anthrax, H.S.
• Viral infection e.g. R.P., Blue tongue.
• Colour of organ/tissue becomes red/cyanotic.
• Exudate contains clots ofblood.
105
• Petechial, echymotic haemorrhages on the
surfaces of organs.
• Mucous membranes become pale / anemic.
• Presence of erythrocytes outside the blood
vessels in extracellular spaces along with
neutrophils/ lymphocytes/ macrophages.
• Serus/serofibrinous exudates.
LYMPHOCYTIC INFLAMMATION
Lymphocytic inflammation is characterized by the
presence of lymphocytes as principal constituent of
the exudate (Fig. 9.36).
Etiology
• Viral/Bacterial infections.
• Toxic conditions.
• No characteristic gross lesion; sometimes there
is formation of small modules on serosa of the
affected organ.
• Enlargement oflymphnodes.
• Congestion.
• Presence of white/grey lymphoid nodules in
organ.
• Presence of lymphocytes in abundant number
as principal constituent of the exudate.
• Congestion.
• Accumulation of lymphocytes around the
blood vessels, "Peri vascular cuffing"
• Aggregation of lymphocytes leading to
lymphofollicular reaction.
GRANULOMATOUS INFLAMMATION
Granulomatous inflammation is a chronic
condition, characterized by the presence of
granuloma in the organs. The granuloma consists of
central caseative necrosis surrounded by
lymphocytes, macrophages, epithelioid cells, giant
cells and fibrous connective tissue (Figs. 9.37 &
9.38).

Fig. 9.34. Photographs o/intestines showing haemorrhagic
inflammation
Fig. 9.35. Photomicrograph o/intestine showing
haemorrhagic inflammatIOn
FIg. 9.36. Photomicrograph o/brain showmg
lymphocytic inflammatIOn
106
Fig. 9.37. Photograph 0/spleen showing
granulomatous inflammation(ARS/uSDA)
Fig. 9.38. Photomicrograph o/lung showing
granulomatous inflammation
Fig. 9.39 Photograph 0/heart showing eosinophIlic
mflammation (ARSIUSDA).
Fig. 9.40. Photomicrograph o/heart showing
eosinophilic inflammation (ARS/uSDA).

Etiology
• Chronic bacterial infection e.g. tuberculosis.
• Fungal infections e.g. blastomycosis.
• Presence ofhard, tiny, nodules in the organ.
• Lungs become hard, patchy.
• Lymphnodes become hard and fibrus.
• Later the affected organ is calcified and gives
cracking sound on cut.
• Presence ofgranuloma in the tissue/ organ.
• Central caseative necrosis, surrounded by
epithelioid cells, macrophages, lymphocytes,
giant cells and covered by fibrous connective
tissue capsule.
• Caseative area contains causative organisms
also, which can be demonstrated by special
staining e.g. Tuberculous organisms by Acid-
fast staining.
• Calcification of necrosed area at later stage
looking black! violet colour on H & E stain.
Table 9.2 Differential features of various types of inflammation
Catarrhal Serus Fibrinous Suppurative Haemorr- Lymphocytic Granulo- Eosinophilic
hagic matous
Macroscop I. Congestion I. Congestion I. Organ 1. Presence of I. Colour of 1. No I. Presence of I. CongestIon
ic features
2. Presence of
becomes firm pus in lesion organ/tissue characteristic hard, tiny,
2. Watery and tense. becomes gross lesion; nodules in the 2. No
increased exudate in 2. Pus is red/cyanotic. sometimes organ. characteristic
amount of cavity/vesicle 2. Surface of white yellow/ there is gross lesion
slimy, stringy fin organ lost its greenish, 2. Exudate formation of 2. Lungs
mucin along intercellular shine. thin, watery contains clot small become hard,
with stool. spaces or viscid/ ofblood. modules on patchy.
3. Produces material.
3. Mucus 3. On rupture adhesions in 3. Petechial, serosa of the 3.
nasal of vesicle between two 3. When pus echymotic affected Lymphnodes
discharge, If clear fluid layers or two present in a haemorrhages organ. become hard
respiratory comes out organs. cavity 11 is on the 2. and fibrous.
mucosa is known as surfaces of Enlargement
involved 4. False abscess. 4. Later the
membrane/
organs. of affectedWhile the
4 Mucous crupous presence of 4. Mucous Iymphnodes organ
vaginal membrane pus diffusely membranes 3. Presence of calcified and
dIscharges, in present, scattered become pale / white/gray gIves
uterine which can be throughout anemic. lymphOId cracking
disorders or removed the nodules In
sound on cut.
as easIly e.g. subcutaneous organ.
physiologIcal fibrinous tissue IS
phenomenon. membrane known as
over heart Phlegmon or
and liver due cellulitis
to
colisepticemi
a In birds.
107

Microscopi I. Increased I. Congestion I. Congestion I. Congestion I. Presence of I. Presence of I. Presence of
c features number of
2. Presence of 2. Presence of
erythrocytes Iymphocytes granuloma in
goblet cells 2. Presence of out side the in abundant the tissue/
on mucous serus fibrin neutrophils as blood vessels number as organ.
surface. exudate- network main in principal
acidophilic in (thread like) constituent of extracellular constituent of 2. Central
2. Increased tissue. on the surface the exudate. spaces along the exudate. caseative
amount of or in the with necrosis,
mucin, which 3. Infiltration organ. 3.
neutrophils/ 2. surrounded
takes basic of Liquifactive Accumulation by epithelioid
stain. neutrophils/ 3. Infiltration necrosis of Iymphocytes/
of cells,
Iymphocytes/ of the cells / macrophage.
Iymphocytes macrophages,
3. mononuclear inflammatory tissue. 2. Serusl around the Iymphocytes,
Hyperplasia cells cells like serofibnnous blood vessels, giant cells
ofepithelial neutrophils, exudates. "Peri vascular and covered
cells on Iymphocytes cuffing" by fibrous
mucous and connective
surface. macrophages. 3. tissue
4. Infiltration
Aggregation capsule.
of
of Iymphocytes 3. Caseative
neutrophils, leading to area contains
Iymphocytes Iymphofollicu causative
and lar reaction. organisms
macrophages. also, which
can be
demonstrated
by special
staining e.g.
Tuberculous
organisms by
Acid-fast
staining.
4.
Calcification
ofnecrosed
area at later
stage looking
black! violet
colour on
H&E stain.
EOSINOPHILIC INFLAMMATION Macroscopic features
• Congestion.It is characterized by the presence of eosinophils as
the main constituents of the exudate (Figs. 9.39 &
9.40).
• No characteristic gross lesion.
I. Presence of
eosinophils in
abundant
numbers
2. Congestion
3. Accumula-
tion of
eosinophils
around the
parasites and/
or blood
vessels.
Etiology • Presence ofeosinophils in abundant numbers
• Allergy/ Hypersensitivity.
• Parasitic diseases.
108
• Congestion.
• Accumulation of eosinophils around the
parasites and! or blood vessels.

Fig. 9.42. Photomicrograph showing healing of
fracture
Flg. 9.43. Diagram showing granulatlon
tlssue m repazr
A
109
--~ F
Fig. 9.44. Dzagram showing fracture repair
A Hematoma B. Inflammatory reactIOn C. Growth
of granulation tl"ue andformatlOn ofsoft callus
D FormatIOn ofprocallus E. FonnatlOn ofo.lseo"s
{allus and F Remodeled bone with complete
heallllg

HEALING
Healing is characterized by the body response to
injury in order to restore normal structure and
function of the damaged organ/tissue. It is of two
types (Figs. 9.41 to 9.44).
Regeneration
Healing is by proliferation of parenchyrnatous cells
leading to complete restoration of the original
tissue.
• No significant gross lesion.
• Proliferation ofparenchyma1cells.
• Hyperplasia of the cells.
Repair
Repair is the replacement of injured tissue by
proliferation offibrous tissue.
• Pink/red granules (granulation tissue) appear
on healing part. These are the indication of
formation ofnew blood vessels.
• It can be seen just beneath the scab.
• Formation of granulation tissue i.e. fibroblasts,
angioblasts, histiocytes, macrophages and
parenchymal cells of organ.
• Fibroblasts are elongated fibrillar cells with
ovoid hyperchromatic nuclei.
• Mitosis is frequently observed.
MODEL QUESTIONS
Q. 1. Fill in the blanks with suitable word(s) to answer thefollowings.
1. The cardinal signs ofinflammation are .........., ............., .........., .......... and .............
2. Acute inflammation is characterized by ..................., while ................. '" changes are the
characteristic feature ofchronic inflammation.
3. Inflammation of mouth cavity is known as ..................., of palate as ...................,
tongue as ................... and of salivary gland as ...................
4. Inflammation starts with transient ..................., followed by ..................., resulting in
coming out of leucocytes which reaches in tissues spaces to release antimicrobial factors such
as ............., ............., ............., ............., ................ and ...................
5. There are three types of lyrnphocytes viz. ..................., ..................., and
..................., of which the later is further classified as ...................,................... and
6. Giant cells are ............................ and formed with fusion of several ............ to kill acid
fast bacteria, and may be of .......................and .............. types.
7. Arachidonic acid is an acid formed in body by conversion of ................. which is acth ated
by ........ to form prostaglandin through ...................and............... pathway.
8. Serot.)nin is also known as ..................... and it is present in tissues of ...................,
..................., ................... and ................... cells and acts on .................. to cause
................... and ................ but is mild in action in comparison to histamine.
9. LysQsomal granules of neutrophils and macrophages are rich in ..............,
.....................,......................... and................. .
10. Cytokines are ................... like substances produced by ........... and ...............mostly
and are of .......... '" ...... in nature.
11. Chemokines are .............. proteins produced by ..........,.........., ............,...............,
, ............,............ and....... and act as chemotactic factor for ..........., ....... and ..........
12. Repair is the substitution of tissue by ......... and is characterized by the presence of ........... .
110

Q.3.
Q.4.
1. ...... Keratitis is the inflammation of eyelid.
2. ...... Inflammation of gums is known as gingivitis.
3. ...... Salpingitis is the inflammation of salivary glands.
4. ...... Inflammation ofpituitary gland is known as posthitis.
5. ...... Densinitis is the inflammation of lamina densa ofglomerular basement membrane.
6. ...... Polymorphonuclear cells are fIrst line of defence in body.
7. ...... Giant cells are multinucleated neutrophils formed to kill the bacteria.
8. ...... Mast cells have basophilic granules rich in histamine
9. ..:... Arachidonic acid is activated by Cs. to form prostaglandin.
10. ...... Interleukins are those cytokines which are required for cell to cell interaction among the
immunocytes.
11. ...... Bacteria are phagocytosed by macrophages and are destroyed by lysosomal enzymes.
12. ...... Nitric oxide produced in phagocytic cells is not toxic to phagocytosed material.
13....... Catarrhal inflammation is characterized by increased mucous as principal constituent of
the exudate on the nucous surface.
14. ...... In colisepticemia, there is false membrane formation over liver and heart composed of
fIbrous cells.
15....... Suppurative inflammation is characterized by the presence of liquifaction and neutrophils.
16. ...... Granuloma consists of central caseative necrosis surrounded by Iymphocytes,
macrophages, epithelioid cells and giant cells.
17. ...... Eosinophilic inflammation is met with bacterial infections.
18....... Granulation tissue is composed offIbroblasts and small blood vessels.
19....... Fibrinous inflammation is seen in herpes virus infection.
20....... Perivascular cuffing is accumulation ofneutrophils around the blood vessels.
Define thefo/lowings.
1. Lampas 13. Cystitis 25. Pavementation
2. Glossitis 14. Carditis 26. Diapedesis
3. Blepheritis 15. Densinitis 27. Giant cells
4. Rhinitis 16. Steatitis 28. Plasma cells
5. Encephalomyelitis 17. Posthitis 29. Monokines
6. Nephritis 18. Funiculitis 30. Lymphokines
7. . Salpingitis 19. Orchitis 31. Chemokines
8. Proctitis 20. Leptomeningitis 32. Chemotaxis
9. Typhlitis 21. Fascitis 33. Phlegmon
10. Cheilitis 22. Spondylitis 34. Granuloma
11. Abscess 23. Balanitis 35. Granulation tissue
12. Phlebitis 24. Neuritis
Write short notes on.
1. Cells in inflammation
2. Chemical mediators of inflammation
3. Cytokines
4. Phagocytosis
5. Healing
111

Q. 5. Select appropriate word(s) from four options given with each question.
1. Inflammation is activation of ........ .
(a) Cardinal signs (b) Blood vascular changes (c) Immunity (d) Fibroplasia
2. Which one ofthe following is not a cardinal sign ofinflammation .........
(a) Redness (b) Pain (c) Oedema (d) Heat
3. Inflammation ofgums in known as........ .
(a) Cheilitis (b) Gingivitis (c) Glossitis (d) Orchitis
4. Inflammation ofovary is known as ........ .
(a) Uveitis (b) Urethritis (c) Oopheritis (d) Metritis
5. Primary granules ofneutrophils contain........ .
(a) Lactoferin (b) Lysozyme (c) Myeloperoxidase (d) Lipase
6. Lecucocytes marginate during vasodilation and come out from blood vessels through
pseudopodia movement; the process is known as........ .
(a) Diapedesis (b) Rhexis (c) Pavementation (d) Leucopenin
7. Macrophages become elongated with marginal nuclei to kill the acid fast bacteria and are
known as .........
(a) Giant cells (b) Epithelial cells (c) Epithelioid cells (d) Plasma cells
8. Langhans type ofgiant cells are observed in lesions in.............
(a) Tuberculosis (b) Neoplasms (c) Leukemia (d) Rinderpest
9. Lymphocytes modified to produce antibodies are known as .........
(a) T- helper cells (b) T-cytotoxic cells (c) Plasma cells (d)Epithelioid cells
10. Fibroblasts proliferate in .........inflammation.
(a) Acute (b) Subacute (c) Per acute (d) Chronic
11. C3a, Csa and C4a are the complement components which are also known as .....
(a) Anaphylotoxin (b) Prostaglandins (c) Vasoactive amines (d) None ofthe above
12. Cytokines are .........in action.
(a) Autocrine (b) Paracrine (c) Endocrine (d) All ofthe above
13. Tumor necrosis factor or cytotoxins are produced by macrophages and T-cells and are
associated with ........ .in tumor.
(a) Necrosis (b) Necrobacillosis (c) Degeneration (d) Apoptosis
14. Coating of foreign particles / bacteria by immunoglobulins to make it more readily palatable by
phagocytic cells is known as ........ .
(a) Opsonization (b) Adherence (c) Chemotaxis (d) Digestion
15. Catarrhal inflammation is characterized by increased number of........ .
(a) Goblet cells (b) Neutrophils (c) Giant cells (d) Epithelial cells
16. Fibrinous inflammation is characterized by the presence of .........as principal constituent of
exudates.
(a) Serum (b) Neutrophils (c) Fibrin (d) Fibroblasts
17. The principal constituent ofpurulent exudates is ........ .
(a) Serum (b) Plasma (c) Neutrophils (d) Eosinophils
18. Granulomatous inflammation is chronic in nature and is found in .........
(a) Tuberculosis (b) Rinderpest (c) Canine distemper (d) H.S.
19. In parasitic and allergic diseases, .........inflammation is mostly seen.
(a) Fibrinous (b) Haemorrhagic (c) Eosinophilic (d) Granulomatous
20. Granulation tissue is found in ........ .
(a) Tuberculosis (b) John's disease (c) Repair (d) Rinderpest
112

•
•
10
CONCRETIONS
Concretions
• Calculi
0 Urinary Calculi
0 Biliary Calculi
0 Salivary Calculi
0 Pancreatic Calculi
0 Enteric Calculi
• Piliconcretions
• Phytoconcretions
• Polyconcretions
Model Questions

CONCRETIONS
Concretions are solid, compact mass of material,
endogenous or exogenous in origin, found in
tissues, body cavities, ducts or in hollow organs.
Concretions are stone-like bodies commonly occur
in urinary system, gall bladder and gastrointestinal
tract. Concretions of endogenous origin are known
as calculi while those formed from exogenous
material are known as piliconcretion (Hair),
phytoconcretion (plant fibres) and polyconcretion
(polythenes).
Calculi
Calculi are formed due to deposition of salts around
the nucleus/nidus consisting ofeither fibrin, mucus,
desquamated epithelial cells or clumps of bacteria.
Due to the gradual and repeated precipitation of
salts, calculi becomes laminated. In the process of
calculi formation, the inner structural arrangement
gets shrinked, producing a rough superficial
surface. Calculi formation is more common in
urinary system and in gall bladder of man and
animals; however, they may also occur in salivary
gland, pancreas and intestines.
URINARY CALCULI
Urinary calculi are formed in renal tubules, pelvis
or in urinary bladder which may be carried away by
urine and may cause obstruction in ureter or
urethra. Urinary calculi is also known as urolith
and the process of formation of calculi is termed as
urolithiasis (Figs. 10.1 & 10.2).
Etiology
• Vit A deficiency.
• Bacterial infection e.g. E. coli, Micrococci,
Streptococci.
• Sulfonamide therapy.
• Hormonal therapy.
• May vary in size from 1 mm to several mm.
• Mostly rounded, pearl-like, laminated.
• Brown, grey and yellowish in colour.
• Enlargement and fibrosis of kidneys.
114
• In kidney sections tiny, laminated bodies of
concretion.
• Hydronephrosis.
• Chemical composition of urinary calculi may
vary in various species ofanimals.
• Horse:- Calcium carbonate, calcium
phosphate, magnesium carbonate.
• Ruminants:- Calcium phosphate, magnesium
phosphate, aluminium phosphate, calcium
oxalate. .
• Pigs:- Ammonium phosphate, magnesium
phosphate, calcium carbonate, magnesium
carbonate, magnesium phosphate, magnesium
oxalate. -
• Dogs:- Calcium carbonate, calcium phosphate,
sodium urate, ammonium urate.
BILIARY CALCULI
Biliary calculi are formed in gall bladder and bile
ducts and are also known as cholelith. These are
common in man; however, in cattle and pigs gall
stones are also seen. They are semisolids but
become hard and brittle on drying.
Etiology
• Bacteria.
• Sand particles.
• Particles ofingesta / intestinal contents.
• Desquamated epithelium.
• In gall bladder and bile duct.
• I mm to 3-4 cm in diameter.
• Numbers vary from 1 to many.
• Obstructive jaundice.
• Cholecystitis and cholangitis.
• In sections, concentric layers of cholesterin,
bilirubin, calcium carbonate and coagulated
material.
• Cholecystitis, cholangitis.

Fig. 101. Photograph 'ifkidney ofbullock ShOWlllg
presence ofcalcult A. Gross illtact kidney B Cro>s
sectIOn ofkidney alld C. MicroscopIc structure of
kidney hal'ing concretlOll
Fig. 10.2. Diagram showing predilection sIte of
calculi in sigmoidf/exure ofurethra in bullocks
Concretions
FIg. 10.4. Photograph ofPlizconcretion
Fig. 10.5. Photograph ofPolyconcretion
115

SALIVARY CALCULI
Salivary calculi are formed in excretory ducts of
the parotid, sublingual and submaxillary salivary
glands. Size of such calculi vary upto 25-30 mm
diameter. They are made up of salts like calcium
carbonate, calcium phosphate, magnesium
carbonate, sodium carbonate, around the plant
fibres. Salivary calculi also known as sialolith.
PANCREATIC CALCULI
Pancreatic calculi or pancrealolith are rare in
occurrence in animals but may be found in cattle.
Pancreatic calculi is grey in colour with size upto
few centimeter. They are made up of calcium
carbonate, calcium oxalate and calcium phosphate
around a nidus ofcholesterol or fatty acids.
ENTERIC CALCULI
Enteric calculi or enterolith are common in horses,
and occur mostly in large intestine 'colon'. In
horse, a nidus is surrounded by wheat and rye bran
containing magnesium phoshphate. The nidus may
be a piece of metal or sand on which concentric
layers are deposited. They may look like a ball of
round or oval in shape (Fig. 10.3). Colour of
enterolith may vary from greyish to dark brown. In
dogs, bone in diet may provide a nidus and such
concretions are known as coproliths.
PILICONCRETIONS
PiIiconcretions are hair balls, that occur in calves or
in adults due to excessive licking of skin. Due to
licking, animals swallow large amount of hairs
which take the shape of ball due to movements of
stomach. Mostly, the hair balls are found in
stomach or in colon (Fig. lOA).
PHYTOCONCRETIONS
Phytoconcretions are formed around the food
materials and may occur in stomach and intestine
of animals and in crop of poultry. They may cause
obstruction of bowel. They are also known as
phytobezoars.
POLYCONCRETIONS
They are made up of polythenes and excessive
deposition of salts around them. They may vary in
size from a few centimeters to several centimeters
and weigh upto kilograms. They cause obstruction
leading to death ofanimals (Fig. 10.5).
Such concretions are observed in cattle wandering
on street in cities and in zoo animals. The
polythene containing vegetable waste or green
leaves and food materials are thrown away on
roads, and are easily available to the animals.
Polythene is not degraded in stomach and remains
there to form a nidus, around which the salts are
deposited and take the shape of calculi leading to
obstruction ofdigestive tract passage.
MODEL QUESTIONS
1. Concretions of endogenous origin are known as ..................... which occurs due to nidus
provided by ................, ............... ,............... and ............
2. In ruminants, the urinary calculi is made up of ............., .........., ........ and ...................
3. Gall stones may cause...............,.............. and ........... which may lead to
4. Enterolith commonly occurs in ................. in horses.
5. Coprolith occurs in ................ due to eating of ....................
1. .........Vitamin B deficiency may lead to formation ofurinary calculi.
2. .. .......Polyconcretions are made up ofpolythenes.
116

Concretions
3. ......... Hair balls are also known as phytobezoars.
4. ......... Choleliths may lead to toxic jaundice.
5. ......... Uroliths may cause hydronephrosis.
1. Urolithiasis
2. Piliconcretions
3. Enteroliths
4. Polyconcretions
Q. 4. Define the followings.
1. Phytobezoars 6. Nidus
2. Coproliths 7. Cholecystitis
3. Piliconcretions 8. Cholangitis
4. Sialolith 9. Hydronephrosis
5. Pancrealolith 10. Obstructive jaundice
Q. 5. Select appropriate word(s) from the four options given with each statement.
1. Calculi are stone-like bodies which have ...............origin.
(a) Endogenous (b) Hematogenous (c) Exogenous (d)None of the above
2. Piliconcretions are made up of ..............
(a) Plant fibres (b) Polythenes (c) Hairs (d) Desquamated cells
3. Urinary calculi are formed in renal tubules and in horse they are made up of ................
(a) Calcium carbonate (b) Calcium phosphate (c) Magnesium carbonate (d)All ofthe above
4. Choleliths may cause ........ .
(a) Toxic jaundice (b) Post-hepatic Jaundice (c) Pre-hapatic jaundice (d)Hemolytic jaundice
5. Sialoliths occur in .............. .
(a) Pancreas (b) Salivary gland (c) Sinus (d)Seminal vesicle
6. Coprolith may occur in dogs due to presence of ............in food.
(a) Sand (b) Muscles (c) Plant fibers (d) Bones
7. Cholelithiasis may lead to inflammation of ........
(a) Gall bladder (b) Intestine (c) Stomach (d) Pancreas
8. Enteric calculi are more common in horse due to feeding of ........ .
(a) Grams (b) Wheat bran (c) Grass (d) Beans
9. Polyconcretions are formed due to accumulation of ............ in G.I. Tract.
(a) Hairs (b) Polysaccharides (c) Polyuria (d) Polythenes
10. Vitamin ....... deficiency may lead to formation of urinary calculi.
(a) A (b)B (c)D (d)K
117

11
IMMUNITY AND
IMMUNOPATHOLOGY
• Immunity
• Immunopathology
• Hypersensitivity
Q Type I
Q Type 11
Q Type III
Q Type IV
• Autoimmunity
• Immunodeficiency
Q Congenital
Q Acquired
• Model Questions

Immunity and Immunopathology
IMMUNITY
Immunity is the resistance of body against
extraneous etiological factors of disease, which is
afforded by the interaction of chemical, humoral
and cellular reactions in body. This is an integral
part of the body without, which one cannot think of
life. During the process of evolution, nature has
provided this defence mechanism in the bodies of
all living creatures particularly of higher animals
and man, that protects them from physical,
chemical and biological threats. It can be classified
as natural or paraspecific and acquired or specific
immunity.
'Natural/paraspecific immunity
There are some species which are resistant to
particular diseases due to presence of natural
resistance against them e.g. horse, pig, cat are
resistant to canine distemper virus; dogs are
resistant to feline panleucopenia virus, chickens are
resistant to anthrax. Even within species, there is
natural resistance that protects some individuals
while others are susceptible e.g. Indian deshi cattle
Zebu (Bos indicus) is quite resistant to
piroplasmosis in comparison to Bos taurus.
Besides, there are the mechanisms or barriers in
body provided by nature. These are:
• Skin and mucous membrane prevent
organisms from gaining entrance in body.
• Mucous prevents from infections by trapping
and keeping them away.
• Saliva, gastric juice and intestinal enzymes
kill bacteria.
• Tears, nasal and GI tract secretions are
bactericidal due to presence oflysozymes.
• Phagocytic cells such as neutrophils kill
bacteria through phagocytosis.
• Macrophages kill organisms through
phagocytosis.
• Natural antibodies act as opsonins and help in
phagocytosis.
• Interferons have antimicrobial properties.
They are host/species specific and arrest viral
replication.
119
• Interleukins, cytotoxins and growth factors
stimulate the immune reactions and
inflammation.
• Natural killer cells kill targets coated with
IgG.
Acquired/specific immunity
Acquired immunity develops in body as a result of
prior stimulation through antigen. it is specific to a
particular antigen against which it was developed.
It can be restimulated on second or subsequent
exposure with antigen and thus, it has memory for a
particular antigen. It differs from natural immunity
in respect of prior stimulation, specificity and
memory. It can be classified as humoral and cell
mediated immunity.
Humoral immunity
This is the immunity present in fluids of body
mainly in blood. There are antibodies in serum of
blood, which protect body from diseases. It is
specific to particular antigen. Antibodies are
formed in blood as a result of exposure of the
foreign substances including bacteria, virus,
parasite and other substances.
Antigen is foreign substance, which is able to
stimulate the production of antibodies in body.
They may be of high molecular weight protein,
polysaccharides, and nucleic acids. Simple
chemicals of low molecular weight are not able to
induce immunity. However, they may be
conjugated with large molecular weight molecules
such as protein to become antigenic and induce
antibody production, such substances are termed as
haptens.
Antibodies are protein in nature present in serum
and produced as a result of antigen. Antibodies are
specific to antigen. Most of the microorganisms
have several antigenic determinants and antibodies
are produced against each antigenic determinant
specifically. The antibody response to antigen can
be enhanced if the antigen is released slowly in
body. There are several substances like oils, waxes,
alum, aluminium hydroxide, WhICh may be added
with antigen so that it is released slowly in body to

Hinge region Ag binding site
Light chain
A
..... , ,,', ...
B
D~
E
FIg.//.I. Diagram showing A. Structure ofantibody with
Its different parts B. Immunoglublin-G (IgG), c.
Immunoglobulm-M (IgM), D. Immunoglobulm-A (/gA)
and E. Immunoglobulm-E (IgE).
120
increase the antibody production. Such substances
are known as adjuvants. Antibodies are also known
as immunoglobulins as they are the part of
globulins. They are glycoprotein in nature and are
of5 types IgG, IgA, IgM, IgD and IgE.
Immunoglobulin G (IgG)
It is the main antibody found in high concentration
(75%) in serum with a mw 150 KD. It is produced
by plasma cells in spleen, lymphnodes and bone
marrow. It has two identical light chains and two
gamma heavy chains. The light chains may be of
kappa or lamda type. IgG is the smallest
immunoglobulin which may pass through blood
vessels with increased permeability. It has the
capacity to quickly bind with foreign substances
leading to opsonization. Its binding with antigen
may also activate the complement.
Immunoglobulin M (IgM)
This is about 7% of total serum immunoglobulins.
It is also produced by plasma cells in spleen,
lymphnodes and bone marrow. It is pentamer, five
molecules of conventional immunoglobulin with
mw 900 KD. These five molecules are linked
through disulfide bonds in a circular form. A
cysteine rich polypetide of 15KD mw binds two of
the units to complete circle and is known as 'J'
chain. It is produced in body during primary
immune response. It is considered to be more
active than IgG for complement activation,
neutralization of antigen, opsonization and
agglutination. IgM molecules are confined to the
blood and have no or little effect in tissue fluids,
body secretions and in acute inflammation.
Immunoglobulin A (IgA)
It is secreted as dimmer (mw 300 KD) by plastpa
cells present under body surfaces like intestinal,
respiratory and urinary system, mammary gland
and skin. Its concentration is very little in blood.
IgA produced in body surfaces is either secreted on
surface through epithelial cells or diffuse in blood
stream. IgA is transported through intestinal
epithelial cells having a receptor of 71 KD which
binds with the secretory component covalently to

form a secretory IgA. This secretory component
protects IgA in the intestinal tract from digestion. It
cannot activate the complement and cannot perform
the opsonization. IgA can neutralize the antigen
and agglutinate the particulate antigen. IgA
prevents adherence of foreign particles/antigen on
the body surfaces and it can also act inside the
cells. It is about 16% of total immunoglobulins
present in serum.
Immunoglobulin E (IgE)
It is also present on body surfaces and produced by
plasma cells located beneath the body surfaces. It is
in very low concentration in serum. It can bind on
receptors of mast cells and basophils. When any
antigen binds to these molecules, it causes
degranulation from mast cells leading to release of
chemical mediators to cause acute inflammation. It
mediates hypersensitivity type I reaction and is
responsible to provide resistance against invading
parasitic worms. It is of shortest half life (2-3 days)
and thus is unstable ~nd can be readily destroyed
by mild heat treatment. It is 0.01% of total
immunoglobulin in serum with 190 KD molecular
weight.
Immunoglobulin D (IgD)
IgD is absent in most domestic animals. However,
it is present in very minute amount in plasma of
dog, non-human primates and rats. IgD can be
detected in plasma. However, it cannot be found in
serum due to lysis by proteases during clotting. It is
only 0.2 % of total immunoglobulin in serum with
mw 160KD.
On the basis of their function, antibodies are
classified as:
Antitoxins have the property to bind with toxins
and neutralise them.
Agglutinins are those antibodies, which can
agglutinate the RBCs and/or particulate material
such as bacterial cells.
Precipitins can precipitate the proteins by acting
with antigen and inhibit their dissemination and
chemical activity.
Lysins can lyse the cells or bacteria through
complement.
121
Opsonins have the property to bind with foreign
particles, non specifically leading to opsonization,
making the foreign material palatable to phagocytic
cells.
Complement fIXing antibodies bind with antigen
and fix the complement for its lysis.
Neutralizing antibodies are those, which
specifically neutralize/destroy the target /antigen;
merely binding with antigen cannot be considered
as neutralizing antibodies.
Immune response
When the antigen enters thebody of an animal is
trapped, processed and eliminated by several cells,
including macrophages, dendritic cells and B-cells.
There are two types of antigen in body i.e.
exogenous and endogenous. The exogenous or
extracellular antigens are present freely in
circulation and are readily available for antigen
processing cells.
The endogenous or intracellular antigens are not
free and are always inside the cells such as viruses.
But when these viruses synthesize new viral
proteins using biosynthetic process of the host
cells, these proteins also act as antigen and are
termed as endogenous or intracellular antigens.
The processing of antigen by macrophages is
comparatively less efficient as most of the antigen
is destroyed by the lysosomal proteases. An
alternate pathway of antigen processing involves
antigen uptake by a specialized population of
mononuclear cells known as dendritic cells located
throughout the body specially in lymphoid organs.
Such dendritic cells have many long filamentous
cytoplasmic processes called dendrits and lobulated
nuclei with clear cytoplasm containing
characteristic granules (Fig. 11.2).
Antigen presenting cells process the exogenous
antigen and convert into fragments to bind with
MHC class 11 molecules. Such processed antigen
along with MHC class 11 molecule and certain
cytokines such as IL-l is presented to antigen
recognizing cells (T-helper cells). Macrophages
also regulate the dose of antigen to prevent
inappropriate development of tolerance and provide
a small dose of antigen to T- helper cells. However,

B-Cell
Antigen
'..; ....f - - -
./
Bone marrow stem cells
(Macrophage)
APC
' /
Plasma cells
Immunoglobulins
Macrophage
Activated macrophage
Histamine
IOflammatIon
Fig 112 Diagram showing mechanism a/inductIOn a/Immunity In body
122
T-cell
Macrophage
+
antigen
Effector
T-cell
(Sensitized)
Cytotoxic/ Killer
cells

.Exlcenul'"
(Exogenous)
APC
(Macrophages
Dendritic cells
B-cells)
~
Antigen
I
InlnlCent,
(Endogenous)
APC
(Macrophages
Dendritic
cells, B-cells)
~Antigen sensitive Antigen sensitive
cells (B-cells) cells (T-cells)
'./
Ab producing
(Plasl' a cells)
Memory cells
(T-cells)
Memory cells
(B cells)
Antigen elimination
Effecter cells
(Tc cells)
if the antigen is presented to T-cells without MHC
class II molecule, the T-cells are turned off
resulting into tolerance. On an average, an antigen
presenting cell possesses about 2x105
MHC class II
molecules. A T-cell requires activation by 200-300
123
peptide-MHC class 11 molecules to trigger an
immune response. Thus, it is estimated that an
antigen-presenting cell may present several
epitopes simultaneously to T-helper cells. A
counterpart of T- helper cell also exists and is
known as suppressor T-cell (Ts cell) which
suppresses the immune response. The viral encoded
proteins, endogenous antigens are handled in a
different manner from exogenous antigens. Such
antigens are bound to MHC class la molecules and
transported to the cell surface. Such antigen and
MHC class la molecule complex triggers a
lymphocytic response i.e. T-cytotoxic cells (Tc-
cells). These cytotoxic T-cells recognize and
destroy virus infected cells. However, there is some
cross priming leading to cell mediated immune
response by exogeno'us antigens and humoral
immune response by endogenous antigens. Some
lymphocytes also function as memory cells to
initiate secondary immune response.
On antigen exposure, there is a latent period of
about four to six days and only after that serum
antibodies are detectable. The peak of antibody titre
is estimated around 2 weeks after exposure to
antigen and then declines after about 3 weeks.
During this primary immune response, majority
antibodies are of IgM type whereas in secondary
immune response, it is always predominated by
IgG.
IMMUNOPATHOLOGY
Immunopathology includes the disorders of
immune system characterized by increased
response or hypersensitivity, response to self
antigens (autoimmunity) and decreased responses
(immunodeficiencies).
HYPERSENSITIVITY
It represents an accelerated immune response to an
antigen (allergen), which is harmful to body rather
than to provide protection or benefit to the body.
Such violent reactions may lead to death. This
condition is also known as allergy or atopy. The
hypersensitive reactions can be classified into four
classical forms including anaphylaxis (Type I),
cytotoxic hypersensitivity (Type-II), Immune

complex mediated hypersensitivity (Type Ill) and
delayed type hypersensitivity (Type-IV) reaction.
ANAPHYLAXIS OR TYPE-I
HYPERSENSITIVITY
Anaphylaxis or type I hypersensitivity reaction is
rapidly developing immune response to an antigen
characterized by humoral antibodies of IgE type
(reagin). These reagins sensitize basophils/mast
cells to release chemical mediators (Histamine,
Serotonin, Prostaglandins, CFA for neutrophils and
eosinophils) of inflammation leading to acute
inflammatory reaction (Fig. 11.3).
Etiology
• Administration ofdrugs.
• Administration of serum.
• Bite of insects, bee etc.
• Dust, pollens etc.
• Bronchial asthma.
• Wheel and flare reaction on skin.
• Oedema, congestion, erythema, itching on
skin.
• Rhinitis.
• Congestion, pulmonary oedema, emphysema,
constriction ofbronchioles.
• Oedema, congestion, haemorrhage on skin.
CYTOTOXIC OR TYPE 11
HYPERSENSITIVITY REACTION
Cytotoxic reactions are characterized by lysis of
cells due to antigen-antibody reaction on the
surface ofcells in the presence ofcomplement.
Etiology/Occurrence
• Blood transfusion.
•
•
•
Hemolytic anemia.
Infections such as Equine
rickettsia, parasites
babesiosis).
Thrombocytopenia.
infectious anemia,
(trypanosomiosis,
124
• Drugs such as penicillin, phenacetin, quinine
cephalosporins.
• Anemia.
• Jaundice.
• Haemoglobinuria.
• Erythrophagocytosis.
• Lysis of erythrocytes/agglutination of
erythrocytes Hemolytic anemia (Fig. 11.4).
• Increased number ofhemosiderin laden cells in
spleen.
IMMUNE COMPLEX MEDIATED OR TYPE-
III HYPERSENSITIVITY REACTION
Type-Ill hypersensitivity reaction is characterized
by the formation of immune complexes as a result
of antigen-antibody reaction and their deposition in
body tissues leading to inflammatory reaction (Fig.
11.5).
Etiology
• Immunoglobulins.
• Tumor antigens, nuclear antigens.
• Environmental pollutants e.g. pesticides.
• Infections such as Leishmaniasis.
• Arthus reaction is focal area of inflammation,
necrosis at the site of infection.
• Serum sickness is necrotizing vasculitis,
endocarditis and glomerulonephritis.
• Chronic immune complex disease is renal
failure due to glomerulonephritis, vasculitis,
chroiomeningitis and arthritis.
• Deposition of immune complexes in wall of
blood vessels.
• Deposition of immune complexes in glomeruli
(Fig. 11.6).

FI
Fig.II.3. Diagram showing IgE mediated Type-I
hypersensitivity reaction A. Mast cell B. Allergen, C.
Allergen binds with two JgE molecules D. Degranulation
and release of histamine, serotonin, mediators of
mflammation JL-2,3,4,5,6,7,13.,TN-a, LTB4, LTC4, PAF
and PGD2 , E. Increased vascular permeability and
F. Bronchoconstriction.
Aa
125
Aa - Positive foal
Aa Positive 1antibodies in
milk
Fig.II 4. Diagram showing type II
hypersensitivity (hemolytic disease in/oal)

Ag
Vasculitis
Immune complex
Arthritis
Removal ofimmune
complexes through
phagocytosis
FIg. J1.5. Dtagram showing Type-1I1 hypersensitiVity reaction. A. Normal architecture ofglomeruli B. Type I,
e. Type 11 and D. Type III Membrano proliferative glomerulonephritis (MPGN).
126

Fig. 11.6. PhotomIcrograph ofimmune complex
mediated glomerulonephirtis
Fig. 11.7. Diagram showing oftuberculin reaction
Fig. 11.9. Photograph showing mallein reaction
127
FIg. 11.10. Ph"tomicrograph showmg DTH reuctlOn-
lymphofolilcular leslOlls
Fig. 11.11. Diagram showing microscopic picture of
DTH reaction
D
c
Fig. 11.12. Diagram Showmg autoimmunity A. RBC
showing presence ofauto antigens B. Recognition of
auto antigen by APC and their processing C. B-cells
for antibody production and D. T-cells for cytotoxicity

• Infiltration of inflammatory cells such as
neutrophils, macrophages and lymphocytes.
• Lesions ofglomerulonephritis, polyarthritis.
DELAYED TYPE HYPERSENSITIVITY
(DTH) OR TYPE IV HYPERSENSITIVITY
REACTION
DTH reaction is mediated by sensitized T-
lymphocytes and is the manifestation of cell-
mediated immune response (Figs. 11.7 to 11.11).
Etiology
• Tuberculin reaction.
• Graft versus host reactions.
• Granulomatous reaction.
• Formation of nodules, which are hard, painful
to touch.
• Rejection oftransplantsigrafts.
• Heavy infiltrations of mononuclear cells
particularly of T-lymphocytes and
macrophages.
• Congestion and oedema.
• Lymphocytic infiltration is more common
around the blood vessels.
• Lymphofollicular reaction.
Table 11.1 Differential features of various types of Hypersensitivity Reaction
Anaphylaxis or Type-I Cytotoxic or Type 11 Immune Complex Delayed Type
Hypersensitivity Hypersensitivity Mediated or Type-III Hypersensitivity (DTH) or
Reaction Reaction Hypersensitivity Reaction Type IV Hypersensitivity
Reaction
Macrosc I. Bronchial asthma. 1. Anemia 1. Arthus reaction is focal I. Formation of nodules,
opic 2. Wheel and flare 2. Jaundice area ofinflammation, which are hard, painful to
features reaction on skin. 3. Haemoglobinuria necrosis at the site of touch.
3. Oedema, infection. 2. Rejection of transplantsi
congestion, erythema, 2. Serum sickness is grafts.
itching on skin. necrotizing vasculitis,
4. Rhinitis endocarditis and
glomerulonephritis.
3. Chronic Immune
complex disease is renal
failure due to
glomerulonephritis,
vasculitis,
chroiomeningitis and
arthritis.
Microsc I. Congestion, 1. Erythrophago- I. Deposition of immune 1. Heavy infiltrations of
opic pulmonary oedema, cytosis complexes in wall of blood mononuclear cells
features emphysema, 2. Lysis of vessels. particularly ofT-
constriction of erythrocytes/ 2. Deposition of immune Iymphocytes and
bronchioles. agglutination of complexes in glomeruli macrophages.
2. Oedema, erythrocytes. 3. Infiltration of 2. Congestion and oedema
congestion, 3. Increased number inflammatory cells such as 3. Lymphocytic infiltration
haemorrhage on skin of hemosiderin laden neutrophils, macrophages is more common around
cells in spleen. and Iymphocytes. the blood vessels
4. Lesions of 4. Lymphofollicular
glomerulonephritis, reaction.
polyarthritis.
128

AUTOIMMUNITY
In autoimmunity (auto=selt) the immune response
is generated against self antigens. It is an aberrant
reaction that serves no useful purpose in body.
Rather, the immunity developed against self
antigens destroys the tissues of body and causes
inflammation leading to death.
Etiology/Occurrence
• Hidden antigens e.g. spermatozoa.
• Alteration of antigens e.g. infections,
mutations, chemicals bind with normal body
proteins recognized as foreign (FIg. 11.12).
• Cross reaction between antigens of self and
foreign nature.
• Forbidden clones ofimmunocytes.
• Autoimmune hemolytic anemia (Fig. 11.4).
• Anti-glomerular basement membrane (GBM)
nephritis.
• Lymphocytic thyroditis.
• Lupus erythematosus- antinuclear antibodies.
• Hemolytic anemia.
• Leukopenia.
• Presence of antinuclear antibodies.
• Infiltration of lymphocytes/ macrophages
(Lymphocytic thryroditis).
• In anti-GBM nephritis, there is immune
complex mediated glomerulonephritis.
IMMUNODEFICIENCY
The alterations in immune system, which decrease
the effectiveness or destroy the capabilities of the
system to respond to various antigens are
designated as immunodeficiency. This precarious
situation may be attributed to poorly developed
immunocompetence or depressed immunity as a
result of genetic and environmental factors.
Immunodeficiences are thus classified as
congenital or primary and acquired or secondary.
Congenital immunodeficiency
In this type of immunodeficiency, the defect in
immunity is genetically determined and is present
in animals since their birth.
EtiologyIOccurrence
• Defect in basic cellular components e.g. stem
cells.
• Defective genes.
• Defect in enzymes.
• Defective expression ofcell components.
Types
Combined immunodeficiency syndrome (CIS)
• Absence ofstem cells of immunocytes.
• Agammaglobulinemia.
• Absence of T and B cells in blood, leucopenia.
• Occurs due to autosomal recessive gene.
• Aplasia or hypoplasia of thymus, lymphnodes,
spleen.
Defects in T-lymphocytes
• Thymic hypoplasia.
• B-cells are normal and adequate amount of
immunoglobulins present in blood.
• Absence of T-dependent regions in
lymphnodes.
• In Danish cattle, exanthema, alopecia,
parakeratosis occurs due to T-cell defect with
A- 46 lethal trait gene.
Defects in B-lymphocytes
• In equines - equine agammaglobulinemia
• Normal T-cell count, absence of B-cells,
absence of all classes of immunoglobulins.
• 'X' linked defects in gene occurs in males.
• Absence of primary lymphoid follicles in
germinal centres in spleen and lymphnodes.
• Selective IgA, IgM and IgG deficiency may
also occur.
• Transient hypogammaglobulinemia in new
born calves.
Partial T and B cell defects
• Partial presence ofT and B lymphocytes.
• Recurrent infections, eczema, purpura.

• Due to 'X' chromosome-linked genetic defect.
• Poor platelet aggregation.
Deficiency ofcomplement
• Rare, associated with abnormal regulation of
immune responses leading to autoimmunity.
• Complement component Cl C2 and C3 are
deficient and deficiency is associated with
systemic lupus erythematosus, polyarteritis
nodosa, glomerulonephritis, rheumatoid
arthritis.
• C5• C6, C7 and Cg deficiency leads to recurrent
infections.
• Absence or deficiency of C3 makes animal
susceptible to bacterial infections due to lack
ofopsonization, chemotaxis and phagocytosis.
Defects in phagocytosis
• Neutropenia, leucopenia.
• Defects in neutrophils, macrophages, platelets,
melanocytes and eosinophils.
• Defective chemotaxis, phagocytosis and
bactericidal activity.
• Persistent bacterial infections, pyogenic
infections.
• Associated with autosomal recessive gene
defect and is also known as "Chediak Higashi
syndrome".
ACQUIRED OR SECONDARY
IMMUNODEFICIENCY
An animal can acquire the suppression of immune
system due to drugs, diseases, deficiency of
nutrition, neoplasm or environmental pollution.
This is clinically manifested by increased
susceptibility to infections, vaccination failures,
recurrent infections and occurrence of new diseases
and neoplasms.
Drugs
• Corticosteroids, azathioprines, alkalating
agents, cyclophosphamide, cyclosporin A,
antibiotics.
• Azathioprines used to suppress graft rejection
• Cyclophosphamides and chlorambucil affect
the DNA reduplication of T- and B-
lymphocytes leading to immunosuppression
with no affect on macrophages.
• Cyclosporin A depresses CMI responses.
• Aspirin decreases phagocytosis and
lymphocyte functions.
• Antibiotics like gentamicin, chloramphenicol,
cephalosporin etc. cause decrease in immunity.
Infections
• Bovine herpes virus-l (BHV-1) decreases
CD/ and CDg+ cells in blood.
• Equine herpes virus (EHV-1) causes reduction
in T-cell functions.
130
• Marek's disease virus acts as lymphocytolytic
agent in lymphoid follicles of spleen, bursa
and thymus.
• Bovine viral diarrhoea virus reduces CD4+ and
CDg+ T-lymphocytes, B-Iymphocytes,
neutrophils and IL- 2 in cattle.
• Respiratory syncytial virus inhibits
lymphoproliferative responses in sheep and
cattle leading to increased susceptibility to
Pasteurella multocida infection.
• Blue tongue virus infects CD4+ and CDg+
lymphocytes and causes their destruction.
• Canine parvovirus causes depletion of
lymphoid cells. Canine distemper virus
activates the T-suppresser cells (Ts cells)
leading to suppression ofimmunity.
• Infectious bursal disease virus selectively
affects B- lymphocytes leading to increased
susceptibility ofbirds.
• Infectious laryngotracheitis virus infects
macrophages and causes their destruction.

