Common Diseases of Goats, Treatment and Preventive Measures

Babagana Alhaji Bukar and Isa Musa Mabu

Submitted: 16 January 2023 Reviewed: 16 January 2023 Published: 05 June 2023
DOI: 10.5772/intechopen.1001377

Abstract
Goat diseases are economically significant and potential to achieve many
national and international assurances on food security, poverty alleviation and
improved nutritional standard. These diseases pose several constraints to the
development of livestock sector to a country where is endemic. This sector
constitutes a quantum of significant livestock production which serves as a source
of meat, milk, wool and source of income to a farmer. Although, most of these
diseases are quite responding to various treatment regimens with the exception
of those few microbes which largely be control through timely recognition,
movement restriction, vector control and moreover the use of effective high
quality vaccines.

1. Introduction
Goat diseases can cause huge economic loss to the farmers due to high intensity
to goat farming with poor management practices. Factors affecting livestock
production in most countries includes diseases, poor management and lack of
proper breeding policies [1]. Disease is an abnormal condition that negatively
affects the structure or function of a body system of an animal. Various organisms
like bacteria, fungal, parasite, protozoa, rickettsia and viruses are said to caused
goat diseases, low quality feeds and poor management practice can predispose
to metabolic disorders, which can caused losses due to reduced productivity and
death [2]. Diseases are very important to farmers and affect the production of
small ruminants in several ways [3]. It incurs increase in the cost of production,
reduces production rate, which directly or indirectly affects the quantity and
quality of animal products and causes a great loss to the farmer. Goats are usually
exposed to vulnerable diseases and harsh conditions due to nonchalant attitudes
of the farmers, where they allowed their animals scavenge freely on the streets
without proper monitoring and sometimes subjected to extreme starvation with
little or no concern to their well-being [1]. Several factors like overpopulated herd
size, less ventilation and poor management system can predispose to disease.
Fomites such as water and feed troughs, as well as bedding can also transmit
disease for a short time, but do not remain infectious for long periods. Goats form
an integral part of animal production in most rural and urban communities, their
economic advantage is primarily associated with the case of handling as it favors
small scale investment minimum risk of loss and high reproductive efficiency.
Livestock production is a tremendous enterprise in East African countries where
about 56% of livestock wealth in Africa is maintained [4]. Goats are mainly kept
for meat, milk, manure, wool and immediate source of income. In most
developing countries, the owner-ship of small ruminants varied from house-holds,
farmers with mixed farming activities to some landless agriculture migrant workers
[5]. A sound management practice is a basic tool to maintain animal health in
the production of goats. There are some human health risks directly associate with
dealing with diseased animals, while some diseases affecting goats do not have
any zoonotic effect to human health. Small ruminants are the main farm animals
owned by the poor in most developing countries which are considered as ‘mobile
banks’ and are reared as source of not only milk and meat for family consumption
but also as source of income that can easily be utilized for paying household
expenditures [6]. Efforts to improve the productivity of goats have been hindered
by a variety of factors including infectious diseases that results in a countless
number of animal deaths [7]. The basic knowledge about diseases and
management practice at the practitioner level on goats production deems
necessary. Productivity of goats is affected due to increased incidence of
diseases and poor management practices. Viral diseases like PPR, goat pox,
contagious ecthyma and viral pneumonia and bacterial diseases like
enterotoxaemia, tetanus, brucellosis, mastitis and metritis, mycotic diseases such
as dermatophytosis and rickettsial infections like conjunctivitis are common
causes of goat’s mortality in rural areas while, Gastrointestinal nematodiasis,
fasciolopses and tape worm infestation causes less mortality but can cause
severe depression in the growth and reproductive performance of goats [8]. This
study therefore seeks to make an attempt to identify some common diseases of
Goats and provide treatment and preventive measures to control goat diseases.
In view of that, the socioeconomic aspect of the farmers, tendency to recognized
common diseases (Table 1) and the professional methods of preventing goat
diseases are established. It is also believed to be useful for scientists, extension
service providers, veterinarians and para-veterinarians in designing appropriate
preventive measures to minimize the risk for diseases in goat production.
 Metabolic and
Bacterial Parasitic Protozoa/Rickettsial Viral
Fungal diseases nutritional
diseases diseases diseases diseases
diseases
Endo
Anthrax Candidiasis Babesiosis PPR Mil fever
parasite
Ecto Goat
Brucellosis Cryptococcosis Coccidiosis Ketosis
parasite pox
CLA Ring worm Theileriosis CAE Grain overload
CCPP Aspergilosis Cowdriosis Orf
Dermatophilosis Anaplasmosis
Mastitis
Foot rot
Table 1.
Summary of common diseases of goats.