Fig. 11.13. Photograph showing atrophy oflymphoid
organs due to A. Pesticide and B. heavy metals in
birds
Fig 11.14. Photomicrograph ofbursa showing
depletion oflymphoid tissue
• Feline leukemia virus causes lymphoid
depletion, glomerulonephritis, defects in
macrophages and complement.
• Feline immunodeficiency virus causes
neutropenia, lymphopenia and inhibits the T-
and B- cells' co-operation.
• Bovine immunodeficiency virus replicates in
macrophages and CD/ lymphocytes leading to
their destruction and immunosuppression. It
also causes lymphadenopathy,
lymphocytolysis, reduction in lymphokine
production.
131
Fig. 11.15. Photomicrograph ofthymus showing
depletion oflymphoid tissue
FIg. 11.16. PhotomIcrograph ofspleen showing
depletion oflymphoid t,ssue
Trauma/surgery
• Trauma or surgical interventions reduce
specific immune responses and functional
capacity ofphagocytic cells.
• Such defects are transient and may reverse
after healing oftrauma! surgery.
• Surgical operation/trauma increases the
number ofT- suppressor cells (Ts cells), which
in turn depresses the immunity.
Environmental pollution (Fig. 11.13 to 11.16)
• Pesticides used in agriculture, animal
husbandry and public health operations remain
in ecosystem and food items for longer period
and enter in body of animals and man through
food, air, water and affect the immune system

leading to its depression and increased
susceptibility to infections.
• Heavy metals are common contaminants of
pesticides, fertilizers and are inadvertently
accumulated in soil, plant, water, which enters
directly or indirectly in the animal's body.
These heavy metals (lead, mercury, cadmium)
may exert their immunotoxic effects leading to
immunosuppression.
• Mycotoxins such as aflatoxin, ochratoxin,
zearalenone etc. also affect the immune system
of animals leading to its suppression resulting
increased susceptibility to infectious diseases.
MODEL QUESTIONS
1. Due to presence of natural resistance in body ....................., ........ ..... ... and
·.... " ........... are resistant to canine distemper virus infection.
2. Adjuvants such as ..................,......................, ..................., and ................. are
absorbed slowly in body and thereby .................. the production ofantibodies.
3. IgM antibodies constitute.................... per cent of total serum immunoglobulins with mw
of about ................... KD and are made up of .............. molecules joined with ............;
this antibody is produced during .............. immune response ofbody.
4. Immunoglobulin D (IgD) is .................... in most ofthe domestic animals.
5. Dendritic cells have ...... ....... ...... filamentous cytoplasmic processes known as
·.... " ......... and ..................nuclei with clear cytoplasm containing....................
6. A counterpart of T-helper cells is ............... cells, which ............... the immune response.
7. AT-cells require .................. peptide- MHC class 11 molecules to trigger an immune
response.
8. In secondary immune response, the main immunoglobulin is .................. while in primary
response it is ...................
9. Immunopathology is defined as ......... in immunity and characterized by ......, ......or
10. Acquired immunodeficiency is characterized by..... '," ... of immune system due to ...........,
·.........., ..........., ........... and/or ........... which is clinically manifested by ...........,
..........., .................., ........... and ...........
11. Deficiency of complement component Ct. C2 and C3 may lead to........, ........, ........ and
........... while absence ofC3 results in lack of ........, ..........., and ........ ..
12. Bovine immunodeficiency virus replicates in ........... and ..........., cells leading to their
........... and ........... which also causes ..........., ........... and ...........
13. Surgical operation may increase the number of ....................... cells.
14. Infectious laryngotracheitis virus causes destruction of ..................
15. Pesticides include ..........., .............., ........... and ...........; residues of which cause
........... in animals leading to ..........., ........... and ...........
1. ......Chickens are resistant to anthrax.
2. ......Feline panleucopenia virus causes decrease in all cell types ofleucocytes in dogs.
3. ..... .Indian cow (Bos indicus) is quite susceptible to piroplasmosis.
132

Q.3.
Q.4.
4. ......Haptens are low molecular weight substances, which are not able to induce immune
response.
5. ..... .IgM is the main antibody found in serum.
6. ..... .IgA antibodies are mostly present on mucosal surfaces secreted in the form ofdimmer.
7. ......lgE is hlso known as reagin.
8. ......Precipitins are those antibodies which precipitate the antigen and thereby enhances the
activity ofantigen.
9. ......Dendritic cells are more efficient in antigen processing in comparison to macrophages.
10. ......The latent period in antibody production on antigen exposure is 8 days.
1l. ......Cyclosporin - A depresses humoral immunity.
12. ......Cyclophosphamide has no effect on phagocytosis by macrophages.
13. ......RSV infection makes animals more resistant to pasteurellosis.
14.......Acquired immunodeficiency occurs in animals due to pesticides.
15.......Feline immunodeficiency virus selectively affects only T-cells.
16.......Trauma reduces activity ofT-suppressor cells.
17. ......Blue tongue virus causes destruction ofCD 4+ and CD 8+ cells.
18...... .Infectious bursal disease virus activates T-suppressor cells to cause immunosuppression.
19.......Pesticides are also responsible to cause immune complex mediated glomerulonephritis.
20.......Cadmium is immunotoxic and nephrotoxic.
Define the following
1. Natural killer cells
2. Antibodies
3. Antigen
4. Adjuvant
5. Haptens
6. Secretory antibody
7. J-chain
8. Agglutinin
9. Precipitin
10. Opsonins
Write short notes on the foliowings.
1. Paraspecific immunity.
11. Antigen presenting cells
12. Dendritic cells
13. T-helper cells
14. T-suppressor cells
15. T-cytotoxic cells
16. Hypersensitivity
17. Autoimmunity
18. Immunosuppression
19. Chediak Higashi syndrome
20. Immunotoxicity
6. Autoimmunity.
2. Immune complex mediated glomerulonephritis. 7. Anaphylaxis.
3. Infections causing immunodeficiency in animals. 8. Humoral immunity.
4. Immunoglobulins. 9. Cell mediated immunity.
5. Immune response. 10. Drugs induced immunosuppression.
Q. 5. Select appropriate word(s) from thefour options given with each statement to answer.
1. This animal is not resistant to feline panleucopoenia virus infections.
(a) Dog (b) Cattle (c) Cat (d) Pig
2. Natural or paraspecific immunity does not include ................. .
(a) Tears (b) NK cells (c) Cytokines (d) Sensitized Tc cells
3. A foreign material capable ofinducing the production ofantibodies in animal is known as ......
(a) Agglutinin (b) Antigen (c) Antipyretic (d) Antidote
l33

4. Antibodies are chemically ..................... in nature.
(a) Lipopolysaccharide (b) Lipid (c) Glycoprotein (d) Protein
5. Which of the following is not an adjuvant.
(a) Oil (b) Wax (c) Alum (d) Glucose
6. Serum contains mainly this antibody..............
W~ ~~ W~ ~~
7. IgD is found abundantly in ..........................
(a) Cow (b) Rat (c) Sheep (d) Horse
8. IgE is found in very low concentration in serum which has the property to bind with receptors
present on ..............cells.
(a) Neutrophils (b) Eosinophils (c) T-Iymphocytes (d) Mast cells
9. IgD in not found in serum due to lysis by ..............during clotting
(a) Bacteria (b) Proteaes (c) Endonucleases (d) Peroxidases
10. Processing of antigen by macrophages is comparatively less efficient due to lysis of antigen by
(a) Proteases (b) Peroxidases (c) Endonucleases (d) Lipases
11. There is a latent period in antibody production on exposure to any antigen which is ..............
(a) 6 days (b) 20 days (c) 25 days (d) 4 weeks
12. The peak antibody titres are found at ..............
(a) 2 days (b) 20 days (c) 2 weeks (d) 4 weeks
13. The exogenous antigen is processed in dendritic cells/macrophages and along with
..............molecule it is presented to Th cells.
(a) MHC class la (b) MHC class 11 (c) MHC class III (d) MHC class Ib
14. T-cytotoxic cells recognize ..............specifically to destroys them
(a) Bacteria (b) Virus (c) Antigen containing cells (d) Fungi
15. Anaphylaxis is also known as ..............hypersensitivity
(a) Type I (b) Type 11 (c) Type III (d) Type IV
16. Equine infectious anemia virus may cause ..............hypersensitivity
(a) Type I (b) Type 11 (c) Type III (d) Type IV
17. Reagin type ofantibody is ......
W~ ~~ W~ ~~
18. DTH reaction is mediated by ........ .
(a) IgA (b) IgG (c) IgM (d) Sensitised T-cells
19. Combined immunodeficiency syndrome occurs as a result of absence of .. '........ .
(a) Stem cells (b) B-cells (c) T-cells (d) Macrophages
20. Autoimmunity developes in body when immune mechanisms are directed towards
................ antigens.
(a) Self (b) Foreign (c) Protein (d) Bacterial
21. In respiratory mucosa secretions, this antibody is mainly found.......'.........
W~ ~~ W~ ~~
22. Corticosteroids bind with receptors present on .........cells leading to decrease in antibody
production.
(a) T- helper (b) Macrophages (c) B-cells (d) T-suppressor
23. Canine distemper virus activates the ..............cells.
(a) T-helper cells (b) T-suppressor cells (c) B-cells (d) Macrophages
134

24. Surgery may enhance the activity of .............cells and therefore modulate the immune
response.
(a) T- helper cells (b) T-suppressor cells (c) T- cytotoxic cells (d) Macrophages
25. Pesticides are common contaminants ofenvironment and may induce .......... in animals.
(a) Immunosuppression (b) Autoimmunity (c) Hypersensitivity (d)All ofthe above
26. Lead, mercury and cadmium are ............ leading to immunosuppression.
(a) Immunotoxic (b) Nephrotoxic (c) Hepatotoxic (d) Neurotoxic
27. Aflatoxin may cause ......................in animals.
(a) Immunopotentiation (b) Immunosuppression
(c) Activation of macrophages (d) Reduction ofcomplement
28. Aspirin decreases ..........
(a) Antibody production (b) Phagocytosis (c) All ofthe above (d) None ofthe above
29. Bovine viral diarrhoea virus reduces..........................
(a) T-suppressor cells (b) IL-l (c) IL-2 (d) Interferon
30. Equine herpes virus (EHV-l) causes reduction in ..... .
(a) B-cell (b) T-cells (c) Macrophages (d) NK cells
135

12
PATHOLOGY OF
CUTANEOUS SYSTEM
• Developmental anomalies
• Acanthosis nigricans
• Dermatitis
• Vesicular dermatitis
• Parasitic dermatitis
• Allergic dermatitis
• Gangrenous dermatitis
• Equine cutaneous granuloma
• Miscellaneous lesions of skin
• Model Questions

Systemic Pathology
DEVELOPMENTAL ANOMALIES
Congenital icthyosis
Congenital icthyosis is scaly epidermis which
resembles the skin of fish and occurs due to a
simple autosomal recessive homozygous gene in
calves. This condition is characterized by scaly,
homy, thick epidermis divided into plates by deep
fissures. Microscopically, there is thick keratin
layer over the epidermis.
Epitheliogenesis imperfecta
Epitheliogenesis imperfecta is a congenital defect
characterized by discontinuity of epithelium on
skin leaving patches without squamous epithelium
mostly at feet, claws and oral mucosa. Such defect
may occur in calves which succumb to infection
after birth or such foetus may abort. This disease
condition is inherited as an autosomal recessive
trait.
Congenital alopecia
Alopecia or hairlessness on the skin with complete
lack of hair follicles has been observed in dog and
other animals. Such hairless sites may follow a
regular pattern or occurs in patches. This is a
hereditary defect recognized in certain breeds.
Congenital albinism
Albinism is absence of melanin pigmentation due
to deficiency of tyrosinase. This congenital
abnormality is encountered sporadically due to a
recessive trait in most species. The melanocytes are
present but there is lack of melanin synthesis due to
tyrosinase deficiency.
Congenital cutaneous asthenia
The collagen fibres are irregular in size and
orientation and become fragmented due to
disorganization of fibrils within the fibres. This
condition occurs due to a deficiency in procollagen
peptidase responsible for formation of collagen.
This condition leads to hyperelasticity and fragility
of skin and hypermotility of joints in cattle, sheep
and dogs.
138
ACANTHOSIS NIGRlCANS
This is increased amount of melanin in skin along
with hyperkeratosis. This condition commonly
occurs in dogs, at ventral abdomen and medial
surface oflegs.
Etiology
• Hormonal imbalance.
• Tumors of testicles and pituitary gland.
• Colour ofskin becomes black.
• Dry and scaly skin due to hyperkeratosis.
• Proliferation ofmelanocytes and melanoblasts.
• Blacklbrown colour pigment intracellular/
extracellular.
• Cells appear as black or brown globular mass.
• Melanin granules are minute, dirty brown in
colour and spherical in shape.
• Hyperkeratinization.
DERMATITIS
Dermatitis is the inflammation of skin
characterized by hyperemia, erythema, serus
exudation and infiltration of neutrophils and
mononuclear cells (Figs. 12.1 to 12.4).
Etiology
• Bacteria, viruses, chemicals, allergy, trauma,
fungi and their toxins.
• Erythematous patches on skin.
• Swelling of skin, itching sensation leads to
damage/scratch due to rubbing.
• Loss ofhairs, patches on skin, alopecia.
• Hyperemia.
• Serus exudate.
• Infilteration of neutrophils and mononuclear
cells.
• Presence of fungus in skin scrapings.

Pathology ofCutaneous System
Fig 12.1. ofa camel showing skin
patches offungal dennatltls
Fig 12.2.Photomlcrograph ofskin scraping showing
presence offungus (Ttrichophyton metagraphite)
FIg 12.3. Photomicrograph ofskm scrapillg showlllg
presence offungus (Trichophyton verzcosum)
Fig 12.4. Photograph ofa calfshowillg
ringworm onface
139
Fig 12.5. Photograph showing vesicle on teat.
Fig 12 6. Photograph showmg vesicles on
skm (ARS/USDA)
FIg 12 7. PhotomIcrograph showmg hydropic
degelleratuJ/l llnd vesicle formation (v)
(ARS/USDA)
FIg 128. Diagram ofvesicle m skin

Systemic Pathology
VESICULAR DERMATITIS
Vesicular dermatitis is excessive accumulation of
clear fluid in dermis and epidermis leading to
vesiclelblister formation. It is also known as
hydropic dermatitis (Figs. 12.5 to 12.8).
Etiology
• Sunburn.
• Heat.
• Foot and Mouth Disease virus.
• Pox virus.
• Oedematous fluid in dermis and epidermis
resulting in thickening ofskin.
• Hyperemia, vesicles.
• Break of vesicles leads to clear fluid discharge.
• Hyperemia.
• Accumulation of clear fluid in epidermis and
dermis, which is characterized by clear spaces
or takes light pink stain ofeosin.
• Some cells show hydropic degeneration.
• Infiltration ofleucocytes.
PARASITIC DERMATITIS (ACARIASIS)
Acariasis or mange is caused by mites and is
characterized by hyperkeratosis and inflammation
of skin leading to itching, rubbing and scratching
(Figs. 12.9 to 12.l8).
Etiology
• Mites
a Sarcoptes scabei
a Psoroptic sp.
a Demodectic sp.
a Chorioptic sp.
• Hyperkeratosis of skin, dry and scaly
appearance ofskin.
• Haemorrhage/trauma due to rubbing!
scratching as a result of intense itching.
• Absence of hairs on lesions.
• Hyperkeratinization ofskin.
• Hyperemia
• Infilteration of neutrophils, lymphocytes,
macrophages, eosionophils
• Presence ofmites at the site oflesions
ALLERGIC DERMATITIS
This is the inflammation of skin sensitized to
certain substances, known as allergens. Such
inflammation can be seen as a result of delayed
type hypersensitivity (DTH) reaction.
140
Etiology
• Chemicals (DNCBIDNFB) (Figs. 12.l9 &
12.20).
• Tuberculin reaction (Figs. 12.21 & 12.22).
• Allergic reaction.
• Soaps, detergents, organic chemicals.
• Parasites- fleas.
• Hyperemia, erythema
• Oedematous/nodular swelling, hard to touch.
• Hot, painful.
• Atopy with vesicular rash, pruritus, serus
exudate.
• Infilteration of eosinophils and mononuclear
cells, macrophages, lymphocytes.
• Hyperemia, oedema, necrosis.
GANGRENOUS DERMATITIS
Gangrenous dermatitis is the inflammation of skin
along with formation of gangrene caused by fungal
toxins and characterized by sloughing of skin, dry
gangrene with break in epidermis.
Etiology
• Fusarium sp. toxins
• Rice straw feeding - Degnala disease.
• Presence ofgangrenous inflammation on
extremities such as legs, udder, ears, tail,
scrotum (Figs. 12.23 to 12.25).

FIg 12.9. Photomicrograph ofSarcoptes scabei
Fig 12.10. Photograph showing mange due to
S. scabei in a camel
Fig 12.11. Photograph ofcamel showmg
orchitIs due to mange
FIg 12.12. Photograph ofa dog showmg
pustular dermatitis due to demodectic mange
141
Fig 12 13. Photograph ofdog showing
demodectic mange
Fig 12.14. Photograph showing pustular dermatitis
due to demodectic mange (ARS/USDA).
Fig 12.15. Photograph ofcow showing
demodecttc mange (ARSIVSDA).
Fig 12.16. Photomicrograph showing
demodectic mites in cyst (ARS/USDA).

Fig 12.17. Photograph ofhorse showing
chorioptic mange
Fig 12.18. Photograph ofhorse showing
chorioptic mange
Fig 12.19. Photograph ofsheep showing
DTH reaction
FIg 12.20. Photomicrograph showmg
DTH reaction in skm
Systemic Pathology
142
Fig. 12.22. Photomicrograph oftuberculOId
dermatitis (ARSIUSDA)
Fig.12.23. Photograph showing dry gangrene on
scrotum ofa buffalo bull due to jusariotoxicosis
Fig.12.24. Photograph showing sloughing of
hoofs m buffalo due to jusariotoxicosis

Pathology of Cutaneous System
Fig. 12.25. Photograph showing sloughing of skm
from udder due to jusariotoxlcosls
Fig.12.26. Photograph showing papule on beak and
around eyes
Fig.12.27. Photograph showing presence of
scab and scar on skin ofcamel.
Fig.12.2B. Photomicrograph ofskin showing
AcanthosIs
143
Fig 12.29 Photomicrograph ofskin showing erosion
Fig.12.30. Diagram ofabscess
Fig.12.31. Photomicrogruph ofulcer
Fig.12.32. Dtagram ofulcer

Systemic Pathology
• Sloughing ofskin leaving raw surface.
• Sloughing ofhoofs with haemorrhage.
• Inflammation ofskin and invasion by
saprophytes causing dissolution ofcells/tissue.
• Infiltration of mononuclear cells at the
periphery of the lesion.
EQUINE CUTANEOUS GRANULOMA
There is development of chronic, ulcerated and
bloody granuloma on limb of horses due to wire
cuts or other cutaneous injury.
Etiology
• Skin cuts/injury.
• Habronemiasis.
• Phycomycosis.
o Hyphomyces destruens
o Entomorphthora coronata
• Granulation oftissue in wound.
• Presence ofyellowish/white specks.
• Summer soreslBursatti.
• Tissue composed of newly formed fibrous
tissue, with large number of capillaries,
infiltration ofeosinophils.
• Presence of necrotic masses, stains deep red
withH&E.
• Presence of helminths in section - cutaneous
habronemiasis.
• Presence ofseptate hyphae offungus.
MISCELLANEOUS LESIONS OF SKIN
Papule: Focal hyperplasia of stratum spinosum
epithelium leading to hard nodular eruption on skin
(Fig. 12.26).
Vesicle: A cavity in epidermis containing fluid and
covered by a thin layer of epidermis elevated from
the surface (Figs. 12.6 & 12.7).
144
Pustule: A vesicle filled with pus (Fig. 12.14).
Acanthosis: Thickening of epidermis due to
hyperplasia of stratum spinosumlprickle cell layer
(Fig. 12.28).
Hyperkeratosis: Thickening of keratin layer
stratum corneum.
Parakeratosis: The retention of nucleus in keratin
layer.
Bullalbleb: Cavitations in epidermis filled with
fluid and larger than vesicle.
ErosionlExcoriation: Superficial loss of
epithelium (Fig. 12.29).
Fissure: Linear defect in epidermis, which may be
crusted at mucocutaneous junctions.
Abscess: A circumscribed cavity filled with pus
(Fig. 12.30).
Ulcer: A break in the continuity of the epidermis
exposing dermis (Fig. 12.31 & 12.32).
Urticaria: A circumscribed area of swelling!
oedema involving dermis.
Folliculitis: Inflammation ofhair follicles.
Acne: Enlargement of sealed off hair follicles or
sebaceous glands and rupture through the
epidermis. It leaves a rounded hole in the epidermis
and a canal down to the dermis.
Eczema: Eczema is a form ofallergic dermatitis of
obscure etiology and characterized by erythema,
vesicular rash, serus exudate and pruritus.

MODEL QUESTIONS
Q. 1. Fill in the blanks with appropriate word(s).
1. ............ is a cavity in epidermis containing fluid and covered by a thin layer of ...... elevated
from the surface. If it is filled with pus, then it is known as....... ,...... .
2. Superficial loss of epithelium in skin is known as ....... ,.... or ...... ...... while thediscontinuity ofepidermis is termed as .............
3. In congenital icthyosis, the skin looks like ............ as offish.
4. Congenital discontinuity ofepithelium of skin leaving patches without squamous epithelium isknown as .............
5. Acanthosis nigricans is increased amount of............caused by............or tumors of
.........and.............
1. ......Urticaria is a circumscribed area ofswelling in dermis.
2. ......Ulcer is filled with fluid in epidermis.
3. ......Parakeratosis is thickening ofkeratin layer.
4. ......Bulla is a large cavity in epidermis filled with fluid.
5. ......Albinism is absence ofmelanin in skin.
6. ......Cutaneous asthenia occurs due to deficiency ofprocollagen peptidase.
7. ......Proliferation ofmelanocytes occurs in Acanthosis nigricans.
8. ......Sunlight may cause dermatitis.
9. ......Mange is caused by mites in animals.
10.......Phycomycosis may lead to cutaneous granuloma in horses.
Q. 3. Define thefollowing.
1. Scaly skin
2. Alopecia
3. Dermatitis
4. Papule
5. Pustule
1. Epitheliogenesis imperfecta.
2. Acanthosis nigricans.
3. Allergic dermatitis.
4. Equine cutaneous granuloma.
5. Eczema.
6. Bleb
7. Parakeratosis
8. Erosion
9. Abscess
10. Urticaria
Q. 5. Select an appropriate word(s) from thefour options given with each question.
1. In congenital icthyosis, the skin ofcalves resembles the skin of ........... .
(a) Toad (b) Fish (c)Tortoise (d) Zebra
2. Acanthosis is ............ ofskin epithelium.
(a) Hypoplasia (b) Aplasia (c) Hyperplasia (d) Anaplasia
3. Vesicle formation occurs in skin as a result of .............,
(a) Cloudy swelling (b) Hydropic degeneration (c) Glycogen storage (d) Fatty change
145

Systemic Pathology
4. Acariasis is caused by ........
(a) Bacteria (b) Virus (c) Chlamydia (d) Mite
5. Enlargement of sealed offhair follicle or sebaceous gland is known as .......
(a) Acne (b) Folliculitis (c) Fissure (d) Bleb
6. A break in the continuity of the epidermis exposing dermis is known as .......
(a) Erosion (b) Ulcer (c) Fissure (d) Vesicle
7. Hyperkeratosis is the thickening of ....................
(a) Prickle cell layer (b) Stratum lucidum (c) Stratum corneum (d) Dermis
8. Superficial loss of epithelium on skin or mucous membrane is known as ........ .
(a) Erosion (b) Abrasion (c) Ulcer (d) Fissure
9. Papule is hyperplasia of .......... Epithelium.
(a) Stratum corneum (b) Stratum lucidum (c) Stratum spinosum (d) Dermis
10. Retention of nucleus in keratin layer of skin is known as ........ .
(a) Hyperkeratosis (b) Parakeratosis (c) Urticaria (d) Acanthosis
146

•
•
•
•
13
PATHOLOGY OF
MUSCULOSKELETAL
SYSTEM
Pathology of muscles
• Equine rhabdomyolysis
• White muscle disease
• Acute myositis
• Haemorrhagic myositis
• Chronic myositis
Pathology of Bones
• Fibrous osteodystrophy
• Rickets
• Osteomalacia
• Osteoporosis
• Osteopetrosis
• Osteomyelitis
• Bone fracture and repair
• Pulmonary osteoarthropathy
• Spondylitis
Pathology ofjoints
• Arthritis
Model Questions

Systemic Pathology
PATHOLOGY OF MUSCLES
EQUINE RHABDOMYOLYSIS
It is also known as Azoturia or Monday Morning
Disease. The disease occurs in well fed horse after
a spell of inactivity. Suddenly after walking a few
steps, the horse is unable to move further and feels
pain with intense sweating and hardening of
muscles.
Etiology
• Accumulation oflactic acid in muscles.
• High glycogen storage.
• Lack ofoxygen supply.
• Hardening of muscle just like wood.
• Urine is dark brown with myoglobin -
myoglobinuria.
• Tonic spasms in muscles.
• Atrophy ofaffected muscles in chronic cases.
• Necrosis of muscle fibres
• Oedema.
• Hyaline degeneration (Fig. 13.1).
• Invasion of sarcolemma by macrophages and
lymphocytes.
• Degeneration and necrosis of tubular
epithelium in kidneys.
WHITE MUSCLE DISEASE
Extensive coagulative necrosis of muscles is
observed in calves possibly due to deficiency of
vitamin E during 6 months of age (Fig. 13.2).
Etiology
• Vitamin E deficiency.
• Selenium deficiency.
• Stress.
• Colour of muscle becomes pale pink,
yellowish red, grey or white (Fig. 13.3).
• Muscle becomes dry, inelastic and firm.
• Urine is brown/red or chocolate brown in
colour because ofmyoglobin.
148
• Coagulative necrosis of muscles.
• In some muscle cells, cloudy swelling can be
observed.
• Neutrophils, macrophages, lymphocytes and
eosinophils may be present.
• Calcium may be deposited in necrosed areas.
ACUTE MYOSITIS
Acute myositis is the acute inflammation of
skeletal muscles characterized by the presence of
serous, fibrinous or haemorrhagic exudate (Figs.
13.4 & 13.5).
Etiology
• Trauma.
• Vitamin E/Selenium deficiency.
• Clostridium chauvei, the cause of black leg in
cattle.
• Muscles become extremely moist.
• Colour becomes red, consistency is firm and
tense.
• Swelling and accumulation of gas in muscles,
crepitating sound on palpation.
• Muscle dark red/ black with gas mixed exudate
(Figs. 13.6 & 13.7) (gangrenous myositis).
• Presence of serous, fibrinous and/or
haemorrhagic exudate.
• Infiltration of neutrophils, macrophages,
lymphocytes, etc.
• Degenerative and necrotic changes in muscles.
• Presence ofGram positive rods in exudate.
HAEMORRHAGIC MYOSITIS
Haemorrhagic myositis is characterized by the
presence of large amount of blood and
inflammation in muscles. It may occur due to
trauma and muscle rupture (Fig. 13.8).
Etiology
• Trauma.
• Clostridial infections.

Pathology ofMusculoskeletal System
Fig. 13. 1. Photomicrograph showlIlg hyaline
degeneratlon in muscle
Fig.13.2. Photograph ofwhue muscle
disease (ARS/USDA)
Fig.13.3. Photograph showing muscular
distrophy
Fig.J3.4. Photomicrograph showing acute
myositis
149
Fig. 13.5. Photomicrograph showing acute
myositl.1 due to clostridia
Fig. 13.6. Photograph showing
gangrenous myc ,itis In poultry
Fig. 13. 7. Photograph showing
gangrenous myositis in heifer
Fig 13.8. Photograph showing
haemorrhagic myositis

Systemic Pathology
• Area becomes red/cyanotic.
• On cut, large amount of blood comes out from
muscles.
• The affected area is hard and painful to touch.
• Regional lymphnodes may become enlarged
and swollen.
• Extravasation of blood in between the
myofibrils.
• Infiltration of neutrophils, macrophages and
lymphocytes in connective tissue between the
muscle cells.
CHRONIC MYOSITIS
Chronic inflammation ofmuscle is characterized by
necrosis, calcification and proliferation of fibrous
connective tissue. In case of tuberculosis and
pseudotuberculosis, there are multiple focal
nodules containing caseation and fibrous capsule.
Etiology
• Mycobacterium tuberculosis.
• Corynebacterium pseudotuberculosis.
• Trichinella spp. infection.
• Sarcosporidia spp. infection.
• Muscles become hard to touch.
• Nodules can be seen (Fig. 13.9).
• On cut the lesions of caseation and
calcification observed.
• Caseative necrosis, infiltration of
macrophages, lymphocytes and proliferation of
fibrous tissue.
• Calcification can also be observed.
• In cases of pseudotuberculosis infiltration of
neutrophils is seen.
• Extensive infiltration of eosinophils in
sarcoporidia infection.
150
PATHOLOGY OF BONES
FIBROUS OSTEODYSTROPHY
Fibrous osteodystrophy occurs as excessive action
ofparathyroid hormone on bones and characterized
by bone resorption with replacement by fibrous
tissue, increased osteoid formation which does not
get sufficient minerals for deposition and formation
ofcysts.
Etiology
• Hyperparathyroidism
• Dietary deficiency of calcium or excess of
phosphorus
• Vitamin-D deficiency
• Excessive bran feeding (Disease in horses of
flour millers).
• Lack ofcalcification in bone
• Resorption ofcalcium from bone, fibrosis
• Bone becomes shoft, flexible and deformed
• Rubbery jaw due to involvement of facial
bones
• Fibrous tissue hyperplasia in bones.
• Enlargement ofHaversian canals.
• Boney tissue is replaced by fibroblasts, with
osteoclastic giant cells lining the remaining
bone tissue.
RICKETS
Rickets is failure of adequate deposition of calcium
in bones of growing animals caused by deficiency
of calcium and vitamin D and is characterized by
bending of limbs, enlargement of ends of long
bones and skeletal deformities (Fig. 13.10).
Etiology
• Vitamin D deficiency.
• Calcium deficiency.
• Deficiency ofphosphorus.
• Bending of legs, bow legs.
• Pot belly.

Flg.J3.9. Photograph showing chromc myosl/ls
(ARSIUSDA)
Fig.13. 12. Photograph showing fracture
151
Flg.J3.13. Photomicrograph offracture healmg
Fig.J3.14 Photograph showing
spondylztis(ARS/USDA)
Fig. 13./6. A. Photograph showing arthrztis B. Dzagram
showing Immune complex deposition in joint

Systemic Pathology
• Enlarged costochondral articulation.
• Softening ofbones.
• Increase in proliferating cartilage adjacent to
the area of ossification and its disorderly
arrangement.
• Disorderly penetration of cartilage by blood
vessels.
• Increased area ofuncalcified osteoid tissue
• Fibrosis ofmarrow.
OSTEOMALACIA
Osteomalacia is also known as adult rickets. It
occurs in bone of adults and is caused by
deficiency of vitamin D and calcium and
characterized by softening ofbones.
Etiology
• Vitamin D deficiency.
• Calcium-phosphorus ratio disturbance.
• Softening ofbones.
• Irregular diffuse thickening ofbones.
• Bone deformities.
• Increase in osteoid tissue with failure of
calcification.
• Increase in osteoclastic activity.
OSTEOPOROSIS
Osteoporosis is atrophy of bones caused by
possibly hormonal imbalance and is characterized
by inadequate deposition of calcium, brittleness of
bones due to its increased porosity.
Etiology
• Vitamin C deficiency.
• Copper deficiency.
• Inadequate calcium deposition.
152
• Bone becomes brittle and porous.
• Increased fragility ofbones.
• Widening ofHaversian canals.
• Increased activity ofosteoclasts.
• Decrease in zona compacta and thickness of
bone trabeculae.
OSTEOPETROSIS
Osteopetrosis is enlargement of bone caused by
fluorosis or avian leukosis virus and is
characterized by increase in bony tissue. It is also
known as marble bone disease.
Etiology
• Avian leukosis virus ofretroviridae family.
• Fluorosis.
• Enlargement of bone towards outside and
inside.
• Reduced marrow cavity.
• Bone becomes brittle, marbelling ofbones.
• Cartilage is also calcified, surrounded by
osteoid tissue.
OSTEOMYELITIS
Osteomyelitis is the inflammation of bone with
bone marrow caused by trauma and pyogenic
bacteria and is characterized by destruction,
replacement and excessive growth of new bone
adjacent to the infected part (Fig. 13.11).
Etiology
• Hematogenous infection.
• Direct infection through trauma/fracture.
• Actinomyces pyogenes, A. bovis.
• Staphylococcus aureus.
• Pseudomonas aeruginosa.
• Metastatic abscess in bone marrow.

• Excessive growth ofbone in adjacent area.
• Exostosis or endostosis.
• Infiltration of neutrophils.
• Proliferation ofosteoid tissue.
• Demonstration ofbacteria in pus.
BONE FRACTURE AND REPAIR
Fracture is the break in the continuity of bone due
to trauma. A fracture may be simple or compound
depending on the severity of trauma. Healing of
fracture occurs by reunion of the broken ends of
bone through development and proliferation of
fibroblasts, angioblasts, osteoid tissue and
infiltration ofcalcium salts (Figs. 13.12 & 13.13).
Etiology
• Trauma.
• Accidents - automobile accidents.
• Fracture can be identified by break in bones.
• Healing of fracture is characterized by
development of callus at the site of reunion of
break ends ofbone.
• Callus may be soft or hard.
• Proliferation of fibroblasts, angioblasts and
metaplasia of connective tissue to osteoid
tissue.
• Areas ofcalcification in osteoid tissue
PULMONARYOSTEOARTHROPATHY
Pulmonary osteoarthropathy is a rare disease of
dog, sheep, cat, horse, and lion caused by
prolonged anoxia and is characterized by cough,
dyspnea, respiratory disturbances and formation of
new bone leading to thickening and deformity of
limbs.
Etiology
• Prolonged anoxia.
• Toxaemia.
153
• Pneumonia.
• New bone formation due to hyperplasia just
beneath the periosteum in long bones.
• The proliferation ofbone is irregular leading to
development of rough surface on bone.
• Bone becomes enlarged twice to its normal
size.
• Heart worms were also seen in case ofdogs.
• Bronchogenic carcinoma.
• Granulomatous lesions oftuberculosis.
• Chronic bronchiectasis.
• Hyperplasia of osteoid tissue with no
indication of any kind of neoplastic growth in
bones.
SPONDYLITIS
Spondylitis is the inflammation of vertebrae caused
by bacteria/fungi and characterized by caseation,
intraosseous abscess formation granulomatous
lesions and fibrosis (Figs. 13.14 & 13.15).
Etiology
• Brucella abortus, Br. ovis, Br. melitensis.
• Actinomyces bovis.
• Coccidioidomyces sp.
• Intraosseous abscess.
• Granuloma encapsulated by fibrous tissue
involving one or two adjacent vertebrae.
• Local enlargement ofbone.
• Granulomatous lesions with caseation.
• Proliferation ofosteoid tissue.
• Infitration of neutrophils in intraosseous
abscess.
PATHOLOGY OF JOINTS
ARTHRITIS
Arthritis is the inflammation of joint caused by
bacteria, virus, chlamydia, mycoplasma and

Systemic Pathology
immune complexes and characterized by serus,
fibrinous, purulent or ankylosing lesions in joints.
• Difficulty in movement.
• In chronic cases fusion of two bony processes
leaving no joint (ankylosing).
Etiology
• Bacteria - E. coli, Erysipelas rhusiopathae,
Streptococus sp., Shigella sp. Corynebacterium
ovis, Brucella sp.
• Synovial fluid diminishes, becomes dirty, thick
in chronic illness.
• Mycoplasma Mycoplasma mycoides,
Mycoplasma sinoviae.
• Virus - Reovims (Tenosynovitis in birds).
• Antigen antibody complexes.
• Trauma.
• Swelling of joints with increase in synovial
fluid (Fig. 13.16).
• Presence of increased number of leucocytes in
synovial fluid.
• Serus, fibrinous or purulent exudate in joints.
• Thickening ofsynovial membrane.
• Presence of plasma cells and immune
complexes in synovial fluid.
MODEL QUESTIONS
1. Gas gangrene is produced by.................... in thigh muscles of heifer which is manifested by
........................sound on palpation due to accumulation of.................... and.....................
2. Equine rhabdomyolysis occurs in horses on.................... after a day's rest and is characterized
by....................,....................,.................... and.................... ofmuscles.
3. Osteomalacia is also known as.................... which is caused by deficiency of.................... and
disturbances in ratio of.................... and.................... characterized by.'" ..............'"
4. ....................,.................... and.................... may led to osteoporosis in animals characterized
by.................... ofbones.
5. Avian leucosis virus may cause........................ in birds characterized by........................ ofbone.
6. Osteomyelitis is inflammation of................... and.................. caused by ...................
and................... and cha:acterized by.................,................ and................. of new bone adjacent
to the infected part.
7. Healing fracture is characterized by the development of.................... at the site of reunion of
break ends ofbone.
8. Arthritis is inflammation of.................... characterized by.................... ofjoints.
Q. 2. Write true andfalse and correct the false statement.
1. ........In white muscle disease the colour of urine becomes redish brown due to presence of
hemoglobin.
2. ........Sarcosporidia causes eosinophilic myositis.
3. ........In rickets, the deficiency ofcalcium may lead to softening ofbones.
4. ........Osteopetrosis is enlargement ofbones.
5. ........Osteoporosis is atrophy ofbones.
6. ........Metastatic abscess are formed in bone marrow due to osteomyelitis.
7. ........Fracture is break in continuity ofbones due to trauma.
154

8. ........Prolonged anoxia may lead to pulmonary osteoarthropathy in dogs.
9. ........Spondylitis is the inflammation of intervertebral disc.
10. ........Rheumatoid arthritis is caused by reovirus infection.
Q. 3. Define thefollowing
1. Myoglobinurea
2. Millers disease
3. Osteitis
4. Osteomyelitis
5. Exostosis
Q.4. Write short notes on thefollowing
1. Azoturia
2. Osteoporosis
3. Gas gangrene
4. Rickets
5. Arthritis
6. Enostosis
7. Callous
8. Spondylitis
9. Tenosynovitis
10. Ankylosis
6. White muscle disease
7. Osteopetrosis
8. Fibrous osteodystrophy
9. Pulmonary osteoarthropathy
10. Fracture healing
1. Equine rhabdomyolysis is also known as ............. morning disease
(a) Sunday (b) Monday (c) Tuesday (d) Wednesday
2. Accumulation of ............. is responsible for hardening ofmuscles in azoturia.
(a) Lactic acid (b) Myoglobin (d) Hemoglobin (d) Glycogen
3. White muscle disease is caused by ............. deficiency.
(a) Vit-A (b) Vit- D (c) Vit-C (d) Vit-E
4. Rickets is caused by deficiency ofvitarnin.............. .
(a) A (b) D (c) C (d) E
5. Osteoporosis is caused by deficiency of .............
(a) Copper (b) Zinc (c) Iron (d) Calcium
6. Osteopetrosis is also known as .................. disease
(a) Brittle bone (b) Marble bone (c) Both a & b (d) None
7. Fibrous osteodystrophy is characterized by ................. condition.
(a) Lockjaw (b) Rubbery jaw (c) Bottle jaw (d) None
8. Osteomyelitis is inflammation of .............
(a) Bone (b) Bone marrow (c) Both a & b (d) None
9. Brucella sp may cause ............. in animals and man.
(a) Pulmonary osteoarthropathy (b) Spondylitis (c) Rickets (d) Osteopetrosis
10. Rheumatoid arthritis is caused by .............
(a) Antigen-antibody complex (b) E. coli (c) Reovirus (d) Brucella sp.
155

14
PATHOLOGY OF
CARDIOVASCULAR SYSTEM
• Cardiac failure
• Acute cardiac failure
• Chronic cardiac failure
• Pericarditis
• Myocarditis
• Endocarditis
• Brisket disease
• Mulberry heart disease
• Arteriosclerosis
• Atherosclerosis
• Medial sclerosis
• Arteriolosclerosis
• Arteritis
• Aneurysm
• Phlebitis
• Lymphangitis
• Model Questions

Pathology ofCardiovascular System
Persistent right aortic arch
This is a developmental anomaly of aorta in which
the aorta develops from right arch present on right
side of trachea and oesophagus. The ductus
arteriosus forms a ring around trachea and
oesophagus by connecting aorta and pulmonary
artery. This ring causes partial obstruction of
trachea and/or oesophagus.
Patent ductus arteriosus
The ductus arteriosus is a short blood vessel which
connects pulmonary artery to aorta in foetal life for
diversion of blood. Normally, soon after birth this
duct is sealed and remains in the form of a
ligamentum arteriosum. But sometimes this ductus
arteriosus remains open and blood is continuously
shunted between aorta and pulmonary artery, after
leading to congestive heart failure, pulmonary
hypertension and cyanosis due to mixing of venous
and arterial blood (Fig. 14.1).
Interventricular septal defects
In foetal life, there is no partition in ventricles and
there is only one chamber which is divided into two
- right and left - by inter-ventricular septum But
when interventricular septum does not develop
completely, or there is defect in formation of
complete partition, there is mixing of blood from
both chambers. It is responsible for thickening of
myocardium, roughening of endocardium and
cyanosis (Fig. 14.2).
Transposition of aorta
THis condition develops if there is a shift in
position of aorta and pulmonary artery i.e. the aorta
arises from right ventricle and pulmonary artery
from left ventricle. This results in arterial blood in
right and venous blood in left side and has no
clinical significance. However, it may create
problems when aorta arises from venous ventricle
and pulmonary artery from arterial side.
Tetrad of Fallot
Tetrad of Fallot includes four developmental
defects of cardiovascular system and is also known
as tetralogy ofFallot (Fig. 14.3).
157
1. Inter-ventricular septal defect.
2. Pulmonary stenosis is characterized by
narrowing of lumen of pulmonary artery at its
origin due to fibrous tissue causing 'jet' effect.
3. Hypertrophy ofright ventricle.
4. Transposition of aorta.
Ectopia cordis
When heart lies outside the thorax under the
subcutaneous tissue of lower cervical region.
Interatrial septal defect
There is a developmental defect in interatrial septa
which remains as incomplete partition of atrium. It
produces continuous overload on the right side of
heart leading to pulmonary hypertension and
hypertrophy of right side myocardium. However, a
small defect in septum may persist throughout the
life of animal without causing any clinical illness
(Fig. 14.4).
CARDIAC FAILURE
Cardiac failure is the inability of heart to maintain
adequate blood supply leading to death. It can be
divided into two types: Acute and chronic heart
failure.
Acute cardiac failure
Acute cardiac failure is sudden failure of
contraction of heart leading to death within
minutes.
Etiology
• Anoxia.
• Drugs/poisons.
• Shock.
• Cardiac temponade.
• Myocardial necrosis.
• Sudden occlusion of aorta and/or pulmonary
artery.
• Cardiac temponade.
• Occlusive thrombus.
• Pulmonary congestion.
• Dialation of heart particularly ofright ventricle

Systemic Pathology
Fig.14.1 Diagram ofheart showing developmental
anomaly patent ductus arteriosus
Fig.14.2. Diagram ofheart showing developmental
anomaly interventricular septal defect
anamalies tetralogy offallot
--
anomaly interatrial septal defect
158
Fig.14.5. Photomicrograph oflung showing lesions
ofheartfailure
Fig.14.6. Photograph ofheart showing necrotic
lesions due to Salmonella gallinarum in poultry.
Fig. 14.7.Diagram showing traumatic reticulo
pericarditis
Fig.14.8. Diagram showingfibrinous
pericarditis

• Myocardial necrosis.
• Centrilobular necrosis in liver "nut meg liver".
• In prolonged cases, congestion and oedema in
visceral organs.
Chronic Cardiac Failure
Chronic cardiac failure is the inability of heart to
maintain balance between its output and venous
return of blood. It can be further divided into two -
left and right sided heart failure.
Left Sided Heart Failure
Left sided heart failure is caused by myocardial
damage and is characterized by congestion and
oedema in lungs with hypertrophy of alveolar
lining cells (Fig. 14.5).
Etiology
• Myocardial degeneration! necrosis
• Aortic and mitral valve disease
• Hypertension
• Congestion and oedema in lungs.
• Chronic dialation of heart.
• Congestion ofalveolar vessels.
• Oedema in lungs.
• Hypertrophy of alveolar lining cells.
• Alveolar macrophages contain hemosiderin
pigment also called" heart failure cells".
Right Sided Heart Failure
Right sided heart failure is caused by a disease of
lungs or pulmonary vasculature and mostly occurs
after a left sided heart failure.
Etiology
• Left sided heart failure.
• Pulmonary lesions, congestion.
• Congestion of visceral organs.
159
• Subcutis oedema and ascites.
• Pulse in jugular vein.
• "Nutmeg appearance" in liver due to
centrilobular necrosis.
• Atrophy, necrosis and fibrosis in liver.
• Congestion in visceral organs.
PERICARDITIS
Pericarditis is the inflammation of pericardium, the
upper layer of heart. It may be serus, fibrinous or
suppurative depending on the type ofexudate.
Etiology/Occurrence
• Pasteurellosis.
• Salmonellosis in poultry (Fig. 14.6).
• Hydropericardium syndrome in poultry.
• Gout in poultry.
• Trauma/foreign body e.g. traumatic reticulo
pericarditis (TRP) (Fig. 14.7).
• Deposition of fibrin in between pericardium
and heart gives an appearance of "bread and
butter" (Fig. 14.8).
• In chronic cases, pericardium becomes thick
due to excessive fibrosis.
• Accumulation of fluid (clear, serus) in
pericardial sac is called Hydropericardium
(Figs. 14.9 & 14.10).
• Presence of blood in pericardial sac is known
as hemopericardium and the excessive
accumulation of blood leading to heart failure
is termed as cardiac temponade (Fig. 14.11).
• Accumulation of pus in pericardial sac is
known as pyopericardium.
• Presence of gas in pericardial sac in known as
pneumopericardium.
• Hyperemia and haemorrhage in pericardium.
• Deposition of fibrin, formation of fibrin
network, infiltration of neutrophils,
macrophages and lymphocytes.

Systemic Pathology
Fig.14.9. Photograph o/hydropericardium
in poultry
Fig. 14.10. Diagram showing hydropericardium
Fig.14.II. Diagram showing hemopericardium
(cardiac temponade)
Fig. 14.12. Photograph showing myocarditis
(ARSIUSDA)
160
Fig.14.J3. Photomicrograph showing myocarditis
Fig.14.14. Photograph showing endocarditis
(ARSIUSDA)
Fig. 14.15. Photomicrograph showing
eosinophilic endocarditis (ARSIUSDA)
R
A
Fig. 14.16. Diagram showing (A) valvular and
(B) mural vegetative endocarditis

MYOCARDITIS
Myocarditis is the inflammation of myocardium,
the middle layer of heart. It may be suppurative,
eosinophlic or lymphocytic depending on the type
of the exudate (Figs. 14.12 & 14.13).
Etiology
• Toxins/ Poisons.
• Bacteria / Virus.
• Parasites.
• Drugs / Chemicals.
• Colour of myocardium may become dark red
or cyanotic due to accumulation ofblood.
• In suppurative myocarditis, one can find
abscesses in myocardium from where yellow/
green pus oozes out.
• Yellowish white streaks of necrosis in
myocardium.
• Presence of cyst encapsulated by fibroplasia
due to cysticercosis.
• Hyperemia and haemorrhages in myocardium.
• Infiltration of neutrophils, eosinophils or
lymphocytes.
• Coagulative necrosis ofmuscle fibres.
• In chronic cases, proliferation of fibrous
connective tissue.
ENDOCARDITIS
Endocarditis is the inflammation of the
endocardium, the inner layer of heart (Figs. 14.14
to 14.19).
• Chronic septicernic diseases
Actinomyces pyogenes,
rhusiopathiae.
• Staphylococci.
• Streptococci.
• Clostridial infections.
like caused by
ErySipelothrix
161
• Lesions in heart valves or wall of atrium!
ventricles.
• Presence of thrombi on endocardium.
• Vegetative/cauliflower like growth on
endocardium either in valves (Valvular
vegetative endocarditis e.g. swine erysepalas)
or in wall (Mural vegetative endocarditis).
• Dilation ofheart chambers.
• Infiltration of thrombocytes, neutophils,
macrophages and lymphocytes.
• Masses ofbacterial organisms can be seen.
• Underlying endocardium and myocardium
shows the presence of fibrin network and
infiltration of RBC, neutrophils and
macrophages.
BRISKET DISEASEIHIGH ALTITUDE
DISEASE
Brisket disease is a condition of slow cardiac
failure, which occurs at 2500 metres above sea
level or higher where pressure of air is low (Fig.
14.20).
Etiology
• Low oxygen in environment.
• Decreased atmospheric pressure ofair.
• In native cattle morbidity rate is only 2% and
in imported cattle at hills it is upto 40%.
Macroscopic feature
• Dilation of heart.
• Hypertrophy of ventricular wall.
• Chronic passive congestion in visceral organs.
• Oedema in sternal region in between forelegs.
Microscopic feature
• Nutmeg liver due to chronic passive
congestion.
• Polycythemia.
• Hypertrophy ofmuscle fibres in myocardium.

Systemic Pathology
Fig.14.17 Photograph showing vegetative
endocarditis (ARSIUSDA)
Fig. 14 19 Photomicrograph showmg endocarditls
'I.
Fig.14.20. Diagram showing Brisket disease in cow
162
::;::::::::::=:=='';
t: -------1i
Flg.14.21. Diagram showing atherosclerosis
leadmg to obstruction o/vessel
Fig.14.22. Photomicrograph showing arteriosclerosis
Fig.14.23. Photograph showmg arterztis (L) Liver (K)
KIdney (ARSIUSDA)
Fig 14.24 Photomicrograph showing arteritis
(ARSIUSDA)

MULBERRY HEART DISEASE
It is characterized by fIrm contraction of heart and
petechial haemorrhage on pericardium giving the
appearance of mulberry.
Etiology
• Notknown
• May be enterotoxaemia/poisoning
• Contraction of heart with petechial
haemorrhage on pericardium looking like
mulberry "Mulbery heart disease"
• Hydropericardium, hydroperitoneum and
pulmonary oedema
• Oedema fluid has high protein content
resulting in clot formation
• Congestion of fundic portion ofstomach.
• Congestion on serosa of visceral organs.
ARTERIOSCLEROSIS
Arteriosclerosis is hardening of arteries causing 3
types of diseases in arteries depending on their size
and etiological factors viz., Atherosclerosis, medial
sclerosis and arteriolosclerosis.
ATHEROSCLEROSIS
Atherosclerosis is characterized by hardening and·
thickening of intimal layer of large arteries and
aorta due to proliferation of connective tissue,
hyaline degeneration, inmteration of fat! lipids and
calcifIcation. These intimal changes may lead to
loss of elasticity of artery (Athere means mushy
substance)(Fig. 14.21 & Fig. 14.22).
Etiology
• Exact cause is not clear
• Hypercholesterolemia and hyperlipidemia
• Hypertension
• Fatty streaks running parallel in the direction
ofthe artery.
163
• Intimal layer of aorta/ coronary arteries is
elevated due to plaques which are white/
yellow, fIbrous and occluding the lumen of
vessel.
• Occlusion of artery may lead to ischemia and
infarction.
• Macrophages are fIlled with lipid droplets
including cholesterol, fatty acids, triglycerides
and phospholipids.
• Fragmented internal elastic lamina in the
intimal layer of artery
• Proliferation of altered smooth muscles may
become metaplastic to macrophages. .
• Deposition of mucoid ground substance and
collagen fIbers
• Hyalinization of connective tissue " Fibrous
plaques".
• Presence of some fat droplets in between the
lesion
MEDIAL SCLEROSIS
Medial sclerosis involve medium sized muscular
arteries and characterized by fatty degeneration and
hyalinization of muscular tissue of medial arteries
leading to necrosis. This is also known as
Monckeberg medial sclerosis.
Etiology
• Old age.
• Excessive administration of epinephrine
(adrenaline).
• Nicotine.
• Vitamin D toxicity.
• Hardening of medium sized arteries.
• Hyaline, fatty changes and calcifIcation of
arterial wall.
• Fatty changes, hyalinization of muscular layer
of medium sized arteries.
• Necrosis ofmyofIbrils.
• CalcifIcation.

Systemic Pathology
Fig.14.25. Diagram showing aneurysm
(a) dissecting (b) sacular
Flg.14.26. Photomicrograph showmg phlebitis
ARTERIOLOSCLEROSIS
Arteriolosclerosis affects arterioles in kidneys,
spleen and pancreas and is characterized by
hyperplasia of intimal cells of arterioles producing
concentric lamellations occluding their lumen.
Etiology
• Hypertension.
• No characteristic macroscopic lesion.
• Atrophy of organ, hardening.
• Proliferation of cells present in intima of blood
vessels.
• Swelling and necrosis of cells in medial layer
leading to occlusion of lumen.
• Calcification in chronic cases.
Fig.14.27. Photograph showing oflymphangitis
ARTERITIS
Arteritis is the inflammation of arteries
characterized by infiltration of neutrophils,
lymphocytes and macrophages in the media and
intima ofarterial wall (Figs. 14.23 & 14.24).
Etiology
• Chemicals.
• Thermal.
• Virus e.g. Equine viral arteritis.
• Pyogenic bacteria.
• Parasite e.g. Strongylus vulgaris.
• Hyperemia.
• Conjunctivitis, oedema ofeye.
• Presence ofthrombi in artery.
164

• Presence of thrombi in artery involving intimal
layer.
• Equine viral arteritis virus causes infiltration of
lymphocytes and macrophages in media.
• Occlusion of lumen of arteries due to
thickening of wall.
• In parasitic arteritis, parasitic thrombi may
present along with inflammatory reaction in
intimal layer.
ANEURYSM
Aneurysm is dilation of an artery or cardiac
chamber leading to formation ofsac (Fig. 14.25).
Etiology
• Aflatoxin.
• Infectious emboli.
• Weak vessel wall due to rupture.
• Fracture or necrosis of medial layer of large
blood vessel.
• Arteriolosclerosis.
• Fracture or necrosis of medial layer of large
blood vessels permitting parallel blood
circulation till the next division of blood vessel
is called as Dissecting aneurysm or false
aneurysm.
• Formation of sac in artery due to dilation, also
known as True aneurysm.
• Rough intimal layer.
• Wall of blood vessel damaged with
inflammatory exudate.
PHLEBITIS
Phlebitis is the inflammation of veins characterized
by presence ofinflammatory exudate, thickening of
the wall and dilation ofthe lumen (Fig. 14.26).
Etiology/Occurrence
• Naval infection in calves.
165
• Uterine infections.
• In jugular vein due to improper intravenous
infection.
• Varicose veins are dilated and elongated veins
following irregular and tortuous course.
• Telangiectasis is marked dilation of veins
particularly of sinusoidal capillaries in one or
more lobules in liver.
Macroscopic feature
• Wall of vein is thickened.
• Vein contain large thick necrotic material
• Lumen dialated
• Inner surface ofvein is rough and hyperemic.
Microscopic feature
• Infilteration of neutrophils in the wal! of veins
• Sometimes calcification may also present.
• Wall of vein becomes thick due to
inflammatory cells and/or proliferation of
fibrous tissue.
LYMPHANGITIS
Lymphangitis is the inflammation of lymph vessels
characterized by aggregation of lymphocytes
around lymphatics, oedema of dependent parts and
distension oflymphatics (Fig. 14.27).
Etiology/Occurrence
• Corynebacterium avis causes caseous
lymphangitis and lymphadenitis
• Equine epizootic lymphangitis
Macroscopic lesions
• Distension of subcutaneous lymph vessels,
nodules oflymphoid aggregates.
• Oedema due to failure oflymphatic drainage.
Microscopic lesions
• Lymphoid aggregation arollld lymphatics.
• Lymphatics distended.
• Oedema ofdependent tissue.

Systemic Pathology
MODEL QUESTIONS
Q.1. Fill in the blanks with suitable word(s).
1. Right sided heart failure is caused by a disease in................and occurs after ................failure
and is characterized by ................pulse.
2. Interventricular septal defects may lead to ................and ................
3. Brisket disease is caused by ................in environment and is characterized by ................,
................and oedema in ................region.
4. Arteriosclerosis is ................ofarteries including ................, ................and ................
5. ................, ................and ................may lead to occurrence ofatherosclerosis.
6. Caseous lymphangitis is caused by............and is characterized by.............., ..............and
7. Hypertension may cause ................characterized by ................producing ................occluding
................ofblood vessels.
8. Macrophages are filled with ................including ................, ................, ................and
................in atherosclerosis oflarge blood vessels.
Q. 2. Write true orfalse and correct the false statements.
1. ..........Transposition ofaorta includes the origin ofaorta from left ventricle.
2. ..........Myocardial necrosis and nutmeg liver are feature ofacute heart failure.
3. ..........Eosinophilic myocarditis is caused by Sarcosporidia.
4. ..........Hypocholesterolemia may cause atherosclerosis.
5. ..........Oedema occurs due to lymphangitis.
6. ..........Phlebitis is inflammation of veins.
7. ..........Excessive administration ofadrenaline may cause medial sclerosis.
8. ..........Arteriolosclerosis may affect medium and large size arteries.
9. ..........Altered smooth muscle fibres may act as macrophages loaded with lipid content.
10...........Lymphangitis may not cause oedema.
Q. 3. Define thefollowing.
1. Ectopia cordis
2. Heart failure cells
3. Hydropericardium
4. Cardiac temponade
5. Pneumopericardium
6. Arteriolosclerosis
7. Arteriosclerosis
8. Nutmeg liver
9. Varicose veins
10. Telangiectasis
1. Tetralogy ofFallot 4. Mulberry heart disease
2. Vegetative endocarditis 5. Atherosclerosis
3. Brisket disease 6. Cardiac failure
Q.5. Match the word(s) from four options given against each statement.
1. Acute heart failure is not caused by ................
(a) Anoxia (b) Shock (c) Cardiac temponade
2. Left sided heart failure is characterized by ................
(a) Heart failure cells (b) Pulse in jugular vein (c) Shock
166
(d) Fever
(d) Oedema

3. "Bread and butter" appearance of heart is due to deposition of ................
(a) Fibrin (b) Neutrophils (c) Fibroblasts (d) Collagen
4. Endocarditis is caused by ................
(a) Actinomyces pyogenes (b) Erysepalas (c) Staphylococci (d)All of the above
5. Vegetative growth in heart is caused by ................
(a) Actinomyces pyogenes (b) Staphylococci (c) Clostridia (d) Erysipalas
6. Arteriolosclerosis affects arterioles in ................
(a) Kidneys (b) Spleen (c) Pancreas (d)All of the above
7. Atherosclerosis is ................ofblood vessels
(a) Hardening (b) Softening (c) Aneurysm (d) Thinning
8. Arteritis is inflammation of arteries caused by ................
(a) Equine viral arteritis (b) E.coli (c) Salmonella (d) Rotavirus
9. Phlebitis is the inflammation of ................
(a) Artery (b) Vein (c) Lymph vessel (d) Capillary
10. Lymphangitis is inflammation of ................
(a) Lymphnode (b) Lymph gland (c) Lymph vessel (d) Lymphocytes
167

15
PATHOLOGY RESPIRATORY
SYSTEM
• Pathology of upper respiratory passage
• Nasal polyps
• Nasal granuloma
• Tracheitis
• Bronchitis
• Pathology of lungs
• Atelectasis
• Emphysema
• Pulmonary oedema
• Pneumonia
• Pulmonary adenomatosis
• Hypersensitivity pneumonitis
• Pneumoconiasis
• Pathology of air sacs
• Air sacculitis
• Pathology of pleura
• Pleuritis
• Model Questions

Pathology ofRespiratory System
PATHOLOGY OF UPPER RESPIRATORY
TRACT
In many infectious diseases, there is inflammation
of mucosa of upper respiratory passage leading to
nasal discharge which is catarrhal, purulent or
fibrinous, depending on the type of infection. The
infection may extend to lower parts of respiratory
tract and reach the lungs causing pathological
alterations. Rhinitis is the inflammation of nasal
mucosa (Fig. 15.1). Sinusitis is the inflammation of
sinuses e.g. frontal sinusitis in dehorned cattle. The
larvae ofbotfly Oestrus ovis enter the nasal passage
and migrate upto frontal sinuses and turbinate
bones and cause mucopurulent inflammation.
Similarly leeches (Dinobdella ferox) is known to
cause nasal cavity inflammation in domestic
animals and suck blood. Rhinitis is caused by
Bordetella bronchiseptica in pigs and IS
characterized by mucopurulent exudate,
disappearance of nasal septum, retarded growth of
snout and plugging ofpassage by solidified exudate
and dead tissue. This condition is known as porcine
atrophic rhinitis. Epistaxis is bleeding from nasal
passage due to trauma, neoplasm and ulcerative
lesions as a result of infections. Pharyngitis is the
inflammation of pharynx while laryngitis is the
inflammation oflarynx.
NASAL POLYPS
Nasal polyps are the inflammatory conditions of
respiratory mucosa resembling neoplastic growth
caused by fungus and characterL'led by formation of
new growth simulating benign neoplasm in nasal
passage.
Etiology
• Rhinosporidium sceberi, a fungus most
commonly prevalent in southern India.
• Formation of a single polyp in respiratory
mucosa, pedunculated, elongated, fills nasal
cavity.
• Cauliflower like growth may cause bleeding.
• Fibrous covering by mucous membrane and
heavily infiltrated by neutrophils,
lymphocytes, eosinophils, macrophages around
fungus.
NASAL GRANULOMA
Nasal granuloma is the granulomatus inflammation
of respiratory mucosa in nasal cavity caused by
blood flukes and characterized by the presence of
granulomatous growth filling the nasal passage
causing obstruction (Figs. 15.2 & 15.3).
Etiology
• Schistosoma nasalis, a blood fluke.
• Type 11 hypersensitivity reaction of nasal
mucosa to plant pollens, fungi, mites etc (Fig.
15.4).
Macroscopic Features
169
• Nasal pruritus.
• Small tiny nodules on nasal mucosa later
becomes cauliflower-like growth filling the
cavity and causing obstruction.
• Oedema in lamina propria.
• Infiltration of eosinophils, mast cells,
lymphocytes and plasma cells and absence of
epithelioid cells.
• Proliferation offibroblasts.
• The lesion is covered by squamous epithelium.
• Mucous glands may have metaplastic
pseudostratified columnar epithelium.
TRACHEITIS
Tracheitis is the inflammation of trachea. In
canines, it is tracheobronchitis while in poultry it is
manifested by laryngotracheitis (Fig. 15.5).
Etiology
• Canine tracheobronchitis caused by
adenovirus, influenza virus and herpes virus.
• Avian infectious laryngotracheitis (lLT) is
caused by herpes virus.

Systemic Pathology
,.:~
Ph'otIJm.iaof!.ra"h showing nasal granuloma
(ARSIUSDA)
~.it"··'r'"-{"':,;~ " j(",
'<, & ' ~,
~~ 'f', ; . ~ i,.,
'.
~
'~
*
Fig.IS.4. Photomicrograph showing causative fungus In
nasal granuloma (ARSIUSDA)
170
Fig.IS.S. Photograph showing haemorrhagic
tracheitis in poultry
Fig.IS.6. Photograph showing presence of
caseous exudate in larynx and trachea.
Fig. IS. 7. Diagram showing presence ofcaseous
exudates In larynx and trachea.
Fig. IS.B. Diagram showing lesions ofinfectious
bronchitis in poultry

• Canine tracheobronchitis or kennel cough
includes congestion of trachea and presence of
catarrhal exudate.
• In poultry, haemorrhage in trachea and caseous
plug in trachea towards larynx causing
obstruction (Figs. 15.6 & 15.7).
• Inclusion bodies in tracheal and bronchial
epithelium in canines.
• Haemorrhagic tracheitis, presence of intra
nuclear basophilic inclusions in tracheal
epithelial cells in infectious laryngotracheitis.
BRONCHITIS
Bronchitis is the inflammation of bronchi,
characterized by catarrhal, suppurative, fibrinous or
haemorrhagic exudate.
Etiology
• Bacteria e.g. Pasteurella.
• . Virus e.g. infectious bronchitis in poultry.
• Parasites.
• Allergy/ Inhalation ofpollens etc.
• Coughing, dyspnoea.
• Mucous exudate in lumen.
• Congestion and/or haemorrhages in bronchi.
• Presence of caseous plugs at the point where
bronchi enters in lungs in infectious bronchitis
ofpoultry (Fig. 15.8).
• Mucous exudate along with inflammatory cells
in the lumen ofbronchi.
• Hyperplasia and/or necrosis of bronchiolar
epithelium.
• Accumulation of mononuclear cells in the
bronchial mucosa and in peribronchiolar area.
PATHOLOGY OF LUNGS
ATELECTASIS
Atelectasis is the failure of alveoli to open or the
alveoli are collapsed and thus do not have air.
171
Etiology
• Obstruction in bronchi! bronchiole.
• Pleuritis.
• Atelectasis neonatorum in new born animals.
In the absence of respiration, lung alveoli
remain closed and thus sink in water indicating
still birth.
• Dull red in colour, hard area of lung like liver
in consistency.
• Atelectic lung sinks in water.
• Compressed alveoli (Fig. 15.9).
• Absence ofair spaces.
• Collapsed bronchioles.
• In inflammatory condition, exudate
compresses alveoli.
EMPHYSEMA
Emphysema is the increase in amount of air in
lungs characterized by dilation of the alveoli. It
may be acute or chronic and focal or generalized.
Etiology
• Bronchitis.
• Atelectasis in adjoining area oflung.
• Pneumonia.
• Allergy to dust, pollens etc.
• Pulmonary adenomatosis.
• Lungs are enlarged and flabby.
• Imprints of ribs can be seen. Colour of lungs
becomes pale.
• Cut surface is smooth and dry.
• Alveoli are distended (Fig. 15.10).
• Some alveoli may rupture and form giant
alveoli.
• Alveolar wall becomes thin due to stretching.
• Mild bronchitis.
• Hyperplasia oflymphoid tissue.

Systemic Pathology
FIg. 15.9. Photomicrograph oflung showlIlg
atelectasIs.
Fig. 15. 10. PhotomIcrograph oflung
showing emphysema
FIg. 15.11. Photograph oflung showing
odema
FIg. 15.12. Photomicrograph oflung showing
oedematous flUId III alveoli
172
Fig.15.13. Photograph oflamb showing signs of
pneumonia
Fig-J5.14. Diagram showing bronchogenous
soread ofcausal a!!ent in lun!!
Fig. 15. 15. Photomicrograph showing
bronchopneumonia
FIg 15 16. Dwgram showing hematogenous
spread ofcausal agent in lung

PULMONARY OEDEMA
In pulmonary oedema, there is accumulation of
serous fluid in alveoli of lungs (Figs. 15.11 &
15.12).
Etiology
• Bacteria.
• Virus.
• Allergy.
• Lungs become enlarged.
• Weight oflungs increases.
• Cut surface releases fluid and frothy exudate in
trachea and/or bronchi.
• Serous fluid accumulation in alveoli oflungs
• Fluid may also be seen in some bronchi!
bronchioles.
• Infiltration ofinflammatory cells.
• Congestion oflungs.
PNEUMONIA
Pneumonia is the inflammation of lungs
characterized by congestion and consolidation of
lungs. Clinically, it is menifested by dyspnoea,
coughing, weakness and nasal discharge (Fig.
15.13). The pathological lesions in lungs are
produced in a similar way irrespective of the type
of etiological agent and includes various stages like
congestion, red hepatization, grey hepatization and
resolution.
Stage of congestion: This stage of lung is
characterized by active hyperemia and pUlmonary
oedema. The capillaries are distended with
engorged blood and alveoli are filled with watery
serous exudate. This requires 2 minutes to few
hours to initiate the congestion.
Stage of red hepatization: This stage of lung is
characterized by the consolidation of lungs due to
accumulation of blood in blood vessels
(congestion). The consolidated lungs are firm and
look like liver and hence the name "red
hepatization". Such affected lung always sinks in
173
water. Alveoli are filled with serous or
serofibrinous exudate giving hardness to lungs. In
inflammatory condition, the neutrophils,
macrophages and lymphocytes along with
erythrocytes infiltrate the affected area of lungs.
This stage of red hepatization takes 2 days for
development offrrmness oflung.
Stage ofgrey hepatization: The lung remains hard
but due to lysis and removal of erythrocytes, it
becomes grey or less red in colour. Firmness/
hardness of lung remains same and thus, the name
grey hepatization. There is increase in infiltration
of inflammatory cells like macrophages,
lymphocytes, epithelioid cells depending on the
virulence ofetiological agents.
Stage of resolution: After a week, the recovery
starts in the form of resorption of fluid; autolized
cells and debris is removed by phagocytic cells.
The causative organism is neutralized or removed
from the lungs through immunity of bl)dy. After a
few days the lung parenchyma becomes normal and
starts functioning. If the causative agent is more
virulent, it may cause death of animal due -to
respiratory failure or may cause permanent lesions
like formation of scar, carnification, granuloma etc.
There are various types of pneumonia caused by
bacteria, virus, fungi, parasites, allergens,
chemicals and all such affections of lungs are
classified as under.
BRONCHOPNEUMONIA
Bronchopneumonia is the inflammation of lungs
involving bronchi or bronchioles along with
alveoli. It is thought to be spread through
bronchogenous route and is the common type of
pneumonia in animals (Figs. 15.14 & 15.15).
Etiology
• Virus.
• Bacteria.
• Chemicals.
• Mycoplasma.
• Chlamydia.
• Parasites.
• Fungus.
• Mainly through bronchogenous route.

Systemic Pathology
Fig.i5.i7. Photomicrograph showing
interstitial pneumonia
Fig.i5.IB. Photomicrograph o/fibrinous
pneumonia
Fig.i5.i9. Photomicrograph showing hyaline
membrane pneumonia
Fig.i5.20. PhotomIcrograph showing verminous
pneumonia
174
Fig.i5.2i. Photomicrograph showing
aspiration pneumonia (ARSIUSDA)
Fig.i5.22. Photograph showmg mycotic
pneumonia
Flg.i5.23. Photomicrograph showing
mycotic pneumonia.
Fig.i5.24. Photograph o/lung showing
tubercle/granulomatous lesIOn (ARSIUSDA)

• Congestion and consolidation of anterior and
ventral parts oflungs (lobular pneumonia).
• Patchy lesions on one or several lobes and
adjacent area showing emphysema.
• Mediastinallymphnodes are swollen.
• Congestion, oedema or haemorrhage in lung.
• Infiltration of neutrophils, mononuclear cells
in and around bronchiolesi bronchi.
• Catarrhal inflammation ofbronchi.
• Proliferation ofbronchiolar epithelium.
Interstitial Pneumonia
Interstitial pneumonia is the inflammation of the
lungs characterized by thickening of alveolar septa
due to serous/fibrinous exudate along with
infiltration of neutrophils and/or mononuclear cells
and proliferation of fibroblasts. It is also known as
lobar pneumonia (Figs. 15.16& 15.17).
Etiology
• Bacteria.
• Virus.
• Chlamydia.
• Parasites.
• Mainly through hematogenous route.
• Lungs are pale or dark red in colour.
• Oedema, dripping of fluid from cut surface.
• Alveoli may have serous or fibrinous exudate.
• Thickening of alveolar septa due to
accumulation of exudate, inflammatory cells
and in chronic cases, proliferation of fibrous
tissue.
• Infiltration of mononuclear cells in alveolar
septa.
Fibrinous Pneumonia
Fibrinous pneumonia is the inflammation of lungs
characterized by the presence of fibrin in alveoli or
175
bronchioles and may give rise to hyaline membrane
formation over the surface ofalveoli or bronchiole.
Etiology
• Bacteria.
• Virus.
• Parasites.
• Toxin/poisons.
• Antero-ventral portion of lung is congested
and consolidation.
• Colour of lungs become deep red due to
congestion.
• Surface of lungs is covered by fibrin sheet.
• Interlobular septa are prominent due to
accumulation ofplasma and fibrin.
• Principal exudate is fibrin, fills alveoli,
bronchioles and bronchi (Fig. 15.18).
• Congestion and/or haemorrhages.
giant cells.
• Formation of eosinophilic false membrane of
fibrin over the surface of alveoli and
bronchiole known as "hyaline membrane
pneumonia" (Fig. 15.19).
Verminous Pneumonia
Verminous pneumonia is caused by parasites and is
characterized by the presence of lesions of
bronchopneumonia along with parasites or their
larva (Fig. 15.20).
Etiology
• Metastrongylus apri in pig.
• Dictyocaulus filariae in sheep and goat.
• D. viviparus in cattle and buffaloes.
• D. arnfieldi in horse and donkeys.
• Capillaria aerophila in dogs and cats.
• Multiple petechial haemorrhage in lungs at the
site ofparasite penetration.

Systemic Pathology
"'*Fig. 15.25. Photomicrograph oflung showing
tubercle
Fig. 15.26. Photomicrograph oflung showing
granulomatous lesions
Fig.I5.27. Photomicrograph oflung showing
granulomatous lesIOns and giant cells
Fig. 15.28. Photograph showing pulmonary
adenomatosis (ARSIUSDA)
176
Fig. 15.29. Photomicrograph showing pulmonary
adenomatosIs (ARSIUSDA)
Fig.15.30. Photograph showing deposition ofcarbon
particles in trachea in chicks
Fig. 15.31. Photomicrograph showing pneumoconiasis
Fig.15.32. Photograph showing air
sacculitis in poultry

• Mature worms in alveoli, bronchioles and
bronchi.
• Mucopurulent exudate in alveolilbronchi.
• Pulmonary oedema, emphysema.
• Dilation ofbronchioleI bronchi
• Lesions ofchronic suppurative bronchiolitis
• Focal areas of inflammation in the vicinity of
parasites and around bronchioles.
• Hyperplasia ofbronchiolar epithelium.
• Infiltration of eosinophils and lymphocytes.
Aspiration Pneumonia
Aspiration pneumonia is caused by faulty
medication through drenching which reaches lungs
instead of targetted place (digestive tract) and
characterized by necrosis and gangrene of lung
paranchyma.
Etiology
• Drugs, food, foreign body and oil drench
which reaches in lungs through trachea.
• Paresis of throat predisposes the animal for
aspiration pneumonia.
• Congestion and consolidation of anterior and
ventral portion oflung.
• Affected part becomes green! black in colour,
moist gangrene.
• Affected lungs are often foul smelling.
• Presence of foreign body like heads of wheats,
parts ofcorn, oil, milk etc.
• Thrombosis ofblood vessels.
• Necrosis in lungs.
• Presence of saprophytes, leucocytes and
bacteria cause liquefaction and gangrene.
• Gangrenous lesions surrounded by intense
inflammation (Fig. 15.21).
• Congestion.
177
Mycotic Pneumonia
Mycotic pneumonia is caused by a variety of fungi
and characterized by the presence of chronic
granulomatous lesions in lungs (Figs. 15.22 &
15.23).
Etiology
• Aspergillusfumigatus.
• Blastomyces sp.
• Cryptococcus sp.
• Coccidioidomyces immitis.
• Nodules in lungs.
• On cut, cheese-like caseative mass comes out
from nodules.
• Caseation involves both bronchiole and
alveoli.
• Such lesions may also be present in trachea,
bronchi and air sacs.
• Presence of granulomatus lesions i.e. caseative
necrosis, macrophages, epithelioid cells,
lymphocytes, giant cells, fibroblasts etc.
• Presence of branched hyphae of fungi in the
necrosed area.
Tuberculous Pneumonia
Tuberculous pneumonia is caused by
Mycobacterium sp. and is characterized by the
presence of chronic granulomatous lesions in the
lungs (Figs. 15.24 to 15.27).
Etiology
• M. bovis.
• Grey, white or light yellowish nodules in
lungs.
• Nodules are hard, painful and/or calcified.
• Animal carcass is cachectic, weak or
emaciated.

Systemic Pathology
Table 15.1 Differential features of various types of Pneumonia
Bronchopneum Interstitial Fibrinous Verminous Aspiration Mycotic Tuberculous
onia
Macroscop 1. Congestion 1. Lungs are I. Antero- 1. Multiple 1. Congestion 1. Nodules in 1. Grey, white
ic features and pale or dark ventral portion petechial and lungs or light
consolidation red in colour. oflung is haemorrhage consolidation
2. On cut,
yellowish
of anterior and congested and in lungs at the of anterior and nodules in
ventral parts of 2. Oedema, consolidated. site ofparasite ventral portion cheese like lungs.
lungs (Lobular dripping of
penetration. oflung. caseative mass
pneumonia).. fluid from cut 2. Colour of comes out 2. Nodules are
surface lungs become 2. Mature 2. Affected from nodules. hard, painful
2. Patchy deep red due to worms in part becomes
3. Caseation
and/or
lesions on one congestion alveoli, green! black in calcified.
or several bronchioles colour, moist involves both
lobes and 3. Surface of and bronchi. gangrene. bronchiole and 3. Animal
adjacent area lungs is alveoli. carcass is
shows covered by 3. 3. Affected
4. Such lesions
cachectic,
emphysema. fibrin sheet. Mucopurulent lungs are often
may also
weak or
exudate in foul smelling. emaciated.
3. Mediastinal 4. Interlobular alveoli/bronchi present in
Iymphnodes septa are 4. Presence of trachea, 4. On cut, the
are swollen. prominent due foreign body bronchi and air cheesy
to 4. Pulmonary like heads of sacs. material comes
accumulation oedema, wheats, parts out from the
of plasma and emphysema. of com, oil, nodules.
fibrin. milk etc.
Microscopi 1. Congestion, I. Alveoli may 1. Principal 1. Dilation of I. Thrombosis I. Presence of I. Presence of
c features oedema or have serous or exudate is bronchiole/ of blood granulomatus tubercle/granul
haemorrhage fibrinous fibrin, fills bronchi vessels. lesions i.e. oma in lungs
in lung. exudate. alveoli,
2. Lesions of 2. Necrosis in
caseative which
bronchioles necrosis, comprises a
2. Infiltration 2. Thickening
and bronchi. chronic lungs. macrophages, central
of neutrophils, of alveolar suppurative
3. Presence of epithelioid necrosed area
mononuclear septa due to 2. Congestion bronchiolitis
saprophytes, cells, surrounded by
cells in and accumulation and/or
3. Focal areas leucocytes and Iymphocytes, macrophages,
around of exudate, haemorrhages
of bacteria cause giant cells, epithelioid
bronchioles/ inflammatory
3. Infiltration inflammation liquefaction fibroblasts etc. cells,
bronchi. cells and in
chronic cases, of neutrophils, in the vicinity and gangrene. 2. Presence of
lymphocytes,
3. Catarrhal proliferation of macrophages of parasites branched
Langhan's
inflammation
fibrous tissue. and giant cells and around 4. Gangrenous
hyphae of
giant cells and
of bronchi. bronchioles. lesions covered by
3. Infiltration 4. Formation surrounded by fungi in the fibrous
4. Proliferation of of eosinophilic 4. Hyperplasia intense necrosed area. covering.
of bronchiolar
mononuclear false of bronchiolar inflammation
epithelium membrane of epithelium. 2. Acid-fast
cells in
fibrin over the 5. Congestion rod shaped
alveolar septa.
surface of 5. Infiltration bacteria may
alveoli and of eosinophils present in
bronchiole and and necrosed area.
then known as lymphocytes.
3. Central area
"hyaline
maybe
membrane
calcified.
pneumonia".
178

On cut, the cheesy material comes out from the
nodules.
• Presence of hIbercle/granuloma in lungs which
comprises a central necrosed area surrounded
by macrophages, epithelioid cells,
lymphocytes, Langhan's giant cells and
covered by fibrous covering.
• Acid-fast rod shaped bacteria may be present
in necrosed area.
• Central area may be calcified.
PULMONARY ADENOMATOSIS
Pulmonary adenomatosis is a slow viral disease of
sheep and is characterized by metaplasia of
alveolar squamous epithelium to cuboidal and lor
columnar epithelium leading to glandular
appearance of alveoli (Figs. 15.28 & 15.29).
Etiology
• Retrovirus.
• Pulmonary adenomatosis virus.
• Multiple focal areas of consolidation in lungs.
• Imprint ofribs on lungs.
• Congestion and hardening of mediastinal
lymphnodes.
• Metaplasia of alveolar epithelium leading to
formation ofglandular structures in alveoli.
• Metaplasia of simple squamous epithelium to
cuboidal or columnar epithelium which gives
alveoli a gland like look.
• Mild inflammatory reaction.
• Proliferation of fibrous tissue.
HYPERSENSITIVITY PNEUMONITIS
Hypersensitivity pneumonitis is the inflammation
of lung caused by an allergic reaction of antigen
(allergen) and characterized by interstitial
pneumonia, emphysema, hyaline membrane
formation and hyperplasia of alveolar epithelium.
179
Etiology
• Allergens.
• Parasites - Dictyocaulus viviparous.
• Moldyhay.
• Fungus - Aspergillus sp.
• Lobes may contain small grey foci.
• Presence of yellow and dense mucus in lumen
ofbronchi.
• Excessive accumulation of air in lungs due to
emphysema.
• Presence ofworms/larvae.
• Extensive infiltration of lymphocytes,
monocytes and eosinophils around the bronchi
and bronchioles.
• Accumulation of catarrhal exudate in bronchi!
bronchiole.
• Emphysema as a result of widening ofalveoli.
• Hyperplasia ofbronchiolar musculature.
• Inflammatory cells in interalveolar septa may
form small granulomas.
• Formation of hyaline membrane over alveolar
and bronchiolar epithelium.
PNEUMOCONIASIS
Pneumoconiasis is the granulomatous inflammation
of lungs caused by aerogenous dust particles of
sand, silica, beryllium, carbon or asbestos. It is also
known as anthracosis (Figs. 15.30 & 15.31).
Etiology
• Silica.
• Asbestos.
• Beryllium.
• Bauxite.
• Graphite.
• Carbon.
• Bronchogenous/aerogenous administration of
particles inhaled with air, mostly around
mines/factories.
• Generator smoke.

Systemic Pathology
• Dense fibrous nodules in lungs.
• Presence of carbon particles in trachealbronchi
mixed with mucous exudate.
• Granuloma formation around the particles of
silica/asbestos infiltrated by macrophages,
lymphocytes and giant cells
• Silica produces cellular reaction 'Silicosis'.
• Beryllium granuloma looks like tubercule
without caseation.
• Asbestosis is characterized by the presence of
club shaped filaments bearing cells in lesion.
PATHOLOGY OF AIR SACS
AIR SACCULITIS
Air sacculitis is inflammation of air sacs caused by
E. coli, Mycoplasma, reovirus etc. and
characterized by thickening of the wall. of air sacs
and presence ofcheesy exudate (Fig. 15.32).
Etiology
• Escherichia coli.
• Mycoplasma gallisepticum.
• Avian reovirus.
• Thickening of the air sac wall, which becomes
dirty and cloudy.
• Presence of cheesy exudate in air sacs,
congestion oflungs.
• Fibrinous pericarditis.
• Liver is covered with thin fibrinous membrane.
• Oedema and infiltration of neutrophils and
lymphocytes in air sacs.
• Caseous exudate in lungs and air sacs.
180
PATHOLOGY OF PLEURA
PLEURITIS
Pleuritis is the inflammation of pleura character-
-ized by serous, fibrinous or purulent exudate. It is
also known as pleurisy.
Etiology
• Mycoplasma mycoides.
• Haemophilus suis.
• Organisms responsible for pneumonia/
traumatic pericarditis may also cause pleuritis.
• Congestion ofpleura.
• Serous, fibrinous or purulent exudate.
• Accumulation of clear fluid in pleura/thoracic
cavity is called as hydrothorax.
• Presence of blood in thoracic cavity is known
as Hemothorax.
• Suppurative exudate in thoracic cavity is
known as pyothorax.
• Presence of air in pleural cavity is termed as
pneumothorax, while presence of lymph in
pleural cavity is called as chylothorax.
• Tuberculous pleuritis is characterized by small
nodules on pleura and is known as ''pearly
disease".
• In chronic cases, development of fibrous tissue
causes adhesions and is known as adhesive
pleuritis.
• Congestion ofblood vessels.
• Infiltration ofneutrophils and lymphocytes.
• Thickening ofpleura due to oedema.
• Proliferation of fibroblasts producing adhesive
lesions.

MODEL QUESTIONS
Q. 1. Fill in the gaps with suitable word(s).
1. ................. is the inflammation oflungs characterized by ................. and ................. oflungs.
2. Lobar pneumonia is characterized by ................. ofinteralveolar septa.
3. Fibrinous pneumonia is characterized by the presence of ................. exu<!ate in alveoli and may
give rise to.............formation which is............of fibrin over the surface of.............and ............
4. Aspiration pneumonia is caused by ................. of drugs/ milk and is characterized by
................. and ................. formation in the lungs.
5. Mycobacterium tuberculosis produces ................. pneumonia in lungs characterized by
................. formation consisting of ................. central area surrounded by .................,
................., ................., ................., and covered by ................. capsule.
6. Pulmonary adenomatosis is caused by ................. and is characterized by ................. ofalveolar
squamous epithelium to ................. or ................. leading to ................. appearance ofalveoli.
7. Allergic reaction due to ................. may cause ................. characterized by .................,
................., ................. and ................. of alveolar epithelium.
8. Pneumoconiasis is ................. inflammation of lungs caused by aerogenous................. of
................., ................. or ................. and it is also known as .................
9. Inflammation of air sacs in poultry is known as.................and is caused by .................,
................. and................. and characterized by................. and .................
10.................. pleuritis is also known as................. while the presence oflymph in pleural cavity is
termed as.................
Q. 2. Write true orfalse against each statement and correct the false statements.
1. ...........Bronchopneumonia is the inflammation oflungs characterized by thickening of
interalveolar septa.
2. ...........Verminous pneumonia is caused by Bordetella bronchiseptica.
3. ...........Gangrenous pneumonia occurs due to faulty drenching ofmedicines.
4. ...........Mycotic pneumonia is caused by E. coli.
5. ...........Granulomatous pneumonia is produced by Blastomyces sp.
6. ...........Pearly disease is caused by Mycoplasma myoides.
7. ...........Atelectic lung floats in water.
8. ...........Oestrus ovis is the cause ofnasal granuloma is sheep.
9. ...........Metaplasia of alveolar epithelium occurs in hypersensitivity pneumonitis.
10............Air sacculitis is caused by E. coli.
Q.3. Define the followings.
1. Rhinitis 14. Tracheobronchitis
2. Sinusitis 15. Pneumothorax
3. Laryngitis 16. Red hepatization
4. Pharyngitis 17. Carnification
5. Hydrothorax 18. Lung worms
6. Pyothorax 19. Atelectasis neonatorum
7. Epistaxis 20. Bronchiolitis
8. Hyaline membrane 21. Beryllium granuloma
9. Silicosis 22. Peribronchitis
181

Systemic Veterinary Pathology
10. Asbestosis 23. Hemothorax
11. Pleurisy 24. Alveolitis
12. Chylothorax 25. Pearly disease
13. Adhesive pleuritis
l. Porcine atrophic rhinitis 9. Infectious laryngotracheitis
2. Nasal polyps 10. Emphysema
3. Nasal granuloma 1l. Pulmonary adenomatosis
4. Atelectasis 12. Bronchopneumonia
5. Pathogenesis ofpneumonia 13. Mycotic pneumonia
6. Lobar pneumonia 14. Granulomatous pneumonia
7. Hyaline membrane pneumonia 15. Air sacculitis
8. Gangrenous pneumonia
Q. 5. Match the word(s) from four options given against each statement.
1. Nasal polyps are caused by ...........
(a) Schistosoma nasalis (b) Rhinosporidium sceberi (c) E. coli (d) Mycoplasma mycoides
2. Canine tracheobronchitis is caused by...........
(a) Adenovirus (b) Influenza virus (c) Herpes virus (d)All ofthe above
3. Presence of caseous plugs ill bronchi at the point of entrance in lungs in characteristic lesions
of ...........
(a) Infectious bronchitis (b) Infectious laryngotracheitis (c) Air sacculitis (d) Pleuritis
4. This is not the pathologic lesion ofpneumonia...........
(a) Congestion (b) Red hepatization (c) Yellow hepatization (d) Resolution
5. Infection through aerogenous route may cause ...........pneumonia
(a) Lobar (b) Lobular (c) Hypersensitivity (d) Fibrinous
6. Verminous pneumonia is caused by ...........
(a) Mycoplasma (b) Chlamydia (c) Dictayocaulus sp. (d) E. coli
7. Langhan's type giant cell is characteristic feature of ...........pneumonia
(a) Tuberculous (b) Verminous (c) Broncho (d) Pulmonary adenomatosis
8. Atelectasis neonatorum is characteristic features of ...........
(a) Premature birth (b) Aborted foetus (c) Still birth (d) None
9. Hypersensitivity pneumonitis is caused by ...........
(a) Allergens (b) Parasites (c) Moldy hay (d)All ofthe above
10. Pneumoconiasis is characterized by ...........lesions in lungs
(a) Serus (b) Fibrinous (c) Haemorrhagic (d) Granulomatous
182

16
PATHOLOGY OF DIGESTIVE
SYSTEM
• Pathology of Mouth cavity
• Pathology of Esophagus and crop
• Pathology of Stomach
• Pathology of Intestines
• Pathology of liver and pancreas
• Pathology of peritoneum
• Model Questions

Systemic Pathology
Epitheliogenesis imperfecta of tongue
Abnormal smooth surface of tongue due to small
filiform papillae. It occurs as a defect in autosomal
recessive gene and occurs in Holstein-Friesian
cattle. This is also known as smooth tongue.
Cleft palate
This is most common congenital abnormality that
occurs due to failure of oral-nasal cavity to divide
leaving cleft. It may also extend towards lips
producing 'harelip' condition.
Mega colon
There is distention of colon which abruptly
terminates in rectum due to mutant gene in dogs.
Duplication of colon
In dog, the colon is duplicated from caecum to
rectum and this defect is associated with
malformation in the body ofvertebrae T4 and T5•
Atresia coli
In calf, the absence of colon occurs and the
intestine terminates in blind caecum.
Atresia ani
This is absence ofanal opening.
PATHOLOGY OF MOUTH CAVITY
STOMATITIS
Stomatitis in the inflammation of mucosa of oral
cavity (Figs. 16.1 to 16.6). It includes:
Gingivitis: Inflammation ofgums.
Glossitis: Inflammation of tongue.
Cheilitis: Inflammation oflips.
Tonsilitis: Inflammation of tonsil.
PalatitislLampas: Inflammation ofpalates.
Etiology
• Trauma due to nails, wire, or any sharp object
like needle.
• Physical due to hot milk, medicines etc.
• Chemical - Alkali / acids.
• Microorganisms - Bacteria, virus, fungi.
184
• Catarrhal stomatitis: Mucous exudation in oral
cavity.
• Vesicular stomatitis: Vesicles in oral mucosal
e.g. FMD.
• Erosive stomatitis: Erosions in oral mucosa
e.g. Rinderpest.
• Fibrinous stomatitis: False membrane in oral
mucosa.
• Ulcerative stomatitis: Presence ofulcers in oral
mucosa e.g. mucosal disease.
• Congestion oforal mucosa.
• Presence oferosions, vesicles or ulcers.
macrophages.
• Presence of fibrinous exudate in the form of
diphtheritic membrane.
PATHOLOGY OF OESOPHAGUS AND
CROP CHOKE
Choke is complete or partial obstruction of
oesophagus either due to any foreign material or
pressure from adjoining areas (Fig. 16.7).
Etiology
• Beets, turnip, carrots, bone.
• Abscess, tumor of neck area.
• Tympany.
• Gangrene, sapremia and toxaemia.
• Sac-like dilatation "Oesophageal diverticulum"
• Perforation due to sharp bone ends.
• Necrosis gangrene at a point ofobstruction.
• Congestion haemorrhage in perforated cases.
OESOPHAGITIS
Oesophagitis is the inflammation of oesophagus
caused by trauma, parasites etc. and is
characterized by catarrhal inflammation, ulceration
or stenosis due to fibrosis.