2. Methodology
This chapter is a detailed summary of the most important common diseases of
goats and this can be a guide to veterinary students, field veterinarians, animal
health workers, animal scientist and goat farmers regarding the impact of these
diseases. This chapter also gives out a hint on the treatment and preventive
measures associated with diseases of goats. Important diseases that are zoonotic
and economically important like anthrax, brucellosis, caseous lymphadenitis,
contagious caprine pleuropneumonia (CCPP), dermatophilosis, foot rot,
candidiasis, cryptococcosis, babesiosis, cowdriosis, anaplasmosis, Peste des petits
ruminants (PPR), goat pox, ecthyma and hypocalcaemia (Table 1) are vividly
discussed. Each disease is dealt with various subsections like definition of the
diseases, etiology, transmission, clinical signs, diagnosis, treatment and preventive
measures.

A. Bacterial disease of goats

a.1 Anthrax
Anthrax is an infectious zoonotic disease of wild and domestic herbivores caused
by a spore- forming bacterium, which is characterized by onset of high fever,
oozing of unclotted blood from natural orifice and sudden death.
Transmission: Susceptible animals get infected by ingesting spores while grazing
in highly contaminated soil or through the bite of certain flies. There is report of
human infection through contact with the infected animals or contaminated
animal tissue or products. The bacterium also penetrates body through lesion and
sometime be acquired through ingestion of poorly cooked meat from infected
animals.
Etiology: the disease is caused by Bacillus anthracis which is an aerobic or
facultative anaerobic capsulated gram-positive, rod shaped spore forming
bacterium. The spores can remain viable on soil for many years.
Clinical signs: Incubation period is typically 1–20 days. Most infections are
noticeable after 3–7 days. Anthrax disease may be per acute, acute, sub-acute
or chronic. The per acute form most often affects cattle, sheep and goats at the
start of an outbreak and is characterized by staggering, trembling, difficulty in
breathing, convulsions and death. Progression of the disease is rapid and
premonitory signs may go unnoticed often animals are found dead with no
rigormortis (Figure 1, Table 1). Blood may fail to clot due to the toxin released by B.
anthracis. The acute or subacute form is common in cattle, sheep and horses and
manifest high fever, increased heart rate, excitement, depression, incoordination,
cessation of rumination, low milk production, bloody discharges, respiratory
distress, convulsion, and death within 48–72 hours. But the chronic form is usually
seen in less susceptible species like swine.

Figure 1.
Absence of rigor mortis in goat with anthrax.

Diagnosis: Careful microscopic examination of stained smears of blood, vesicular

fluid, or edema may reveal the presence of B. anthracis. Biochemical and
microbiologic tests provide a definitive diagnosis. It can also be isolated from skin
lesions or respiratory secretions.
Treatment: Treatment of per acute case is usually untimely because of sudden
death. Good recovery can be achieved through the use of anthrax antiserum in
the early stage of the disease. Oxytetracycline at the dose rate of
5miligram/kilogram body weight parenterally can be effective if used from
anthrax is most often seen in less susceptible species such as swine, but it has also
been reported as developing in cattle, horses, dogs and cats. Route of infection
in animals is most often ingestion, rather than inhalation or inoculation via skin
lesions, initial suspicions of anthrax may be raised when livestock are found dead,
bloated the onset of the disease. Penicillin streptomycin (Penstrep) also found
effective if given concurrently with antiserum for 5 consecutive days.

Prevention: Anthrax can be prevented through annual vaccination programs.

Rapid detection and reporting, quarantine, treatment of sub clinically affected
animals (post exposure prophylaxis) and burning or burial of suspect and
confirmed cases may prevent spore formation.

a.2 Brucellosis
Brucellosis is a bacterial infection that can affect goats and other livestock such
as sheep and cows and wild ruminants such as deer, elk and bison. Brucellosis
causes abortion or stillbirth in animals. Brucellosis is one of the widest spread
zoonosis transmitted by animals and in endemic areas, human brucellosis has
serious public health consequences.

Etiology: Brucellosis in goats is normally caused by a Gram-negative

coccobacillary rod, Brucella melitensis although Brucella abortus may also cause
clinical brucellosis.

Clinical sign: Brucella melitensis is the most common cause of brucellosis in sheep
and goats. It can cause abortion, retained placenta and swelling of the testicles.
Abortion usually occur in late pregnancy in sheep and during the fourth month of
pregnancy in goats (Figure 2, Table 1). Communicably, brucellosis is contagious
to humans. Bacteria are present in milk, placenta, fetal fluids, fetus, vaginal
discharges, semen and urine. Ruminants and other animals can shed bacteria
long-term or lifelong.
Figure 2.
Abortion complicated with uterine prolapse in brucellosis.

Diagnosis: History and clinical signs may be suggestive of the brucellosis.