Pathology ofDigestive System
Fig. 16.1. Photograph ofmouth cavity ofa bird
showing stomatitis due to avian pox
Fig 16:2. Photograph ofmouth cavity ofa buffalo
having erosive palatitis
Fig 16.3. Photograph ofmouth ofa camel
showing cheilitis
Fig 16.4. Photograph oftongue showing
granulomatous lesIOns (ARS/USDA)
185
ulcerative glossitis (ARSlUSDA)
Fig 16.6. Photograph oftongue showing glossitis
due to cysticercosis.(ARS/uSDA)
Fig 16.7. Diagram ofalimentary tract ofdog
showing choke in oesophagus due to bone
Fig 168. Photograph ofoesophagus showing
presence ofcysts due to sarcosporidiosis
(ARS/USDA)

Systemic Pathology
Etiology
• Trauma due to foreign bodies.
• Chemicals - Acids, alkalies.
• Infection - Mucosal disease virus.
• Parasite - Spirocerca lupi, sarcosporidiosis
(Fig. 16.8).
• Nutritional- Vit. A deficiency.
• Congestion.
• Ulcer formation (Fig. 16.9).
• Red streaks ofcatarrhal inflammation.
• Stenosis due to fibrous nodules or
inflammatory exudate.
• Enlargement of glands due to Vit A. defi. (Fig.
16.10).
• Congestion, haemorrhage.
• Ulceration.
• Infilteration of neutrophils, lymphocytes.
• Sub-epithelial fibrosis/nodules by Spirocerea
lupi.
INGLUVITlS
Ingluvitis is the inflammation of crop caused by
fungi and characterized by ulcerative or diphtheritic
lesions (Fig. 16.11).
Etiology
• Candida albicans.
• Monilia albicans.
• Turkis towl-like appearance in crop mucosa.
• Round and raised ulcers.
• In moniliasis, formation of diphtheritic
membrane.
• Necrotic and ulcerative lesions.
• Fibrinous inflammation with infiltration of
mononuclear cells.
PATHOLOGY OF STOMACH
TYMPANY
Tympany is accumulation of gases in rumen due to
failure of eructation as a result of obstruction or
due to excessive production of gases characterized
by distended rumen and dyspnoea. It is also known
as bloat (Fig. 16.12).
186
Etiology
• Choke ofoesophagus.
• Sudden change in animal feed with high
content oflegumes.
• Excessive lush green fodder.
• Rumen is distended due to excessive
accumulation ofgases (C02, H2S, CO).
• Distended rumen compresses diaphragm to
hinder respiration.
• Tarry colour blood, pale liver and rupture of
diaphragm.
• On rupture of rumen gas comes out (dry
tyrnpany).
• The gas is trapped in small bubbles in the
ruminal fluid forming foams and is not easily
removed. This is known as ''frothy bloat",
which is produced by saponin and water
soluble proteins and due to reduction in surface
tension in the absence of fatty acids that
favours froth formation.
• Haemorrhage in lungs, pericardium, trachea
and lyrnphnodes.
• Atelectasis in lungs.
RUMENITIS
Rumenitis is the inflammation of rumen in
ruminant animals caused by change in diet,
chemicals or drugs and characterized by
seropurulent exudate or ulcer formation with or
without parakeratosis.
Etiology
• Change in diet, corn or alfaalfa hay.
• Chemicals/drugs e.g. potassium antimony
tarterate.
• Spherophorus necrophorus infection

Fig. 16.9. Photograph showing ulcerative esophagitis due
to bovine viral diarrhoea.virus
Fig. 16.10. Photograph ofoesophagus showing
nutritional roup
Fig. 16.11. Photograph ofcrop showing ingluvitis
Fig. 16.12. Diagram showing tympauy in a cow
187
Fig. 16.13. Diagram showing penetration ofneedle
from reticulum (Traumatic reticulitis)
Fig. 16.14. Photograph showing ulcerative
abomasitis
Fig 16.15. Photograph showlllg proventriculitis
Fig 16 16 Photograph ofcalfshowing diarrhoea

Systemic Pathology
• Ulcers.
• Spherical white nodules of 1-2 cm diameter
size.
• Sloughing of mucosa.
• Seropurulent exudate.
• Ulcers
• Infiltration oflymphocytes and neutrophils.
• Fibrous nodules due to hyperplasia of
fibroblasts.
• Parakeratosis.
RETICULITIS
Reticulitis is the inflammation of reticulum in
ruminant animals caused by trauma/perforation by
foreign body including sharp object like needles,
wires, etc. and characterized by abscess formation,
adhesions, peritonitis and pericarditis (Fig. 16.13).
Etiology
• Foreign body - sharp objects like needles,
wires etc.
• Perforation ofreticulum by foreign body.
• Abscessation/suppuration.
• Peritonitis, adhesions of reticulum with
diaphragm.
• Pericarditis due to foreign body (traumatic
reticulo pericarditis).
• 'nfiltration of neutrophils, macrophages,
lymphocytes.
• Proliferation of fibroblasts producing
adhesions.
• Liquifactive necrosis.
OMASITIS
Omasitis is the inflammation of omasum in
ruminant animals caused by Actinobacillus sp. and
characterized by granulomatous inflammatory
reaction.
188
Etiology
• Actinobacillus ligneiresi.
• Granulomatous nodules in omasum.
• Typical granuloma formation.
• Sulphur granules of Actinobacillus in the
centre oflesion.
ABOMASITIS
Abomasitis is the inflammation of abomasum in
ruminants caused by chemicals/drugs, bacteria,
virus or parasites and characterized by congestion,
oedema and/or haemorrhagic ulcers (Fig. 16.14).
Etiology
• Chemicals/drugs.
• Bacteria e.g. Clostridium septicum cause of
braxy.
• Virus e.g. Hog cholera, mucosal disease.
• Parasites e.g. Theileria sp.
• Presence of ulcers (button ulcers in Hog
cholera).
• Congestion, oedema of abomasal folds,
haemorrhage in braxy.
• Catarrhal, haemorrhagic abomasits.
• Presence of Gram positive rods in case of
braxy.
• Neutrophilic and lymphocytic infiltration.
• Congestion and haemorrhages.
• Ulceration with lymphocytic infiltration.
IMPACTION OF RUMEN AND RETICULUM
Impaction of rumen and reticulum is common in
cattle and buffaloes. It is caused by heavy
carbohydrate diet and characterized by atony of
rumen, indigestion, acidosis and haemorrhage on
serous membranes.

Fig. 16.17. Photograph showing enteritis
Fig. 16 18 Photograph showzng catarrhal enteritis
Fig 16.19. PhotomIcrograph sholVzng catarrhal enterztis
FIg. 16.20. PhotomIcrograph ShOWlllg nonnal
length oj vil/z III lIlte5tzne
189
Fig. 16.21. Photomicrograph showing reduced
length ofvillI due to rotavirus
Fig. 16.22. Scannmg electron mIcrophotograph
showing normal length ofl'llll
FIg. 16.23 Scanning electron mIcrophotograph ShOWlllf,
reduced lenf,th of VIll, with rough ;urface
Flf, 1624. SWlllllllg electroll nll<Tophotograph
showmg smooth surface oj villi

Systemic Pathology
Etiology
• Overfeeding ofcarbohydrate feed.
• Lack of water.
• Defective teeth or damaged tongue.
• Paralysis ofrumen.
• Atony of rumen due to lactic acid production.
• Rumen is filled with hard, caked undigested
food with foul odour.
• Hemoconcentration, anuria, blood becomes
dark in colour.
• Haemorrhage in lungs.
• Desquamation of ruminal epithelium.
• Lesions ofacidosis/toxicosis.
GASTRITIS
Gastritis is the inflammation of stomach in non-
ruminant animals having simple stomach caused by
chemicals/drugs, bacteria, virus, parasite and
characterized by congestion, oedema, haemorrhage
and ulceration. Inflammation of proventriculus in
poultry is termed as proventriculitis (Fig. 16.15).
Etiology
• Physical - overfeeding, trauma.
• Chemicals - Acid/alkali.
• Microorganisms such as bacteria, virus, fungi.
• Parasites e.g. Trichostrongyles sp., Hemonch.us
sp.
• Urernia.
• Congestion, oedema and haemorrhage of
mucosal surface.
• Thick mucous exudate in stomach.
• Presence of vesicles/ulcers on gastric mucosa.
• Congestion and haemorrhage of gastric
mucosa.
• Presence of ulcersinecrosis.
• Infiltration ofmononuclear cells.
• Lymphoid hyperplasia.
PATHOLOGY OF INTESTINES
CATARRHAL ENTERITIS
Catarrhal enteritis is characterized by increased
number of goblet cells, congestion and infiltration
of neutrophils and mononuclear cells in mucosa of
intestine (Figs. 16.16 to 16.25).
Etiology
• Physical- Foreign bodies and corase feed
• Chemical - drugs
• Microorganisms - E.coli, Salmonella sp.,
viruses
• Parasites - Coccidia
• Presence of catarrhal exudate in lumen of
intestine and congestion.
• Thickening ofthe wall of intestine.
• Diarrhoea.
• Presence ofparasites in lumen of intestine.
• Increased number of goblet cells in intestinal
villi, reduced length ofvilli.
190
• Congestion.
• Infiltration of polymorphonuclear and
mononuclear cells.
HAEMORRHAGIC ENTERITIS
Haemorrhagic enteritis is characterized by
inflammation of the intestines along with
haemorrhagic exudate (Figs. 16.26 to 16.28).
Etiology
• Bacteria - E. coli, Bacillus anthracis,
Salmonella sp.
• Virus - Coronavirus, BVD, MD, RP.
• Parasites - Coccidia.
• Haemorrhagic exudate in intestines; blood
mixed intestinal contents.
• Petechial or echymotic haemorrhage in mucosa
and submucosa of intestine.
• Presence oferosions/ulcers in mucosa.

Fig. 16.25. Scanning electron microphotograph
showing rough surface ofVIlli
Fig. 16.26. Photograph showing haemorrhaglc
enteritis
Fig. 16.27. Photomicrograph showing haemorrhagic
enteritIs
Fig. 16.28. Photograph showzng linear
haemorrhage (Zebra markzng) in large intestzne
191
Fig. 16.29. Photograph showing corrugations in
large intlstzne indicative ofchromc enteritis
FIg. 16.30 Photograph ,howing necrotic ellteritls
in birds due to clostrzdia
Fig. 16.31 Photomicrograph showing
necrotic enteritis
necrotic enteritIS

Systemic Pathology
• Haemorrhage in the mucosa ofintestine.
• Infiltration of neutrophils and mononuclear
cells.
• Erosion or ulcers in intestinal mucosa.
• Presence ofcoccidia in the mucosa.
CHRONIC ENTERITIS
Chronic enteritis is the chronic inflammation of
intestine characterized by proliferative changes like
proliferation of fibrous tissue, infiltration of
mononuclear cells and plasma cells in lamina
propria leading to hardening ofintestinal wall.
Etiology
• Mycobacterium paratuberculosis in bovines
• Intestinal helminths
• E. coli in poultry (Hjarre's disease)
• Thickening of the wall of intestine
(corrugations in Johne's disease) (Fig. 16.29).
• Thick mucous cover over mucosa ofintestine
• Transverse corrugations in the large intestine.
• Granulomatous nodules in duodenum.
• Small, round, raised necrotic foci on serosal
surface of intestine covering whole length of
intestine.
• Proliferation of fibrous tissue in lamina
propria.
• Infiltration of macrophages, lymphocytes,
plasma cells.
• Atrophy ofintestinal glands.
NECROTIC ENTERITIS
Necrotic enteritis is characterized by necrosis of
mucosal epithelium of intestine leading to
erosions/ulcer formation and exposition of
underlying tissues (Figs. 16.30 to 16.32).
Etiology
• Salmonella.
192
• Rinderpest, rotavirus, cornovirus, Hog cholera
virus.
• Coccidia, Histoplasma.
• Niacin deficiency.
• Clostridium sp. after coccidial infection in
birds.
• Necrotic patches in intestines.
• Fibrinous deposits over necrotic patches like
bran deposits.
• Swelling ofmesenteric lymphnodes.
• Ulcers in intestine.
• Congestion and infiltration of mononuclear
cells.
• Necrosis and desquamation of intestinal villus
epithelium, leading to exposed underlying
tissue.
• Ulcers in mucosa.
• Proliferation of crypt epithelium, presence of
abnormal epithelium over villus surface.
PARASITIC ENTERITIS
Parasitic enteritis is caused by parasites and is
characterized by catarrhal and/or haemorrhagic
exudate in intestine, presence of ova/adult parasite
and thickening of the wall of intestine (Figs. 16.33
& 16.34).
Etiology
• Helminths :
• Roundworms
• Tapeworms
• Protozoa:
• Coccidia
• Histoplasma
• Presence of parasite helminths in the lumen of
intestine.
• Thickening ofthe wall ofintestine.
• Catarrhal or haemorrhagic exudate in intestine.

Fig.16.33.Photograph showing parasitic
enteritis (Coccidiosis)
Fig.16.34.Photomicrograph showing
parasitic enteritis (Coccidiosis)
Fig.16.35.Photograph showing
fibrinous enteritis
Fig.16.36.Photograph showing granulomatous
lesion in duodenum ofpoultry
193
Fig.16.37. Photograph showing small tiny
necrotic granulomatous lesion on intestine
Fig. 16.38. Photograph showing piliconcretions
(hair balls) recoveredfrom stomach ofcalves
Fig. 16.39.Photograph showing polybezoars
recovered from stomach ofa barking deer
Fig.16.40.Diagram (A) and photograph (B)
showing intussusception in intestine

Systemic Pathology
• Presence of large number of goblet cells in
mucosa of intestine.
• Congestion and!or haemorrhage.
• Presence of parasite/ova in the intestinal
lumen.
• Infiltration of eosinophils in mucosa and
submucosa of the intestines.
• Coccidia can be seen on mucosal scrapings
under microscope.
FIBRINOUS ENTERITIS
Fibrinous enteritis is the fibrinous inflammation of
intestine characterized by presence of fibrinous
exudate comprising of pseudomembrane in the
mucosa of intestine (Fig. 16.35).
Etiology
• Salmonella choleraesuis.
• Spherophorus necrophorus.
• Presence of diphtheritic membrane over
mucosa of intestine.
• Button ulcers.
• Sometimes, diphtheritic membrane covers the
faeces.
• Congestion and haemorrhage in intestine.
• Thickening of intestinal wall due to fibrinous
exudate.
• Fibrin network in mucosa.
GRANULOMATOUS ENTERITIS
Granulomatous enteritis is caused by bacteria or
fungi and is characterized by granuloma formation
in the intestines (Figs. 16.36 & 16.37).
Etiology
• Coli granuloma - E. coli in poultry (Hjarre's
disease).
• Coccidioidomycosis / candidiasis.
• Granulomatous about cm diameter elevated!
raised areas on the serus surface of intestine.
• Thickening of the wall of intestine.
• Small, tiny, white necrotic nodules on serosa.
• Granuloma formation COnsIStIng of central
necrosed area covered by lymphocytes,
macrophages, epithelioid cells, giant cells and
fibrous connective tissue.
• Extensive proliferation of fibrous tissue.
• Presence ofbacteria / fungus in the lesion.
Table 16.1 Differential features of various types of Enteritis
Catarrhal Haemorrhagic Chronic Necrotic Parasitic Fibrinous Granulomato
us
Macroscop 1. Presence 1. 1. 1. Necrotic 1. Presence 1. Presence I.
ic features ofcatarrhal Haemorrhagic Thickening patches in ofparasite of Granulomato
exudate in exudate in ofthe wall of intestines. helminths in diphtheritic us about one
lumen of intestines; intestine 2. Fibrinous the lumen of membrane cm diameter
intestine and blood mixed (Corrugation deposits over intestine. over mucosa elevated/
congestion. intestinal s in Johne's necrotic 2. Thickening of intestine. raised areas
2. contents. disease). patches like ofthe wall of 2. Button on the serus
Thickening 2. Petechial or 2. Thick bran deposits intestine. ulcers surface of
intestine.ofthe wall echymotic mucous 3. Swelling 3. Catarrhal 3.
of intestine. haemorrhage cover over ofmesenteric or Sometimes, 2. Thickening
194

3. Presence in mucosa and mucosa of Iymphnodes haemorrhagic diphtheritic of the wall of
of parasites submucosa of intestine 4. Ulcers in exudate in membrane intestine.
in lumen of intestine. 3. Transverse intestine. intestine. covers the 3. Small,
intestine. 3. Presence of corrugations faeces. tiny, white
erosions/ in the large necrotic
ulcers in intestine. nodules on
mucosa. 4. serosa.
Granulomato
us nodules in
duodenum.
5. Small,
round, raised
necrotic foci
on serosal
surface of
intestine
covering
whole length
of intestine.
Microscop I. rncreased I. I. 1. Congestion 1. Presence 1. Congestion 1. Granuloma
ic features number of Haemorrhage Proliferation and of large and formation
goblet cells in the mucosa of fibrous infiltration of number of haemorrhage consisting of
in intestinal of intestine tissue in mononuclear goblet cells in intestine. central
villi, 2. Infiltration lamina cells. in mucosa of 2. Thickening necrosed area
reduced of neutrophils propria. 2. Necrosis intestine. of intestinal covered by
length of
and 2. Infiltration and 2. Congestion wall due to Iymphocytes,
villi. mononuclear of desquamation and! or fibrinous macrophages,
2. cells. macrophages of intestinal haemorrhage. exudate. epithelioid
Congestion. 3. Erosion or villus 3. Presence 3. Fibrin
cells, giant,
cells and
3. ulcers in Iymphocytes, epithelium, of network in fibrous
Infiltration intestinal plasma cells. leading to parasite/ova mucosa. connective
of mucosa 3. Atrophy of exposed in the tissue
polymorpho intestinal underlying intestinal
nuclear and glands. tissue. lumen 2. Extensive
mononuclea 3. Ulcers in 4. Infiltration
proliferation
r cells. offibrusmucosa. of tissue.
4. eosinophils in
3. PresenceProliferation mucosa and
ofcrypt submucosa of of bacteria!
epithelium, the intestines. fungus in the
presence of lesion.
5. Coccidia
abnormal can be seen
epithelium on mucosal
over villus scrapings
surface. under
microsc~e.
195

Systemic Pathology
INTESTINAL OBSTRUCTION
Obstruction of intestines may occur as a result of
foreign body, enterolith, piliconcretions,
phytobezoars, polybezoars or due to hypermotility
ofintestines leading to intussusception, volvulus or
torsion.
Piliconcretions
Piliconcretions are hair balls mostly found in
stomach/intestines of animals having habit of
licking. This vice is more common in suckling
calves and in animals with pica related to
phosphorus deficiency. The hairs are accumulated
in stomach which become in rounded shape due to
movements of stomach and look like balls. Such
hair balls are not degradable in gastrointestinal tract
and may cause obstruction (Fig. 16.38).
Phytobezoars/Polybezoars
Concretions formed in gastrointestinal tract as a
result of deposition of salts around a nidus of
undigested plants or polythenes. They may cause
obstruction in gastrointestinal tract (Fig. 16.39).
Foreign bodies
Foreign bodies like rubber balls, nuts, bones,
stones, plastic and rubber materials, polythenes
may obstruct the intestinal tract as they are not
degradable in the gastrointestinal tract.
Hernia
Hernia is presence of intestinal loop in umbilical
area, scrotum or inguinal cavity which causes
passive congestion, oedema and obstruction in
intestines.
Intussusception
Intussusception is telescoping of intestine means a
portion of intestine enters in caudal segment due to
196
violent peristaltic movement. It causes obstruction,
passive congestion and oedema (Fig. 16.40).
Volvulus
In volvulus, the loop of intestine passes through a
tear in mesentry. It causes obstruction at both ends
ofloop (Fig. 16.41).
Torsion
Torsion is twisting of intestine upon itself causing
obstruction (Fig. 16.42).
Enterolith
Concretions in intestines particularly in horses are
responsible for obstruction of intestinal tract and
cause "colic in horse" and enterocolitis (Fig.
16.43).
TYPHLITIS
Typhlitis is the inflammation of caecum. It is
particularly important in poultry, caused by
protozoan parasites and characterized by
haemorrhage, thickening of the wall, presence of
cheesy exudates and/or necrotic ulcers (Fig. 16.44).
Etiology
• Eimeria tennel/a.
• Histomonas meleagridis.
• Haemorrhage in caecum, blood mixed
contents.
• Thickening of the wall, with congestion and
cheesy exudates.
Presence of necrotic ulcers in caecum in case of
histomoniasis which is further supported by round,
depressed, yellowish-green areas of necrosis in
liver.

Fig. 16.41. Diagram showing volvulus in intestine
Fig.16.42.Diagram showmg torsion in intestme
Frg.16.43.Photograph showing A. enterolith
recoveredfrom colon ofa horse B. cross section of
enterolith showing lamillated deposition ofsalts
197
Fig. 16.44.Photograph showing typhlitis in
poultry
Fig.16.45.Photograph ofliver showing
hepatitis with focal necroSIS
Fig.J6.46.Photograph showing presence of
fibrinous membralle on liver (Colisepticemia.)
Fig.J6.47.Photomicrograph showing focal necrosis

Systemic Pathology
• Congestion, haemorrhage, necrosis.
• Presence ofprotozoan parasites.
• Necrotic hepatic lesions.
HEPATITIS
Hepatitis is the inflammation of liver. It may be
acute or chronic. Acute hepatitis is characterized by
the presence of degeneration and necrosis of
hepatocytes and infiltration of neutrophils and
mononuclear cells along with hyperemia and/or
haemorrhage (Figs. 16.45 to 16.48).
Etiology
• Bacteria - Necrobacillosis, Salmonella, E. coli.
• Virus - ICH.
• Chemicals - Carbon tetrachloride.
• Parasites - Fasciola gigantica, Fasciola
hepatica.
• Enlargement of liver.
• Congestion and/or haemorrhage.
• Presence ofnecrotic patches in liver.
• Presence of fibrinous diphtheritic membrane
on liver.
• Cloudy swelling and/or fatty changes in liver.
• Congestion in blood vessels and in sinusoidal
area.
lymphocytes.
• Necrosis ofhepatic parenchyma.
In acute toxic hepatitis there is necrosis of
hepatocytes. According to location it can be
classified as under which is helpful in making
diagnosis.
• Diffused necrosis covers a considerable area
crossing over the lobular boundaries.
• Focal necrosis occupying only a part of lobule
e.g. EHV induced aborted foetal liver.
• Peripheral necrosis is characterized by
necrosis at the periphery of lobule which
occurs due to presence of strong toxins in
blood.
• Midzonal necrosis have necrosis of cells in
midway ofperiphery and centre oflobule.
• Centrilobular necrosis is characterized by
necrosis of hepatocytes around the central vein
and occurs due to stagnation of blood with
toxaemia.
198
• Paracentral necrosis is characterized by
necrosis of hepatocytes at one side of central
vein e.g. Rift valley fever.
CIRRHOSIS
Cirrhosis is the chronic inflammation of liver
characterized by extensive fibrosis, hepatic
degeneration and necrosis (Fig. 16.49 to 16.51).
Etiology
• Bacteria Salmonella, Spherophorus
necrophorous.
• Virus - Infectious canine hepatitis.
• Chemicals - Carbon tetrachloride.
• Parasites - Fasciola hepatica, F. giantica.
• Poisons/toxins - Aflatoxins.
• Once cirrhosis of liver starts, it is not checked
even after removal of the cause as the newly
formed fibrous tissue itself acts as an irritant to
cause further proliferation offibroblasts.
• Liver becomes hard and firm.
• Surface ofliver becomes uneven and nodular.
• Size ofliver becomes reduced due to atrophy.
• Colour becomes yellowish, grey.
• Increase in fibrous tissue within and around
lobules.
• Infiltration ofmacrophages and lymphocytes.
• Central vein is either absent or placed
eccentrically.
• Hepatocytes show degenerative and necrotic
changes.

Fig. 16.48.Photomicrograph ofliver showing
diffuse necrosis
Fig.16.49.Photograph showing cirrhosis in liver
Fig. 16.50.Photomicrograph showmg
cirrhosis in liver
Fig. 16.51.Photomicrograph showing
cirrhosis in liver
199
Fig. 16.52.Photograph showing cholecystitis in birds
Fig. 16.53.Photograph showing cholangitis
(ARSIUSDA)
Fig. 16 54.Photograph showmg pearly
disease
Fig.16.55.Photograph showing
haemorrhage in mesentry due to peritonitis

Systemic Pathology
Biliary cirrhosis is characterized by
proliferation of fibrous tissue around the bile
ducts encircling them e.g. Fasciola giantica.
• Glissonian cirrhosis is mostly confined to
areas at a short distance beneath the capsule.
• Pigment cirrhosis is associated with yellow
discolouration.
• Central or cardiac cirrhosis is increase in
fibrous tissue around the central vein as a
result ofchronic passive congestion.
• Parasitic cirrhosis occurs due to damage
caused by migration of parasites e.g. Ascaris
lumbricoid~s, Schistosoma sp.
CHOLECYSTITIS
Cholecystitis is the inflammation of gall bladder
characterized by congestion, thickening of wall and
infiltration of mononuclear cells. Cholangitis is the
inflammation ofbile duct (Figs. 16.52 & 16.53).
Etiology
• Parasites - Fasciola sp.
• Foreign body - Stones
• Bacteria - E. coli.
• Thickening ofthe wall ofgall bladder.
• On opening of gall bladder, there may be
parasites/stones/foreign body.
• Contents of gall bladder may be watery or
thick oily.
• Congestion.
• Proliferation of fibrous tissue in the wall of
gall bladder.
• Infiltration of mononuclear cells.
• Increased number of mucus secreting cells.
PANCREATITIS
Pancreatitis is the inflammation of pancreas
characterized by necrosis of pancreatic tissue,
infiltration of neutrophils and mononuclear cells
and fibrous tissue proliferation.
200
Etiology
• Bacteria.
• Virus- Reovirus in poultry.
• Parasites.
• Pancreas becomes pale, swollen, oedematous.
• In chronic cases, atrophy ofpancreas.
• Pancreas becomes hard, firm, and fibrous.
• Necrosis ofpancreatic cells.
• Oedema, infiltration of leucocytes,
haemorrhage.
• Fibrosis characterized by proliferation of
fibroblasts.
PATHOLOGY OF PERITONIUM
Peritonitis is the inflammation of peritoneum
characterized by hemorrhagic suppurative,
serofibrinous or nodular lesions (FIg. 16.54 &
16.55).
Etiology
• Bacteria - Staphylococci, Mycobacterium sp.
• Virus.
• Neoplasia.
• Parasites .
• Serofibrinous, fibrinous, haemorrhagic,
suppurative or granulomatous lesions.
• Accumulation of clear fluid is known as
Hydroperitoneum or Ascites.
• Presence of nodules in tuberculosis is also
termed as "Pearly disease".
• Serofibrinous, suppurative or granulomatous
lesions.
• Thickening of peritoneum, adhesions due to
fibrosis.

MODEL QUESTIONS
1. In esophagus sub-epithelial fibrous nodules are produced by ..................
2. Esophageal choke may lead to .................. in ruminants characterized by .................. rumen.
3. Omasitis is the inflammation of..........caused by...............and characterized by............nodules.
,4. Clostridium septicum may cause .................. in sheep characterized by .................., ..................
and .................. ofabomasal folds.
5. Haemorrhagic enteritis is the inflammation of .................. along with .................. exudates
caused by .................., .................. and .................. bacteria and characterized by .................. or
.................. haemorrhage in the intestinal wall.
6. Chronic enteritis is the..............inflammation of intestine characterized by...............changes like
................, .................and .................. in lamina propria leading to .................. of intestinal wall.
7. In poultry necrotic enteritis is caused by ............after the primary damage caused by ................
8. Coligranuloma is also known as .................. in poultry and is caused by ..................
9. .................. is the cause of ingluvitis in poultry which produce .................. like lesions.
10. In acute toxic hepatitis, necrosis occupying a considerable area in lobule is known as ...............
Q. 1. Write true orfalse, correct thefalse statements.
Q.3.
Q.4.
1. ...........Ulcerative stomatitis is a feature of mucosal disease in cattle.
2. ...........Impaction ofrumen may lead to alkalosis.
3. ...........Hog cholera virus produces punched out ulcers in abomasum.
4. ...........Actinobacillosis in omasum is characterized by haemorrhagic lesions.
5. ...........Focal necrosis ofliver covers a considerable area oflobules.
6. ...........Cirrhosis is the extensive fibrosis ofliver.
7. ...........Once cirrhosis starts it can't be checked in spite ofremoval ofcausative agent.
8. ...........Parasitic cirrhosis is caused by Fasciola gigantica.
9. ...........Cholangitis is the inflammation ofgall bladder.
10............Midzonal necrosis occurs in rift valley fever.
Define the followings.
1. Necrotic enteritis
2. Atresia ani
3. Piliconcretions
4. Glossitis
5. Cleft palate
6. Intussusception
7. Phytobezoars
8. Cardiac cirrhosis
9. Cholangitis
10. Pearly disease
Write short notes on.
1. Frothy blot
2. Hjarre's disease
11. Ingluvitis
12. Polybezoars
13. Cheilitis
14. Volvulus
15. Gingivitis
16. Torsion of intestine
17. Atresia coli
18. Typhlitis
19. Glissonian cirrhosis
20. Parasitic cirrhosis
9. Hernia
10. Necrosis in liver
201

Systemic Pathology
3. Enteroliths 11. Peritonitis
4. Cholecystitis 12. Chronic enteritis
5. Traumatic reticulitis 13. Acute toxic hepatitis
6. Fibrinous enteritis 14. Developmental anomalies ofdigestive system
7. Impaction 15. Choke in esophagus
8. Cirrhosis
Q. 5. Select appropriate word(s) from the four options given with each statement.
1. Turkish towel like lesions are observed in ..................
(a) Candidiasis (b) Histomoniasis (c) Moniliasis (d) Coccidiosis
2. Vesicular stomatitis is seen in cases of ..................
(a) Rinderpest (b) Mucosal disease (c) Hog cholera (d) FMD
3. Choked oesophagus may cause .................. in ruminants.
(a) Impaction (b) Vomition (c) Tympany (d) Gastritis
4. Rumen is distended due to accumulation of .................. in bloat.
(a) H2S (b) CO2 (c) CO (d)All ofthe above
5. Traumatic reticulitis may lead to ...................
(a) Pericarditis (b) Peritonitis (c) Pleurisy (d)All ofthe above
6. Increase in .................. cells is observed in catarrhal enteritis.
(a) Mast cells (b) Eosinophils (c) Goblet (d) Neutrophils
7. Punched out ulcers are produced by ...................
(a) Theileria (b) Babesia (c) Hog cholera (d) Clostridium sp.
8. Granulomatous lesions in intestine ofpoultry are observed in ...................
(a) Coli granuloma (b) E. coli infection (c) Hjarre's disease (d)All ofthe above
9. Telescoping ofintestine is also known as ..................
(a) Torsion (b) Volvulus (c) Intussusception (d) None
10. Eimeria tennella causes .................. in intestines.
(a) Typhlitis (b) Enteritis (c) Colitis (d) Proctitis
11. Necrosis ofhepatocytes at one side ofcentral vein in liver is known as .................. necrosis.
(a) Centrilobular (b) Midzonal (c) Paracentral (d) Focal
12. Parasitic cirrhosis is caused by ...................
(a) Hemonchus sp. (b) Ascaris lumbricoides (c) Fasciola sp. (d) Amphistomes
13. Cholecystitis is the inflammation of ...................
(a) Urinary bladder (b) Bile duct (c) Gall bladder (d) Pancreas
14. Reovirus causes .................. ofpancreas.
(a) Hypertrophy (b) Atrophy (c) Hyperplasia (d) Hypoplasia
15. 'Pearly disease' is caused by ...................
(a) Streptococci (b) Staphylococci (c) Mycobacterium sp. (d) None
16. Erosive stomatitis is seen in ...................
(a) Rinderpest (b) Mucosal disease (c) Pox (d) FMD
17. Ingluvitis is the inflammation of ...................
(a) Colon (b) Rectum (c) Jenjunum (d) Crop
18. Sub-epithelial fibrous nodules are produced in .................. esophagitis.
(a) Traumatic (b) Bacterial (c) Viral (d) Parasitic
19. Sudden change in feed with lush green fodder is the cause of ...................
(a) Impaction (b) Tympany (c) Reticulitis (d) None
202

20. Acute abomasitis characterized by oedema, congestion and haemorrhage of abomasal folds is
feature of ...................
(a) Enterotoxaemia (b) Black disease (c) Braxy (d) Blue tongue
21. Corrugations in large intestines are observed in ...................
(a) Tuberculosis (b) Paratuberculosis (c) Pseudotuberculosis (d)All ofthe above
22. Pica may lead to formation of ...................
(a) Piliconcretions (b) Polybezoars (c) Both a & b (d) None
23. Enterolith may cause ...................in horses.
(a) Enterotoxaemia (b) Colic (c) Lameness (d) Diarrhoea
24. Frothy bloat occurs in buffaloes due to ....................
(a) Saponin (b) Fatty acids (c) Carbohydrate (d) None
25. Button ulcers are produced in abomasum due to ....................
(a) Salmonella sp. (b) Staphylococci (c) E. coli (d) FMD
203

17
PATHOLOGY OF
HEMOPOITIC AND IMMUNE
SYSTEM
• Anemia
• Hemolytic
• Haemorrhagic
• Deficiency
• ToxidAplastic
• Autoimmune Hemolytic
• Polycythemia
• Leukocytosis
• Leukopenia
• Pathology of Spleen
• Pathology of Lymphnodes
• Pathology of Thymus
• Pathology of Bursa
• Model Questions

Pathology ofHemopoietic and Immune System
Hereditary anemia
Hereditary anemia has been reported in mice due to
defects in erythropoiesis or reduced vitality of
erythrocytes. Erythropenia along with leucopenia
occurs in mouse foetus on 20th
day of gestation due
to defective autosomal chromosome 4. Sex linked
anemia in mouse is hypochromic with deficient
bone marrow and occurs in hemizygus males or
homozygus females. This anemia occurs due to
deficiency of iron as a result of poor absorption
from gastrointestinal tract.
Autoimmune hemolytic anemia in foals
It occurs due to incompatible blood group antigens
of male and female parents. The mare does not
have that blood group antigen but foetus acquires it
from father. The foetal blood exposed to dam
through placental exchanges leads to induction of
antibody production in mares against foetal blood
group antigen. These antibodies accumulate in
colustrum and when foal suck the milk from mares,
they are readily absorbed through G.!. tract of foals
in blood and cause destruction of erythrocytes
leading to anemia.
Congenital defects in lymphocytes
Congenital defects in lymphocytes are classified
under stem cell aplasia/agenesis leading to
combined immunodeficiency with absence of both
T- and B-lymphocytes in Arabian foals. It occurs
either due to inherited gene defect or
differentiation/maturation defects in lymphocytes.
It is characterized by agammaglobulinemia,
lymphopenia, hypoplasia of thymus, lymphnodes
and spleen.
Chediak-Higashi Syndrome
This syndrome is related with defects in phagocytic
cells such as defective neutrophils and monocytes.
The defects are in chemotaxis, engulfment and
killing of bacteria and associated with defective
assembly of cytoplasmic microtubules responsible
for degranulation and release of lysosomal
enzymes, there is depression of superoxide anions
leading to persistent bacterial infections.
205
ANEMIA
Anemia is the decrease in number of erythrocytes
or hemoglobin concentration in erythrocytes per
unit of blood and is characterized by pale mucus
membrane, dyspnoea, cardiac hypertrophy and
weakness. Anemia is classified according to
morphological characteristics of erythrocytes and
on the basis of causative factors. Morphologically,
anemia is classified as macrocytic, normocytic and
microcytic depending on the size of red blood cells
and normochromic and hypochromic based on the
presence of quantity of hemoglobin in RBC.
Macrocytic anemia is characterized by increased
size of RBC and occurs due to acute blood loss or
hemolysis resulting in excessive production and
availability of immature erythrocytes in blood.
Such cells also have reduced amount of
hemoglobin and are termed as hypochromic.
Macrocytic normochromic anemia is increase size
of RBC with normal hemoglobin and has been
observed in deficiency of folic acid, niacin and
vitamin B12. Normocytic anemia is most common
in animals occurs due to neoplasia, irradiation and
is also known as aplastic anemia as a result of
aplasia or agenesis of RBC. In Normocytic
normochromic, normal size of RBC with normal
hemoglobin occurs as a result of depression of
erythrogenesis. Microcytic anemia is reduction in
size of erythrocytes with decreased hemoglobin
(Microcytic hypochromic) and occurs in deficiency
ofiron and pyridoxine or chronic blood loss.
In anemia, the size of RBC varies markedly, some
being of large size and some of small size and is
known as anisocytosis. The presence of abnormal
shape (elongated, angular, ovoid, distorted) ofRBC
is termed as poikilocytosis. In some blood smears,
there are nucleated RBC's which are immature due
to increased production to meet the demand.
Sometimes, the erythrocytes have minute dark
spots known as basophilic stippling which occurs
in acute blood loss. Some erythrocytes stain
unevenly with some dark and light colour spots and
are known as polychromatophilia which is an
indication of active erythrogenesis. The
denaturation and precipitation of hemoglobin leads
to appearance ofpurplish granules in RBC near the

A
B
Systemic Pathology
Aa- positive foal
( ) ( RBC With
U ~ surface Ag
Z::;;, /
~ ~l
'> :.-L., Processing of
~
., .' AgbyAPC'1 • ,
j ,
/' .,
I 'l '---'
Generation of f'e' Generation of
T-cytotoxic plasma cells
cells
/--'-" /~"
Hemolytlc disease in foal
Fig.17.1.Dwgram showing autoimmune
hemolytic anemia In foal
Fig.17.2. Photograph showing toxic aplastic
anemw A. Normal B. Yellow bone marrow
206
( /."", <.
/
/'
,;
I,
' ' >'
'''--_/
Fig. 17.3. Diagram showmg autoimmune
hemolytic anemia
Fig. 17.4. Photograph showing atrophy in spleen
(A. Normal, B, C and D Progressive atrophied of
spleen)
Fig.17.5. Photograph showing depletion
oflymphoid tissue

Pathology ofHemopo;et;c and Immune System
cytoplasmic membrane which are known as "Heinz
bodies". According to etiological factors, anemia is
classified as hemolytic, haemorrhagic or deficiency
anemia.
HEMOLYTIC ANEMIA
Hemolytic anemia occurs due to excessive lysis of
erythrocytes and is characterized by icterus,
hemoglobinuria and presence of nucleated
erythrocytes in blood and hemosiderosis in spleen.
Etiology
• Infections e.g. Anaplasma spp. Babesia spp.,
Equine infectious anemia virus.
• Toxins/ poisons e.g. snake venom, chronic lead
poisoning.
• Immune mechanisms e.g. autoimmunity
against erythrocytes (Fig. 17.1).
• Pale mucus membranes.
• Icterus.
• Blood is thin, watery.
• Hemoglobinurea.
• Decreased number oferythrocytes.
• Presence ofnucleated/immature RBC in blood.
• Hemosiderin laden cells in spleen.
HAEMORRHAGIC ANEMIA
Haemorrhagic anemia occurs due to severe
haemorrhage, extravasation of blood and is
characterized by pale mucus membrane and
haemorrhage in body.
Etiology
• Infections e.g. Acute septicemic diseases.
• Toxins/poisons e.g. Bracken fern poisoning.
• Parasites e.g. Hemonchus contortus.
• Deficiency e.g. vitamin C deficiency.
• Petechiae or echymotic haemorrhage.
• Pale mucus membrane.
• Hematuria.
207
• Haemorrhage in various tissues /organs.
• Macrocytic or nomlOcytic characters ofRBC.
• Poikilocytosis.
• Hyperplasia ofbone marrow.
DEFICIENCY ANEMIA
Deficiency anemia occurs as a result of deficiency
of iron, copper, cobalt and vitamins and 1S
characterized by pale mucus membrane, weak and
debilitated body and decreased number of
erythrocytes with hypochromasia in blood.
Etiology
• Deficiency ofiron.
• Deficiency ofcopper.
• Deficiency ofcobalt.
• Deficiency of vitamin B12, Pyridoxine,
riboflavin and folic acid.
• Parasitic infestation may lead to deficiency.
• Thin watery blood with light red colour.
• Weak and debilitated carcass.
• Heavy parasitic load in gastrointestinal tract.
• Microcytic hypochromic erythrocytes.
• Poikilocytosis.
TOXIC APLASTIC ANEMIA
Toxic aplastic anemia is agenesis or aplasia of
hemopoietic tissues in bone marrow and there is
lack of erythrocyte production. It is characterized
by the absence of developmental stages of
erythrocytes viz., norrnoblasts, megaloblasts etc.
Etiology
• Radiation e.g. X-rays, y rays, or UV rays.
• Sulfonamides.
• Bracken fern toxicity.
• Uremia.
• Feline panleukopenia.

Systemic Pathology
Fig. I 7.6. Photograph ofspleen showing
tubercles/granulomatous lesions (ARSIVSDA)
Fig.17.7. Photograph showing lymphadenitis
in horse due to glanders
Fig.l7.B. Photograph showing caseous
lymphadenitIs (ARS/USDA)
Fig.l7.9. Photomicrograph oflymphnode
showing acute lymphadenitIs
208
Fig.17.10. Photomicrograph oflymphnode
showing chronic lymphadenitis
A B c D
Fig.l7.II. Photograph showing atrophy ofthymus
A. Normal B. C and D. progressive atrophy
.Fig.17 12. Photomicrograph ofthymus showing
depletion oflymphoid tissue.
Fig.17.J3. Photograph showmg oedema in bursa
ofFabncius due to Gumboro disease.

• Weak and debilitated animal.
• Dyspnoea.
• Bone marrow becomes yellow/fatty (Fig.
17.2).
AUTOIMMUNE HEMOLYTIC ANEMIA
Autoimmune hemolytic anemia occurs as a result
of destruction of erythrocytes by immune
mechanisms developed against erythrocytes.
Etiology
Microscopic features • Autoimmune hemolytic anemia in foals.
• Absence of developmental stages or RBC such
as norrnoblasts, megaloblasts etc.
• Antibodies produced against own RBC of an
• Agranulocytosis i.e. reduction of WBC in
circulating blood.
animal (Fig. 17.3).
• Equine infectious anemia.
• Anaplasmosis.
• Bone marrow becomes fatty. • Systemic lupus erythematosus.
Table 17.1 Differential features of various types of Anaemia
Hemolytic Haemorrhagic Deficiency Toxic/ Aplastic Autoimmune
Hemolytic
Macrosco I. Pale mucus I. Petechiae or I. Pale mucus I. Pale mucus I. Pale mucus
pic membranes Echymotic membrane membrane membrane
features 2. Icterus haemorrhage 2. Thin watery 2. Weak and 2. Enlargement of
3. Blood is thin, 2. Pale mucus blood with light debilitated animal liver, spleen and
watery. membrane red colour 3. Dyspnoea Iymphnodes
4. Hemoglobinurea 3. Hematuria 3. Weak and 4. Bone marrow 3. Hemoglobinuria
debilitated carcass becomes 4. Lameness due to
4. Heavy parasitic yellow/fatty rheumatoid
load in arthritis
gastrointestinal
tract.
Microsco I. Decreased 1. Haemorrhage in 1. Microcytic 1. Absence of 1.
pic number of various tissues hypochromic developmental Erythrophagocytos
features erythrocytes /organs erythrocytes. stages or RBC is
2. Presence of 2. Macrocytic or 2. Poikilocytosis such as 2. Demonstration
nucleated/immatur normocytic normoblasts, of antibodies
e RBC in blood characters ofRBC megaloblasts etc. against own RBC
3. Hemosiderin 3. Poikilocytosis 2. Agranulocytosis in sera of animals.
laden cells in 4. Hyperplasia of
i.e. Reduction of 3. Active
spleen WBC in circulating erythropoiesisbone marrow blood.
4.
3. Bone marrow Glomerulonephritis
becomes fatty.
209

Systemic Pathology
• Enlargement of liver, spleen and lymphnodes.
• Hemoglobinuria.
• Lameness due to rheumatoid arthritis.
• Erythrophagocytosis.
• Demonstration of antibodies against own RBC
in sera of animals.
• Active erythropoiesis.
• Glomerulonephritis.
POLYCYTHEMIA
Polycythemia is increase in number of erythrocytes
in circulating blood. It may be relative increase as a
result of dehydration or decrease in plasma volume
or absolute due to anoxia.
Etiology
• Dehydration due to diarrhoea, vomiting and
loss of fluid in oedema/inflammation.
• Anoxia in high altitudes.
• Heart diseases e.g. patent ductus arteriosus.
• Severe pulmonary emphysema.
Flg.17.14 Photograph showing haemorrhage in bursa of
Fabricius due to Gumboro disease
210
• Erythroid leukemia.
• Dehydration, mucus membrane dry, sticky.
• Pulmonary emphysema, fibrosis in lungs.
• Increase hemoglobin concentration.
• Increased number oferythrocytes
• Severe damage in lungs, congestion,
emphysema, fibrosis
LEUCOCYTOSIS
Leucocytosis is increase in number of leucocytes in
circulating blood caused by various infections.
There is also increase in white blood cells in blood
due to neoplastic condition and is known as
Leukemia. As the leucocytes consist ofneutrophils,
lymphocytes eosinophils, monocytes and basophils;
the increase in number of neutrophils is termed as
neutrophilia, eosinophils as eosinophilia,
Iymphocytes as lymphocytosis, basophils as
basophilia and of monocytes as monocytosis.
Flg.17.15. Photograph ofbursa ofFabricius
showzng atrophy andfibrosis (A. Normal. B,C and
D. progressive atrophic changes)
Fig.17.16. PhotomIcrograph ofbursa of
Fabricius showing depletIOn oflymphoid tIssue

Etiology
• Infections.
• Bacterial infection - neutrophilia.
• Viral infections and chronic bacterial
infections - lymphocytosis.
• Parasites - eosinophilia.
• Allergies - basophilia, lymphocytosis.
• No characteristic lesion.
• Reactive lymphnode hyperplasia.
• Enlargement of lymphoid organs such as
spleen, thymus and bursa.
• Increase in number of total leucocytes in
blood.
• Increase in absolute lymphocyte, absolute
neutrophil, absolute eosinophil counts.
• Hyperplastic lesions in lymphoid organs.
LEUCOPENIA
Leucopenia is decrease in number of white blood
cells. The leucocytes are neutrophils, lymphocytes
monocytes, eosinophils and basophils. If there is
decrease in number of all 5 cells of leucocytes, it is
known as panleucopenia. The 'decrease in number
of neutrophils is termed as neutropenia and
lymphocytes as lymphopenia.
Etiology
• Congenital e.g. Chediak-Higashi Syndrome.
• Infections e.g. Feline panleucopenia virus,
infectious bursal disease virus.
• Chemicals e.g. Pesticides, heavy metals.
• Radiation e.g. X-rays.
• Atrophy oflymphoid organs.
• Recurrent infections, vaccination failures,
pyogenic disorders.
• Oedema, haemorrhage in bursa, atrophy of
bursa due to fibrosis in IBD infection.
• Decrease in total leucocyte count and absolute
neutrophil and absolute lymphocyte counts.
• Degeneration and necrosis of lymphoid cells in
follicles oflymphoid organ.
211
• Oedema, necrosis, proliferation of fibrous
tissue in bursa in IBD infection.
PATHOLOGY OF SPLEEN
SPLEENITIS
Spleenitis is the inflammation of spleen
characterized by enlargement, infiltration of
inflammatory cells, proliferation of lymphoid
follicles, congestion and oedema followed by
proliferation of fibrous tissue (Figs. 17.4 to 17.6).
Etiology
• Infections e.g. bacteria, virus.
• Deficiency of vitamins and minerals.
• Amyloidosis.
• Immunodeficiency e.g.environmental pollution
• Enlargement ofspleen.
• Necrotic patches on spleen.
• In chronic cases or in immunological
disorders.
• There is atrophy of spleen due to fibrosis.
• Necrotic patches and congestion leading to
mottling.
• Congestion in spleen.
• Proliferation oflymphoid follicles/cells.
• Oedema.
• In atrophied spleen, proliferation of fibrous
tissue, depletion oflymphoid cells/follicles.
PATHOLOGY OF LYMPHNODES
LYMPHADENITIS
Lymphadenitis is the inflammation of lymphnodes
characterized by enlargement/atrophy, congestion
proliferation of lymphoid cells/depletion of
lymphoid cells, oedema and fibrosis of lympbnodes
(Figs. 17.7 to 17.10).

Systemic Pathology
Etiology
• Infections e.g. Rinderpest.
• Immunological disorders e.g. immuno-
deficiency.
• Deficiency e.g. deficiency ofprotein.
• Environmental pollution e.g. pesticides, heavy
metals.
• Tumors/neoplasm e.g. lymphosarcoma.
• Enlargement oflymphnodes.
• Congestion.
• Oedema.
• In chronic cases- fibrosis.
• Atrophy.
• Congestion, oedema, proliferation of lymphoid
cells.
• In chronic cases, proliferation of fibrous tissue,
depletion of lymphoid cells.
PATHOLOGY OF THYMUS
THYMOMA ITHYMIC HYPERPLASIA
It is characterized by congestion and hyperplasia of
lymphoid cells in thymus. The inflammation of
thymus in chronic cases is characterized by atrophy
and proliferation of fibrous tissue (Figs. 17.11 &
17.12).
Etiology
• Immunological disorders.
• Environmental pollution e.g. pesticide, heavy
metals.
• Toxins/poisons.
• Aging e.g. in adult poultry thymus regresses.
• Congestion, reddening of thymus.
• Oedema.
• Increase in size.
• Atrophy, thinning like thread.
• Congestion, oedema.
• Proliferation of lymphoid cells.
• Depletion of lymphoid cells.
• Proliferation of fibrous tissue.
PATHOLOGY OF BURSA
BURSITIS
Bursitis is the inflammation ofbursa of Fabricius in
poultry characterized by oedema, congestion,
haemorrhage or atrophy and depletion of lymphoid
cells (Figs. 17.13 to 17.16).
Etiology
• Infectious Bursal disease virus (Birnavirus).
• Environmental pollution e.g. Pesticides, heavy
metals.
• Enlargement ofbursa.
• Oedema.
• In chronic cases, atrophy and fibrosis.
• Oedema.
• Depletion oflymphoid tissue.
• Degeneration and necrosis of lymphoid cells.
• Proliferation fibrous tissue.
MODEL QUESTIONS
1. Hereditary anemia occurs in mice due to defects in ............... or ............... of erythrocytes
leading to............... and...............
2. Chediak-Higashi Syndrome is related with defects in........... including............ and............... .
The defect are in..............., ............... and............... ofbacteria.
212

3. Morphologically, anemia is classified as.........., ......... and......... while on the basis of presence
ofhemoglobin in RBC, it is divided into............ and...........
4. Hemolytic anemia occurs due to............... of erythrocytes in............... and is characterized
by............... and...............
5. ............... (parasitic infection) may cause haemorrhagic anemia.
6. Deficiency anemia occurs due to deficiency of.............., ............., ............ and vitamin ...........,
............, ..............., ............... and characterized by............., ............. and.............
7. Leucocytosis is............... number of WBC in............... caused by............... and............... .
Q. 2. Write true orfalse against each statement, correct the false statement.
Q.3.
1. .........Leukemia is increase in number of allleucocytes in blood.
2. .........Polycythemia is decrease in RBC in blood.
3. .......:.Inflammation of spleen may lead to immunosuppression.
4. .........Pesticides do not cause lymphadenitis.
5. .........Lymphopenia is a feature ofcongenital defects of stem cells.
6. .........Bima virus causes thymic hyperplasia
7. .........Atrophy ofbursa occurs due to heavy metal toxicity
8. .........Chediak-Higashi Syndrome is decrease in WBC in blood
9. .........Sex linked anemia in mouse is hypochromic in nature due to iron deficiency.
10. .........Anisocytosis is variation in size ofRBC
Define the followings.
1. Polycythemia
2. Poikitocytosis
3. Panleucopenia
4. Leukemia
5. Anisocytosis
6. Macrocytic normochronic
7. Neutropenia
8. Microcytic
9. Polychromatophilia
10. Lymphopenia
1. Hemolytic anemia.
2. Anemia due to nutritional deficiency.
3. Impact ofenvironmental pollution on lymphoid organs.
4. Leucopenia.
5. Chediak Higashi syndrome.
Q. 5. Select most appropriate word(s) from the four options given against each statement.
1. Congenital defects in lymphocytes may result into .........
(a) Lymphopenia (b) Agammaglobulinemia (c) Hypoplasia of spleen (d)All of the above
2. The size ofRBC varies from small to large in peripheral blood and this condition is known as...
(a) Poikilosytosis (b) Anisocytosis (c) Polychromatophilia (d) Heinz bodies
3. Hemolytic anemia is caused by .........
(a) Anaplasma spp. (b) Coccidia (c) Hemonchus (d) Proteus sp.
4. Hematuria is an example of .........anemia
(a) Hemolytic (b) Autoimmune (c) Haemorrhagic (d) Deficiency
5. Eosinophilia occurs in .........infection
(a) Bacterial (b) Prion (c) Viroid (d) Parasitic
213

Systemic Pathology
6. Decrease in number of all components of leucocytes is known as .........
(a) Leucopoenia (b) Panleucopenia (c) Leucocytosis (d) Leukemia
7. Pesticides may cause .........
(a) Neutropenia (b) Lymphopenia (c) Hypogammaglobulimia (d)All of the above
8. Depletion oflymphoid tissue from follicles ofbursa ................
(a) Gumboro disease (b) Rinderpest (c) Coccidiosis (d) Salmonellosis
9. Macrocytic normochromic anemia is.........
(a) Large size RBC (b) Decreased Hb
(c) Small size RBC (d) Large size RBC & normal Hb
10. Erythrocytes having minute dark spots are known as .........
(a) Heinz bodies (b) Theleiria (c) Basophilic stippling (d) None
214

18
PATHOLOGY OF URINARY
SYSTEM
• Functional disturbances
• Pathology of kidneys
• Glomerulonephritis
• Interstitial nephritis
• Pyelonephritis
• Nephrosclerosis
• Urolithiasis
• Pathology of ureter
• Pathology of urinary bladder
• Cystitis
• Pathology of urethra
• Urethritis
• Model Questions

Systemic Pathology
Aplasia
Absence of one or both kidneys. Absence of one
kidney is observed in animals with compensatory
hypertrophy of another kidney and such animals
may survive well.
Hypoplasia
The size of kidneys remain small as they don't
grow properly due to defect in a single recessive
autosomal gene.
Cyst in kidney
Single or multiple cysts in pig and dog kidney are
reported with tinged yellow colour. They may arise
from nephron due to its distension. Presence of
multiple cysts is also termed as congenital
polycystic kidney.
• Type-I cysts are formed due to dilation and
hyperplasia of collecting tubules resulting in
spongiform kidneys. In such neonates cystic
bile ducts are also present.
• Type-II polycystic kidney is formed due to
absence of collecting tubules and
developmental failUIe of nephron. The cysts
are thick walled with dense connective tissue
•
and may involve one or both kidneys.
Type-Ill cysts in kidneys occur due to multiple
abnormalities during development. Cysts
develop from tubules or Bowmen's capsule
with part ofglomeruli in cyst. This condition is
bilateral and causes considerable enlargement
of kidney due to clear fluid or blood mixed
fluid containing cysts.
FUNCTIONAL DISTURBANCES
Proteinuria
Presence of protein particularly albumin in urine.
Protein is found as smooth, homogenous, pink
staining precipitate also called as 'cast'. The
presence of albumin in urine is indicative of
damage in glomeruli. It is also characterized by
oedema due to protein deficiency.
216
Hematuria
Presence of blood in urine giving bright red colour.
It may occur due to damage in glomeruli, tubule or
haemorrhage anywhere from glomeruli to urethra.
The most important cause of hematuria is bracken
fern toxicity (Fig. 18.1).
Hemoglobinuria
When hemoglobin is present in urine without
erythrocytes due to intravascular haemolysis. The
urine becomes browriish red in colour. It must be
differentiated from hematuria in which intact
erythrocytes are present and settle down after some
time leaving clear urine as supematant.
Hemoglobinuria is caused by various infections
such as Leptospira sp.• Babesia sp. or phosphorus
deficiency in animals (Fig. 18.1).
Anuria
Absence of urine is known as anuria which may be
due to:
• Absence of urinary secretion due to
glomerulonephritis.
• Inelastic renal capsule unable to exert
sufficient pressure required for glomerular
filtration leading to nephrosis.
• Due to hydronephrosis or calculi urine already
secreted puts back pressure to prevent further
secretion.
• Low blood pressure.
• Dehydration.
• Necrosis oftubular epithelium.
Polyuria
Increased amount of urine leading to frequent
urination caused due to diabetes insipedus,
hormonal imbalance and polydipsia. In this
condition, waste products are successfully
eliminated.
Uremia
The presence of harmful waste products like uric
acid, creatinine and urea in blood. Normally such
waste products are removed by excretion through
kidneys. But due to damage in kidneys or
obstruction by inflammation, neoplasm, abscess