Demonstration of the bacteria in smears made from the samples of blood, bone
marrow and other bod fluids can help confirming the diagnosis of the disease.
Brucella can be isolated from the abomasal contents and lungs of the fetus,
mammary glands, supramammary, retropharyngeal, parotid and mandibular
lymph nodes and seminal vesicles by culturing on 5–10% blood or selective serum
agar. Other serological methods like Serum Agglutination Test, Rose Bengal Plate
Test, Enzyme Linked Immuno-Sorbent Assay (ELISA), Agar Gel Immuno-Diffusion
(AGID) and Complement Fixation Test can be diagnostically used in the
confirmation of brucellosis.

Treatment: There is no specific treatment of brucellosis that is successful, but long

term antibiotics treatment can eliminate B. melitensis infections in valuable goats
but the reproductive performance may be poor.

Prevention: Prompt vaccination of cattle, sheep and goats is recommended

especially in endemic areas. Good hygiene practice such as milk pasteurization,
proper meat processing, correct handling of stillbirths and animal carcasses are
important strategy for the prevention of brucellosis in goats.
a.3 Caseous lymphadenitis (CLA)
Caseous lymphadenitis is an infectious disease caused by the
bacterium Corynebacterium pseudotuberculosis, that affects the lymphatic
system, resulting in abscesses in the lymph nodes (Figure 3, Table 1) and internal
organ of Goats and Sheep.

Figure 3.
Lymphnode abscess seen in clinical CLA in goat.

Transmission: The disease is highly contagious that affects sheep and goats [9].
When abscess ruptures, it releases a huge number of bacteria on to the skin and
wool and it results to the consequent contamination of the surrounding
environment. Animals may get infected when come in contact with the affected
animals or indirectly via already contaminated fomites [10]. Infected animals may
contaminate feed and water, which may become source of infection. The
disease is also easily spread through the materials that are used during the
operation of the animals such as castration, identification with ear tags or by
tattooing. It is thought to also be spread by coughing or even by flies [11].

Etiology: CLA is caused by a gram-positive, nonmotile pleomorphic rods

bacterium known as Corynebacterium pseudotuberculosis that has a
characteristic Chinese letter arrangement in the smear. When this organism
successfully established in the host, it surrounds and subdue the immune system,
as a result it causes chronic infection that may remain in the animal for life but not
pestilent [10].

Clinical signs: In CLA, there is abscessation in the region of peripheral lymph

nodes especially the submandibular, parotid, prescapular and prefemoral nodes,
which is termed superficial or cutaneous form. The internal form of CLA more
commonly presents as dyspnea, loss of weight and failure to thrive. Other clinical
signs include large pus-filled cyst on the neck, sides and udders, cough, purulent
nasal discharge, fever and tachypnea with abnormal lung sounds may be
observed.
Diagnosis: A provisional diagnosis of the disease can be based on clinical features
and physical examination of lesions associated with lymph nodes. Confirmation
of the disease is achieved by bacterial culture of suspected lesions and purulent
materials from an intact abscess. Serologic tests are available but their reliability
is unrealistic.

Treatment: Treatment of CLA is often unsuccessful, but supportive care can be

helpful. However, CLA abscesses must be treated to prevent ruptures and further
contamination of other animals and environment. Parenteral antibiotics may be
used in severe cases. Surgical drainage of the affected lymph nodes is
recommended.

Prevention: The prevention of CLA can be achieved through strict biosecurity

measures, immediate isolation of the affected animals from the flock. Surgical
procedures such as castration, shearing or mass vaccination should be carried
out through aseptic means and affected premises should be disinfected
thoroughly.

a.4 Contagious caprine pleuro-pneumonia (CCPP)

Contagious caprine pleuro-pneumonia (CCPP) is a highly contagious and rapidly
spreading mycoplasmal disease that affects a vast majority of goat’s population,
which is characterized by severe respiratory distress associated with sero-mucoid
nasal discharge, dyspnea, coughing, pyrexia and general malaise.

Transmission: Main route of transmission occurs through inhalation of infected

aerosol. Airborne transmission can result in distant spread [12]. Transmission by
direct contact is also reported [13]. Infected objects, vectors, fomites and animal
products are yet to be known in transmission role [14].

Etiology: Contagious caprine pleuro-pneumonia is a highly fatal disease that is

caused by Mycoplasma capricolum capripneumoniae or Mccp
(previously Mycoplama biotype F38), in Africa, Asia and the Middle East.
Morbidity is often 100% and mortality may reach 80%.
Clinical signs: The disease is characterized by anorexia, dullness, depression,
weakness and lethargy, pyrexia, weight loss and decreased production. Also
have respiratory signs of bilateral nasal discharge (Figure 4, Table 1), dyspnea,
tachypnea and coughing. Occasionally, the only sign seen is sudden death.