Pathology of Urinary System
Fig. 18.1. Photograph showing (A) Normal (B)
hematuria and (C) hemoglobinuria
Fig. 18.2. Photograph showing nephrosis
Fig. 18.3. Photomicrograph showing nephrosis
(coagulative necrosis)
Fig. 184. Photomicrograph showing nephrosis
217
Deposition
in glomeruli
1~~
~~~~
Subendothelial Membranus
Ab
Removal
through
phagocytosis
Subepithelial
Fig. 18.5. Dtagram o/immune complex mediated
glomerulonephritis

Systemic Pathology
and most importantly by presence of calculi, urine
remains in the system and causes uremia. Uremia is
characterized by headache, vomiting,
hyperirritability, convulsion, ulcers in oral cavity
and stomach, normochromic and normocytic
anemia, hemosiderosis and thrombocytopenia.
Glycosuria
Presence of glucose in urine. This is also known as
diabetes mellitus, a metabolic disorder. It may
occur due to insulin deficiency. This condition is
not common in animals. However, it may occur in
dogs as a result of hypoglyecemia. It may occur in
sheep due to enterotoxaemia caused by Clostridium
welchii type D.
Pyuria Presence of pus in urine due to suppurative
inflammation in urinary tract.
Ketonuria
Presence of ketone bodies in urine, which is
common in diabetes mellitus, acetonemia,
pregnancy toxaemia and in starvation.
Oliguria
In this condition, there is decreased amount of
urine, which occurs due to glomerulonephritis,
obstruction in urinary passage, dehydration, low
blood pressure and tubular damage.
NEPHROSIS
Nephrosis is the degeneration and necrosis of
tubular epithelium without producing inflammatory
reaction. It mostly includes acute tubular necrosis
as a result of ischemia or toxic injury to kidney.
Nephrosis is characterized by necrosis and
sloughing of tubular epithelial cells exhibited by
uremia, oliguria, anuria (Figs. 18.2 to 18.4).
Etiology
• Hypotension.
• Heavy metals.
• Mycotoxins e.g. Ochratoxin.
• Antibiotics e.g. Gentamicin.
218
• Swelling ofkidneys.
• Capsular surface smooth, pale and translucent.
• Vacuolation in tubular epithelium.
• Coagulative necrosis.
• Sloughing oftubular epithelium.
GLOMERULONEPHRITIS
Glomerulonephritis is the inflammation of
glomeruli primarily characterized by pale and
enlarged kidneys with potential haemorrhage,
oedema of glomeruli, congestion and infiltration of
inflammatory cells. Due to presence of mesangial
proliferation, it is also called mesangio proliferative
glomerulonephritis (MPGN) (Figs. 18.5 to 18.7).
Etiology
• Streptococci infection.
• Immune complexes.
• Environmental pollutants such as
Organochlorine pesticides.
• Enlarged kidneys.
• Oedema, pale kidneys.
• Petechiae on kidneys.
• Proteinuria, uremia, hypercholesterolemia and
increased creatinine level in blood.
• Oedema of glomeruli leading to increase in
size.
• Infiltration ofneutrophils, macrophages.
• Compression of blood capillaries and absence
of erythrocytes.
• Thrombosis and necrosis of glomerular
capillaries.
Based on type of lesions, it can be divided into 5
subtypes.
1. Type-I MPGN
• Proliferation ofmesangiaI cells.

Fig. 18.6. Diagram showing different locations
ofdeposits ofimmune complexes A.
subendothelial B. Membranous and C. Sub
epIthelial deposits ofimmune complexes.
Fig. 18.7. Photomicrograph showing immune
complexes in glomerult (Immunoperoxidase staining)
interstitial nephritis
Fig. 18.9. Photomicrograph .,hawing mterstitial
nephritis with severe haemorrhages In lIltersflum.
219
FIg. IS. 10. Photomicrograph showing
suppura/ive nephritis
Fig. 18 11. Photomicrograph ofkidney showing
nephrosclerosis
Fig. 18.12. Photograph ofkIdney showmg
nephrolithiasis
FIg 18.13. Photograph oj kIdney showll1g
nephrolithiasis

Systemic Pathology
• Deposition of immune complexes containing
IgG, IgM, IgA and C3.
• Immune complexes penetrate vascular
endothelium but not the basement membrane
and are deposited in subendothelial region.
• Proliferation and swelling of endothelial cells.
• Immune complexes induce production of
transforming growth factor (TGFB1) which
increases production of fibrinolectin, collagen
and proteoglycans leading to thickness of
basement membrane; this is also known as
"wire loop" lesions.
2. Type-Il MPGN (Membranous)
• Deposition of immune complexes in basement
membrane (lamina densa).
• Due to uncontrolled activation ofcomplement.
• Proliferation of endothelium and mesangial
cells.
• Demonstration of C3 component, no
immunoglobulin.
3. Type III MPGN (Acute Proliferative)
• Subepithelial deposits of immune complexes
and disruption ofbasement membrane.
• Swelling of epithelium and its proliferation
forming "Epithelial cresent".
• Demonstration of IgG in subepithelial region.
• Congestion and oedema of glomeruli.
lymphocytes.
4. Chronic glomerulonephritis
• Proliferation ofepithelial and endothelial cells.
• Reduplication, thickening and disorganization
ofglomerular basement membrane.
• Lumen ofcapillaries occluded.
• Entire glomerulus is replaced by Hyaline
connective tissue.
5. Focal embolic glomerulonephritis
• Focal zone ofnecrosis in glomeruli.
• Infiltration of neutrophils.
• Proliferation of epithelial cells and formation
ofcrescent.
220
INTERSTITIAL NEPHRITIS
Interstitial nephritis is the inflammation of kidney
characterized by degeneration and necrosis of
tubular epithelium, oedema and infilteration of
inflammatory cells in interstitium (Figs. 18.8 &
18.9).
Etiology
• Ochratoxins and atrinin.
• Leptospira.
• Toxins/ poisons e.g. pesticides.
• Herpes virus.
• Endogenous toxaemia e.g. ketosis.
• Immune complexes.
• Enlargement ofkidneys.
• Necrosis, congestion and haemorrhage.
• Oedema, congestion, haemorrhage.
• Necrosis and degeneration of tubular
epithelium.
• Infiltration of inflammatory cells like
neutrophils, macrophages and lymphocytes in
interstitium.
• Loss of tubules, foci of mononuclear cells,
fibrosis in chronic cases.
• Immune complexes are deposited in granular
form causing degeneration ofepithelial cells of
tubules and mononuclear cell infiltration.
PYELONEPHRITIS
Pyelonephritis is the inflammation of renal pelvis
and parenchyma i.e. tubules characterized by
congestion, suppurative inflammation and fibrosis.
Etiology
• Corynebacterium renale.
• E. coli.
• Actinomyces pyogenes.

FIg. IS.I4. Photomicrograph ofkIdney
showing nephrolithIasis
Fig. IS. 15.Photograph showing ureteritis due
to deposition ofsalts
Fig. IS.16. Photograph showing cystitis
Fig. IS.I7. Diagram showing retelltion of
calculi in urethra ofbovines
• Suppurative inflammation of pelvis and kidney
• Congestion, haemorrhage and abscess parenchyma (Fig. 18.10).
formation in renal cortex, pelvis and ureters. • Necrosis of collecting ducts.
• Pyuria - pus mixed urine in bladder.
• Enlargement of kidneys.
• Purulent exudate in pelvis.
plasma cells in interstitium.
a e I eren la ea ures 0T bl 181 D'n f I ~ t f tvarious types 0 fN h Tepl rt IS
Glomerulonephritis Interstitial Pyelonephritis
Macros 1. Enlarged kidneys 1. Enlargement of kidneys 1. Congestion, haemorrhage
copic
2. Oedema, pale kidneys 2. Necrosis, congestion and
and abscess formation in renal
features
haemorrhage
cortex, pelvis and ureters.
3. Petechiae on kidneys
2. Pyuria- Pus mixed urine in
4. Proteinuria, uremia, bladder.
hypercholesterolemia and
3. Enlargement of kidneys
increased creatinine level in
blood.
221

Systemic Pathology
Microsc 1. Oedema of glomeruli 1. Oedema, congestion, 1. Congestion, haemorrhage
opic leading to increase in size. haemorrhage
2. Suppurative inflammation
features
2. Infiltration ofneutrophils, 2. Necrosis and degeneration ofpelvis and kidney
macrophages. oftubular epithelium parenchyma.
3. Compression ofblood 3. Infiltration of inflammatory 3. Necrosis of collecting
capillaries and absence of cells like neutrophils, ducts.
erythrocytes. macrophages and
4. Purulent exudate in pelvis.
4. Thrombosis and necrosis of
lymphocytes in interstitium.
glomerular capillaries. 4. Loss oftubules, foci of
5. Infiltration ofneutrophils,
mononuclear cells, fibrosis in
lymphocytes and plasma cells
chronic cases
in interstitium.
5. Immune complexes are
deposited in granular form
causing degeneration of
epithelial cells oftubules and
mononuclear cell infiltration.
NEPHROSCLEROSIS
Nephrosclerosis is chronic fibrosis of kidney
characterized by loss of glomeruli and tubules and
extensive fibrosis (Fig. 18.11).
UROLITHIASIS
Urolithiasis is the formation of stony precipitates
anywhere in the urinary passage including kidneys,
ureter, urinary bladder or urethra.
Etiology
• Glomerulonephritis.
• Interstitial nephritis.
• Arterioloscleresis.
• Hard, atrophied kidneys.
• Fibrous nodules on kidneys.
• Thickening of capsule.
• Small white firm kidneys.
• Ischemia, tubular atrophy.
• Loss of glomeruli and tubules.
• Extensive fibrosis.
• Deposition of hyaline mass.
• Infiltration of mononuclear cells.
222
Etiology
• Bacterial infections.
• Metabolic defects.
• Vitamin A deficiency.
• Mineral imbalance.
• Nephrosis, hydronephrosis.
• Distension ofureters.
• Distension ofureters and urinary bladder.
• Hard enlarged kidneys.
• Presence of calculi! stone in kidney, ureter,
bladder or urethra (Figs. 18.12 & 18.14).
There are various types of calculi, which differ in
size, shape and composition. Some of them are as
under:
Oxalate calculi are hard, light yellow, covered with
sharp spines, found in urinary bladder and formed
by calcium oxalate. They cause damage in urinary
bladder leading to haemorrhage.

Pathology ofUrinary System
Uric acid calculi are composed of ammonium and
sodium urates and uric acids, are yellow to brown
in colour, formed in acidic urine, are spherical and
irregular in shape and are not radioopaque.
Phosphate calculi are white or grey in colour,
chalky in consistency, soft, friable and can be
crushed with mild pressure. They are mostly
multiple in the form of sand-like granules. They are
composed of magnesium ammonium phosphate
and occur as a result ofbacterial infection.
Xanthine calculi are brownish red, concentrically
laminated, fragile and irregular in shape. They
rarely occur in animals.
Cystine calculi are small, soft with shiny and
greasy in appearance, yellow in colour which
becomes darker on exposure to air. Insoluble amino
acid cystine precipitates in bladder to form calculi.
Such calculi may cause obstruction of urethra with
cystinuria.
• Presence ofcrystals/stone in lumen oftubules.
• Degeneration and necrosis of tubular
epithelium.
• Haemorrhage.
• Proliferation offibrous tissue.
PATHOLOGY OF URETER
URETERITIS
Ureteritis is the inflammation of ureter
characterized by enlargement, thickening of wall
due to accumulation of urates, or calculi,
pyonephrosis and pyelonephritis (Fig. 18.15).
Etiology
• Tuberculosis.
• Calculi.
• Hydronephrosis.
• Pyelonephritis.
• Pyonephrosis.
• Deposits of whitish/yellowish urates in ureter
in poultry.
• Obstructions ofureter due to calculi leads to its
enlargement and formation of diverticulum.
223
• Thickening of the wall due to congestion and
infiltration ofinflammatory cells.
• Extensive fibrosis with infiltration of
mononuclear cells in chronic cases.
PATHOLOGY OF URINARY BLADDER
CYSTITIS
Cystitis is the inflammation of urinary bladder
characterized by congestion and fibrinous, pumlent
or haemorrhagic exudate (Fig. 18.16).
Etiology
• Urinary calculi.
• Tuberculosis.
• Blockage in urethra.
• Bracken fern poisoning.
• Enlargement ofurinary bladder.
• Thickening of the wall.
• Presence ofsmall nodules on wall.
• Thickening of wall due to infiltration of
neutrophils and macrophages.
• Granuloma in tuberculosis.
• Fibrosis
• Presence ofneoplasm.
PATHOLOGY OF URETHRA
URETHRITIS
Inflammation of urethra is known as urethritis,
which occurs as a result of catheter injury or
calculi. It is characterized by congestion,
obstruction, hydronephrosis and strictures (Fig.
18.17).
Etiology
• Calculi.
• Catheter injury.
• Trichomonas foetus infection.
• Picoma virus infection.

Systemic Pathology
Macroscopic features • Obstruction due to calculi, presence of calculi.• Transient inflammation, congestion and
haemorrhage. Microscopic features
• Strictures (male), diverticulum (female). • Thickening due to inflammatory exudate.
MODEL QUESTIONS
1. Increased amount of urine leading to..........urination is known as ..........which is caused by
.........., ..........and .......... to remove the ..........at a faster rate.
2. Uremia is presence of ..........like .........., ..........and ..........in blood.
3. Presence ofketones bodies in urine has been observed in.........., ......., ..........and .........
4. ............. are fungal toxins which may cause interstitial nephritis.
5. Environmental pollutants such as ..........may induce the formation of ..........in body leading
to ..........in animals characterized by proteinuria.
6. Pyelonephritis is caused by .........., .........., .........., ..........and ..........; of which
..........is the main etiological agent causing disease in cattle.
7. Nephrosclerosis is ..........ofkidney characterized by .........., ..........and ..........and mostly
occurs as a sequaelae to .........., ..........and ..........
Q.2. Write true orfalse against each statement and correct thefalse statement.
Q.3.
1. ..........Glycosuria occurs in enterotoxaemia in sheep.
2. ..........Arteriolosclerosis may lead to pyelonephritis.
3. ..........In cattle, Corynebacterium ovis causes pyelonephritis.
4. ..........Oxalate calculi are hard and composed ofdiammonium and sodium oxalates.
5. ..........Urolithiasis is presence offoreign body in kidneys.
6. ..........In poultry, ureteritis is common feature ofvisceral gout.
7. .. ........Urinary calculi may cause urethritis in bullocks.
8. ..........Low blood pressure may cause polyuria
9. ..........Epithelial cresent is feature of interstitial nephritis.
10. ..........Hypovitaminosis A may predispose the animal for calculi formation in urinary tract.
Define thefollowing
1. Hematuria
2. Pyuria
3. Cystitis
4. Anuria
5. Hemoglobinuria
6. Polyuria
7. Ketonuria
8. Oligouria
9. Epithelial crescents
10. Bracken fern toxicity
1. Uremia
2. Glomerulonephritis
3. Pyelonephritis
4. Nephrosclerosis
5. Urolithiasis
6. Cystic kidney
224

Pathology ofUrinary System
Q. 5. Select the most appropriate word(s) from thefour options given against each statement.
1. C3 component of complement is found in which type of glomerulonephritis (MPGN).
(a) Type-I (b) Type-II (c) Type III (d) Type-IV
2. In cattle, pyelonephritis is caused by ........ ..
(a) E. coli (b) Proteus spp. (c) Corynebacterium renale (d) Actinomyces pyogenes
3. Nephrosclerosis is .............. disease of kidney
(a) Acute (b) Chronic (c) Subacute (d) Peracute
4. Hypovitaminosis ..........may cause urolithiasis
(a) A (b)B (c)C (d)D
5. Ureteritis is the inflammation of ..........
(a) Uterus (b) Uterine glands (c) Ureter (d) Uterine tube
6. .......... amino acid forms calculi in animal which causes obstruction in urethra.
(a) Arginine (b) Lucine (c) Cystine (d) Gsolucine
7. Bracken fern causes ..........
(a) Hematuria (b) Pyuria (c) Hemoglobinuria (d) Anuria
8. Urethra may become infected by ..........virus.
(a) Picoma (b) Picobima (c) Bima (d) Adeno
9. Hyperplasia ofcollecting tubes with their dilation causes ..........cysts in kidneys.
(a) Type-I (b) Type-II (c) Type-Ill (d) Type-IV
10. Uremia is caused by the increased level of .................... in blood.
(a) Urea (b) Uric acid (c) Creatinine (d)All of the above
225

19
PATHOLOGY OF GENITAL
SYSTEM
• Female Genital System
• Cystic ovaries
• Oophoritis
• Salpingitis
• Metritis
• Pyometra
• Endometritis
• Cervicitis
• Vaginitis
• Abortion
• Placentitis
• Mastitis
• Male genital system
• Orchitis
• Epididymitis
• Funiculitis
• Seminal vesiculitis
• Prostatitis
• Balanoposthitis
• Model Questions

Pathology ofGenital System
FEMALE GENITAL SYSTEM
Agenesis
Absence of ovary, uterus, oviduct and cervix in
females. It may be unilateral or bilateral.
Hypoplasia
Complete or partial lack of germ cells in ovaries.
Hypoplasia of uterus is related with agenesis of
gonads. Ovaries of freemartin are also hypoplastic.
Hermaphrodite animal has ovary and testicular
tissue both in the gonads.
Hermaphroditism
In hermaphrodites, there is presence of organs of
both sexes in same individual animal. Both ovarian
and testicular tissue occur in one animal leads to
sterility in animal (true hermaphrodite) while in
pseudohermaphrodite the gonadal tissue of only
one sex is present but there is some degree of
development ofopposite sex organs.
Uterus unicornis
Uterus unicornis is presence of only one horn of
uterus instead of two, seen in animals with white
heifer disease.
White heifer disease
White heifer disease occurs due to a single sex
linked gene defect responsible for white coat
colour. In such animals, there are normal ovaries,
oviduct but uterus is incomplete and may lack
communication with cervix. There is hypoplasia of
cervix and vagina.
Uterus didelphys
Uterus didelphys is the occurrence of two cervix
with two uterine bodies and single or double
vagina. It occurs due to failure ofmullerian ducts to
fuse at their distal end. Sometimes failure of fusion
may affect only cervix and there are two cervix
which termed as Cervix bifida.
227
CYSTIC OVARIES
Cystic ovaries are defined as an ovary, which
contains one or more clear cysts ranging from one
to several centimeters in size (Fig. 19.1).
Etiology
• Hormonal imbalance
• Presence ofcysts in ovaries.
• Hormonal imbalance of animal leads to
sterility, continuous estrus, nymphomania due
to follicular cyst.
• Lutein cysts may cause pyometra leading to
pseudopregnancy.
• Follicular cyst.
• Ova absent several layers of granulosa or a
single layer ofepithelium.
• Many follicular cysts are present.
• Lutein cyst covered by fat containing
granulosa cells.
OOPHORITIS
Oophoritis is the inflammation of ovary caused by
trauma, infection and characterized by
granulomatous or lymphocytic inflammation of
ovary (Figs. 19.2 to 19.4).
Etiology
• Herpes virus.
• Hard, nodular lesions in ovary, encapsulated
with fibrous tissue.
• Granuloma of tuberculosis through
hematogenous infection.
• Infiltration of lymphocytes leading to
lymphofollicular reaction in follicles.
• Atrophy or absence ofova.

Systemic Pathology
cystic ovary (ARSIUSDA)
Fig. 19.2 Photograph showmg oophoritis
and salpingti'
Fig. 19.3 Photonucrograph showlllg oophorifl'
Fig. 19.4. Photomicrograph showing oophoritis
228
FIg. 19.5 Photomicrograph showmg metritis
Fig. 19.6. Photograph showmg proiap,e oj vagina
Fig. 19. 7. Photomicrograph showing oedema and
congestion in placenta (Placentitis) due to brucellosis
Fig. 19.8. Photomicrograph showingjimgal
placenlltis (ARSIUSDA)

SALPINGITIS
Salpingitis is the inflammation of oviduct or
fallopian tube characterized by congestion,
catarrhal or purulent exudate leading to distended
lumen (Fig. 19.2).
Etiology
• Mycoplasma.
• Streptococci.
• Tuberculosis (Mycobacterium tuberculosis).
• Trichomoniasis (Trichomonas foetus).
• Congestion, abscess formation
• Distension of oviduct lumen due to
accumulation of serous exudate which is
known as Hydrosalpinx.
• Accumulation of pus in oviduct is termed as
Pyosalpinx.
• Fibrosis, hardness.
• Occlusion of lumen due to inflammatory
exudate resulting in sterility.
• Inflammatory exudate is toxic to ova as well as
sperms leading to sterility.
• Congestion.
• Suppurative inflammation.
lymphocytes.
• Debris of desquamated cells.
METRITIS
Metritis is the inflammation of uterus characterized
by suppurative exudate, haemorrhage and necrosis
ofuterus (Fig. 19.5).
Etiology
• E. coli.
• Staphylococci.
• Streptococci.
• Trichomonas foetus.
• Campylobacterfoetus.
229
• Congestion, catarrhal or purulent exudate.
• Haemorrhage.
• Enlargement, oedema.
• Oozing out of pus from uterus on pressure.
• Seropurulent exudate in uterine wall.
• Oedema.
• Infiltration ofmacrophages and lymphocytes.
• Desquamation of lining epithelium.
PYOMETRA
Pyometra is an acute or chrl)nic suppurative
inflammation of uterus resulting in accumulation of
pus in the uterus.
Etiology
• Occurs under the influence ofprogesterone.
• E. coli.
• Proteus spp.
• Discharge of thin cream like pus from vulva
soiling the tail and perineal region.
• Pus discharge is more on sitting position of
animal.
• Enlargement of abdomen due to distension of
uterus.
• Uterus looking like a pregnant uterus as a
result ofaccumulation ofpus. This condition is
also known as Pseudocyesis or
pseUdopregnancy.
• Rention of lutein cyst.
• Congestion, infiltration of neutrophils,
lymphocytes and plasma cells.
• Necrosis ofmucosal epithelium ofuterus.
• Proliferation ofendometrial epithelium.
• Oedema, glandular hyperplasia.

Systemic Pathology
ENDOMETRITIS
Endometritis is the inflammation of endometrium,
the mucosa of uterus. It may be catarrhal or
purulent and may occur after metritis.
Etiology
• Staphylococci.
• Streptococci.
• Organism enters in uterus as a result of coitus,
artificial insemination or as iatrogenic
infection.
• Strong chemicals/medicines administered in
uterus.
• Catarrhal discharge from uterus containing
desquamated cells.
• Sterility due to toxic environment of uterus to
sperms.
• Congestion.
• Congestion.
• Moderate infiltration of lyrnphocytes, plasma
cells and neutrophils in mucosa.
CERVICITIS
Cervicitis is the inflammation of cervix as a result
of either descending infection from uterus or
ascending infection from vagina and characterized
by catarrhal inflammation.
Etiology
• Etiological agents are similar as in
endometritis.
• Congestion.
• Enlargement ofcervix.
• Catarrhal inflammation ofcervical mucosa.
• Hyperplasia of mucous glands with tall mucin
containing epithelial cells.
• Presence ofmucin in lumen.
VAGINITIS
Vaginitis is the inflammation of vagina
characterized by congestion, granularity as a result
of elevations in mucosa. This is also known as
infectious pustular vulvovaginitis in cattle caused
by herpes virus.
Etiology
• Mycoplasma bovigenitalium.
230
• Bovine herpes virus-l (BHV-1).
• Picorna virus.
• Granular elevation in vaginal mucosa.
• Congestion.
• Prolapse due to limitation (Fig. 19.6).
• Accumulation of lyrnphocytes in sub-epithelial
region.
• Congestion.
ABORTION
Abortion is expulsion of dead embryo or foetus
before attaining normal gestation. There are two
other terms related to abortion i.e. stillbirth and
premature birth. Stillbirth is defmed as expulsion
of dead foetus on its full maturity while premature
birth is birth of a live foetus before attaining full
gestation period.
Etiology
• Brucellosis (Brucella abortus, B. meletensis, B.
ovis).
• Salmonella abortus-equi - mares.
• Equine herpes virus - mares.
• Bovine herpes virus-l - cattle.
• Chlamydia psittasci.
• Listeria monocytogenes (Listeria ivanovii).
• Leptospria spp.
• Toxoplasma gondii.

• Mycoplasma mycoides.
• Fungi - Aspergillus spp., Coccidioides spp.
Absidia spp.
• Toxins / poisons.
• Expulsion of dead foetus in early stage (3-4
month) ofgestation (Trichomoniasis).
• Abortion in middle of gestation
(Campylobacteriosis).
• Late abortions (7-9 months) occur due to
Brucellosis, BHV-1 infection.
• Liver offoetus has necrotic foci, congestion.
• Stomach contents used for confrrmation of
etiology.
• In some cases of abortion, there is retention of
placenta (e.g. Brucellosis).
• Placenta becomes oedematous and necrotic
(Placentitis).
• If the foetus dues and is not expelled outside
the body due to non-opening of cervix, the
dead foetus remains in uterus under sterile
conditions. Such foetus undergoes autolysis
and is liquified. Liquid material is absorbed in
uterus through lymph or blood but bones/skin
etc. remain in uterine horn sometimes causing
irritation or damage to endometrium. Such
foetus becomes shrunken with wrinkled skin
and dried as mummy and is known as
"Mummifiedfoetus".
• Necrotic hepatitis with lymphofollicular
reaction in foetus (Brucellosis, BHV-1
infection).
• Granulomatous lesions (tuberculosis, fungal
infection), lymphofollicular reaction
(mycoplasma, chlamydia).
• Demonstration/isolation of causative
organisms in foetal stomach contents.
• Liver offoetus icteric (leptospirosis).
• Endometritis in dam.
• Bronchopneumonia in foetus e.g. brucellosis.
231
RETAINED PLACENTAlPLACENTITIS
Retention of placenta occurs after abortion or
parturition as a result ofinflammation characterized
by swelling, oedema or fibrosis which prevent the
separation of chorion from endometrium (Figs.
19.7 & 19.8).
Etiology
• Lack ofprogesterone.
• Infection e.g. Brucellosis, Trichomoniasis.
• Retained placenta undergoes autolysis,
putrefaction.
• Toxaemia in dam.
• Endometritis, pyometra.
• Placenta is oedematous and congested.
• Infiltration ofneutrophils, mononuclear cells.
• Proliferation offibroblasts.
MASTITIS
Mastitis is the inflammation of mammary gland
characterized by oedema, haemorrhage and fibrosis
of udder. Mastitis is always infectious and is a
disease of lactating glands. There is no
hematogenous infection and infections enter
through teat canal to cause mastitis (Figs. 19.9 to
19.12).
Etiology
• Bacteria e.g. Streptococcus agalactiae,
Streptococcus dysgalactiae, Staphylococcus
aureus, Actinomyces pyogenes, Pseudomonas
aeruginosa, Brucella abortus, Mycobacterium
tuberculosis, E. coli, Pasteurella multocida
and many more.
• Virus e.g. FMD virus, pox virus, BHV-l.
• Mycoplasma e.g. Mycoplasma mycoides.
• Fungi e.g. Candida ablicans, Trichosporon
spp. Nocardia asteroids, Cryptococcus
neoformans.
• Oedema ofudder.

Systemic Pathology
Fig. 199. Photograph 5hoWlllg mastiti' due to
fusarium tOXICOSIS
FIg. 19.11. PhotomIcrograph showmg chronic
granulomatous maslllls (ARS/USDA)
FIg. 19.12 Photonllcrograph showmg mycoplasmal
mastitis
232
FIg. 19.13. Photograph showing orchllls in a ram
Fig. 19.f.! Photograph ofte,tirles showing
(A) normal (b) AClIte orchllls.
Fig. 19.15. Photograph o/testicles o/poultry
showing orcllltis due to slamonellosis
Fig. 19.16. Photomicrograph showing orch1l1s

• Flakes (coagulated milk proteins) in milk.
• Blood mixed milk.
• Watery dirty grey or dark colour milk in
animals. In dry period it is caused by
Actinomyces pyogenes and is known as
"summer mastitis".
• Terminal atrophy or shrunken quarter.
• Gangrene formation.
• Infiltration of neutrophils, macrophages,
lymphocytes.
• Necrosis of alveolar epithelium, hyperplasia of
epithelial lining.
• Increase in WBC count in milk (more than
100/ml milk).
MALE GENITAL SYSTEM
Testicular hypoplasia
Testicular hypoplasia occurs in animals with
chromosomal abnormality such as XXV
chromosomes or Klinefelter's syndrome.
Hypoplasia is also seen in hermaphrodites and in
animals with cryptorchidism.
Spermatocele
There is failure of development of mesonephric
tubules and it does not connect with vas deferens
resulting in blind tubules filled with spermatozoa.
Rupture of tubules may lead to spermatic
granuloma.
Cryptorchidism
The testicles fail to descend in scrotum through
inguinal canal after birth and remains in abdominal
cavity. This permanent retention of testicles in
abdominal cavity causes their hypoplasia leading
to lack ef spermatogenesis. Such testes are more
prone to development ofneoplastic growth.
233
Phimosis
Phimosis is the failure of extension of penis from
its sheath.
Paraphimosis
Paraphimosis is the failure of withdrawal of
extended penis.
Hypospadias
In hypospadias, there is urethral opening in ventral
side ofthe penis.
Epispadias
There is urethral opening on the dorsal side of the
penis.
Phallocampsis
Phallocampsis is the deviation ofpenis, which may
be spiral (Cork screw penis) or ventral deviation
(rainbow penis).
ORCIDTIS
Orchitis is the inflammation of testes characterized
by oedema, necrosis and infiltration of neutrophils,
macrophages, lymphocytes and proliferation of
fibrous tissue leading to atrophy in chronic cases
(Figs. 19.13 to 19.16).
Etiology
• Brucella spp.
• Campylobactor spp.
• Salmonella spp.
• Trichomonas spp.
• Corynebacterium pseudotuberculosis.
• Actinomycess pyogenes.
• Pseudomanas aeruginosa.
Macroscopic feature
• Enlargement oftestes, oedema.
• Accumulation of sems fluid in scrotal
sac/tunica vaginalis is called as hydrocele.
• Enlargement ofscrotum.
• Congestion.
• Atrophy and hardening in chronic cases.

Systemic Pathology
• Congestion.
• Infiltration of neutrophils and mononuclear
cells.
• Necrosis of germinal cells.
• Proliferation of fibrous tissue and infilteration
of mononuclear cells.
•
•
Granulomatous lesions in
actinomycosis and tuberculosis.
Aspermatogenesis.
EPIDIDYMITIS
case of
Epididymitis is the inflammation of epididymis
characterized by catarrhal or suppurative exudate
with necrosis of lining epithelium.
Etiology
• Brucella avis in sheep.
• Other organisms that cause orchitis which is
preceded by epididymitis.
• Enlargement of epididymis.
• Oedema ofscrotum.
• Accumulation of mucus and/or purulent
exudate in epididymis.
• Accumulation of serus exudate in scrotum.
• Necrosis of lining epithelium ofepididymis.
lymphocytes.
• Oedema.
• Formation of granuloma in chronic cases.
FUNICULITIS
Funiculitis is inflammation of scirrhous cord
characterized by enlargement of scrotum due to
chronic abscess.
Etiology/Occurrence
• Botryomycosis.
• Actinomycosis.
• Castration.
• Unsamtary conditions.
234
• Enlargement ofscrotum.
• Hard swelling! chronic abscess.
• Chronic hyperplastic/proliferative changes.
• Fibroplasia.
• Infiltration of macrophages, lymphocytes,
neutrophils around sulphur granules forming
rosette.
SEMINAL VESICULITIS
Seminal vesiculitis is the inflammation of seminal
vesicle characterized by metaplasia ofthe columnar
epithelial lining to cornfied stratified squamous
epithelium.
Etiology
• Chlamydia psittasci.
• Mycoplasma bovigenitalium.
• Brucella abortus.
• E. coli.
• Melanosis in bulbourethral glands.
• Enlargementlhardness ofseminal vesicle.
• Metaplasia of columnar epithelium into
severely cornified stratified squamous
epithelium.
• Proliferation of melanoblasts/melanocytes.
PROSTATITIS
Prostatitis is the inflammation of prostate gland by
formation of painful abscess, atrophy, hyperplasia
of epithelial cells, proliferation of fibroblasts and
formation ofcysts. It occurs in dogs.
Etiology
• Pyogenic staphylococci, streptococci.

• Presence of abscess encapsulated by fibrous
tissue.
• Enlargement of prostate causing obstruction of
urethra.
• Obstruction in rectal passage.
• Hematuria.
• Infiltration of neutrophils and liquefied
necrosis.
• Chronic inflammation is characterized by
hyperplasia ofglandular epithelium, fibroblasts
and smooth muscle fibres.
• Cystic glandular hyperplasia.
• Infiltration of lymphocytes.
BALANOPOSTHITIS
Balanoposthitis is the inflammation of prepuce and
glans penis characterized by phimosis or
paraphimosis and pain during copulation. Balanitis
is inflammation of glans penis and posthitis IS
inflammation ofprepuce.
Etio)ogy
• BHV-1 virus.
• Vesicular exanthema virus.
• Mycoplasma spp.
• Phimosis and paraphimosis due to pain,
adhesions.
• Congestion.
• Fibrinopurulent exudate.
• Lymphocytic infilteration, congestion.
MODEL QUESTIONS
1. Cystic ovary occurs due to...........imbalance and is characterized either by...........cyst
manifested by.............., .......... and............or..........cyst that leads to ............ confused with ........
2. Pyometra is ................. inflammation of uterus characterized by accumulation of ................. in
uterus under the influence of ................. hormone secreted by..................
3. Endometritis is mostly characterized by ................. inflammation.
4. Early abortions in cattle are caused by................. while late abortions are caused by
................., ................. and .................
5. Fungal infection causes ................. inflammation of placenta that leads to abortion and
................. formation in foetal river.
6. Infectious VUlvovaginitis is caused by ................. which is transmissible to male counter part
through coitus and characterized by ................. and jointly this disease is known as.................
Q. 2. Write true orfalse against each statement. Correct thefalse statement.
1. ..........Mastitis is caused by chemical poisons.
2. ..........Acute placentitis leads-to abortion.
3. ..........Hypoplasia ofcervix and vagina is seen in uterus unicornis.
4. ..........Pseudocyesis is seen during endometritis.
5. ..........Brucellosis causes early abortion in cows.
6. ..........Salpingitis may cause death ofsperms and zygote.
7. ..........Balanitis may cause vaginitis through coitus.
8. ..........Hematogenous infection ofPasteurella multocida infection causes mastitis.
9. ..........Retention ofplacenta occurs in trichomoniasis.
235

Systemic Pathology
10...........Rainbow penis is seen as a developmental defect characterized by spiral shape ofthe
penis.
Q.3. Define the following
1. Uterus unicornis 14. Cervicitis
2. Vulvovaginitis 15. Mummified foetus
3. Hydrosalpinx 16. Hypospadias
4. Stillbirth 17. Uterus didelphys
5. Pseudohermaphrodite 18. Shrunken udder
6. Pseudocyesis 19. Pseudopregnancy
7. Placentitis 20. Phallocampsis
8. Premature birth 21. Paraphimosis
9. Cervix bifida 22. Funiculitis
10. Spermatocele 23. Balanitis
11. Pyosalpinx 24. Posthitis
12. Phimosis 25. Corkscrew penis
13. Epispadias
Q.4. Write short notes on
1. Cystic ovary 6. Cryptorchidism
2. Pyometra 7. Orchitis
3. Endometritis 8. Prostatitis
4. Late abortions 9. Mastitis
5. Summer mastitis 10. Epididymitis
1. Cryptorchidism may lead to ................. of testicles.
(a) Hypoplasia (b) Aspermatogenesis (c) Neoplasia (d)All ofthe above
2. Ventral deviation ofpenis is known as .................
(a) Corkscrew penis (b) Phallocampsis (c) Rainbow penis (d) None
3. Hydrocele is accumulation ofserus fluid in .................
(a) Oviduct (b) Testes (c) Mammary gland (d) Tunica vaginalis
4. Funiculitis is the inflammation of .................
(a) Scirrhous cord (b) Seminal vesicle (c) Glans penis (d) Prepuce
5. Phimosis is caused by .................
(a) Balanitis (b) Posthitis (c) Balanoposthitis (d)All ofthe above
6. Presence offollicular cysts in ovary may lead to .................
(a) Sterility (b) Nymphomania (c) Continuous oestrus (d)All ofthe above
7. Inflammation ofoviduct leads to sterility due to ................. nature ofthe exudate to sperms.
(a) Toxic (b) Obstructive (c) Penetrative (d) None
8. Mastitis is mostly caused by .................
(a) Trauma (b) Hematogenous infection (c) Toxins/poisons (d) Infection
9. Summer mastitis is caused by .................
(a) Staphylococci (b) Actinomyces pyogenes (c) Streptococci (d) Candida albicans
10. Parturition ofa dead foetus on its full development and gestation is termed as .................
(a) Abortion (b) Stillbirth (c) Premature birth (d) Normal birth
236

20
PATHOLOGY OF NERVOUS
SYSTEM
• Encephalitis
• Encephalomalacia
• Spongiform Encephalopathy
• Meningitis
• Neuritis
• Model Questions

Systemic Pathology
Nervous system is composed of brain, spinal cord,
and peripheral nerves. The neuron is a basic
functional unit of nervous system. Necrosis of
neurons in brain is known as encephalomalacia
while necrosis of neurons in spinal cord is termed
as myelomalacia. If the necrosis occurs in grey
matter it is known as polioencephalomalacia while
necrosis of neurons in white matter is called as
leukoencephalomalacia. There are three types of
scavenger cells in nervous system known as
microglial, oligodendroglial and astrocytes.
Microglial cells surround the necrotic neurons and
are known as satellite cells and the process is called
as satellitosis. As the neuron dies, it is engulfed by
microglial cell and this process is termed as
neuronophagia. The necrosis of nerve fibres starts
from myelin sheath and this change is called
demyelination or Wallerian degeneration.
The brain and spinal cord is covered by meninges.
The inflammation of meninges is termed as
meningitis. Meningoencephalitis. The term is used
for inflammation of both meninges and brain.
Inflammation of duramater is known as
pachymeningitis and of piamater is termed as
leptomeningitis. Hydrocephalus means
accumulation of clear fluid in ventricles and in sub
arachnoid space due to obstruction in drainage.
Hydrocephalus occurs in neonatal calves due to
influenza and parainfluenza virus and is termed as
congenital hydrocephalus.
Some nutritional deficiency like vitamin A, folic
acid, vitamin B12, niacin and zinc may also lead to
hydrocephalus. Cerebeller hypoplasia has been
observed due to bovine virus diarrhoea, hog cholera
and feline panleukopenia virus. Some other
congenital malformations are as under.
Anencephaly means absence ofbrain.
Microencephaly means small size of brain.
Cranioschisis is failure of cranium to fuse which
results in hernia of meninges known as
meningocele. Hernia of meninges and brain is
known as meningoencephalocele.
Encephalitis
characterized
ENCEPHALITIS
is the
by
inflammation of brain
purulent/lymphocytic or
238
proliferative changes. Encephalomyelitis is the
inflammation of brain as well as spinal cord (Figs.
20.1 to 20.11).
Etiology
• Bacteria
• Listeria monocytogenes (L. ivanovii) main
cause
• Haemophius spp.
• Pasturella spp.
• Virus.
• Mycoplasma.
• Strychnine poisoning.
• Congestion.
• Haemorrhage.
• Small, tiny abscess.
• Necrosis also known as encephalomalacia.
• Involvement of spinal cord leads to
encephalomyelitis and of meninges and is
termed as meningoencephalitis.
• Tiny or micro abscess in cerebrum.
• Infiltration by neutrophils and lymphocytes.
• Perivascular cuffing in Virchow Robin space
by lymphocytes.
• Necrosis ofneurons.
• Satellitosis, neuronophagia.
• Pleocytosis- Increase in number of white blood
cells in cerebrospinal fluid.
ENCEPHALOMALACIA
Encephalomalacia is the necrosis of nervous tissue
in brain characterized by loss of normal
architecture and soft friable liquefied mass (Figs.
20.12 & 20.13).
Etiology
• Deficiency ofcopper, thiamine, vitamin E.
• Poisons: Bracken fern, lead, mercury, salt
poisoning, enterotoxaemia, mycotoxins.

Pathology ofNervous System
FIg. 20.1. Photograph ofbrain showmg
congestion in poultry
Fig. 20.2. Photograph showing abscess
in brain (ARSIUSDA)
Fig. 20.3. Photograph ofcerebeller hypoplaslG
Fig. 20.4. Photograph showing staggerlllg gait
in buffalo calfdue to strychnine pOIsoning
239
FIg. 20.5 Photograph showing spasms in neck due
to strychnine pOlsonillR
Fig. 20.6. Photograph showing torticollis in buffalo
calfdue to strychmne poisoning
Fig. 20.7. Photomicrograph shml'mg perivascular
cuffing in brain
Fig. 20.S. Photomicrograph sllOwmg
menigoencepilalitis

Systemic Pathology
• Encephalomalacia - necrosis in brain.
• Myelomalacia - necrosis in spinal cord.
• Poliomalacia - necrosis in brain gray matter.
• Leukomalacia - necrosis in brain white matter.
• Soft, friable liquefied mass in brain.
• Congestion.
• Liquefactive necrosis.
• Surrounded by neurological cells/scavenger
cells.
• Proliferation ofsmall new capillaries
SPONGIFORM ENCEPHALOPATHY
Spongiform encephalopathy is characterized by the
presence of vacuoles in grey and/or white matter.
Etiology
• Prion proteins.
• Scrapie in sheep.
• BSE in cattle.
• No characteristic gross lesion.
• Oedema ofbrain or hydrocephalus.
• Congestion.
• Vacuolation in white and grey matter.
• Vacuoles are usually in neurons, glial cells and
in myelin.
• Vacuoles are more extensive in medulla, pons
and mid brain and give brain "spongy form".
MENINGITIS
Meningitis is the inflammation of meninges,
usually occurs along with encephalitis or
encephalomyelitis and is characterized by
congestion and infiltration of neutrophils and
240
mononuclear cells. Pachymeningitis is
inflammation of dura mater while leptomenigitis
involves the pia mater.
Etiology
• Virus e.g. swine fever.
• Trauma.
• Bacteria e.g. Pasturella, Listeria.
• Toxoplasma.
• Leptospira.
• Congestion.
• Thickening ofmeninges.
• Petechial haemorrhage.
• Congestion.
• Infiltration of neutrophils and lymphocytes.
• Fibrosis.
NEURITIS
Neuritis is the inflammation of nerves along with
degenerative changes characterized by oedema,
infiltration of inflammatory cells (Fig. 20.14 to
20.16).
Etiology
• Toxins.
• Trauma.
• Virus e.g. Marek's disease MD.
• Lead and Mercury.
• Bacteria e.g. Strangles.
• Deficiency of vitamin E.
• Wallerian degeneration.
• Infiltration of neutrophils and lymphocytes.
• More destruction at distal end ofthe neuron.

Fig. 20.9. Photomicrograph showing congestion and
infiltration ofinflammatory cells in brain
Fig. 20.10. Electronmicrophotograph ofbrain showing
increase in endoneural space and Wallerian
degeneration in nerve fiber.
Fig. 20.11. Electronmicrophotograph ofbrain
showing phagocytosis ofdegenerated nerve cell by
phagocytic cell (Neuronophagia)
encephalomalacia in a chick
241
Fig. 20.13. Photomicrograph showing
encephalomalacia
Fig. 20.14. Photograph showing neuritis
due to Marek's disease
Fig. 20.15. Electronmicrophotograph ofsciatic nerve
showing degeneration of myelinatedfibres with
swelling andfragmentation
;~·~~G
Fig. 20.16. Electtronmicrophotograph ofsciatic
nerve showing advanced Wallerian degeneration and
increased endoneural space.

Systemic Veterinary Pathology
MODEL QUESTIONS
1. Necrosis of neurons in brain is known as ................ while that of spinal cord in termed as
2. Encephalitis is the ................ of brain caused mainly by ................ and characterized by
................, ................, ................, ................ and ................
3. Necrosis of nerve cells in grey and white matter is known as ................ and ................,
respectively. The necrosed neurons are surrounded by ................ cells and the process is termed
as ................ while they are eaten away by these cells and the process is known as................
4. Vacuoles in ................, ................ and ................ and which are more prominent in ................ ,
...............and..............and give the brain ................ are only diagnostic lesions ofBSE in cattle.
5. The inflammation ofpia mater is ................ and of dura mater is ................
1. ............Meningoencephalomyelitis is the inflammation ofbrain and meninges.
2. ............Vitamin B12 deficiency may cause cerebral hydrocephalus.
3. ............Neuronophagia is necrosis ofnerve fibres.
4. ............Inflammation of dura mmter is known as patchymeningitis
5. ............Polioencephalomalacia is inflammation of white matter ofbrain.
6. ............Spongiform encephalopathy is caused by a virus.
7. ..........Vacuoles in neurons in brain are main diagnostic lesion which helps in diagnosis ofBSE.
8. ............Leptospira may cause meningitis and myelitis.
9. ............Neuritis can be observed in Marek's disease.
10.............Mycotoxins may cause encephalomalacia in calves.
Q.3. Define thefollowing
1. Myelomalacia 9. Cerebellar hypoplasia
2. Satellitosis 10. Leptomeningitis
3. Neuronophagia 11. Leukomalacia
4. Pleocytosis 12. Wallerian degeneration
5. Cranioschisis 13. Poliomalacia
6. Microencephaly 14. Pachymeningitis
7. Anencephaly 15. Perivascular cuffing
8. Meningoencephomyelitis
Q. 4. Write short notes on
1. Bovine spongiform encephalopathy
2. Encephalomalacia
3. Encephalitis
4. Meningitis
5. Hydrocephalus
242

Q. 5. Select the most appropriate word(s) from the four options given against each statement.
1. Neuritis is observed in ............
(a) Mucosal disease (b) Infectious bursal disease (c) Marek's disease (d) ILT
2. Necrosis ofbrain in known as ............
(a) Encephalomalacia (b) Polioencephalomalacia(c) Myelomalacia (d) None of the above
3. Removal ofdead neurons through microglial cells in known as ............
(a) Satellitosis (b) Neuronophagia (c) Perivascular cuffing (d) None
4. Increase in number of white blood cells in cerbrospinal fluid in termed as ............
(a) Encephalitis (b) Satellitosis (c) Pleocytosis (d) Leucoencephalomalacia
5. Spongiform encephalopathy is caused by ............
(a) Virus (b) Viroids (c) Prions (d) Deficiency ofvit B2
6. Inflammation ofdura mater is known as ............
(a) Leptomeningitis (b) Pachymeningitis (c) Meningitis (d) Meningoencephalitis
7. Congenitally small size brain is termed as ............
(a) Anencephaly (b) Hydrocephalus (c) Microencephaly (d) Cranioschisis
8. Phagocytic cells ofbrain are ............cell(s)
(a) Astrocytes (b) Microglial (c) Oligodendroglial (d)All of the above
9. Increase in CSF in sub arachnoid space is known as ............
(a) Pleocytosis (b) Hydrocephalus (c) Microencephaly (d) Hypoplasia
10. Hernia of meninges through cranioschisis is known as ............
(a) Hydrocele (b) Meningocele (c) Meningoencephalocele (d) None
243

21
PATHOLOGY OF ENDOCRINE
SYSTEM, EYES AND EAR
• Pathology of Endocrine System
• Pathology of Hypothalamus
• Pathology of Pituitary
• Pathology of Thyroid
• Pathology of Parathyroid
• Pathology of Adrenal glands
• Pathology of Pancreas
• Pathology of Pineal gland
• Pathology of Eyes
• Keratoconjunctivitis
• Cataract
• Pathology of Ear
• Otitis externa
• Otitis media
• Otitis interna
• Model Questions

Pathology ofEndocrine System, Eyes and Ear
PATHOLOGY OF ENDOCRINE SYSTEM
PATHOLOGY OF HYPOTHALAMUS
The lesions in hypothalamus may cause diabetes
insipedus characterized by polydipsia and polyuria
with low specific gravity of urine. It occurs due to
deticiency ofantidiuretic hormone vasopressin.
• Lesions in hypothalamus and/or pituitary.
• Adenoma and adenocarcinoma ofpituitary.
• Necrosis of hypothalamic nuclei due to larval
migration.
PATHOLOGY OF PITUITARY GLAND
HYPERPITUITARISM
Hyperpituitarism is increased secretion of
hormone(s) from pituitary gland such as excessive
secretion of somatotropic hormone which may
cause gigantism characterized by increased length
of long bones, heavy and thick bones leading to
large hands, feet, skull bones (acromegaly).
Hyperpituitarism also increases adrenal cortical
stimulating hormone leading to hyperplasia of
adrenal cortex. Pituitary adenoma or adeno-
carcinoma is responsible for hyperpituitarism.
HYPOPITUITARISM
Hypopituitarism is decrease in pituitary hormone
secretions due to atrophy, aplasia or hypoplasia of
pituitary. Systemic diseases such as meningitis of
bacterial or viral origin may also cause lesions in
pituitary e.g. infectious canine hepatitis, hog
cholera. It is characterized by dwarfism, genital
hypoplasia and prolonged gestation period.
PATHOLOGY OF THYROID
HYPERTHYROIDISM
Hyperthyroidism is increased activity of thyroid
gland leading to increased production of thyroxin
characterized by tachycardia, increased basal
metabolic rate, bulging of eyeballs and early
maturity. It occurs due to presence of tumor in
thyroid. Other signs include polydipsia, polyuria,
and loss of weight, weakness, fatigue and
hyperthermia.
245
HYPOTHYROIDISM
Hypothyroidism is reduced activity of thyroid
gland characterized by decreased basal metabolic
rate, obesity, retardation of growth and sexual
development leading to cretinism. In adult, it is
characterized by myxomatous mucoid degeneration
in subcutaneous region giving floppy and
oedematous appearance. Hypothyroidism is caused
by aplasia or hypoplasia ofthyroid gland.
Goiter
Goiter is enlargement of thyroid gland, which may
be accompanied by hypo- or hyperthyroidism. The
enlargement of thyroid is due to hyperplasia,
inflammation, or proliferation of connective tissue.
The hyperplasia of gland is characterized by
increased height and number to epithelial cells in
acini of gland. It may be caused by deficiency of
iodine, thiouracil toxicity and by use of
goiterogenic substances such as soybean and
cabbage. The goiter has been classified into 6
forms described as under:
Hyperplastic goiter
Due to iodine deficiency, there is hyperplasia of
thyroid gland with reduction in thyroxin
production. It occurs due to increased level of
thyrotropic hormone from pituitary gland.
Familial goiter
There is hyperplasia of thyroid gland with reduced
thyroxin secretion caused by defective or absence
of enzymes responsible for thyroxin synthesis. It is
not related with iodine deficiency but has
congenital basis of occurrence
Colloid goiter
Colloid goiter is enlargement and distention of
acini filled with colloid and flat epithelium caused
by deficiency ofiodine.
Adenomatous goiter
This is characterized by nodular enlargement of
thyroid gland, with one or many hard nodules of
variable size and characteristic adenoma ofgland.

Systemic Pathology
Fig.21.1. Photograph showing conjunctivitis
in pigeon due to poxvirus infection
Fig.21.2. Photograph showing conjunctivitis
in pIgeon due to poxvirus infectIOn
Fig.21.3. Photograph showing mucopuruiant
dIscharge from eyes due to mallein test in horse
Frg.21.4. Photograph ,/IOWlIlg mllcopllruiant
exudate in eye
246
Fig.21.6. Photograph showing cataract
Fig.21.7. Photograph showing corneal opacity
Fig 21.S. Photograph showing otills extenza III pig.

Toxic goiter
Toxic goiter is characterized by exophthalmus due
to hyperthyroidism, enlargement of thyroid due to
hyperplasia, and occurs as a hypersecretion of
thyrotropic hormone from pituitary.
Equine goiter
Equine goiter is caused by excessive iodine levels
in feed and occurs in new born foals with weakness
from a goiterous mare. These foals have enlarged
thyroid gland.
LYMPHOCYTIC THYRODITIS
Lymphocytic thyroditis is characterized by
infiltration of lymphocytes in gland causing
destruction and is caused by autoimmune
mechanism. The infiltration of lymphocytes is so
severe that it gives lymphofollicular appearance.
PATHOLOGY OF PARATHYROID GLAND
HYPOPARATHYROIDISM
Hypoparathyroidism is decreased activity of
parathyroid gland characterized by decreased
concentration of blood calcium and tonic spasms of
muscles. It occurs due to infection, neoplasms, low
calcium diets and hypersecretion of thyrocalcitonin.
HYPERPARATHYROIDISM
Hyperparathyroidism is the increased activity of
parathyroid gland characterized by weakness,
polydipsia, polyuria, hypercalcemia
nephrocalcinosis, demineralization of bones,
metastatic calcification in soft tissues and fibrous
osteodystrophy. It may occur in adenoma or
adenocarcinoma of parathyroid and hyperplasia of
gland. Hyperparathyroidism is also associated with
renal disease and chronic hypocalcemia and
produces more parathormone hormone.
PATHOLOGY OF ADENAL GLANDS
HYPOADRENOCORTICISM
Hypoadrenocorticism is decreased activity of
adrenal cortex characterized by atrophy, necrosis
and decreased hormones leading to low blood
pressure, decreased blood volume, hypoglycemia,
gastrointestinal malfunction and hyperpigmentation
247
m skin. It may occur in tuberculosis,
histoplasmosis, amyloidosis, neoplasms and drug
toxicity.
HYPERADRENOCORTICISM
Hyperadrenocorticism is increased activity of
adrenal cortex characterized by hyperplasia and
neoplasia of the gland leading to alopecia, muscle
weakness, pendulous abdomen, obesity, polyuria,
polydipsia, lymphopenia, eosinophilia, neutrophila
and excessive secretion of 17- ketogenic steroids.
PATHOLOGY OF PANCREAS
Pancreatic islets or islets of Langerhans' are
responsible for production of insulin, deficiency of
which may cause hyperglycemia or diabetes
mellitus. It is characterized by polyuria, glycosuria,
hyperglycemia, polydipsia, loss of secretory
granules in ~-cells of pancreatic islets. It is caused
by inflammation of pancreas causing excocrine
pancreatitis. This condition may lead to
arteriosclerosis in blood vessels ofanimals.
PATHOLOGY OF PINEAL GLAND
The pineal gland is responsible for secretion of
melatonin hormone which inhibits gonadotropic
hormone synthesis and release by pituitary and thus
plays an important role in seasonal
estrus/reproductive capacity of animals.
Degeneration and necrosis of gland may cause its
decreased function but it is not well reported.
Adenoma of gland may be associated with
increased sexual libido and activity.
PATHOLOGY OF EYE
Blepheritis is the inflammation of eyelids while the
term conjunctivitis is used to describe the
inflammatory condition ofconjunctiva and keratitis
for cornea. In ward turning of eyelid is known as
entropion which may result in keratitis or
conjunctivitis. Conjunctivitis is also caused by
double row ofeye lashes (disctichiasis).
Aphakia is the absence oflens.
Microphakia is the small size of lens.

Systemic Pathology
Hypoplasia of optic nerve is underdeveloped optic
nerve with absence of optic nerve layer and
ganglion cell layer of retina.
Agenesis ofoptic nerve is absence ofoptic nerve.
Coloboma is the congenital defect in the continuity
of one of the tunics of the eye i. e. iris.
Congenital anophthalmos is the absence of the eye
which may occur due to vitamin A deficiency in
dam.
Congenital microphathalmos is the decreased size
of eyes and may occur due to maternal vitamin A
deficiency
Congenital opacity of cornea occurs in cattle and
dogs due to effect ofinherited recessive gene trait.
Hemeralopia is day blindness which may occur in
dogs due to single autosomal recessive gene.
KERATOCONJUNCTIVITIS
Keratoconjunctivitis is the inflammation of cornea
and conjunctiva characterized by congestion of
eyes, blindness, opacity and corneal oedema (Figs
21.1 to 21.7).
Etiology
• Penetrating foreign objects e.g. Awns of
wheat.
• Moraxella bovis.
• Mycoplasma spp.
• BHV-1, poxvirus.
• Rickettsia conjunctivae.
• Chlamydia spp.
• Thelazia spp.
• Allergy.
• Congestion of conjunctiva leading to redness
"pink eye".
• Oedema, pain
• Increased lacrimation (decreased lacrimation
also causes conjunctivitis).
• Corneal opacity.
CATARACT
Cataract is opacity of lens and IS classified as
under:
248
Subcapsular cataract is the opacity of lens due to
abnormal proliferation of lens epithelium in
anterior end as a result of injury.
Posterior polar cataract is opacity of lens due to
abnormal growth of lens epithelium at posterior
face oflens
Cortical cataract is opacity of lens due to
disorganization of the lens fibres.
Nuclear cataract is the incrt;ased density of fibres
oflens at the centre and occurs in old animals.
Morgagnian cataract is the liquefaction of cortical
substance and has not been observed in animals.
Congenital cataract is seen in neonatal animals
and occurs due to failure of closure of primary lens
vesicle at the periphery of lens vesicle and is
associated with chediak - Higashi Syndrome.
RETINITIS
Retinitis is the inflammation of retina caused by
trauma, iritis, iridocyclitis and choroiditis. When it
is associated with inflammation of choroids, it is
known as chorioretinitis. It may lead to detachment
of retina. Iritis is inflammation of iris. Iridocyclitis
is the inflammation of iris and uvea. Choroiditis is
inflammation ofchoroid plexus.
The chorioretinitis is characterized by glaucoma
occurs in canine distemper, feline panleukopenia,
toxoplasmosis, tuberculosis, coccidioidomycosis,
deficiency of vitamin A and bracken fern
poisoning.
GLAUCOMA
Glaucoma is the intraoccular hypertension due to
occlusion of the filtration angle and is caused by
trauma, iridocyclitis, intraoccular haemorrhage and
neoplasm. It may be unilateral or bilateral. It is
characterized by enlargement of eye ball, opaque
cornea and increase aqueous humor.
PATHOLOGY OF EAR
OTITIS EXTERNA
Otitis externa is inflammation of external ear
caused by Actinomyces bovis, parasites and fungus'
and characterized by granulomatous inflammation
(Fig. 21.8).

Etiology
• Psoroptes communis - mite.
• Otobius megnini - tick.
• Fungi - (otomycosis).
• Grass of wheat awns.
• Swelling and congestion leading to obstruction
ofear canal.
• Excessive production of thick, tenacious and
brownish wax.
• Granulomatous lesions filling the external
auditory meatus
• Granulomatous lesions of actinomycosis in
subcutaneous region around the cartilage.
OTITIS MEDIA
Otitis media is inflammation of middle ear
including tympanic cavity and eustachian tube.
Etiology
• Infections from otitis externa or nasopharynx.
• Mites.
• Awns of wheat.
• Pasteurella spp.
• Occlusion ofeustachian tube.
• Purulent inflammation.
OTITIS INTERNA
Otitis interna is the inflammation of inner ear
including membranous and osseous labyrinth. This
is also known as labyrinthitis.
Etiology
• Infection from otitis media.
• Mycoplasma spp.
• Mumps.
• Measles.
• Disturbance in equilibrium.
• Deafness.
MODEL QUESTIONS
1. Pathological lesions in hypothalamus may cause...................characterized by................... and
...................with low specific gravity of...................
2. Hyperpituitarism is excessive secretion of............hormone which may cause............