Figure 4.
Sign of bilateral nasal discharge in CCPP.

Diagnosis: The simplest and quickest procedure in field diagnosis is the detection
of antibodies by Latex agglutination (LAT) as is easy to run and has a long shelf
life. Other diagnosis include growth inhibition disc tests (GI), direct and indirect
fluorescent antibody tests, complement fixation test (CFT), indirect
hemaglutination test, ELISA and PCR. Isolation of M. capricolum
capripneumonia from clinical samples is the only way to definitively diagnose the
infection but is not normally performed as it is difficult and time consuming.

Treatment: Macrolides, tetracycline and quinolones are very active against M.

capricolum capripneumonia. Antibiotics like tylosin at 1 ml/10 kg and
enrofluxacin at 1 ml/20 kg body weight can be helpful in the treatment of CCPP.

Prevention: Vaccination has been an important aspect of CCPP prevention in a

country where it is prevalent. Quarantine of affected animals and strict biosecurity
measures for the introduction of new animals is necessary to reduce transmission
and losses due to CCPP.
a.5 Dermatophilosis
Detmatophilosis is contagious bacterial disease of skin that affects sheep and
goats. It is an infection affecting multiple species of animals world-wide, most
common in young or immunosuppressed animals or in animals that are
chronically exposed to wet conditions.

Transmission: Dermatophilosis is believed to be spread by direct contact between

animals, through contaminated environments or possibly through biting insects.
Etiology: The disease is caused by a dimorphic bacterium, Dermatophilus
congolensis that has two characteristic morphologic forms: filamentous hyphae
and motile zoospores. Is a gram positive, non-acid fast, facultative anaerobic
actinomycete, which is the only currently accepted species in the genus but, a
variety of strains can be present within a group of animals during an outbreak
[15].

Clinical signs: In severe generalized dermatophilosis, there is often loss of

condition and motion, scab formation on the lips, muzzle, nose, ears (Figure
5, Table 1), feet and scrotom which if severely affected make prehension difficult.
The scabs can become detached and reveal a yellow, creamy or hemorrhagic
exudate. Allopecia can occur if the scabs are rubbed off. There is tufted papules
and crusts that resembles paintbrushes. Concurrent infection with orf virus and
other stress factors like malnutrition, pregnancy and lactation exacerbate the
disease [16]. Most infections are mild thus render susceptible animal with normal
functioning immune system spontaneously recover in time.

Figure 5.
Scab formation on the lips, muzzle and nose.
Diagnosis: Clinical and cytological examinations of fresh lesions are suggestive of
the disease. A definitive diagnosis is made by demonstration of the organism in
cytological preparations, isolation on culture and/or via skin biopsy. Indirect
fluorescent antibody technique and a single dilution ELISA test have been
developed for large serologic and epidemiologic surveys.
Treatment: The causal organism is susceptible to a wide range of antimicrobials.
High doses of penicillin-streptomycin are effective in severely affected animals, if
administered in early stage of the disease. Heavy doses of long acting tetra cline
(20 mg/kg) may be used and topical application of lime sulfur is a cost-effective
adjuvant to antibacterial therapy. Insect repellent can be use externally to
control biting insects.

Prevention: Isolation and culling of clinically affected animals can be helpful in

preventing the disease. Ectoparasites control is a method used in breaking the
infective cycle of the parasite. Keeping susceptible animals dry and frequent
checking of the zinc sulphate and copper sulphate level in feeds have been
found useful in reducing the spread and incidence of the disease.

a.6 Mastitis
Mastitis is an inflammation of mammary gland due to physical injury, stress,
bacterial or viral infections. It can either be clinical or subclinical. It is
characterized clinically by clots or serum formation in the milk, swollen udder
(Figure 6, Table 1), hot and tender to touch. Sub clinically, can be detected using
California Mastitis Test (CMT), milk culture or Somatic Cell Count (SCC).

Figure 6.
Swollen udder in mastitic goat. By author.
Transmission: In goats, both vertical and horizontal transmissions are likely to
occur. But vertical transmission presents very low occurrence. The introduction of
mastitis is favored mainly by the factors that intervene in the horizontal
transmission of pathogen. The pathogens can be eliminated by milk, feces, urine
and oronasal secretions. The hands of the milker, milking equipment, vectors and
fomites as a general way. The most often entry is via the galatogenic route [17].
All animals are susceptible, increasing the predisposition mainly according to age
and number of lactations [18].
Etiology: The disease has a multiple etiolo gy but Staphylococcus
aureus and Streptococcus agalactiae are the commonest bacteria isolated
from cases of mastitis in small ruminants. Other bacteria identified
include Corynebacterium pyogenes, Klebsiella spp, Mycobacterium
spp and Brucella spp [16].

Clinical signs: The clinical manifestations of acute mastitis include edema,

elevated fever above 1050 F, increased pulse rate, loss of appetite, depression,
apathy, dyspnea, swelling and redness of the mammary gland, enlargement of
the retro-mammary lymph nodes and lethargic movement are observed.
Agalactia or lack of milk and hard lumps are common features of chronic mastitis.
Claudication is a common sign in which small ruminants limps in order not to
tamper with the inflamed mammary gland [19]. However, in subclinical mastitis,
there is no evidence of clinical signs, but alterations in milk composition can occur
and positive respond to CMT or other suggestive tests [20].

Diagnosis: History and clinical features are suggestive for tentative diagnosis.
Microbiological culture can be reliable to determine the presence of organism in
milk sample; California Mastitis Test (CMT) and somatic cell count (SCC) are
commonest tests for mastitis. Other tests like multiplex-PCR and Enzyme-Linked
Immuno Sorbent Assay (ELISA) are important techniques used in the diagnosis of
mastitis.

Treatment: Glucocorticoids is recommended in the early course of disease,

antibiotics like penicillin streptomycin (penstrep) at 200 mg/ml for 3–5 consecutive
days is effective, oxytetracycline, benzylpenicillin, cloxacillin, amoxicillin,,
ampicillin, or erythromycin have been recommended to treat mastitis. Some
strains of S. aureus have found to be resistant to penicillin, hence drug sensitivity
test is recommended before the use of such drugs on the treatment of mastitis.
Topical application of antibiotic cream can be helpful.
Prevention: Proper milking practices, good hygiene for milking utensils and culling
persistent infectors can help in reducing the incidence of the disease. Kidding
pens and Bedding should be disinfected daily to avoid growth of pathogenic
bacteria. Abscess draining and proper wound dressing can be carried out
regularly. The hygienic-sanitary management aimed at preventing mastitis
involves a number of factors including the choice of antimicrobial, microorganism
susceptibility, duration of treatment, dosage employed, and the animal’s immune
status [21].

a.7 Foot rot

Foot rot is a contagious disease of the hooves in goats and sheep, characterized
by ulceration and necrosis of the sensitive laminae of the foot (Figure 7, Table 1)
and lameness. This disease is prevalent in the Southern region of the United States
due to wetness and humidity of the environment.

Figure 7.
Ulceration and necrosis of laminae of foot in goat.

Transmission: Transmission is mainly enhanced by genetics, stocking rate and

environmental factors. The disease can be spread from infected animal to non-
infected susceptible animals (direct transmission). Incidence of overgrown
hooves can predispose animals to foot rot. During the rainy season, infected
animals can contaminate the soil and muddy pens which can enhance disease
transmission to other animals If not treated; sick animals can become
permanently infected [22]. The organism can also be transported to the soil by
visitor’s shoes.
Etiology: Foot rot is disease caused by a large Gram-negative rod-shaped
bacterium, Fusobacterium necrophorum and Dichelobacter nodosus which are
mostly common in contaminated soil.

Clinical signs: Foot rot results in lameness, inappetence, loss of weight, and
necrotic lesions in the interdigital space with foul smelling of the foot, there is
elevated temperature and reduced production performance, lethargy, grazing
on knees and abnormal gait. This condition may result increase in production
losses, cost of treatment and prevention. Affected animals will lose value due to
the infection [23]. The disease is very difficult to eradicate when it affects a
herd/flock.

Diagnosis: The first signs of hoof rot are limping, holding limbs above the ground,
grazing on knees, and abnormal gait, should be sufficient for diagnosis. If
laboratory confirmation is required, submit smears and swabs of interdigital
exudate and necrotic tissue from multiple animals for bacteriology.

Treatment: Systemic administration of antibiotics (penicillin streptomycin or

oxytetracycline) and dry underfoot conditions usually resolve even severe
lameness after a few days without the need to pare away dead horn. To curate
in-between hooves with potassium per manganite and topical application of
aerosol sprays of cetrimide or oxytetracycline may be helpful. Foot bathing in
formalin or zinc sulphate (with surfactant) is another success achievable option.

Prevention: Quarantine all newly purchased animals before introducing in to the

flock, isolate affected animals and give a deserving treatment, keep barn dry
and clean to avoid contamination, Provide good drainage to areas of pastures
and paddock, trim hooves regularly, supplement trace minerals and vitamins and
give adequate nutrition.

B. Fungal disease of goats

b.1 Candidiasis
Candidiasis is a mucocutaneous fungal disease caused by a yeast-like fungus. It
is a normal inhabitant of gastro intestinal tract, nasopharynx and outer genitalia
of different species of animals.
Etiology: Candidiasis is caused by a yeast-like candida specie most
commonly Candida albicans that usually affects immunocompromised animals
and opportunistic in causing diseases. The disease is distributed worldwide in a
different spp. of animals [24].