characterized by..................., ................leading to large..................., ...................and..................
3. Goiter is...................ofthyroid gland accompanied by...................or...................
4. Hypoparthyroidism is characterized by...................and...................and caused by...................,
..................., ...................and...................secretion of thyrocalcitonin.
5. Hypoadrenalism may occur in...................,...................,...................,................... and...................
Q. 2. Write true orfalse against each statement. Correct the false statement.
1. ...........Hypoadrenocorticism may cause lymphopenia.
2. ...........Disctichiasis is protrusion ofeyelid.
3. ...........Moraxella canis causes pink eye.
4. ...........Diabetes mellitus is related with insulin deficiency.
249

Systemic Pathology
5. ...........Hemeralopia is night blindness
6. ...........Aphakia is absence ofeyelid.
7. ...........BHV-1 virus is responsible for keratoconjunctivitis.
8. ...........Iridocyclitis is inflammation ofiris and lens.
9. ...........Bracken fern poisoning may cause chorioretinitis
10. ...........Cretinism is related with hypothyroidism.
Q. 3. Define the following
1. Aphakia
2. Disctichiasis
3. Labyrinthitis
4. Glaucoma
5. Conjunctivitis
6. Microphakia
7. Retinitis
8. Lymphocytic thyroditis
Q. 4. Write short notes on
1. Goiter
2. Cataract
3. Pink eye
4. Otitis externa
5. Hyperparathyroidism
9. Iritis
10. Keratitis
11. Hypothyroidism
12. Iridocyclitis
l3. Coloboma
14. Gigantism
15. Hemeralopia
Q. 5. Select the most appropriate word(s) from the four options given against each statement.
1. Metastatic calcification occurs in...................
(a) Hyperthyroidism (b) Hyperparathyroidism (c) Hypothyroidism (d) Hypoparathyroidism
2. Goiter is related with...................
(a) Hypothyroidism (b) Hyperthyroidism (c) Both a & b (d) None
3. Otitis media is the inflammation of middle ear including.............
(a) Tympanic cavity (b) Eustachian tube (c) Both a & b (d) None
4. Disturbance in equilibrium occurs in animals with disease of ...................
(a) External ear (b) Eyes (c) Middle ear (d) Inner ear
5. Glaucoma is caused by...................
(a) Neoplasm (b) Trauma (c) Haemorrhage (d) All ofabove
6. Thelazia spp worms may cause...................
(a) Keratoconjunctivitis (b) Microphakia (c) Aphakia (d) Coloboma
7. Cleft in iris is known as...................
(a) Intis (b) Microphakia (c) Aphakia (d) Coloboma
8. Equine goiter is caused by...................
(a) Iodine deficiency (b) Iodine excess (c) Cabbage (d) Radiation
9. Exophthalmos is a feature oL................ goiter
(a) Colloid (b) Adenomatous (c) Toxic (d) Familial
10. Acromegaly is caused by...................
(a) Hyperpituitarism (b) Hypopituitarism (c) Hypothyroidism (d) Hyperthyroidism
250

22
APPENDICES
I. Techniques of post-mortem examination
11. Steps in post-mortem examination
Ill. Writing of post-mortem report
IV. Collection, preservation and dispatch of
specimens for laboratory diagnosis
V. Histopathological techniques
VI. Post-mortem examination of veterolegal
cases
VII. Collection, preservation and dispatch of
material to forensic laboratory
VIII. Examination of blood, urine and faeces
IX. Self assessment

Appendices
Appendix I
TECHNIQUES OF POST-MORTEM EXAMINATION (NECROPSy)
Necropsy is examination of animal after death. It
helps in diagnosis ofdiseases and their control. It is
said that "Necropsy is a message of wisdom from
dead to living". Necropsy include systemic
examination of dead animal, recording of
pathological lesions and their interpretation to
make diagnosis of disease. Sometimes it is difficult
to arrive at any conclusion merely based on gross
examination'of dead animal. Then one should seek
the help of laboratory examinations from other
branches of pathology such as Histopathology,
Microbiology, Immunology and Toxicology for
confirmation.
Necropsy examination is an integral part of disease
investigation. Therefore, veterinarians must have
the knowledge of the techniques of post-mortem
examination, recording of lesions, collection of
proper material for laboratory and most importantly
their correlation to arrive at conclusive diagnosis.
The technique of post-mortem examination is as
under:
•
•
•
•
•
•
•
•
POST-MORTEM EXAMINATION OF
LARGE ANIMAL
Place animal on left side (ruminants) (Fig.
22.1).
Place horse on right side and dog on vertebral
column (Figs. 22.2 & 22.3).
Make midventral incision with knife from chin
to anus.
Surround the prepuce, scrotum/mammary
gland.
Remove skin dorsoventrally. Remove skin at
face, neck, thorax and abdomen.
Cut the muscles and fascia in between scapula
and body; remove fore legs.
Raise hind legs, cut the coxofemoral ligament.
Examine sIc tissue, muscles, superficial
lymphnodes prescapular, prefemoral
supramammary, etc.
252
• Open abdominal cavity by cutting muscles and
peritoneum.
Fig. 22.1. D/agram showingpost-mortem examinatIOn of
ruminant (A) position ofcow and the marklngfor incIsIOn
(8) after removal ofskin and (e) after exposure of
abdominal cavity

Appendices
• Open thoracic cavity by cutting xiphoid
cartilage at sternum; lift ribs and press them to
break at joints with vertebral column.
• Examine the visceral organs in both cavities:
Thorax Heart, Lungs, Trachea,
Abdominal cavity
Ruminants
Other animals
In all animals
Pelvic cavity
Oesophagus, Mediastinal
lymphnodes, Diaphragm
Rumen, Reticulum,
Omasum, Abomasum
Stomach
Liver, Pancreas, Intestines,
Mesenteric lymphnodes,
Spleen, Kidneys, Ureter
Urinary bladder, uterus
POST-MORTEM EXAMINATION
(POULTRY, Figs. 22.4 to 22.21)
• Dip the dead bird in antiseptic solution or in
water to avoid feather contamination.
• Keep the bird on post-mortem table at
vertebral column and look for any lesion or
parasite on skin.
• Examine the eyes, face and vent.
• Remove skin through a cut with knife and with
the help of fingers. Expose thymus,' trachea,
oesophagus in neck.
• Break the coxofemoral joint by lifting the legs.
Examine the chest and thigh muscles.
• Cut on lateral side of chest muscles. Lift the
chest muscle dorsally and break bones at joints
with thorax. Cut bones at both sides and
remove muscles, bones to expose thorax,
abdomen.
• Examine different organs.
• Cut proventriculus and pull the organs of
digestive tract out. Separate liver, spleen,
intestines, caecum, proventriculus, gizzard, etc.
• Expose bursa just beneath the cloaca.
• Cut beak at joint, examine mouth cavity and
expose oesophagus and trachea.
• Remove skin of head and make a square cut on
skull to expose brain.
253
• Take a forceps and place in between thigh
muscles, remove fascia and expose the sciatic
nerve.
• Separate each organ, examine them for the
presence of lesion.
'-~~::-.?---...
FIg. 22,2. Diagram showingpost-mortem
examination ofhorse (A) position ofhorse and
markmgfor incision (B) after removal ofskm and
(C) after exposure ofabdominal cavity
c

Appendices
,
,,
'.,.
:.
1:
I,,
rr A
Fig. 22.3. Diagram showing post-mortem examination ofdog (A)
position ofdog and marking for incision (B) after exposure of
thoracic and abdominal cavity
254
bird on post-mortem table
Fig. 225. Photograph showmg external
examination for presence oflice, mite; & ticks
Fig. 22.6 Photograph ;howing external
examinatIOn ofeyes
Fig. 22.7. Photograph showing examinatIOn
ofvent

Fig. 22.8. Photograph showing removal ofskin
Fig. 22.9. Photograph showing breaking
ofcoxofemoral joint
Fig. 22.10. Photograph showmg exposure of
musclesfor examination
Fig. 22.11. Photograph showing removal ofbreast
muscles
Appendices
255
Fig. 22.13. Photograph showing exposure
ofinternal organs
Fig. 22.14. Photograph showing kidneys, ovary,
oviduct after removal ofdigestive system and heart

Fig. 22.15. Photograph showing examination
ofmouth cavity
Fig. 22.16. Photograph showing examination of
intestmes including caeca and proventriculus
female genital tract.
Appendices
256
~ ~
testes
Fig. 22.20. Photograph showing examination ofnervous
system (A) brain (B) sciatic nerve
B
,0
Fig. 22.21. Photograph showing (A) Heart, (B)Spleen
(e) Bursa ofFabricious and (D) Thymus

Appendices
Appendix II
STEPS IN POST-MORTEM EXAMINATION
Post-mortem examination should be conducted
only after receiving a formal request from the
owner of animal having details of anamnesis and
date and time of death. Without a formal written
request, one should not do post-mortem
examination of animal. The post-mortem record
includes the animal's identification, illness,
therapeutic and preventive measures adopted and
date and time of death. This information is
provided by the owner or person requesting
autopsy, which helps in post-mortem examination
and recording of lesions to make a conclusive
diagnosis.
Various steps in post-mortem examination are as
under:
1. External examination
Animal should be examined externally before
opening the body for the presence of lesions on
body surface. Eyes, ear, anus, vulva, mouth, nares
etc. should be specifically examined for the
presence of blood and any other lesion. If the blood
is coming out from natural orifices, it should be
examined for the presence of anthrax bacilli and
such carcasses must not be opened for post-mortem
examination. Following points should be taken into
consideration while conducting external
examination.
• Trauma, wound, fracture, cuts, etc.
• Fungal infection e.g. ringworm.
• Parasitic infestation e.g. mange, lice, ticks.
• Side ofanimal lying down on earth..
• Discharges from openings.
• Bum, ulcers, erosions etc.
2. Subcutaneous tissue and musculature
Examine the subcutaneous tissue and musculature
after removal of skin for the presence of lesions
such as:
• Congestion, haemorrhage, oedema, nodule,
anemia, icterus.
• Fat deposits.
• Necrosis on muscles, hardening, calcification.
257
3. Abdominal and thoracic cavity
Just after opening the carcass, one should observe
the presence of any lesion in abdominal and
thoracic cavity and following points must be kept
in mind.
• Accumulation of fluid (serus, serosanguinous,
blood, pus etc.).
• Fibrinous or fibrous adhesions.
• Parasites.
• Abscess, tumor etc.
4. Respiratory system
Organs/tissues to be examined
External nares, nasal passage, larynx, trachea,
bronchi, lungs, air sacs (poultry) mediastinal
lymphnodes.
Lesions to be observed
• Discharge from external nares.
• Growth (granulornalpolyp) in nasal passage if
there is blood mixed nasal discharge.
• Trachea and Bronchi Congestion,
haemorrhage, presence of caseous exudate,
frothy exudate etc.
• Lungs - Congestion, consolidation, nodules,
presence of exudate on cut surfaces, oedema,
atelectasis, emphysema, haemorrhage,
necrosis.
• Mediastinal
hardening,
haemorrhage.
lymphnodes
calcification,
5. Cardiovascular system
Oedema,
congestion,
Heart, aorta, arteries, veins and lymphatics.
• Fluid, blood, pus etc. in pericardial sac.
• Adhesions, fibrin, fibrosis.
• Congestion, haemorrhage, necrotic foci.
• Hardening of blood vessel, obstruction,
thrombi.
• Presence ofparasites.

Appendices
• Post-mortem clot/thrombi.
6. Digestive system
Mouth cavity, oesophagus, crop, proventriculus,
gizzard (poultry), rumen reticulum, omasum,
abomasum (ruminants), stomach, intestine
(duodenum, jejunum, ileum, caecum, colon,
rectum), cloaca, vent (poultry), anus, liver,
pancreas, gall bladder, mesenteric lymphnodes etc.
• Erosions, ulcers, vesicles.
• Congestion, haemorrhage, oedema.
• Necrosis.
• Icterus.
• Abscess/pus.
• Perforation, needles or hard objects in
reticulum.
• Intussusception, torsion, volvulus.
• Parasites.
• Atrophy, hardening, nodules.
• Contents, catarrhal, blood mixed, digested!
undigested feed material, thickening of wall of
intestines.
• Cut surface ofliver for parasites, lesions in bile
duct.
7. Cardiovascular system
• Kidneys, ureter, urinary bladder, urethra
• Congestion, haemorrhage, infarction, oedema.
• Necrosis, hardening, nodules.
• Deposition of salts, calculi.
• Obstruction.
8. Genital system
Organs/tissues (female)
• Ovaries, oviduct, uterus, cervix, vagina.
Male
• Testicles, Epididymis, penis, prepuce.
• Cysts in ovary.
• Congestion, haemorrhage, oedema.
• Foetus in uterus, pus, fluid.
• Necrosis, overgrowth, nodules.
• Atrophy, adhesions, granularity.
9. Immune system
• Spleen, lymphnodes, bursa and thymus
(poultry), bone marrow.
• Peyer's patches, GALT, RALT.
• Size, shape, atrophy, hardening.
• Oedema, congestion, haemorrhage.
258
10. Nervous system
• Brain, spinal cord, nerves, meninges.
• Congestion, haemorrhage, hematoma.
• Oedema, swelling.
• Abscess.
• Hypoplasia.
11. Miscellaneous observation
• Adhesions in pleural/peritoneal cavity.
• Any other left over information pertinent to
post-mortem examination/diagnosis.
12. Post-mortem diagnosis
• Diagnosis should be made on the basis of
above findings about any system or organ. The
most involved organ based diagnosis should be
written with suggestion of etiological factors
or etiology based diagnosis.

Appendices
Post-mortem report consists of two parts, post-
mortem record and post-mortem examination as
given in the format on next page. The ftrst part i.e.
post-mortem record contains information related to
animal and is supplied by the owner or person
requesting post-mortem examination. Actually, it is
a part of request form of the case for post-mortem
examination. This is necessary for the identiftcation
of animal. It should be ftlled in before conducting
post-mortem examination. The proper record will
be helpful in establishing accurate diagnosis based
on post-mortem examination.
POST-MORTEM RECORD
1. Species: Here one should write the species of
animal such as bovine, porcine, equine,
poultry, etc.
2. Date: Date ofthe post-mortem examination.
3. Case number: The serial number of your post-
mortem book. It shows cumulatively how
many animals are examined by you in
necropsy.
4. Breed: Mention the breed of animal, if known
or supplied, in the request form, such as
Murrah buffalo, Jersey cattle, etc.
5. AgelDate of birth: Age of animal or its date
of birth. In case the exact age is not known
then mention young, adult or chick, grower,
adult in case ofpoultry.
6. Sex: Sex ofanimal (male or female).
7. Identification number/mark: It must be
ftlled with utmost care; the number (tattoo
number or brand number) should be the same
as on animal. If the identiftcation number is
not available/illegible then write the
characteristic mark of animal.
8. Owner: Here, the name of owner with
complete address must be ftlled clearly. The
Appendix III
WRITING OF POST-MORTEM REPORT
address should be complete enough so that the
report can reach the owner through post also.
9. Referred by: In this column, the name of
Veterinary Offtcer/any other offtcer who has
referred the case for post-mortem examination
should be written. Sometimes owner
himselflherself is interested in post-mortem
examination of animal; in such cases the name
ofowner should be written.
10. History of the case: This includes the clinical
illness of animal, duration of illness,
epidemiological data, tentative diagnosis,
therapeutic and preventive measures adopted.
This is very important and information of this
column has an important role in making the
diagnosis.
11. Reported date and time of death: It should
have the exact date and time of death of
animal. Sometimes, it is difftcult to note the
exact time then one can write morning, noon,
evening, midnight etc. to approximate the
timing ofdeath of animal. In some large farms,
it is very difftcult to record information with
regard to each individual animallbird so here
one can write "previous night" as time of
death.
259
12. Date and time of post-mortem examination:
Pathologist conducting post-mortem
examination should write here the exact time
and date ofthe post-mortem examination.
The above information is very important to arrive
at any conclusive diagnosis. The correct
information enhances the speciftcity of post-
mortem diagnosis. Some points might appear to be
insigniftcant but one should not overlook them and
write as correct information as he/she can gather
from the owner's request letter/form.

Appendices
POST-MORTEM REPORT
POST-MORTEM RECORD
1. Species: 2. Date: 3. Case No.:
4. Breed: 5. Age/Date ofbirth: 6. Sex:
7. Identification No.:
8. Owner's name with address: 9. Referred by:
10. History ofthe case: 11. Reported date & time ofdeath:
12. Date and time ofpost-mortem examination:
1. External appearance :
2. Subcutaneous tissue and musculature:
3. General observations after opening the carcass:
4. Respiratory system:
5. Cardiovascular system:
6. Digestive system:
7. Urinary system:
8. Genital system:
9. Immune system:
10. Nervous system:
11. Miscellaneous observations:
12. Post-mortem diagnosis
Signature ofofficer conducting post-mortem
Date:
Place:
260

Appendices
It includes the observations made by the
pathologist conducting post-mortem examination.
This part of report should be filled in as soon as
possible after the post-mortem examination. It is
advisable to record some points on a small paper or
diary during post-mortem examination and fill
them in report after the necropsy/autopsy.
1. External appearance: Record the lesions
observed in intact animal before opening it.
One should place on record the side of animal
lying down, lesions on skin, external parasites,
trauma etc.
2. Subcutaneous tissue and musculature: The
observations made after removal of skin, on
subcutaneous tissue and muscle should be
included in this column.
3. General observations after opening the
carcass: It contains the general information or
lesions present in abdominal and thoracic
cavity such as accumulation of fluid, pus,
blood, clot of blood, post-mortem changes
such as pseudomelanosis, etc.
4. Respiratory system: Record the lesions
observed in respiratory system right from
external nares, nasal passage, trachea, bronchi
and lungs along with mediastinallymphnodes.
5. Cardiovascular system: Record the lesions
present in heart, aorta, arteries, veins and
lymphatics.
6. Digestive system: Record the lesions observed
in digestive tract from mouth cavity,
oesophagus, crop, proventriculus, gizzard
(poultry), rumen, reticulum, omasum
abomasum (ruminants), stomach, intestines,
rectum, anus, cloaca, vent (poultry), liver,
pancreas, gall bladder etc.
7. Urinary system: Place on record the lesions
present on kidneys, ureter and urethra.
261
8. Genital system: Record the lesions present in
ovaries, uterus, oviduct, cervix and vagina in
females and testes, penis etc. in males. Be
careful in recording lesions in this column as it
should match with the sex of animal written in
post-mortem record section.
9. Immune system: Record the lesions present in
spleen, bursa, thymus, lymphnodes, respiratory
associated lymphoid tissue (RALT), gut
associated lymphoid tissue (GALT) etc.
Careful recording of lesions in these organs
will be helpful in diagnosis.
10. Nervous system: Place on record the lesions
present in brain, spinal cord and nerves. Most
of the pathologists overlook this system and
often do not taken pain to examine the brain. It
should not be done and every effort should be
made to examine and place on record the
lesions present in this system.
11. Miscellaneous observations: Here one can
record any missing observation which has not
been covered above.
12. Post-mortem diagnosis: This is very
important. Based on the history and lesions
present in different systems, pathologist, by
using his experience and conscience,
concludes the diagnosis. He/she may also write
suggestions along with diagnosis or some
points to suggest the diagnosis and/or contain
the disease in other animals.
13. Signature of officer conducting post-
mortem: Each and every report must be
signed by the officer doing post-mortem
examination. Without signature of competent
officer, it has no validity.
14. Place and date: The person signing the post-
mortem report must also write date and place
ofpost-mortem examination.

Appendices
Appendix IV
COLLECTION, PRESERVATION AND DISPATCH OF SPECIMENS
FOR LABORATORY DIAGNOSIS
Tissue samples are collected from dead or live
animals for laboratory examination to confirm the
tentative diagnosis.
Purpose
• Diagnosis of disease or for identificatlon of
new disease.
• Confirmation of tentative diagnosis.
• Prognosis.
• To observe the effect of treatment and give
directions for future therapy.
Precautions
• Collect the tissues as early as possible after
death ofanimal.
• Representative tissue/sample should be
collected.
• Sharp knife should be used for cutting tissue.
• Collect the tissues directly in fixative.
• Size of tissue should not be more than 1 cm for
histopathology in 10% formalin.
• Hollow organs should be taken on paper to
avoid shrinkage.
• Hard organs like liver, kidneys etc. should be
collected along with capsule.
COLLECTION OF SPECIMENS FOR
BACTERIOLOGICAL EXAMINATION
• Collect the tissues under sterile condition.
• Sterilize knife/ scalpel! spatula on flame or in
boiling water.
• Surface sterilized by hot spatula.
• Cut with knife and collect sample from inner
tissue.
• Body fluidslblood should be collected in
sterilized syringe or in Pasteur pipette.
262
• Specimens should be collected directly in
media (liquid media-nutrient broth, peptone
water, tetrathionate broth or even in normal
saline solution/phosphate buffer saline).
• Seal, pack and transport the collected material
to laboratory in ice/under refrigeration
conditions.
BACTERIAL DISEASES
Abscesses
• Swab in sterile conditions/pus in vials.
• Collect material from margin ofabscess.
Actinobacillosis! Actinomycosis
• Tissues from affected parts in 10% formalin.
• Pus in sterile test tube/from edge oflesion.
• Slides from pus for sulphur granules.
Anthrax
• Blood smear from tip of the ear.
• Blood for cultural examination.
• Muzzle piece for biological test.
• Mark the specimen as "Anthrax suspect".
Black QuarterIBlack leg
• Smear from swelling.
• Affected muscle piece in ice.
Brucellosis
• Serum after 3 weeks of miscarriage.
• Foetal stomach tied off.
• Swabs from uterine discharge.
• 5 to 10 ml milk in ice.
Glanders
• Smear from discharge.

Appendices
• Lung, liver and spleen in 10% formalin.
• Serum.
Johne's disease
• Bowel washings in sterile bottle.
• Smear from rectal mucosa.
• Mesenteric lymphnode in 10% formol saline.
Leptospirosis
• Serum 21 days after miscarriage.
• Milk/urine in vials (1 drop of formalin in 20
ml).
• Liver, kidney tissue in 10% formalin.
Listeriosis
• Halfbrain in ice.
• Halfbrain in 10% formalin.
Mastitis
• 10 ml milk in sterile vial in ice.
Pasteurellosis
• Heart blood.
• Lung, spleen and mediastinal lymphnodes in
ice.
• Affected tissues in 10% formalin.
Salmonellosis
• Liver, spleen, kidney and intestine tied off in
ice.
Strangles
• Smear, swab ofpus in ice.
Erysipelas
• Blood.
• Spleen, kidney, liver in ice.
Vibriosis/Campylobacteriosis
• Foetal stomach tied off.
• Vaginal mucosa in ice.
263
• In pig, intestine and liver in 10% formalin.
Colibacillosis
• Heart blood in sterile vial.
• Tissues from intestine and lymphnodes in 10%
formol saline.
Tuberculosis
• Lungs, mediastinal and bronchial lymphnodes
in ice and in 10% formalin.
VIROLOGICAL EXAMINATION
• Collect tissue under sterilized condition.
• Body fluidslblood in sterilized syringe or in
Pasteur pipette.
• Tissues in buffered glycerin.
o PBS pH 7.2- 50%
o Glycerin- 50%
• Avoid s!lmples in glycerin from sensitive
viruses e.g. Rinderpest, canine distemper.
• Seal and mark the specimen bottle and
transport to laboratory.
VIRAL DISEASES
Foot and mouth disease
• Tongue epithelium, vesicular fluid, saliva,
pancreas in 50% buffered glycerine.
• Serum.
Hog cholera/ swine fever
• Serum under refrigeration.
• Spleen, liver, kidney in 50% glycerin/ice.
• Tissues from intestine, mesenteric lymphnode
and half of the brain stem in 10% formol
saline.
Infectious Canine Hepatitis
• Several pieces of liver, gall bladder and kidney
in 10% formol saline.
Pox
• Scabs in ice and in 10% formol saline.

Appendices
Rabies
• Intact head should be soaked in 1% carbolic
acid.
• Fracture the skull with hammer.
• Remove skin and bones.
• Halfbrain in 10% formalin.
• Halfbrain in 50% neutral glycerin.
• Tissues from cerebellum and hippocampus in
Zenkers fluid for 20 hrs, wash in tape water for
24 hr and keep in 80% ethyl alcohol for
Negribodies.
Ranikhet disease
• Liver, spleen in 50% neutral glycerin.
• Proventriculus in 10% formalin.
• Brain in ice.
Rotaviral enteritis
• Faecal sample.
• Interstinal tissue in 10% formol saline.
Gumboro disease
• Bursa of Fabricious, kidney, muscles in 10%
formol saline.
• Bursa, kidney in 50% buffered glycerine.
SYSTEMIC DISEASES
DiarrhoealEnteritis
• Faecal sample in sterile vial.
• Serum.
• Tissues of intestine, mesenteric lymphnodes in
10% formol saline.
MiscarriagelMetritis
• Foetal stomach content tide off or in sterile
vials.
• Serum of dam after 21 days of miscarriage.
• Vaginal discharges in sterile conditions.
• Tissues of placenta, foetal liver, stomach,
kidney in 10% formol saline.
264
Pneumonia
• Nasal discharge/nasal swabs.
• Lung tissue/pieces in sterile vials.
• Lung tissue and mediastinal lymphnode in
10% formol saline.
Dermatitis
• Skin scrapings in 10% KOH.
• Skin tissue in 10% formol saline.
Encephalitis
• Cerebrospinal fluid in heparinised vials.
• Brain tissue in 10% formol saline.
• Brain tissue in 50% glycerol.
Nephritis
• Urine sample in sterile vial.
• Kidney tissue in 10% formol saline.
TOXICOLOGICAL EXAMINATION
• Stomach/intestinal contents.
• Liver, kidneys, heart blood.
• Urine.
• In clean glass jars.
• In ice/refrigeration without any preservative.
• Seal, label, transport to laboratory.
• In veterolegal cases all specimens must be
collected in presence ofpolice.
• Type of poison suspected along with detailed
history, signs, lesions/treatment etc. should be
written on letter with specimens.
TOXICOSIS/POISONING
Heavy metal poisoning
• Hg, Pb, Bi, Ag.
• Liver, kidney, stomach content in ice 10
separate containers.
Alkaloids
• Liver, stomach contents and brain tissue in ice.

Appendices
Nitrate
• Fodder.
• Stomach contents, blood in ice.
Strychnine poisoning
• Stomach contents, intestinal contents, urine,
liver, kidney in ice.
Hydrocyanic acid
• Plants.
• Stomach contents, blood, liver.
• Preserved in 1% solution ofmercuric chloride.
Pesticides
• Fatty tissue, liver, stomach contents, blood in
ice.
• Subcutaneous, omental, mesenteric fat.
IMMUNOLOGICAL EXAMINATION
• Heart blood in syringe/ Pasteur pipette.
• CSF/Synovial fluid /peritonial fluid.
• Tissues in formol sublimate or in buffered
formalin.
• Blood/serum/others should be sent to
laboratory under refrigeration conditions.
265
• Add one drop of 1:10000 merthiolate in 5 ml
serum as preservative.
DISPATCH OF MATERIAL
Following points must be kept in mind while
dispatching the material to laboratory for diagnosis.
1. Describe the clinical signs, lesions, tentative
diagnosis and treatment given to animal in
your letter. Also mention the type of test you
want with your tentative diagnosis.
2. Write correct address on letter as well as on the
parcel preferably with pin code, if the material
is sent through post.
3. Mark the parcel 'Biological Material', 'Handle
with care', 'Glass material', 'Fragile' etc. in
order to avoid damage in parcel. Also mark the
side to be kept on upper side with arrows.
4. Seal the container so that it does not leak in
transit.
S. Try to send the material soon after its
collection from animal.
6. Keep one copy of cover letter inside the parcel
and send aIlother copy by hand or post in a
separate cover.
7. Keep adequate material like thermocol etc. in
the parcel which will save the material from
outside pressures/jerks.
8. Use dry ice, if available, otherwise use ice in
sealed containers.

Appendices
Histopathology is the branch of pathology which
concerns with the demonstration of minute
structural alterations in tissues_ as a result of
disease. Most of histopathological techniques
simulate those of applied for study- the normal
histological structures. For the demonstration of
minute histological changes, the tissue must be
processed in such a manner that it will provide
maximum information. The histopathological
diagnosis is an overlooked area specially in
Veterinary Sciences. Many times it has been
observed that the procedures are not properly
followed or the qualified person trained for
histopathology is not available, which in turn
affects the interpretation and/or diagnosis.
Histopathological procedures are described for the
benefit of readers which will help them in
diagnostic laboratory.
Scope
Though the histopathological techniques are labour
intensive, cumbersome and time consuming,
particularly when there are automation equipments
are not available; their use in diagnosis of diseases
is unequivocal. Some of the areas where
histopathological diagnosis is helpful are described
as follows:
• This is useful in establishing the pathogenesis
and pathology of any disease caused by
bacteria, virus, chlamydia, rickettsia,
mycoplasma, parasite, toxin, poisons etc.
• There are certain diseases in which
histopathological examination of tissues is the
only alternative to diagnose the disease. e.g.
Bovine spongiforrn encephalopathy. The agent
of this disease has a very long incubation
period and very difficult to isolate and there is
no immune response and inflammation in
animal. Therefore, histopathology remains the
only alternative for confirmatory diagnosis.
• In some cases, the tissues from dead animals
are the only available material for laboratory
diagnosis. This may occur either due to lack of
Appendix V
HISTOPATHOLOGICAL TECHNIQUES
266
time or due to negligence for not collecting the
material for serological tests or isolation
studies. Sometimes the transportation of
material from remote areas destroys the other
material and the tissues fixed in formalin only
remains for making diagnosis. In all such cases
the histopathological examination has its
pivotal role.
• The histopathological procedures produce
permanent slides, which can be stored for a
longer period and one cannot manipulate the
findings; therefore, it is considered the best
reliable technique.
• The histopathological techniques are useful in
carrying out retrospective studies. The
unstained slides and blocks can be stored for
indefinite period; which can be examined even
after many years for further studies.
• The presence of causative agents can also be
demonstrated in tissue sections using routine
histopathological techniques or special
stainings, In the Gram's staining, procedures
are used for demonstration of bacteria while
viral presence is demonstrated using
hematoxylin and eoxin or other staining
techniques like Macchiavello's stain or Mann's
methylene blue eosin method. The Negri
bodies are demonstrated by Seller's stain in
case of rabies in animals. In such cases, the
isolation of causative agent or their serological
examination not required; since the presence of
causal agent in infected tissues gives a
confirmatory diagnosis.
• The detection of chemicals in tissues like
enzymes, lipids etc. is included in
histochemical examination; which not only
describes the structural changes but also gives
an idea about the functional status ofthe organ.
Histopathological procedures
The microscopic examination of t~ssues or organs
can be achieved by their smears or using vital

Appendices
staining or by sectioning; the latter method being
more commonly used in histopathological
laboratories.
Smears
The microscopic examination using smears of any
organ/tissue/cells is very rapid method which gives
the results within hours. A drop of blood is placed
on clean glass slide and with the help of another
slide, the smear is prepared (Fig. 22.22). In this the
tissue pieces from organs are cut using a sharp
knife and the cut surface is mildly touched with
clean glass slides with some gentle pressure. Which
gives an impression on the slide (Figs. 22.23 &
22.24). This is also known as impression smear;
generally 2-5 smears are prepared on a slide. If the
collected tissue material is too less then it is
pressed between two slides and the impressions
thus obtained on both the slides are used for study.
The wet smears are fixed with methanol and can be
stored or transported to laboratory for examination.
The impression smears of hippocampus,
cerebellum and cerebrum of brain are very useful
for demonstration of Negri bodies in rabid animals
for diagnosis of rabies. The impression smears are
stained with seller's stain for a few seconds,
washed and air dried and examined under oil
immersion microscope for the presence of inclusion
bodies also known as Negri bodies. These
inclusions are characterized by intracytoplasmic,
eosinophillic appearance with basophilic granules
and round to oval in shape with a clear hallo.
In case of pox infection in animals, the impression
smears are prepared from scabe or pustule for
demonstration of intracytoplasmic inclusions.
Sometimes the viral inoculum is inoculated on
chorioallantoic membrane (CAM) of embryonated
eggs; the impression smears of CAM may yield the
viral inclusions. In certain bacterial diseases like
haemorrhagic septiemia and enterotoxaemia, it
becomes very difficult to demonstrate the organism
in blood or in tissues. For confirmatory diagnosis,
the material is inoculated in laboratory animals like
mice, guinea pigs etc. The impression smears are
then prepared from liver, spleen and other relevant
organs of laboratory animals for demonstration of
the organism. .
267
FIg. 22.22. Photograph shOWing preparatIOn ofbload smear
Fig 2223. Photograph shOWingpreparatIOn of
Impression smear
FIg. 22.25. Photograph shOWing collectIOn of
tissue Infixallve

Fig. 22.26. Photograph showing collection of
tissue in fixative
FIg 22.27 Photograph showing the collectIOn
ofmtestme on a p,ece ofpaperfor fixatIOn.
FIg. 22.28. Photograph showing the dehydratIOn of
blocks in ascending series ofethanol
R
Fig. 22.29. Photograph showmg (A) Mould
(B) Tissue capsule and (C) Block holder.
Appendices
268
Fig. 22.30. Photograph showmg section cutting
on mu.:rotome
Fig. 22.31. Photograph showing lifting oftissue
section from floatation bath
Fig. 22.32. Photograph showing staming
oftissue sections
mounting ofslides with DPX

Appendices
Vital Staining
Vital staining procedures are not much in use
directly in the diagnosis. However, for detection of
phagocytic cells in body the vital stains are used. In
the living animals when vital staining procedures
are used for localization of phagocytic cells, these
are known as intravital. In vitro use of vital stains
is called as spravital staining which is being done
for the live and dead lymphocyte count in leucocyte
migration inhibition test (LMIT), lymphocyte
stimulation test (LST), macrophage migration
inhibition test (MMIT) and macrophage function
tests (MFT).
Routine Histopathological Techniques of
sectioning
The tissue pieces from morbid animals should be
collected properly and fixed in a suitable fixative.
Then these are processed and sections of 4-5
microns are cut and taken on slides. These sections
are stained and mounted to make the permanent
preparations of slides. The different steps required
for making the tissue slides are described briefly as
follows.
1. Collection of tissue
The collection of tissues is an important step,
which is many times not given proper attention.
The whole diagnostic process depends upon the
collection of tissue pieces. A representative tissue
should have been collected carefully and should
have the normal as well as abnormal (lesion) part.
The tissues must be collected by qualified person
after a thorough examination of each organ/system.
Sometimes it has been observed that the collection
of tissues is done by attendants or very casually by
the qualified persons and proper attention is not
paid. It should be kept in mind that a representative
tissue sample will only give the correct diagnosis
which cannot be corrected/altered afterwards. At
the time of tissue collection following points must
be kept in mind which will be beneficial for
making a correct diagnosis.
• The tissue pieces from morbid animal should
be collected as early as possible after the death
of animal. Once the autolytic changes starts in
269
the dead body; it will not give true picture of
microscopic lesions due to autolysis.
• At the time of tissue collection, it should be
kept in mind that the representative tissue
piece should include a part of lesion and a part
of normal tissue, which facilitates the
identification of organ/tissue at the time of
microscopic examination.
• The tissue pieces should be cut with sharp
knife and using only one stroke. Blunt edged
knife may require many attempts for cutting,
which destroys the normal architecture of
tissues.
• Tissue pieces for histopathological
examination should be collected from all the
organs. Sometimes it has been noticed that the
tissue sample is taken from those parts ofbody
which show gross lesions; merely absence of
gross lesion does not mean that there will not
be microscopic alteration. In many disease
conditions only microscopic changes occur
which do not exhibit grossly. Such selective
collection of tissues gives a biased
interpretation, so it is better to have tissues
from all the organs for proper interpretation
and unbiased conclusions of histopathological
studies.
• Tissues should be collected directly in the
fixative and not in any other pot or water (Figs.
22.25 & 22.26). Sometimes it has been
observed that at the time of post-mortem
examination, the tissue samples are collected
in petridishes or in bottles and brought to the
laboratory, then fixative is added. This seems
to be a wrong practice. The tissue bottles filled
with 2/3 fixative must be available at the time
of necropsy and tissue pieces should be
collected directly in the fixative.
• The size of tissue piece should not be more
than 5 mm; it facilitates the homogenous and
smooth fixation. Large size tissues do not get
fixed properly and in the middle, the tissue
gets autolysed.
• The tissue pieces from hollow organs like
intestines, oviduct etc should be cut

Appendices
transversely and placed on a hard paper, then it
should be cut longitudinally in such a way that
the serosal layer sticks to paper and mucosal
layer gets free. Thereafter, it should be placed
in fixative along with paper. This allows a
good fixation and avoids the shrinkage and
folding of tissue (Fig. 22.27).
• At the time of post-mortem examination, it has
been noticed that the faecal matter is removed
from the intestines by pressing/squeezing them
or after opening the lumen by sharp objects
like knife, slides etc., which causes damage in
the mucosal layer. The representative tissue
should not be collected from such damaged
portions.
• The tissues from encapsulated organs should
be collected along with capsule or covering.
like brain should be collected along with
meninges; kidneys and liver should be
collected with their capsules. The coverings of
such organs also yield useful information on
histopathological examination.
2. Fixation
The fixation of tissues is required for preventing
the post-mortem changes like autolysis and
putrefaction by saprophytes, preservation of
cellular constituents in life-like manner and for
hardening of tissues by way of conversion of
semisolids to solid material. For a proper
histopathological preparation and their
interpretation, the role of fixative is very crucial.
Any faulty fixation cannot be remedied at any later
stage. An ideal fixative should be one that fixes the
tissues quickly and does not interfere with the
refractive index of the tissue components.
The choice of fixative depends on the type of
investigation required, the formol saline (10%
formaldehyde in 0.85% sodium chloride solution)
is considered best fixative for routine
histopathological studies. The buffered formalin
has certain advantages over formol saline and now
a days it is recommended for routine use in
histopathological laboratories. The buffered
formalin can also be used for immunopathological
studies. Buffered formalin is widely used and
270
preferred because of its tolerance; tissues can be
left for longer period without excessive hardening
or damage and sectioned easily. Since it has neutral
pH, the formalin pigment is also not formed in the
tissues. However, for immunopathological studies
like immunoperoxidase staining techniques, the
fixative of choice is formol sublimate. But in its
absence buffered formalin may also be used. The
time required for proper fixation is 6-12 hrs for 5
mm thick block oftissue.
3. Washing
After 6-12 hours fixation the tissue pieces are taken
out from fixative and cut into 2-3 small pieces of 2-
3 mm size blocks. These blocks are then kept in
tissue capsules (Fig. 22.29 B) or in a gauge tide off
with the help of thread. The identification marks
written by copying pencil are also kept along with
tissues. These capsules/gauge containing tissues
should be kept in running tap water overnight for at
least 12 hours.
4. Dehydration
In routine practice, the dehydration is done in
ascending series of graded ethanol. The tissue
blocks are kept in 50% ethanol and then in 70%,
80% 90% 95% absolute ethanol I and absolute
etha~ol 11 for one hour each. These ethanol graded
series should be kept in tight glass stoppered bottle
or in screw cap jars to prevent evaporation. In the
last bottle of ethanol 11 sometimes the copper
sulfate is layered in the bottom, covered with filter
paper, which increases the life of ethanol as it
absorbs the water from alcohol. But care should be
taken, as soon as the copper sulfate turns bluish due
to absorption of water, the ethanol should be
changed (Fig. 22.28).
To increase the process of dehydration, the tissue
blocks should be agitated either mechanically in an
automatic tissue processor or by shaking the
container periodically. The volume of alcohol
should be at least 50 times more than the tissue
placed for dehydration.
5. Clearing
Usually the clearing of tissue blocks is done in
xylene. Like ethanol, xylene should also be kept in

Appendices
tightly stoppered bottle to prevent evaporation.
After dehydration the tissue blocks should be kept
in ethanol and xylene (1: 1) mixture for one hour,
then the blocks should be transferred to xylene I
and xylene 11 for one hour each. If xylene is not
available then benzene may be used for 3 hours as
its action of clearing is slower than xylene. On
complete clearing, the tissue becomes transparent.
It should then be transferred in paraffm wax for
impregnation.
6. Impregnation
For the impregnation of tissue blocks, paraffin wax
is used either in paraffin embedding bath or in oven
fixed at 60-62°C temperature. Both the oven and
embedding bath are electrically operated with
thermostat to adjust the desired temperature. At the
time of transfer of tissue blocks from xylene 11, the
paraffin wax must be kept at 60-62°C in liquid
form for impregnation. Three changes are given in
paraffin wax; each of one hour duration. The
paraffin wax should be free from dust or other
gross impurities; which can be removed by
filteration through muslin cloth.
7. Casting ofblocks
After 3 hours' impregnation of tissue blocks in
paraffin wax, the blocks are formed in moulds
using molten wax. The tissues are placed in moulds
(Fig. 22.29A) in such a way that desired surface
remains downward, on the base of mould. The
sections are cut from this surface, so care must be
taken to keep the tissue in a proper manner and
should be cut into sections homogenously. The
mould is then filled with molten paraffin wax and
then the blocks are cooled either at room
temperature or in cold water. Various types of
moulds, like 'L' shaped or ring shaped, can be
used. If the moulds are not availa~le, the blocks can
be prepared in glass petridishes or in empty slide
boxes. But care should be taken to lubricate the
surface of such petridishes and other moulds with
liquid paraffin or glycerine which facilitates the
easy removal of blocks after cooling and hardening
ofparaffin wax.
271
8. Trimming
The blocks are removed from the moulds and are
cut so as to give one tissue per block and the wax is
trimmed by knife or by rubbing on a hot plate in
order to remove the extra wax on either side of
tissue. The tissue is exposed, which helps in
determining the side on which the section is to be
cut. The identification of tissue should by fixed on
one side of the block by touching the block with the
small paper kept on it with hot forcep or knife,
bearing the number. Then the blocks are fixed on
block holder (Fig. 22.29C). Care should be taken
that the number of marking of block is kept on
upper side at the time of trimming of the block on
microtome to remove the extra wax and expose the
whole surface of tissue. The trimming of blocks is
done at 10-1511 and a separate knife should be used
for trimming and section cutting.
9. Section cutting
Before the sectioning, the tissue blocks are cooled
on ice or by keeping them in refrigerator. The
tissue floatation bath should be cleaned and filled
with water having a temperature of about 60-70°C.
The blocks along with block holders are fixed in
the microtome (Fig. 22.30) in such a way that the
marking number is on upper side, giving a similar
position to the blocks as it was during trimming.
Usually the sections are cut at 4-611 thickness on
rotary microtome using a plain edge knife. The
knife should be sharp enough to cut the desired
thickness sections in the form of a ribbon while not
causing damage to the tissue. By using a brush and
forceps, the ribbon of tissue sections are placed in
tissue floatation bath (Fig. 22.31). The tissue
sections will spread here due to melting of paraffin
wax and will take the shape similar to the tissue of
that block. One can make out the selection here; the
best looking 1-5 sections can be lifted on a sticky
glass slide, which should be kept in a tray at an
angle so that the water is removed. The glass slides
are made sticky by applying on clean glass slides a
sticky material consisting of egg white and
glycerine in 1:1 (VN) ratio. The sticky material

Appendices
"Flow Chart Showing Processing of Tissue for Histopathology
Collection oftissues in
Dry in incubator
10% formol saline 1-2 days
Cleaning in water Lift section on slide
10 - 12 hrs pasted with adhesive
50 % ethanol Place in flotation bath
1 hr 62° C
( 70 % ethanol
) Cut sections
1hr 4-5 ~m
l
80 % ethanol Trimming to expose
1 hr tissue
90 % ethanol FIxing of blocks on block
1 hr holders
95% ethanol
Numbering on blocks1 hr
Absolute ethanol
Trimming ofblocks
lhr
Alcohol + Xylene
Casting of blocks
1 hr
( Xylenel
) Paraffin III 62° C
Ihr 1hr
l
Xylene JI Paraffin II 62° C
1 hr Ihr
Paraffin I 62° C
I hr
272

Appendices
facilitates the sticking of sections on slides, so that
they are not damaged or removed during further
processing of staining. Generally, 4-5 slides are
made from each block and air dried in incubator or
at room temperature. The following precautions
should be taken at the time of section cutting:
i. Adjust the microtome gauge at right place,
generally it is adjusted at 4-5Jl for routine
histopathological examinations.
ii. Knife should be properly fixed with the help of
screws at an angle of about 45 degree. Ensure
that all the fittings are tightly fixed.
iii. The knife should be sharp enough to cut
sections free from nicks. If the nicks are
present on sections, the position of knife
should be changed or the knife should be
properly stropped.
iv. The temperature of tissue floatation bath
should neither be low nor should it be higher
than the prescribed limit. In low temperature,
the tissue will not spread properly and its
compressions and creased will not be removed,
while at high temperature the paraffin wax of
tissue will melt quickly making the tissue
fragments and destroying the original shape of
section.
v. Lift the tissue sections on slide at an angle
(45°) of slide so that the air bubbles does not
appear in between the slide and section.
vi. Use little sticky material on slide, if it is more
then drying process will take more time.
vu. If the ribbon of sections is large then it should
be cut at the junction of two sections with a
sharp knife or blade and small pieces made of
it.
viii. During summer, when temperature is above
40°C, the tissue sections should be cut either in
a room or laboratory having air-conditioner or
desert cooler. If such facilities are not available
then make moisture in the environment by
sprinkling water on ground. It is necessary
because at high environmental temperature, the
tissue sections stick to the knife and the ribbon
is not properly formed.
ix. Drive the microtome smoothly at a regular
speed; jerks should not be given.
273
x. For marking the slides, use the diamond pencil.
The marking should be made at the time of
section cutting itself.
10. Staining
(A) Routine procedure
After drying the slides are kept in slide cabinets.
One slide of each- block is selected for staining
using the following procedures (Fig. 22.32):
(a) Removal o/paraffin
The slides are slightly warmed either in incubator
or by the flame of a spirit lamp and placed in jar
having xylene. Replace the xylene after 10-15 min
with fresh xylene for another 10-15 min. This
removes the paraffin from the tissue sections.
(b) Rehydration
After removal of paraffin, the slides are kept in
descending series of alcohol. For this first they
should be kept in absolute ethanol and xylene (1: 1)
mixture for 5 min; then in absolute ethanol, 95%,
90%, 80%, 70%, 50% ethanol for 5-6 min in each
dilution. After that the slides are taken in water.
(c) Cleaning o/slides
With the help of muslin cloth, clean the slides at
both the sides. Leave only 1 or 2 section on a slide
and remove the extra sections and/or paraffm wax.
Wash the slides in running tape water.
(d) Staining in hematoxylin
Place the slides in Harris hematoxylin or Meyer's
hematoxylin for 10-15 min. Shake the slides 2-3
times for proper staining. Remove the hematoxylin
solution and wash the slides in running tap water,
then dip in acid alcohol for few seconds, which
helps in differentiation. Wash in tap water and
place the slides in ammonia water for few seconds
for blueing and place in running tap water in order
to remove the ammonia.
(e) Staining in eosin
Place the slides in 2% aqueous eosin or alcoholic
eosin for 2-5 min. After staining in eosin, quickly
proceed for dehydration.

Appendices
Flow Chart Showing Staining Procedure
Deparaffinize the sections Mounting on DPX
on flame / hot plate
)( Xylene I Xylene 11 10-15 min
10-15 min
~
( )( Xylene 11
) Xylene I 10-15 min
10-15 min
f~
Xylene + ethanol Xylene + ethanol 5 min
5 min
Absolute ethanol Absolute ethanol 5 rilin
5min
J(95 % ethanol 95 % ethanol 5 min
5min
f
( )90 % ethanol 95 % ethanol 5 min
5min
f
( )80 % ethanol 90 % ethanol 5 min
5min
f
70 % ethanol
( 80 % ethanol 5 min )5min
f
water / cleaning ( 70 % ethanol 5 min
)
f
Hematoxylin
( Eosin 2-5 min )10-15 min
f
( Water
~
) ( Water
f
)
Dip in acid alcohol Dip in Ammonia water
Water
274

Appendices
(I) Dehydration
The slides are placed in 70%, 80%, 90% 95%
absolute ethanol for dehydration for at least 5 min
in each solution; then they are placed in absolute
ethanol: xylene mixture (1: 1) for 5 min.
(g) Clearing
Clear the sections in xylene and give 2 changes at
least for 10-15 min each. The clearing in xylene II
can be extended for even upto one hour.
(h) Mounting
Mount the slides with coverslip using Canada
balsam or DPX mountant. For this the cover slips
of desired size and shape are kept on filter paper
and one or two drop of mountant is placed on
coverslip. Takeout the slides from xylene and place
on coverslip in such a way that the section touches
with mountant, press gently and lift the slide (Fig.
22.33). Remove air bubble, if any, by pressing the
coverslip with fine forcep and keep the slides in
horizontal position in a tray for drying.
(i) Cleaning and labelling
After drying, clean the slides with muslin cloth and
xylene. Remove the extra mountant using a blade.
Label the slide with a piece of paper and stick it on
one corner of slide using gum or other adhesive. At
the time of examination, the histopathologist
should put the name of organ, main changes in
sections/disease condition with other remarks on
this label for future identification ofthe slide.
G) Examination
On hematoxylin and eosin staining, the nuclei of
the cells take blue stain while the cytoplasm is pink
or red. Examine the' tissue section using 10 x
objective and, if required, in high power or oil
immersion. Precautions and important tips which
should be considered at the time of staining:
1. Check the sections for staining after blueing in
ammonia water for hematoxylin stain and after
dehydration for eosin stain. If under stained
then repeat the process and in case of
overstaining, the sections can be differentiated
for some more time in acid alcohol to remove
275
the excess hematoxylin and in ethanol for
removing the excess eosin.
11. Clean the slides thoroughly in water and
remove all patches/spots of paraffin; which
gives a good look to slides.
iii. If on clearing in xylene, cloudyness appears
then repeat the dehydration process in absolute
ethanol for 10-15 min. The cloudyness appears
due to presence of water in the sections which
reacts with xylene.
iv. At the time of mounting, ensure that the tissue
section does not get dried. To eliminate the
chance of drying, proceed fast. Ensure the
proper mounting of section on slides.
Sometimes the opposite side of the section is
mounted and the section becomes dry. To
ensure proper mounting, one should feel/touch
the diamond pencil marking present on the
same surface and then mount the sections. This
can also be checked by touching the slide on
reverse side for the presence/absence of tissue
sections.
v. Labelling with paper should be done on same
side on which the section is present; which will
be helpful at the time of examination.
(B) Special procedures
In histopathological techniques, one can
demonstrate bacteria, fungus, chlamydia, rickettsia
or viral inclusions in the tissue sections by using
special staining procedures. These special staining
techniques, however, require special expertise but
can be used in diagnostic laboratory as routine
methods. Some important special staining
techniques are described as under:
I. Staining for acid fast bacilli
The acid fast bacilli are demonstrated in
tuberculosis or Johne's disease in animals. The
tissues are collected in formol saline or buffered
formalin and processed in same manner as for
routine histopathological techniques. For special
staining of acid fast bacilli following procedures
are followed:

Appendices
1. Deparaffinize the sections and hydrate in
descending series of ethanol as described
earlier.
2. Clean the slides in water and give a wash in
distilled water for 5 min.
3. Place the slides in carbol fuchsin solution and
keep the chamber of slides in a water bath at
56°C for 1 hr.
4. Thereafter, remove the slides from water bath
and keep at room temperature for a few min,
wash in running tap water. Dip in acid alcohol
for differentiation till the colour of tissue
becomes pale pink.
5. Wash in running tap water.
6. Place the slides in methylene blue working
solution for a few seconds, wash in tap water
till the colour of sections becomes pale blue.
7. Dehydrate in ascending series of ethanol, clear
in xylene and mount in DPx as described
earlier in histopathological procedures.
Examine the slides under oil immersion. The
acid fast bacilli will be of bright red colour
with a light blue back ground.
S. Precautions
(a) Care should be taken that at 56°C for 1 hr, the
stain does not get dry so it is always advisable
to keep it in a covered jar in water bath to
prevent drying.
(b) Differentiation with acid alcohol is a very
crucial step and should be controlled carefully;
it depends on experience of a histopathologist
to stain the slides properly.
11. Demonstration of Gram-positive/Gram
negative bacteria in tissue sections
i. Deparaffinize and hydrate the sections in
water, clean them.
11. Stain the slides with crystal violet for 2 min.
iii. Wash in distilled water.
iv. Keep the slides in Gram's iodine solution for
5 min.