Clinical signs: Signs noticed are defined patch of red itchy skin, pustules and
scabs (Figure 8, Table 1). There is a local overgrowth of candida spp. on the
tongue and mucosa of the mouth that appears as white plaques. Anorexia,
dehydration, watery diarrhea, loss of weight and sometime death. Affected kids
may develop listlessness, inappetence and stunted growth.

Figure 8.
Area of pustules and scabs in goats with candidiasis.

Diagnosis: Diagnosis can be made by microscopic examination of scrapings or

biopsy specimens from mucocutaneous lesions. The fungus can be seen visibly on
staining with Wrights, methylene or Gram stain techniques. It can also be
confirmed on culture of a sample in blood or tissue agar.

Treatment: Antifungal like amphotericin B or nystatin ointment can be effective

when use topically, 1% iodine solution may also be used in the treatment of
cutaneous candidiasis.
b.2 Cryptococcosis
Cryptococcosis is a dimorphic potential fungal disease of mainly the lung and
brain that is distributed worldwide and affects immunocompromised animals
especially goats and sheep causing pneumonia and or meningitis [25].

Etiology: At least 322 species of the genus Cryptococcus (Tremellales,

Agaricomycotina) have been described [26]. However, only Cryptococcus
neoformans (var. neoformans and var.grubii) and C. gattii have been described
as causing disease in humans and domestic animals [27]. The pathogenic species
of Cryptococcus are the only species of the order Tremellales able to grow well
at temperatures >30°C, and their capacity to grow at 37°C is one of their main
virulence factors [28].

Clinical signs: In cryptococcosis signs observed are; pyrexia, paraplegia,

depression, severe dyspnea due to the obstruction of the nostrils, swelling of the
nasal region, purulent nasal discharge, with abundant granulation tissue and
hemorrhagic exudate in the nostrils [29]. Goats may have severe respiratory
disease, including cough, anorexia, fever and severe weight loss [27]. Neurologic
signs may also be observed in goats [30] and or meningitis (Figure 9, Table 1). The
infection is sub-acute to chronic, with a clinical course of 2–6 week in goats and
sheep [29].

Figure 9.
A sign of cryptococcal meningitis in goat.
Diagnosis: Diagnosis. A definitive diagnosis can be achieved by cytologic
evaluation of cerebrospinal fluid, skin and nasal exudates or isolation of C.
neoformans from blood or body fluids such as CSF. Cryptococcal antigen latex
agglutination serology (CALAS) can be performed on serum or body fluids but
only provides presumptive evidence [31]. Gram stain is also useful.

Treatment: Prompt anti-fungal treatment such as Amphotericin B plus flucytosine,

fluconazole, itraconazole or ketoconazole was found effective in the treatment
of Cryptococcus in goats especially when treatment with antibiotics did not give
any result. Success with oral fluconazole (5 mg/Kg/day orally for 6 months) was
established in a goat with abdominal wall infection with C. gatti [32].

Prevention: It is difficult to prevent exposure to Cryptococcus in goats, since it is

commonly found in the environment. Avoidance and environmental control of
bird droppings (especially pigeons) are important [33]. Good hygiene and
environmental sanitation is paramount in the prevention of the Cryptococcus.

b.3 Ringworm
Ringworm is a skin lesion usually circular and hairless, caused by a fungal infection
of the hair follicle and outer layer of skin. Ringworm is a zoonotic disease. Sheep
and goats develop crusty, scaly, circular patches that may or may not be pruritic
(itchy).

Transmission: It is transmitted by close contact between animals or via animals

contracting infective spores in the environment or by direct or indirect contact
with contaminated equipment or environment.

Etiology: Ringworm is sometime called wool fungus, which is typically from

the Trichophyton or Mycosporum genera. Ringworm is highly contagious and
zoonotic in nature.

Clinical Signs: The primary signs observed are alopecia, scaling, crusting and poor
growth. Sheep and goats develop moist and reddened skin, but later gray, scaly
and dry, circular patches (Figure 10, Table 1) which is due to coalesced lesions
that may or may not be pruritic (itchy). In more severely affected animals, lesions
become confluent to produce an extensive areas of infection. Sheep and goats
used for exhibition are at a much higher risk of contracting ringworm due to
shearing practices, which cause exposure of the skin and the spread of fungal
spores [34].

Figure 10.
Gray scaly dried circular area consumed by ringworm.

Diagnosis: Diagnosis is typically made by visual examination and/or microscopic

examination of biopsy of lesions, hair or skin scrapings. A definitive diagnosis and
identification of the organism is made by a fungal culture.

Treatment: Treatments may not shorten the time to complete healing of lesions.
Treatment with ketoconazole is found effective. Topical application of charmil gel
can be helpful. The use of imidazole spray may stop progression of lesions and
lower the spread to other animals.

Prevention: It is important to isolate infected animals so as not to spread ringworm

to the rest of the flock or herd. Minimize mixing of animals in pre-confinement
periods. Not only is it important to treat the animal, it is important to disinfect pens
and anything with which the infected sheep or goat may have been in contact
[34]. Thorough hand washing is also recommended after treating the animals.
b.4 Aspergillosis
Aspergillus spp. may cause infections in a variety of domestic animals. They are
saprobes that are widely distributed in nature. Spread occurs via aerosols of
spores present in soil, decaying vegetation, and occasionally animal tissues [35],
a specialized hyphal structure of some fungi that produce conidia (asexually
produced spores borne externally to the cells), can be observed in highly
oxygenated tissues, such as those of the respiratory system [36].

Etiology: Aspergillosis is caused by several species of aspergillus, and there are

more than 300 species of Aspergillus [37]. A. fumigatus is known to be directly
associated with infection. Other spps like A. niger, A. flavus, A. terreus, and A.
nidulans are opportunistic pathogens that are being recognized commonly with
the use of molecular techniques.

Clinical signs: In ruminants, signs include moist cough, nasal discharge, pyrexia
and shallow respiration. Pulmonary aspergillosis in sheep and goats is
characterized clinically by anorexia, dyspnea, apathy, cough and nasal
discharge [38]. The lungs are mottled, firm and heavy. There may be loss of
condition associated with necrosis of the nasal mucosa in goats with nasal form
of aspergillosis which may result in severe dyspnea (Figure 11, Table 1).

Figure 11.
Nasal and cutaneous aspergillosis in goat. By author.
Diagnosis: Aspergillosis can be confirmed by immunohistochemical, molecular
and culture-based diagnostic methods. Macroscopic and histologic lesions can
be used as presumptive diagnosis. There is another alternative diagnostic
approach which involves the use of pan-fungal PCR on animal tissues [39].
Immunodiffusion, complement fixation, and ELISA can be used to detect
antibodies against Aspergillus spp [40].

Treatment and prevention: Antifungal agents are currently unlicensed, but

management of the disease usually relies on preventative measures such as
ensuring clean bedding, good hygiene and good husbandry.

C. Parasitic diseases of goats

Parasites commonly found in goats can be divided into two general categories:
Internal (Endo) and External (Ecto) parasites:

C.1 Endo parasites of goats

Endo parasites are worms that live in the body or inside an organ and there are
multiple types. The most common internal parasites in goats are: Nematodes
(roundworms) e.g. lung worms (Dictyocaulus spp. or Muellerius capillaris),
Tapeworms, for example, moniezia, Liver flukes, for example, Fasciola hepatica,
and intestinal parasites like Coccidia, for example, Eimeria or Isospora and
Cryptosporidia. Parasites grow and reproduce in certain environments. Goats
that live in those environments are at high risk of becoming infested [41].

Clinical signs: The clinical signs of endoparasitism in goats include: reduced

weight gain, decreased milk yield, Diarrhea, Rough hair coat (Figure 12, Table 1),
loss of condition, Weakness, Anemia, Fever, hyperpnea, Coughing and Bottle jaw.
Figure 12.
Diarrhea and rough haircoat in goat affected by internal parasite.

Diagnosis: Endo parasite of goats can be diagnosed mainly based on laboratory

tests. The commonly used laboratory tests for the diagnosis of endo parasitic
diseases include blood packed cell volume, etiological examination, which
involves the detecting of the parasitic larvae or eggs from stool, blood, nasal
secretions as well as tissue of the animals, serological assay such as Enzyme linked
immunosorbent assay, indirect hemagglutination test or fluorescence
immunoassay and molecular diagnostic techniques such as polymerase chain
reaction (PCR) or DNA sequencing.

Treatment: Benzimidazoles (oxfendazole, febantel, fenbendazole and

albendazole) Macrocyclic lactones: Avermectins (ivermectin, doramectin and
eprinomectin) Milbemycins Cholinergic agonists: Imidazothiazoles (levamisole)
Tetrahydropyrimidines (pyrantel and morantel) are found effective for internal
parasite. However, only morantel, thiabendazole, fenbendazole, albendazole
and phenothiazine are approved for goats [42]. Dewormer resistance occurs
when there is less than 95% reduction in fecal egg count 14 days after
administration. Resistance has risen due to anthelmintics being used often,
rotated too frequently or under dosed.