v. Wash in distilled water.
vi. Differentiate in cellosolve (Ethylene glycol
monomethyl ether) until blue colour no
longer comes out from sections.
V11. Wash in distilled water.
276
viii. Place in basic fuchsin for 5 min and wash in
distilled water.
IX. Place the slides in differentiating solution for
5 min., wash in distilled water and blot dry.
x. Dip the slides in tetrazine for a few seconds.
xi. Place the slides in cellosolve, 3 changes of 6
dip in each.
XII. Clear in xylene I and 11 for 15 min each.
xiii. Mount in DPX
xiv. Examine the slides under oil immersion. The
Gram-positive bacteria will be of blue colour
while Gram-negative will take a red colour
against a yellow background.
Ill. Demonstration of spirochaetes
1. During post-mortem examination, cut about 1
mm thick slice of tissues from several sites of
an organ and fix them in 10% buffered
formalin for 24hrs, wash in running tap water
overnight and place in 95% alcohol for 24hr.
2. Transfer the tissues in distilled water and keep
till the tissues sink to bottom.
3. Stain in silver nitrate at 37°C in dark for 3-5
days and change the solution daily.
4. Wash in distilled water and place the tissues in
reducing solution for 1-3 days.
5. Rinse in distilled water and dehydrate In
ascending series ofethanol.
6. Clear in cedar wood oil for 2 hrs.
7. Impregnation/embedding is done in paraffin
wax as in case of routine histopathology, cut
sections at 4-51l, dry and deparaffinise in
xylene (3 changes of5 min each)
8. Clean the slides, remove artifacts and spots of
paraffin wax
9. Mount 1-2 sections per slide with DPX
10. Examination is done under microscope; the
spirochaete will be ofblack colour with yellow
to light brown background.
IV. Demonstration of fungi
1. Collect the tissues in formol saline or buffered
formalin and process the samples in a same
way as in routine histopathology and cut the
section at 4-5Il, deparaffmize and hydrate to
water.

Appendices
2. Place the slides in 4% chromic acid for 1 hr.
3. Wash in running tap water and keep the slides
in 1% sodium bisulfite solution for 3-5 min.
4. Wash in running tape water and then in
distilled water.
5. Stain with methanamine-silver nitrate working
solution at 60°C in water bath till sections
become yellowish brown.
6. Wash in distilled water and place in gold
chloride solution for 5 min.
7. Wash in distilled water and place in sodium
thiosulfate solution for 5 min and wash in
runmng tap water.
8. Stain with light green for 1 min, wash in water;
dehydrate in ascending series of ethanol, clear
in xylene and mount in DPX.
9. Examine the sections under microscope, the
fungi will take a black colour, mycelia and
hyphae will be of rose coloured with a pale
green back ground.
V. Demonstration of rickettsia
1. Tissues are fixed in formol saline or buffered
formalin and processed in same manner,
sections of 4-5/l thick are cut, dried,
deparaffinized and hydrated in water.
2. Place in methylene blue solution for overnight
and decolourize in 95% ethanol for a few
seconds or till blue colour is lost.
3. Wash in distilled water and place the slides in
basic fuchsin solution for 30 min.
4. Decolourize in citric acid solution for 1-2 sec.
5. Differentiate in absolute ethanol for a few min,
clear in xylene and mount in DPX.
277
Examine the slides, the ricketts~a will be ofbrigr.'
red colour and nucleus ofthe cell will take blue
colour.

Appendices
Appendix VI
POST-MORTEM EXAMINATION OF VETEROLEGAL CASES
The post-mortem examination of veterolegal cases
is performed as described in previous sections.
However, following points must be kept in mind
during post-mortem examination and while
preparing the report.
1. For veterolegal cases, post-mortem request
should be signed by a police officer not below
the rank of inspector or by magistrate; without
this no post-mortem examination should be
done.
2. Always collect maximum information on
history, date and time of death of animal and
treatment given. Use self knowledge and
experience to determine the time of death such
as rigor morits, autolysis, putrefaction,
pseudomelanosis etc.
3. Animal identification, including species, breed,
age and number or mark, must be clearly
established before starting post-mortem
examination. It is specially necessary in case
of insured animals as well as in religion-related
disputes..
4. All the lesions present on skin surface should
be clearly defined as laceration, wound,
trauma, incision, erosion, vesicle, ulcer, and if
there is suspected sharp edge wound or bullet
injury its depth and width (diameter), as the
case may be, should also be stated. Also
mention the side on which the animal is lying
down (ventral portion touching earth).
5. In case of dispute whether it was still birth or
the calf was born alive, a piece of lung should
be placed in water. The lung piece will sink in
278
water in case of atelectasis neonatum while it
will float if the calf was born alive.
6. If the case is suspected for toxic
condition/poisoning, try to mention the type of
poison in your report. This will help the police
authorities to establish/confirm the type of
toxin/poison in forensic laboratory.
7. The post-mortem examination of wild animals
should be conducted as a special case. One
should conduct the post-mortem examination
only when DFO or higher officer makes
request for post-mortem examination. It should
be noted on the report that all the viscera,
including skin, bones, teeth, etc. have been
returned to the person who requested for the
necropsy and no item has been left behind.
8. Fill the post-mortem report clearly with neat
handwriting and in clear language and avoid
ambiguity in presentation. Avoid writing
general sentences. Be specific in your findings
and conclusions. Sign the report with date and
keep a copy of it with you for record and
future evidence in the court of law.
9. Post-mortem examination should be conducted
in daylight. In darkness, where the pathologist
is not able to recognize the lesions, the post-
mortem examination should not be conducted.
10. At the time of post-mortem examination
outsiders should not be allowed in. To avoid
them, and wild birds and animals, post-mortem
examination should be done in closed
premises.

Appendices
Appendix VII
COLLECTION, PRESERVATION AND DISPATCH OF MATERIAL TO
FORENSIC LABORATORY
The collection, preservation and dispatch of
different tissues/organs, fluids and viscera should
be done as described in section 4 of appendix.
However, in veterolegal cases, these materials
should be sent to forensic laboratory under sealed
packings.
• In suspected cases of toxic condition or
poisoning, the stomach and intestinal contents
should be sent after proper ligation at both the
ends and in ice to prevent putrefaction.
Besides, samples of blood, liver, spleen and
kidneys should be sent in separate container.
• All the materials should be collected in leak
proofglass or plastic bottles.
• Tissues for histopathological examination
must be collected in 10% formalin or formol
saline, this can be sent to laboratory under
normal temperature.
• The materials suspected for toxicity should be
sent in ice without adding any preservative.
• The bottles or containers should be sealed and
labelled properly indicating the name of
owner, identification ofanimal (number, name,
mark etc.), type of tissue collected and
279
preservative used. The examination requested
and disease or poisoning suspected should also
be written.
• A copy with details of post-mortem report
containing above information should be sent
separately under separate cover.
• The address of the forensic laboratory should
be clearly written.
• All the containers should be packed with cloth
and sealed with sealing wax and should
preferably be sent through person in order to
avoid any breakage in transit.
• One copy of the forwarding letter should be
kept in file for future reference, one copy
should accompany the material and one copy
should be sent by post. The forwarding letter
bearing number and date should have the
information about materials sent, type of
preservative used, type of examination
requested and identification of animals,
including other details ofowner.

Appendices
Appendix VIII
EXAMINATION OF BLOOD, URINE AND FAECES
BLOOD EXAMINATION
TOTAL ERYTHROCYTE COUNT
• Clean New Bauer's counting chamber/
hemocytometer counter and place clean
coverslip on ruled areas.
• Suck fresh or anticoagulant mixed blood in
RBC diluting pipette (red ball in bulb) upto 0.5
mark and fill the pipette with RBC diluting
fluid upto 101 mark.
• Hold pipette in horizontal position and remove
rubber tube. Mix the contents by rotating the
pipette in between palms.
• Discard first few drops from pipette and then
place a drop near the edge of cover slip to fill
the space between cover slip and counting
chamber.
• Keep counting chamber 1-2 min for settling of
the cells.
• Count the cells under high power of the light
microscope.
• Cells are counted in 5 medium squares of the
central large square or 80 tertiary squares.
• Cells on top of square or left side are included
in count.
• Calculate RBC per ~l of blood by multiplying
10 000 to the total number of cells counted in
80'tertiary squares. It can be converted into ml
by further multiplying by 1000 and in litre by
10,00,000.
TOTAL LEUCOCYTE COUNT
• Clean the New Bauer's chamber/
hemocytometer. Put the cover slip on the area
demarcated for counting.
• Suck fresh/anticoagulant mixed blood in WBC
diluting pipette (white ball in bulb) upto 0.5
mark and fill the pipette with WBC diluting
fluid upto 11 mark.
280
• Hold the pipette in horizontal position and
remove rubber tube. Mix the contents by
rotating the pipette in between palms.
• Discard first few drops from pipette and then
place a drop near the edge of cover slip to fill
the space between cover slip and chamber.
• Keep counting chamberl-2 min for settling of
the cells.
• Count the cells under low power in four large/
primary corner squares ofthe ruled area.
• Cells on top of square and left side are
included in count.
• Calculate WBC per ~l of blood by multiplying
the total number of cells counted in 4 primary
squares by 50. It can be converted into ml by
multiplying by 1000 and in litre by 10,00,000.
PACKED CELL VOLUME
(HEMATOCRIT VALUE)
• Clean and dry the wintrobe tube.
• With the help of a long needle (6") and syringe
fill the blood in wintrobe tube upto mark 100.
• Take precaution to prevent air bubble from
entering the tube.
• Centrifuge the wintrobe tube at 3000 rpm for
30 min.
• Record the reading of packed cell volume in
percent i.e. mass of erythrocytes settling down
in tube.
ERYTHROCYTE SEDIMENTATION RATE
• Clean and dry Westergren pipette.
• Suck anticoagulant mixed blood in Westergren
pipette upto mark '0' and fix it in stand in
vertical position.
• Leave this for one hour in room temperature.
• Record the reading on pipette, it is the mm fall
oferythrocytes per hour.

Appendices
HEMOGLOBIN
• It is measured by using Hellige- Sahli
hemoglobinometer.
• Clean and dry the graduated tube of the
hemoglobinometer.
• Take 5 drops of Nil 0 hydrochloric acid in
tube.
• Suck the anticoagulant mixed blood in pipette
upto 20 marks.
• Place the pipette in tube containing N/lO HCI
and transfer the blood into acid.
• Suck acid in pipette and leave in tube.
• Keep the tube for 5 min in dark.
• Add distilled water in the tube drop-by-drop
using dropper, mix with stirring rod and match
the colour with standard. Add water till the
colour matches with standard.
• Read the scale on tube; it is the value of
hemoglobin gram per 100 ml ofblood.
DIFFERENTIAL LEUCOCYTE COUNT
(DLC)
• Prepare a thin blood smear on clean glass slide.
Place a drop of blood on one end of slide and
spread as smear with the help of another slide
using its edge at 45° angle.
• Dry the smear in air and mark identification
number in the thick portion of smear.
• Fix the smear in methanol for at least 5 min
and dry in air.
• Stain the smear with Giemsa stain diluted to
1: lOin distilled water for 30 min or with
Leishman's stain without fixing the smear.
• Wash the slide, dry in air and examine under
oil immersion microscope. Count at least 200
cells by battlementlzigzag method. Cells
counted are lymphocytes, neutrophils,
monocytes, eosinophils and basophils. (Figs.
9.12 - 9.16) Cell count is presented in percent.
281
, -t,
~~_,W~
Fig. 22.34 Neubauer s chamber
(W=Counting areafor leucocytes;
R= Counting area for erythrocytes)
,
I
I
Fig. 22.35 Smear preparationfor dijJerential
leucocyte count

Appendices
ABSOLUTE LYMPHOCYTE COUNT
(ALC)
The absolute lymphocyte count is calculated by
using the data of DLC and TLC through following
formula:
% Lymphocyte x TLC (103
/)11)
ALC =--------------------
(103
/)11) 100
ABSOLUTE NEUTROPHIL COUNT
(ANC)
The absolute neutrophil count is calculated by
using the neutrophil percentage of differential
leucocyte count and total leucocyte count using
following formula:
% Neutrophils x TLC (103
/)11)
ANC = - - - - - - - - - - -
(103
/)11) 100
MEAN CORPUSCULAR VOLUME
(MCV)
Mean corpuscular volume is determined by
dividing the packed cell volume (PCV) by the total
erythrocyte count in millions/)11 and multiplied by
10. The MCV is expressed in cubic microns.
PCV
MCV = ---x 10
(Cubic )1) TEC
MEAN CORPUSCULAR HEMOGLOBIN
CONCENTRATION (MCHC)
Mean corpuscular hemoglobin concentration is
calculated by dividing the hemoglobin in grams per
100 ml ofblood by the PCV and multiplied by 100.
It is expressed in percent.
Hb
MCHC = - - x 100
(%) PCV
282
MEAN CORPUSCULAR HEMOGLOBIN
(MCH)
Mean corpuscular hemoglobin is calculated by
dividing hemoglobin in grams per 100 ml by TEC
in millions per )11 ofblood and multiplying by 10.
MCH
(10.12
g)
Hb
--xl0
TEC
ALTERATIONS IN HEMATOLOGICAL AND
BIOCHEMICAL ATTRIBUTES IN VARIOUS
DISEASE CONDITIONS OF ANIMALS
A. Hematological profile
1. Erythrocytosis
Brucellosis, Campylobacteriosis, Leptospirosis,
Rinderpest, Haemorrhagic septicemia.
2. Erythropenia
Leukemia, Haemorrhage, Aflatoxicosis,
Theileriosis, Babesiosis, Anaplasmosis.
3. Leucocytosis
Pyogenic infections, Rabies, Tuberculosis,
Strangles, Leptospirosis, Theileriosis Babesiosis,
Anaplasmosis, Haemorrhagic septicemia.
4. Leucopenia
Canine distemper, Infectious canine hepatitis,
Swine fever, Brucellosis, Tuberculosis, Infectious
bovine rhinotracheitis.
5. Neutrophilia
Acute inflammation, Pyogenic infections,
Pyometra.
6. Neutrophiliamth (shift to left)
Leptospirosis, Metritis,
reticulopericarditis (TRP), Canine
Glanders.
7. Neutropenia
Traumatic
distemper,
Pasteurellosis, Infectious canine hepatitis.
8. Lymphocytosis
Leukemia, after vaccination, viral infections.

Appendices
9. Lymphopenia
Canine distemper, Infectious canine hepatitis,
Infectious bovine rhinotracheitis, Foot and Mouth
Disease.
10. Eosinophilia
Allergy, Parasitic diseases.
11. Hypohemoglobinemia
Anemia, Theileriosis, Strangles, Anaplasmosis,
Degnala disease, Fascioliosis.
12. Increased ESR
Carcinoma, Nephritis, Chronic granulomatous
infection, Tuberculosis, Canine distemper,
Trypanosomiasis.
13. Increased Hematocrit ValuelPCV
Dehydration.
14. Decreased hematocrit ValuelPCV
Anemia, Theileriosis, Strangles, Anaplasmosis,
Blue tongue.
B. Biochemical attributes
1. Hyperglycemia
Diabetes mellitus, Chronic nephritis.
2. Hypoglycemia
Hepatic insufficiency, Ketosis.
3. Hyperproteinemia
Shock, Dehydration, Plasmacytoma, Infectious
diseases.
4. Hypoproteinemia
Bum Diarrhoea, Renal dysfunction, Hepatic
disorders, Tuberculosis.
5. Hypergiobulinema
Dehydration, Leukemia, bacterial, viral and
parasitic infections.
6. Hypogammaglobulinemia
Anemia, Haemorrhage, Immunodeficiency.
283
7. Hypercalcemia
Hyperparathyroidism, bone cancer, Nephrolithiasis.
,8. Hypocalcemia
Hypoparathyroidism,
Ketosis.
Ricketts, Osteomalacia,
9. Hyperphosphatemia
Renal failure, Hypoparathyroidism, Healing of
fracture.
10. Hypophosphatemia
Chronic diarrhoea, Pica, Rheumatism-like
syndrome, Hemoglobinuria. Hyperparathyroidism.
11. Increased levels of blood urea nitrogen
Renal impairment, nephritis, Urinary obstruction.
12. Decreased levels of BUN
Acute hepatic insufficiency, nephrosis, Chronic
wasting diseases
13. Increased level of creatinin
Severe nephritis, urinary obstruction, severe toxic
nephrosis.
14. Hypermagnesemia
Chronic infection, Oxalate poisoning.
15. Hypomagnesemia
Grass tetany, Lactation tetany, Wheat pasture
poisoning.
16. Increased levels of SGOT
Hepatic necrosis, Myocardial infarction, Muscular
degeneration/necrosis in dog and cat, Azoturia.
17. Increased levels of SGPT
Hepatic necrosis, Infectious canine hepatitis.
18. Increased levels of alkaline phosphatase
Obstructive jaundice, hepatitis,
Hyperparathyroidism.
19. Decreased level of alkaline phosphatase
Chronic nephritis.

Appendices
20. Increased level of acid phosphatase
Prostate carcinoma, Leukemia.
21. Increased level oflactic dehydrogenase
Malignant lymphoma.
22. Increased level of serum isocitric
dehydrogenase
Hemolytic anemia in horses.
23. Increased level of ornithine carbamyl
transferase
Liver disorders in dogs.
URINE EXAMINATION
PHYSICAL EXAMINATION
1. Colour:
• Note the colour ofurine as
0 Watery/colourless
0 Amber colour
0 Red
0 Brown
0 YellowlYellowish green
0 Black
0 Pale
2. Odour
• Record the smell ofthe urine
o Uremic
o Sweetish! Fruity
o Fetid
3. Turbidity
• Look for the presence of suspended material in
urine
o Clear
o Turbid +, ++, +++, +++
o Cloudy
4. Foaming
• Shake the urine in a test tube
o No/slight foams
o Yellow/Green foams
o Redlbrown foams
5. Specific Gravity
• This is measured by urinometer
o Urine is filled in cylinder and urinometer
is left in the urine.
o Record the specific gravity in urinometer.
CHEMICAL EXAMINATION
1. Reaction
• Reaction is determined by using pH strips or
pH meter.
284
• For this take a pH strip and dip in urine.
• Read the change in colour on scale given with
pH strips.
2. Glucose
• Take 0.5 ml urine in a clean and dry test tube.
• Mix 5.0 ml Benedict's reagent in the urine and
keep it in boiling water bath!flame for 5 min.
• Remove the tube and cool it on test tube stand.
• Record the changes of colour in tube as
follows:
0 Blue (-) : No glucose
0 Blue to green (+): Mild glucose
0 Yellow with heavy sediment (++):
Moderate glucose
o Orange with heavy sediment (+++):
Highly positive for glucose
3. Protein
• Take 2 ml of urine in a clean and dry test tube.
• Place 2 ml Robert's reagent over urine.
• If protein is present in urine, then a white ring
will appear at the interjunction of two fluids. It
is graded as follows:
o No ring (-): Negative
o Mild ring (+): Mild positive
o A wide ring (++): Moderate positive
o Heavy ring (+++): Positive
o Very heavy ring (++++): Highly positive

Appendices
Ketone bodies
1. Acetone
• Take 1.0 gm mixed powder of sodium
nitropruside and ammonium sulfate (Sod.
Nitropruside 1 part, Amm. Sulfate 100 parts)
in a test tube.
• Add 5 rnl urine in the salts and mix them
properly.
• To this slowly overlay 20% ammonium
hydroxide solution.
• Record the colour at the interjunction of two
fluids.
• If it is red to purple then it is acetone positive.
2. Acetoacetic acid
• Take 10 rnl urine in a clean and dry test tube.
• Add 5 drops of Lugol's iodine and 3 rnl
chloroform, mix them and allow to stand.
• Record the colour ofurine
Colour less Positive
Red! violet colour : Negative
3. Beta hydroxybutyric acid
• Take 20 rnl urine in a small beaker and add 20
rnl distilled water and a few drops of acetic
acid.
• Boil the contents over flame till it remains 10
rnI, add distilled water to make it 20 rnl and
place in two test tubes, 10 rnl in each.
• In one test tube add 1 rnl H20 2 and warm it for
1 min, cool it.
• Add 1 rnl glacial acetic acid, 1 rnl freshly
prepared sodium nitropruside solution in both
tubes, mix thoroughly.
• To this overlay strong ammonia water and
allow to stand for 3-4 hrs.
• Record the change in colour in H20 2 added
tube if it is purple colour ring then it is
positive.
285
Bile salts
• Take 4-5 rnl urine in a test tube and shake it. If
persistent foams are present then it is positive
for bile salts.
• Add sulphur granules over surface of urine. In
case of positive, sulphur granules will sink in
urine.
Blood
• Take 2 rnl urine in test tube I.
• Take 1 rnl saturated solution of Benzidine in
test tube 11. Add 1 rnl 3% H20 2 and mix well.
• Mix the contents oftubes I and 11.
• Record the development of colour. In positive
case a green to blue colour will appear.
Hemoglobin/Myoglobin
• Take 5 rnl urine in a test tube.
• Add 2.8 gm ammonium sulfate.
• Shake well and allow to stand for a few min.
• If urine becomes clear/ watery in colour. Then
it is positive for hemoglobin. If colour remains
same as before the test then it is positive for
myoglobin.
Microscopic examination
• Take 5-10 rnl urine in a centrifuge tube and
centrifuge it at 1000 rpm for 10 min.
• Discard supematant and place a drop of
sediment on clean, dry glass slide.
• Cover it with a cover slip and examine it under
microscope for the followings:
o Epithelial cells
o Leucocyte
o Erythrocytes
o Microorganisms
o Casts
FAECAL EXAMINATION
GROSS EXAMINATION
• Collect faeces in clean and dry petridish or in
small sample bottle.

Appendices
• With clean spatula and glass rod spread the
faeces and note the following:
o Colour
o Consistency
o Odour
o Presence ofblood
o Presence ofparasite/segments ofparasite
MICROSCOPIC EXAMINATION
Direct smear method
• Place a drop ofdistilled water on clean and dry
glass slide.
• Add small amount of faeces in distilled water
on slide.
• Mix with glass rod/tooth pick! matchstick.
• Place a cover slip on it.
• Examine under microscope for the presence of
parasitic ova.
Qualitative concentration method
(Simple floatation method)
• Take about 1.0 gm faeces and mix it in small
amount ofdistilled water.
• Filter it through sieve/muslin cloth.
• Filterate is mixed with 4-5 ml of saturated salt
solution.
286
• Place the mixture in a tube or cylinder and fill
it upto the top.
• A clean coverslip or glass slide is placed on the
mouth oftube/cylinder.
• Keep it for 30 to 60 min at room temperature.
• Remove the coverslip or slide and examine it
under microscope for parasitic ova.
Qualitative concentration method
(Centrifugation floatation method)
• Take about 1.0 gm faeces and mix it in small
amount ofdistilled water.
• Mixture is filtered through fine sieve/muslin
cloth.
• Mix the filterate with saturated salt solution
(1 :3) in a centrifuge tube.
• Centrifuge it at 1500 rpm for 5 min.
• Take a drop of superficial contents on a clean
glass slide and examine under micr~scope.
• Sediment is examined for eggs ofliver flukes.

Appendix-IX
SELF ASSESSMENT
1. INTRODUCTION
,
Q. 1. (1) S% (2) 3% (3) 37.5% (4) 16 days (S) (a) Clitiical Pathology (b) Post-mortem Pathology (c)
Chemical Pathology (d) Histopathology (e) Humoral Pathology (t) Clinical Pathology.
Q.3. (1) Renatus Vegetius (2) Comelius Celsus, Redness, Swelling, Heat, Pain, Loss of function,
Claudius Galen. (3). Comparative Pathology (4) Immune mechanisms, immunodeficiency,
Autoimmunity, Hypersensitivity. (S) Subjective, objective (6) Pathogenesis, entry/action, recovery,
death (7) Biopsy.
Q.S. (l)b, (2) a, (3)b, (4)d, (S)b, (6) a, (7)d, (S)d, (9) a, ·(lO)b
2. ETIOLOGY
Q. 1. (1) Immunosuppression, Neutrophils (2) Dividing, ovary, testicles/ sperm, lymphocytes, Intestine/
Bone marrow (3) DNA, RNA, nucleic acid (4) Tuberculosis, Paratuberculosis, Leprosy, (S)
Iatrogenic (6) Phospholipase A2, hyaluronidase, phosphodiesterase, peptidase, hemolytic anemia,
shock (7) Paddy straw, Degnala (S) Aflatoxin, ochratoxin. (9) Insecticides, weedicides, fungicides,
rodenticides insecticide (10) Lead, cadmium, mercury (11) Skeletal muscle, myocardium, brain (12)
young (13) Deprivation, Fatty degeneration of liver, anemia, skin diseases (14) Acetoatcetate,
hydroxybutyrate, acetone, (1S) Testicles, ovary, thymus, lymphoid tissue (16) lysin, tryptophane
(17) Linolenic acid, linoleic acid, arachdonic acid (IS) Conjunctivitis, keratitis (19) E (20) Biotin,
choline, manganese.
Q.2. (1) T, (2) F, (3) F, (4) F, (S) T, (6) F, (7) T, (S) T, (9) F, (10) T, (11) F, (12) T,
(13) F, (14) F, (1S) T, (16) F, (17) T, (IS) T, (19) F, (20) T.
Q. S. (1) a, (2) b, (3) c, (4) c, (S) d, (6) d, (7) c, (S) c, (9) a, (10) d, (11) d, (12) b
(13) c, (14) d, (IS) c, (16) a, (17) b, (1S) d, (19) d, (20) b.
3. GENETIC DISORDERS, DEVELOPMENTAL ANOMALIES AND MONSTERS
Q. 1. (1) Length, location of centromere, Karyotyping (2) Translocation, reciprocal, non-reciprocal (3)
cranium, abrachia (4) Atresia, atresia ani (5) Chelioschisis, harelip (6) Cleft, cleft palate (7)
Dextrocardia, right side (S) Single ovum, incomplete ( 9) Pyopagus (10) Renarcuatus, horseshoe
kidneys.
Q.2. (1) F, (2) F, (3) F, (4) T, (S) T, (6) T, (7) F, (S) F, (9) T, (10) F.
287

Appendices
Q.5. (1) a, (2)b, (3) c, (4) d, (5) c, (6) a, (7) d, (8) c, (9) b, (10) c. (11) c, (12) a (13) d,
(14) c, (15) c, (16) a, (17) d, (18) c, (19) b, (20) a .
4. DISTURBANCES IN GROWTH
Q.1. (1) Abnormal, improperly, development (2) Reduced, full size (3) Decreased (4) More (5)
Hyperplasia (6) Hypertrophy, myometrium (7) Change (8) Embryonic, differentiated (9) Anaplasia
(10) Metaplasia.
Q.2. (1) T, (2) F, (3) T, (4) F, (5) T, (6) F, (7) F, (8) F, (9) T, (10) T.
Q.5. (1) c, (2) c, (3) a, (4) d, (5) a, (6) a, (7) d, (8) c, (9) a, (10) d.
5. DISTURBANCES IN CIRCULATION
Q. 1. (1) Congestion! hyperemia (2) Hematuria, hemoptysis, melena (3) Linear (4) Anasarca, hydrocele
(5) Hydropericardium, HPS(6) Total blood volume, blood flow, hemoconcentration (7) Sludged
blood, emboli, obstruction of blood vessel, ischemia, infarction (8) Metrorrhagia, hematemesis.
Q.2. (1) F, (2) T, (3) F, (4) F, (5) T, (6) T, (7) T, (8) F, (9) F, (10) T.
Q.3. (1) a, (2) b, (3) d, (4) d, (5) b, (6) d, (7) d, (8) c, (9) d, (10) c.
6. DISTURBANCES IN CELL METABOLISM
Q. 1. (1). Hydropic degeneration, stratum spinosum, food & mouth (2) pustules (3) Mildest, mild / any,
first (4) Thyroid, cachexia, Starvation, parasitism, chronic wasting disease (5) Cystadenoma,
cystadenocarcinoma, transparent, slimy, (6) Starch, black / brown / blue, Protein polysaccharide (7)
Old scars, nutrients, homogenous, strong acidophilic (8). Keratinized epithelium, horn.
Q.2. (1) F, (2) T, (3) F, (4) F, (5) T, (6) T, (7) T, (8) T, (9) F, (10) T.
Q.3. (1) a, (2) c, (3) d, (4) b, (5) a, (6) c, (7) b, (8) d, (9) c, (10) a.
7. NECROSIS, GANGRENE AND POST-MORTEM CHANGES
Q. 1. (1) Caseative, proteins, lipids (2) Chromatin (3) Living, pyknosis, karyorrhexis, karyolysis (4)
liquifactive, pyogenic (5) Pancreas, chalky white ( 6) Moist (7) Fusarium, dry (8) Clostridia,
oedema, blackening, crepitating sound (9) Digestion, own (10) Pseudomelanosis, saprophyte,
hydrogensulfide, iron.
Q.2. (1) F, (2) T, (3) F, (4) F, (5) T, (6) F, (7) F, (8) F, (9) T, (10) F.
Q.3. (1) d, (2) d, (3) c, (4) b, (5) a, (6) b, (7) a, (8) b, (9) b, (10) c.
288

Appendices
8. DISTURBANCES IN CALCIFICATION AND PIGMENT METABOLISM
Q. 1. (1). Hypercalcemia, hyperparathyroidism, renal failure, Excess of vit. D, Increased calcium
intake (2) Bright yellow, macrophages (3) Brown/black, skin, hairs, retina (4) Bile, hemolysis,
damage to liver, obstruction in bile duct, yellow, mucous membranes (5) Glucuronic acid,
bilirubin diglucuronide, urobilinogen, urobilin, stercobilin.
Q.2. (1) T, (2) T, (3) F, (4) T, (5) T, (6) F, (7) T, (8) T, (9) F, (10) F.
Q.3. (l)d, (2) a, (3)c, (4)b, (5) a, (6)c, (7)b, (8)d, (9) a, (IO)d.
9. INFLAMMATION AND HEALING
Q. 1. (l). Redness, heat, swelling, pain, loss of function (2) Vascular changes, proliferative (3) Stomatitis,
Lampas/palatitis, glossitis, Sialadenitis. (4) Vasoconstriction, vasodilation, cationic proteins,
hydrogen peroxide, hydrolytic enzymes, lysozymes, proteases, cytokines (kinins, histamine,
serotonin, heparin, complement are also true) (5) B-Iymphocytes, N.K. Cells, ·T-Iymphocytes, T-
helper, T-cytotoxic T-suppressor cells (6) Multinucleated cells, macrophages, Langerhans, foreign
body (7) Linoleic acid, Csa, cyclo-oxygenase, lipo-oxygenase (8) 5- hydroxytryptamin,
gastrointestinal tract, spleen, mast, blood vessels, vasodilatation, increased permeability. (9) Acid
proteases, collagenases, elastases, plasminogen activator (10) Hormone, lymphocytes, monocytes,
glycoprotein (11) Small macrophages, fibroblasts, endothelial cells, lymphocytes, granulocytes,
hepatocytes, keratinocytes, basophils, neutrophils, T-cells (12) Fibrous tissue, granulation tissue/
fibroblasts.
Q.2. (1) F, (2) T, (3) F, (4) F, (5) F, (6) T, (7) F, (8) T, (9) T, (10) T. (ll)T, (12)F,
(13)T, (14) F, (I5)T, (16) T, (17) F, (18) T, (19) T, (20) F.
Q.3. (1) c, (2) c, (3) b, (4) c, (5) c, (6) a, (7) c, (8) a, (9) c, (10) d, (11) a, (12) d,
(13) a (14) a, (15) a, (16) c, (17) c, (18) a, (19) c, (20) c.
10. CONCRETIONS
Q. 1 (1) Calculi, fibrin, mucus, desquamated epithelial cells, bacterial clumps (2) Calcium phosphate,
magnesium phosphate, aluminium phosphate, calcium oxalate (3) cholecystitis, cholangitis
obstruction ofbile duct, post hepatic /obstructive jaundice (4) Colon (5) Dogs, bones
Q.2. (1) F, (2) T, (3) F, (4) F, (5) T.
Q.3. (1) a, (2) c, (3) d, (4) b, (5) b, (6) d, (7) a, (8) b, (9) d, (10) a.
289

Appendices
11. IMMUNITY AND IMMUNOPATHOLOGY
Q. 1. (1) Horse, pig, cat (2) Oil, wax, alum, aluminium hydroxide, increa:;e (3) 7,900, S, J-chain, Primary
(4) Absent (S) Long, dendrites, lobulated, cytoplasmic granules (6) T-suppression, suppresses (7)
200-300 (8) IgG, IgM (9) Alteration, Immunodeficiency autoimmunity, hypersensitivity. (10)
Suppression, drugs, diseases, deficiency of nutrition, neoplasm, environmental pollution, increased
susceptibility to infections, vaccination failures, recurrent infections, occurrence of new diseases,
neoplasms (11) Systemic lupus erythematosus, polyarteritis nodosa, glomerulonephritis, rheumatoid
arthritis, opsonization, chemotaxis, phagocytosis (12) Macrophages T-helper cells, destruction,
immunosuppression, lymphadenopathy, lymphocytolysis, reduction in lymphokine production (13)
T-suppressor cells (14) Macrophages (1S) Insecticide, weedicide, fungicide rodenticide,
Immunopathology, immunosuppression, autoimmunity, hypersensitivity.
Q.2. (1) T, (2) F, (3) F, (4) T, (S) F, (6) T, (7) T, (8) F, (9) T, (10) F, (11) F, (12) T,
(13) F, (14) T, (IS) F, (16) F, (17) T, (18) F, (19) T, (20) T.
Q.3. (1) c, (2) d, (3) b, (4) c, (S) d, (6) a, (7) b, (8) d, (9) b, (10) a, (11) a, (12) c, (13)
b, (14) c, (IS) a, (16) b, (17) d, (18) d, (19) a, (20) a,' (21) c, (22) a, (23) b, (24) b,
(2S) d, (26) a, (27) b, (28) c, (29) c, (30) b.
12. PATHOLOGY OF CUTANEOUS SYSTEM
Q. 1. (1) Vesicle, stratum lucidum! corneum, pustule (2) Erosion, excoriation, ulcer (3) Scaly, (4)
Epithliogenesis imperfecta (S) Melanin, hormonal imbalance, testicles, pituitary gland.
Q.2. (1) T, (2) F, (3) F, (4) T, (S) T, (6) T, (7) T, (8) T, (9) T, (10) T.
Q.3. (1) b, (2) c, (3) b, (4) d, (S) a, (6) b, (7) a, (8) a, (9) c, (10) b.
13. PATHOLOGY OF MUSCULOSKELETAL SYSTEM
Q. 1. Clostridia, crepitating, gas, water/fluid (2) Monday, pain, sweating, unable to more, hardening.
(3) Adult rickets, vit-D, calcium, phosphorus, softening of bones (4) Hormonal imbalance,
copper deficiency/vit-c deficiency, atrophy (S) Osteopetrosis, increase (6) Bone, bone marrow,
trauma, pyogenic bacteria, destruction, replacement, excessive growth of new bone (7) Callus
(8) Joints, swelling.
Q.2. (1) F, (2) T, (3) T, (4) T, (S) T, (6) T, (7) T, (8) T, (9) F, (10) F.
Q.3. (1) b, (2) a, (3) d, (4) b, (S) a, (6) b, (7) b, (8) c, (9) b, (10) a.
290

Appendices
14. PATHOLOGY OF CARDIOVASCULAR SYSTEM
Q. 1 (1) Lungs, left sided heart, juglar (2) Hypertrophy of myocardium, cyanosis (3) Low oxygen,
dilation of heart, chronic passive congestion, sternal (4) Hardening, atherosclerosis, medial
sclerosis, arteriosclerosis. (5) Hypercholesterolemia, hyperlipidemia, hypertension (6)
Corynebacterium ovis, inflammation of lymph vessels, aggregation of lymphocytes, oedema (7)
atherosclerosis, hypercholesterolemialfatty streaks, plaques, lumen (8) Lipid, cholesterol, fatty
acids, triglycerides, phospholipids.
Q.2. (1) F, (2) T, (3) T, (4) F, (5) T, (6) T, (7) T, (8) F, (9) T, (10) F.
Q.5. (1) d, (2) a, (3) a, (4) d, (5) d, (6) d, (7) a, (8) a, (9) b, (10) b.
15. PATHOLOGY OF RESPIRATORY SYSTEM
Q. 1 (1) Pneumonia, congestion, consolidation (2) Thickening (3) Fibrinous, hyaline membrane
diposition, alveoli, bronchiole (4) Drenching, necrosis, gangrene (5) Granulomatous, tubercle,
caseative, macrophages, epithelioid cells, giant cells, fibrous (6) Retrovirus, metaplasia, cuboidal,
columnar, glandular (7) Moldy hay/ fungus, hypersensitivity pneumonitis, interestitial pneumonia,
emphysema, hyaline membrane formation, hyperplasia, (8) Granulomatous, dust particles, sand,
silica /beryllium, carbon/asbestos, anthracois, (9) Air sacculitis, E. coli Mycoplasma gallisepticum,
avian reovirus, thickening ofair sac wall, cheesy exudate (10) Tuberculous pearly disease,
chylothorax.
Q.2. (1) F, (2) F, (3) T, (4) F, (5) T, (6) F, (7) F, (8) F, (9) F, (10) T.
Q.5. (1) b, (2) d, (3) a, (4) c, (5) b, (6) c, (7) a, (8) c, (9) d, (10) d.
16. PATHOLOGY OF DIGESTIVE SYSTEM
Q. 1 (1). Spirocerca lupi (2) Tympany, distended (3) Omasum, Actinobacillus ligneiresi,
granulomatous (4) Braxy, congestion oedema, haemorrhage (5) Intestine, haemorrhagic, E. coli,
Bacillus anthracis, Salmonella sp., Petechiae, echymotic (6) Chronic, proliferative, proliferation
of fibrous tissue, infilteration of mononuclear cells, plasma cells, hardening (7) Clostridium sp.
Coccidia (8) Hjarre's disease, E. coli (9) Candida albicans, Turkish towel (l0) Diffused necrosis.
Q.2. (1) T, (2) F, (3) F, (4) F, (5) F, (6) T, (7) T, (8) T, (9) F, (10).
Q.5. (1) a, (2) d, (3) c, (4) d, (5) d, (6) c, (7) a, (8) d, (9) c, (10) a(ll) c, (12) c, (13) c,
(14)b, (15)c, (16) a, (17)d, (18)d, (19)b, (20)c, (21)b, (22)c, (23)b, (24) a,
(25) a.
291

Appendices
17. PATHOLOGY OF HEMOPOIETIC AND IMMUNE SYSTEM
(1). Erythropoiesis, reduced vitality, erythropenia, leucopenia (2) Phagocytic cells, neutrophils,
macrophage, chemotaxis, engulfment, killing (3) Macrocytic, normocytic, microcytic,
normochromic hypochromic (4) L)sis, blood vessel, icterus, hemoglobinuria.(5) He"lonchus
contortus (6) Iron, copper, cobalt, B12, pyridoxine, riboflavin, folic acid, pale mucus membrane,
weakness, decreased number oferythrocytes. (7) Increased, blood, infections, neoplasms.
Q.2. (1) F, (2) F, (3) T, (4) F, (5) T, (6) F, (7) T, (8) F, (9) F, (10) T.
Q.5. (1) d, (2) b, (3) a, (4) c, (5) d, (6) b, (7) d, (8) a, (9) d, (10) c.
18. PATHOLOGY OF URINARY SYSTEM
Q. 1. (1) Frequent, polyuria, diabetes insipedus, hormonal imbalance, polydipsia, wasteproduct (2)
Harmful wasteproducts, urea, uric acid, creatinine (3) Diabetes mellitus, acetonemia, pregnancy
toxaemia, starvation (4) Ochratoxins (5) Pesticides, immune complexes, glomerulonephritis (6)
Corynebacterium renale, Staphylococcus aureus, E. coli. Actinomyces pyogenes, Pseudomonas
aeruginosa, corynebacterium. renale. (7) Chronic fibrosis, loss of glomeruli, loss of tubules,
extensivefibrosis, glomerulonephritis, interstitial nephritis, arteriolosclerosis.
Q.2. (1) T, (2) F, (3) F, (4) F, (5) F, (6) T, (7) T, (8) F, (9) F, (10) T.
Q.5. (1) b, (2) c, (3) b, (4) a, (5) c, (6) c, (7) a, (8) a, (9) a, (10) d.
19. PATHOLOGY OF GENITAL SYSTEM
Q. 1. Hormonal, follicular, sterility, continuous oestrus, nymphomania, lutein, pyometra, pseudopregnancy
(2) Acute or chronic, pus, progesterone, llltein cyst /corpus luteum (3) catarrhal (4) Trichomonas foetus,
Brucella spp, BHV-l, Leptospira spp (5) chronic, granuloma (6) BHV-l virus, Epididymitis, Epi-vag.
Q.2. (1) F, (2) T, (3) F, (4) F, (5) F, (6) T, (7) T, (8) F, (9) T, (10) F.
Q.5. (1) d, (2) c, (3) d, (4) a, (5) d, (6) d, (7) a, (8) d, (9) b, (10) b.
20. PATHOLOGY OF NERVOUS SYSTEM
Q. 1. (1) Encephalomalacia, myelomalacia, (2) Inflammation, Listeria monocytogenes, congestion,
haemorrhage, tiny abscess, necrosis, meningoencephalomyelitis (3) Polioencephalomalacia,
leucoencephamalacia, microglial cells, satellitosis, neuronophagia, (4) Neurons, glial cells,
myelin, medulla pons, mid brain, spongy form (5) Leptomeningitis, pachymeningitis.
292

Appendices
Q.2. (1) F, (2) T, (3) F, (4) T, (5) F, (6) F, (7) T, (8) F, (9) T, (10) T.
Q.5. (1) c, (2) a, (3) b, (4) c, (5) c, (6) b, (7) c, (8) d, (9) b, (10) b.
21. PATHOLOGY OF ENDOCRINE SYSTEM EYES AND EAR
Q. 1. (1). Diabetes insipedus, polydipsia polyuria, urine. (2) Somatotropic, gigantism, long bones, heavy and
thick bones, hands, feet, skull bones (3) Enlargement, hypothyroidism, hyperthyroidism
(4) Hypocalcemia, tonic spasms of muscles, infections, neoplasms, low calcium diet, hyperl
increased (5) Tuberculosis, histoplasmosis, amyloidosis, neoplasms, drug toxicity.
Q.2. (1) F (2) F, (3) T, (4) T, (5) F, (6) F, (7) T, (8) F, (9) T, (10) T.
Q.5. (1) b, (2) c, (3) c, (4) d, (5) d, (6) a, (7) d, (8) b, (9) c, (10) a.
293

Index
A Acrania 38
Abomasitis 85,188 Adactylia 38
Abortion 230 Agnathia 38
Abortion T7
Anencephalia 38
Abrasions 14
Anophthalmia 38
Atresia 38
Abscess 66,105,144 Hemicrania 38
Acanthosis nigricans 138 Fissures 38
Acanthosis 144 Chelioschisis 38
Acne 144
Cleft palate 38
Acromegaly 245
Cranioschisis 38
Acute myositis 148
Harelip 38
Palatoschisis 38
Adhesive pleuritis 180 Rachischisis 38
Adjuvants 120 Schistosomus 38
Adult rickets 152 Schistothorax 38
Aflatoxins 24 Fusion 38
Air sacculitis 180 Cyclopia 38
Albnism-congenital 138 Hose shoe kidneys 39
ALe 282 Renarcuatus 39
Algor mortis 73 Anophthalmos T7
Allergic dermatitis 140 Anthracosis 81
Allergy 123 Antibody 121
Alopecia-congenital 138 Agglutinins 121
Amyloid infiltration 61 Antitoxins 121
Anaphylaxis 123,124 Complement fixing 121
Anaplasia 46
Lysins 121
Anasarca 54
Neutralizing 121
ANC 282
Opsonins 121
Anencephaly 238
Precipitins 121
Antigen 119
Anemia 205 Anuria 216
Aplastic 205 Aphakia 247
Macrocytic 205 Aplasia 44,216
Macrocytic normochromic 205 Aplastic anemia 205
Microcytic 205 Apoptosis 68
Normocytic 205 Arachidonic acid metabolites 94
Aneurysm 165 Arteriosclerosis 163
Dissecting I false 165 Arteriolosclerosis 164
True 165 Atherosclerosis 163
Anisocytosis 205 Medial sclerosis 163
Anomalies 38 Arteritis 85,164
Agenesis 38,44 Arthritis 85,153
Abrachia 38 Arthropods 21
Abrachlocephalia 38 Asbestoses 81,180

Index
Ascites 54,200 Bronchitis 85,171
Aspiration pneumonia (f) Bronchopneumonia 173
Atelectasis 171 Brucellosis - 231
Atopy 123 Bruises 14
Atresia ani 184 Bulla/bleb 144
Atresia coli 184 Bullet wound 16
Atrophy 44 Bums 16
Autoimmunity 129 Bursitis 85,212
Autoimmune hemolytic anemia 205,209
Autolysis 72 C
Azoturia 148 Clinical pathology 2
Chemical pathology 2
B Comparative pathology 2
Bacteria 21 Cytopathology 2
Bacterial toxins 23 Course of disease 4
Balanitis 85,235 Case fatality rate 4
Balanoposthitis 235 Contusions 14
Basophilia 210 Compression 16
Basophilic stippling 205 Chlamydia 21
Basophils 91 Chemical causes 23
Berylliumgranulouma 180 Crazy chick disease 27
Bile pigment 79 Chastek paralysis 29
Biliary calculi 114 Curled toe paralysis 29
Biliarycirrhosis 200 Canine pellegra 29
Biochemical attributes 283 Cyanocobalamin 29
Biological causes 16 Choline 29
Biological toxins 23 Chromosomes 36
Atlatoxins 24 Autosomes 36
Bacterial toxins 23 Sex chromosome 36
Ergot 24 Cytogenetics 36
Fungal toxms/mycotoxins 24 Codon 36
FusarIum toxins 24 Chimerism 37
Ochratoxins 24 Cranioschisis 38,238
Plant toxins 24 Chelioschisis 38
Snake venom 23 Cleft palate 38,184
Biopsy 6 Cyclopia 38
Biotin 29 Craniopagus 39
Black Quarter 71 Cepha1othoracopagus 39
Blast injury 16 Congestion 50
Blepheritis 85,247 Cardiac temponade 50
Bloa 186 Cardiac thrombus 52
Frothy bloat 186 Cloudy swelling 59
Blood examination 280 Connective tissue hyaline 61
Bone fracture and repair 153 Chromatolysis 66
Brisket disease 161 Coagulative necrosis 66
295

Index
Crepitating sound 71 Cardiac failure 157
Calcification 77 Acute 157
Dystrophic 77 Chronic 159
Metastatic 77 Left sided heart faIlure 159
Crystals 81 Right sided heart failure 159
Cholangitis 85,200 Cardiac temponade 159
Cervicitis 85,230 Chylothorax 180
Colonitis 85 Choke 184
Conjunctivitis 85,247 Catarrhal enteritis 190
Cellulitis 85, 105 Chronic enteritis 192
Cholecystitis 85,200 Cirrhosis 198
Carditis 85 Biliary 200
Cheilitis 85,184 Central/cardiac 200
Cystitis 87,223 Glissonian 200
Cytokines 94 Parasitic 200
Chernokines 97 Pigment 200
Cytotoxins 97 Cardiac cirrhosis 200
Growth factors 97 Central cirrhosis 200
lnterferons 96 Chediak-Higashi Syndrome 205
Interleukins 95 Cyst in kidney 216
Lymphokines 94 Cystine calculi 223
Monokines 94 Cervixbifida 227
Turnor necrosis factor 97 Cystic ovary 227
Cytotoxins CJ7 Cervicitis 230
Chemokines CJ7 Campylobacteriosis 231
Clotting mechanism 98 Cryptorchidism 233
Complement system 99 Cork screw penis 233
Catarrhal inflammation 103 Coloboma 248
Concretions 114 Congenital anophthalmos 248
Biliary 114 Congenital microphthalmos 248
Enteric 116 Cataract ,248
SalIvary 116 Congenital 248
UrInary 114 Cortical 248
Cystine 223 Morgagnian 248
Oxalate 222 Nuclear 248
Phosphate 223 Posterior polar 248
Uric acid 223 Subcapsular 248
Xanthine 223
Choroiditis 248
Cholelith 114
Chorioretinitis 248
Coprolith 116
Cytotoxic hypersensitivity 124
D
Congenital icthyosis 138
Dacryadenitis 85
Congenital alopecia 138
Deficiency anemia 207
Congenital albinism 138
Delayed type hypersensitivity 128
Congenital cutaneous asthenia 138
Demyelination 238
Chronic myositis 150
Dendritic cells 121
296

Index
Dermatitis 87,138 Eustachitis 85
Allergic 140 Enteritis 85,189
Gangrenous 140 Catarrhal 190
Parasitic 140 Chronic 192
Vesicular 140 Fibrinous 194
Dennoid cyst 39 Granulomatous 194
Desrnitis 85 Haemorrhagic 190
Dextrocardia 39 Necrotic 192
Diagnosis 4 Parasitic 192
Diapedesis 50,87 Endometritis 85,230
Dicephalus 39 Eosinophils 91
Diprosopus 39 Epithelioid cells 93,101
Dipygus 39 Eosinophilic inflammation 108
Disctichiasis 247 Enteric calculi 116
Disease 4 Enterolith 116,196
Displacement oforgan 73 Epitheliogenesis imperfecta 138
DLC 281 Tongue 184
DNA 36 Equine cutaneous granuloma 140
Down's syndrome 38 Excoriation 144
Drenching pneumonia (f) Eczema 144
Drug toxicity 24 Equine rhabdomyolysis 148
Dry gangrene 68 Emphysema 171
Duplication ofcolon 184 Eosinophila 210,283
Dysplasia 46 Epispadias 233
Dystrophic calcification 77 Encephalitis 238
Entropion 247
E Erythrocyte sedimentation rate 280
Experimental pathology 2 Erythrocytosis 282
Etiology 4,14 Erythropenia 282
Extrinsic 14
lntrisic 14 F
Erosion 14,144 Faecal examination 285
Electrical injury 16
Gross examination 285
Ergot 24
Microscopic examination 286
Environmental pollutants 24
DIrect smear method 286
Encephalomalacia 27,238
QuantitatIve concentration Method 286
Ectopia cordis 39,157
Fascitis 85
Ecchymoses 50
Fat necrosis 36
Epistaxis 50,169
Fatty changes 62
Embolism 52
Fibrinolytic system 99
Epithelial hyaline 61
Fibrinous enteritis 194
Encephalitis 85
Fibrinous inflammation 103
Endocarditis 85, 161
Fibroblasts 93
Esophagitis 85,184
Fibrous osteodystrophy 150
Epididymitis 85,234
Fissures 38,144
Folate 29
297

Index
Folliculitis 144 Moist 69
Food deprivation 25 Gout 81
Forensic pathology 4 Gingivitis 85 184
Fracture and repair 153 Gastritis 87,190
Freemartinism 38 Glossitis 87,184
Fungi 21 Giant cells 93
Funiculitis 87,234 Foreign body 93
Fusarium toxins 24 Langhan's 93
Fusion 38 Touton 93
Tumor 93
Granulomatous inflammation 105
G Granuloma 105
General pathology 2 Equine cutaneous 140
Gluconeogenesis 26 Granulation tissue 110
Grass tetany 30 Gall stones 114
Grass staggers 30 Gangrenous dermatitis 140
Goiter 31,245 Grey hepatization 173
Adenomatous 245 Granulomatous enteritis 194
Colloid 245 Glissonian cirrhosis 200
Equine 237 Glycosuria 218
Familial 245 Glomerulonephritis 218
Hyperplastic 245 Chronic 220
Toxic 247 Focal embolic 220
Genetics 36 Mesangio proliferative (MPGN) 218
Gene 36 Type I 218
Genetic code/codon 36 Type 11 220
Genetic disorders 37 Type III 220
Aberration in chromosome 37
Chimerism 37 Glaucoma 248
Deletion 37
Down's syndrome 38 H
Free martinism 38 Humoral pathology 2
Heteroploidy 37 Health 4
Intersexes 38 Homeostasis 4
Klinefelter's syndrome 37 Historical milestones 6
Monosomy 37
Mosaicism 37 Hypothermia 16
Testicular feminization 38 Hyperthermia 16
Tortoiseshell male cat 37 Helminths 21
Translocation 37 Horizontal transmission 21
Trisomy 37 Coitus 23
Turner's syndrome 38 Contact 23
Goblet cells 59 Iatrogemc 23
Glycogen storage disease 63 Ingestion 23
Gangrene 68 Inhalation 23
Dry 68 Inoculation 23
Gas 71 Hemoglobinuria 30,216
298

------------
Index
Heteroploidy 37 Hereditary anernia 205
Hemicrania 38 Hemolytic anernia 207
Harelip 38 Haemorrhagic anernia 207
Horse shoe kidney 38 Herrnaphroditism 227
Hypoplasia 44 Hydrosalpinx 229
Hypertrophy 44 Hypospadias 233
Hypetplasia 44 Hypetpituitarism 245
Hyperemia 50 Hypopituitarism 245
Haemorrhage 50 Hyperthyroidism 245
Hematoma 50 Hypothyroidism 245
Hemothorax 50, 180 Hypoparathyroidism 247
Hemopericardiwn 50,159 Hypetparathyroidism 247
Hemoperitoniwn 50 Hypoadrenocorticism 247
Hemoptysis 50 Hyperadrenocorticism 247
Hematuria 50,216 Hemeralopia 248
Hematemesis 50 Histopathological techniques 266-277
Hydroperitoniwn 54,199 Procedures 266,269
Hydropericardiwn 54,159 Scope 266
Hydrocele 54,233 Section cutting 271
Hydrocephalus 54,238 Smears 267
Hydrothorax 54,180 Special procedures 275
Hydropic degeneration 59
Staining 273
Vital staining 269
Hyaline 61 Hemoglobin 281
Connective tissue hyaline 61 Hematological profile 282
Epithelial hyaline 61
Hematocrit 280
Kerato hyaline 62
Hypostatic congestion 73
I
Hemosiderosis 77
Immunopathology 2,123
Hyperbilirubinernia 79
Hepatitis 85,197
Hypersensitivity 123
Heterophils 89
Type I 124
Type II 124
Histamine 94 Type III 124
Haemorrhagic inflammation 105 Type IV 128
Healing 110 Illness 4
Regeneration 110 Incubation period 4
Repair 110 Infection 6
Hair balls 116 Infestation 6
Hapten 119 Idiosyncracy 14
Hyperkeratosis 144 Incised wounds 16
Haemorrhagic myositis 148 Injury 16
High altitude disease 161 Blast 16
Hypersensitivity pneumonitis 179 Electrical 16
Haemorrhagic enteritis 190 Radiation 16
Hjarre's disease 192 Intestinal involution 26
Hernia 195 Intersexes 38
299

Index
Ischiopagus 39 Arthus reaction 124
Ischemia 52 Chronic immune complex disease 124
Infarction 52 Serum sickness 124
Imbibition ofbile 73 Immunodeficiency 124,129
Icterus 80 Acquired 130
Hemolytic 80 Drugs 130
Obstructive 80
Environmental pollution 131
Toxic 80 Infections 130
Inflammation 85
Surgery 131
Trauma 131
Cardinal signs 85 Congenital 124
Cellularchanges 89 Combined immunodeficiency
Chemical changes 93 syndrome 129
Pathogenesis 87 Defects in B-Iymphocytes 129
Terminology 85 Defects in phagocytosis 130
Vascular changes 89 Defects in T-Iymphocytes 129
Acute 85, 103 Deficiency of complement 130
Catarrhal 103 Partial T- and B-cell defects 129
Chronic 85, 103 Icthyosis, congenital 138
Eosinophilic 108
Interventricular septal defect 157
Fibrinous 103
Granulomatous 105 Interarterial septal defect 157
Haemorrhagic 105 Infectious laryngotracheitis-
Lymphocytic 105 Ingluvitis 186
Serus 103
Impaction 188Subacute 103
Suppurative 105 Rumen/reticulum 188
Types 101 Intestinal obstruction 196
Iritis 85,248 Intussusception 196
Interleukins 95 Interstitial nephritis 220
Interferons 96 Infectious pustular vulvovaginitis 230
Immunity 119 Iridocyclitis 248
Acquired 119
Cell mediated 123
Humoral 119 J
Natural 119 Jaundice
Paraspecific 119
Specific 119
K
Immunoglobulins 120
Karyolysis 66
IgA 120
IgD 121 Karyorrhexis 66
IgE 121 Karyotyping 36,37
IgG 120 Kennel cough 171
IgM 120 Keratitis 85,247
Immune response 121 Keratoconjunctivitis 248
Autoimmunity 123,129 Keratohyaline 62
Immunodeficiency 123,129 Ketonuria 218
Immune complex mediated- Kinin system 98
hypersensitivity 124 Klinefelter's syndrome 37
300

Index
L Mongolism 38
Labyrinthitis 249 Mosaicism 37
Laceration 16 Monsters 39
Lampas 87,184 Metaplasia 44
Laryngitis 85,169 Metrorrhagia 50
Leptomeningitis 85,238 Melana 50
Leptospirosis 231 Mural thrombus 52
Lesion 4 Mucinous degeneration 59
Leucocytosis 210,282 Mucus 59
Leucoencephalomalacia 238 Mucoid degeneration 61
Leucopenia 211,282 Moist gangrene (f)
Leukemia 210 Metastatic calcification 77
Linearhaemorrhage 50 Meningitis 87,238,240
Lipids 26 Myositis 87
Lipolysis 26 Myocarditis 87,161
Liquifactive necrosis (Xj Myelitis 87
Livor mortis 73 Metritis 87,229
Lobar pneumonia 175 Macrophages 91
Lobularpneumonia 175 Mast cells 91
Local anemia 52 Monokine 94
Lymphadenitis 85,211 MPGN 126
Lymphangitis 85,165 Monday morning disease 148
Lymphocytes 89 Myoglobinurea 148
B-cells 91 Myositis 148
NK cells 91 Acute 148
T-cells 89,91 Chronic 150
Lymphocytic inflammation 105 Hemorrhagic 148
Lymphocytic thyroditis 247 Marble bone disease 152
Lymphocytosis 210,282 Mulberry heart disease 163
Lymphokine 94 Medial sclerosis 163
Lymphopenia 211,283 Mega colon 184
Lysosomal components 94 Macrocytic anemia 205
Macrocytic normochromic anemia 205
M Microcytic anemia 205
Microscopic pathology 2 Monocytosis 210
Morbidity rate 4 Mesangio proliferative
Mortality rate 4 glomerulonephritis (MPGN) 218
Mycoplasma 21
Type I MPGN 218
Type Il MPGN 220
Maintenance of infection 23 Type III MPGN 220
Microbial toxins 23 Membranous glomerulonephritis 220
Mycotoxins 24 Mummified foetus 231
Minerals 29,31 Mastitis 231
Microphathalmos 27 Summer mastitis 233
Myoglobinuria 27 Myelomalacia 238
Milk fever 30 Meningoencephalitis 238
301

Index
Microencephaly 238 Neutrophils 89
Meningocele 238 Nasal polyps 169
Meningoencephalocele 238 Nasal granuloma 169
Microphakia 248 Necrotic enteritis 192
MCV 282 Normocytic anernia 205
MCHC 282 Neutrophilia 210,282
MCH 282 Neutropenia 211,282
Nephrosis 218
N Nephrosclerosis 222
Nutritional pathology 2 Neuronophagia 238
Nutritional causes of diseases 25 Necropsy 252
Calorie deficiency 25 Largeanimal 252
Deficiency of Iipids 26 Poultry 252
Deficiency ofminerals 29 Veterolegal cases 278
Calcium 30 Nicks 1:13
Cobalt 31
Copper 31 0
Fluorine 31
Oncology 2Iodine 31
Iron 31 Ochratoxins 24
Magnesium 30 Osteomalacia Zl
Manganese 31 Occlusive thrombus 52
Phosphorus 30
Oedema 52Selenium 31
Osteomyelitis 8SSodium chloride 30
Zinc 31 Osteitis 8S
Deficiency ofvitamin 26 Otitis 8S
Vitamin A 26 Ophthalmitis 85
Vitamin B 29 Otitis externa 85,248
Vitamin C 29 Otitis interna 85,249
Vitamin D 27 Otitis media 87,249
Vitamin E 27
Omasitis 87,188Vitamin K 27
Deficiency ofwater 26 Oophoritis 87,227
Food deprivation 25 Orchitis 87,233
Protein deficiency 26 Osteodystrophy, fibrous 150
Starvation 25 Osteomalacia 152
Nutritional roup 27,46 Osteoporosis 152
Nyctalopia Zl Osteopetrosis. 152
Niacin 29 Osteomyelitis 152
Neoplasia 46 Oliguria 218
Necrosis 66 Oxalate calculi 222
Caseative 66 Ovaries
Coagulative 66 Cyst 227
Fat 66
Liquifactive 66 p
Necrobiosis 66 Pathology 2
Nephritis 85 Chemical 2
Neuritis 87,240 Clinical 2
302

Index
Comparative 2 Hypostatic congestion 73
Experimental 2 Imbibition ofbile 73
Forensic 4 Livor mortis 73
General 2 Post-mortem clot 73
Humoral 2 Post-mortem emphysema 73
Microscopic 2 Pseudomelanosis 72
Nutritional 2 Putrefaction 72
Physiological 2 Rigor mortis 73
Post-mortem 2 Putrefaction 72
Specific 2 Pseudomelanosis 72
Systemic 2 Post-mortem emphysema 73
Pathogenesis 4 Post-mortem clot 73
Prognosis 4 Pneumoconiasis 81
Pathogenicity 6 Pyelonephritis 85
Physical causes 16 Pneumonia 85,173
Prions 21 Aspiration pneumonia 177
Parasite 21 Bronchopneumonia 173
Arthropods 21 Fihrinous pneumonia 175
Helminths 21 Hyaline membrane pneumonia 175
Protozoan 21 Interstitial pneumonia 175
Plant toxins 24 Mycotic pneumonia 177
Protein deficiency 26 Tuberculous pneumonia 177
Pellegra 19 Verminous pneumonia 175
Pyridoxine 19 Pneumonitis 85
Pantothenic acid 19 Palatitis 87,184
Pica 30 Pancreatitis 87,200
Perosis 31 Pericarditis 87
Palatoschisis 38 Peritonitis 87,200
Polyotia 39 Pharyngitis 87,169
Polyodontia 39 Pachymeningitis 87
Polymelia 39 Pleuritis 87,180
Polydactylia 39 Posthitis 87,235
Polymastia 39 Proctitis 87
Polythelia 39 Phlebitis 87
Pyopagus 39 Pavementation 87
Prosopothoracopagus 40 Polymorphonuclear cells 89
Pulmonary adenomatosis 46,179 Platelets 91
Petechiae 50 Plasma cells 93
Pustule 59,144 Platelet activating factor 9t
Pseudomucin 61 Phagocytosis 100
Pyknosis 66 Chemotaxis 100
Pus 66 Digestion 100
Post-mortem changes 72 Lysosomal enzymes 101
Algar mortis 73 Respiratory burst 101
Autolysis 72 Ingestion 100
Displacement oforgans 73 Opsonization 100
303

Index
Phlegmon 105 Prostatitis 234
Perivascular cuffing 105 Polioencephalomalacia 238
Piliconcretions 114,116,196 Pachymeningitis 238
Phytoconcretions 114,116,196 Pinkeye 248
Polyconcretions 114,116,196 Post mortem examination 252
Pancreatic calculi 116 Collection, preservation and
Pancrealolith 116 dispatch ofmaterial to laboratory 262
Phytobezoars 116,196 Bacterial diseases 262
Parasitic dermatitis 140 Forensic laboratory 279
Papule 144
Systemic diseases 264
Toxic conditions 264
Parakeratosis 144 Viral diseases 263
Pulmonary osteo arthropathy 153 Immunological examination 265
Persistant right aortic arch 157 Large animal 252
Patent ductus arteriosus 157 p.m. examination ofveterolegal cases 278
Pericarditis 159 Poultry 253
Pyopericardium 159 Steps in p.m. examination 257
Pneumopericardium 159 Writing of p.m. reports 259
Phlebitis 165 Packed cell volume 280
Porcine atrophic rhinitis 169
Pulmonary oedema 173 R
Pneumoconiasis 179 Rachipagus 40
Pleurisy 180 Rachischisis 38
~yothorax 180 Radiation injury 16
Pneumothorax 180 Rainbow penis 233
Pearly disease 180,200 Red hepatization 173
Parasitic enteritis 192 Regeneration 110
Parasitic cirrhosis 200 Renarcuatus 39
Pigmentcirrhosis 200 Repair 110
Poikilocytosis 205 Reticulitis 87,188
Polychromatophilia 205 Retinitis 87,248
Polycythemia 210 Rheumatism like syndrome 30
Panleucopenia 211 Rhexis 50,87
Proteinuria 216 Rhinitis 87,169
Polyuria 216 Riboflavin 19
Pyuria 218 Rickets 27, 150
Phosphate calculi 223 Adult 152
Pyosalpinx 229 Rickettsia 21
Pyometra 229 Rigor mortis 73
Pseudocyesis 229 Rumenitis 87, 186
Pseudopregnancy 229 Russell body 93
Premature birth 230
Placentitis 231 S
Phimosis 233 Saddle thrombus 52
Paraphimosis 233 Sago spleen 61
Phallocarnpsis 233 Salivary calculi 116
304

Index
Salpingitis 87,229 Horizontal 21
Satellitosis 238 Vertical 23
Schistosomus 38 Congenital 23
Schistothorax 38 Hereditary 23
Seminal vesiculitis 234 Thiamine ~
Septic thrombus 52 Turner's syndrome 38
Serotonin 94 Testicular feminization 38
Serus inflammation 103 Teratoma 39
Shock 54 Thoracophagus 40
Sialadenitis 'if! Thrombosis 50
Sialolith 116 Thrombus 52
Signs 4 Cardiac 52
Silicosis 81, 180 Mural 52
Sinovitis 'if! Occlusive 52
Sinusitis 87,169 Saddle 52
Slipped tendon 31 Septic 52
Sludged blood 54 Valvular 52
Snake venom 23 Typhlitis 85, 196
Specific pathology 2 Tendinitis 'if!
Spermatocele 233 Tracheitis 87, 169
Spirochaete 21 Transposition of aorta 157
Spleenitis 87,211 Tetrad ofFallot 157
Spondylitis 87,153 Tetralogy ofFallot 157
Spongiform encephalopathy 240 Telagiectasis 165
Squamous metaplasia TI Tracheobronchitis 169
Stab wound 16 Tonsilitis 184
Stargazing ~ Tympany 186-
Starvation 25 Torsion 1%
Steatitis 85 Toxic aplastic anemia 207
Stifflamb disease TI Thymoma 212
Stillbirth 27,230 Thymic hyperplasia 212
Stomatitis 87,184 Trichomoniasis 231
Subviral agents 21 Testicular hypoplasia 233
Suffusions 50 Total erythrocyte count 280
Summer mastitis 233 Total leucocyte count 280
Suppurative inflammation 105
Symptoms 4 U
Syndrome 4 Ulcer 144
Systemic pathology 2 Upper respiratory tract 169
Uremia 216
T Ureteritis 87,223
Toxopathology 4 Urethritis 87,223
Trauma 14 Uric acid calculi 223
Temperature 16 Urinary calculi 114
Transmission of pathogens 21 Urine examination 284
305

Index
Chemical 284 Vasoactive amines 94
Microscopic 285 Histamine 94
Physical 284 Serotonin 94
Urolith 114 Vesicular dermatitis 140
Urolithiasis 27,222 Vegetative endocarditis 161
Urticaria 144 Mural 161
Uterus didelphys 227 Valvular 161
Uterus unicomis 227 Varicose veins 165
Volvulus 196
V W
Virulence 6 Wallerian degeneration 238
VIrus 16 Water deficiency 26
DNA virus 21 White heifer disease 227
RNA virus 21 White muscle disease 27, 148
Viroids 21 Wounds 16
Vitamins 26,29 Bullet 16
Valvular thrombus 52 Incised 16
Vesicle 59,144 Stab 16
Vaginitis 87,230
Vasculitis 87 X
Vulvitis 87 Xanthine calculi 223
306

Illustrated veterinary pathology (General & systemic pathology)

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