Prevention: The best prevention is to alternate livestock species grazing, avoiding

overcrowding of pens or premises, genetic improvement and pasture rotation.
Balanced nutrition is very important to keep animals healthy and help them
develop appropriate resistance to external pathogens, especially for dams
before and after lambing/kidding. Also practice the use of effective dewormers.

c.2 Ectoparasite of goats

Ectoparasites feed on body tissues like skin, hair or blood, and they include fleas,
flies, lice, mites, nose botfly and ticks. The wounds and skin irritation produced by
these parasites result in discomfort and irritation to the animals. Parasites can
transmit diseases from sick to healthy animals, which can reduce weight gains
and milk production.

Clinical signs: Mites infect the head, legs, body or tail region causing the skin to
become crusted and cause loss of hair and wool (Figure 13, Table 1). The infected
area itches and the animal scratches. The host does not feed well. The infections
cause skin damage to a goat. Lice, flea and flies are found where animals are
kept in overcrowded confined environment and cause irritation of the skin,
anemia and damage to the skin. It causes loss of weight and condition to the
host. The can transfer from one animal to another through close contact. Ticks
are very important parasites that can harm its host by bites resulting in anemia,
weakness and debility. Ticks can be classified according to groups; one-host, two-
host and three-host ticks. Ticks that are known to infest goats are those belonging
to three-host tick as they parasitize three different hosts in their life cycle that make
their control very difficult. Ticks also spread diseases (tick borne diseases) that are
so fatal to its host. Nose botfly infests the nostril of goats causing irritation, sneezing,
shaking of the head, nasal discharge, respiratory distress, loss of appetite and
grinding of the teeth.
Figure 13.
Loss of hair caused by ectoparasite.

Diagnosis: Identification of ectoparasites can prove difficult because detailed

clinical examination can fail to confirm the presence of some ectoparasites. It
may be necessary to take skin stub samples to investigate whether arthropods
such as mites are in residence. Ticks, flea, flies and biting lice usually can be seen
with the naked eye. The presence of mites can be confirmed by examining mites,
eggs and fecal pellets in skin scrapings under the stereoscopic microscope.

Treatment: Mites and lice are controlled by washing the infected area, spraying
or dipping the animal with a suitable treatment. If an animal has only a few ticks
these can be carefully pulled off making sure the mouth parts of the tick are
removed. Dipping is very effective if large numbers of livestock need to be
treated. Ivermetin injection and pour on are also effective in the treatment of
ectoparasite, but accurate dose must be maintained.

Prevention: Monitoring program should be exercise to insure early identification.

Sanitation and regular cleaning of facilities using appropriate detergent and
disinfectant is helpful in the prevention of ectoparasite. Eliminate areas where
external parasites can breed and develop (e.g. elimination of standing water
reservoirs decreases mosquito levels). The use of Insecticides and fly predators
may be necessary.
D. Protozoa/Rickettsial diseases of goats

d.1 Babesiosis
Babesiosis is an infectious tickborne, obligate, intraerythrocytic protozoan
parasites from the phylum Apicomplexa, order Piroplasmida affecting a wild and
domestic animals which include cattle, sheep and ggoats. It is typically fatal
disease that is characterized by hemoglobinuria, fever, icterus and intravascular
hemolysis resulting to anemia. Variety of animals. Susceptible animals may suffer
high rate of mortality but recovered animals that are latently infected has an
immunity for a certain period of time. It is transmitted transovarially by ticks. By the
ingestion of the parasite, the female tick becomes infected during engorgement,
upon drops off of the babesial agents on the host, it reproduce within the tick’s
tissues which is incorperated within the embryo of the developing ticks resulting
to the transmission of the disease to the new hosts by feding of ensuing tick larvae,
nymphs, or adults [43].

Transmission: Babesiosis is transmitted by

ticks Boophilus, Hemaphysalis, Hyalomma, Dermaentor and Ixodus spp are the
vetor in the transmission of Babesia of different species. It is transmitted in both
transovarially and transstadially. Babesia spp affecting goats and sheep may be
maintained in non-susceptible hosts such as wild animals [16].

Etiology: Although small ruminants can be infected by several species of Babesia,

the two most important species associated with Babesiosis in goats are B.
ovis and B. motasi, transmitted by Rhipicephalus bursa and Haemaphysalis
spp, respectively. Infection is of importance in the Middle East, southern Europe,
and some African and Asian countries.

Clinical signs: B. motasi can cause an acute or chronic Babesiosis in goats,

generally runs a course of 1 week or less. In acute infection, the first clinical signs
are anorexia, lethargy, depression, and fever (frequently ≥41°C]), which persist
throughout, and these are accompanied later by inappetence, anemia and
jaundice (Figure 14, Table 1), hemoglobinemia and hemoglobinuria occur in the
final stages. Chronic infection is manifested by emaciation, coughing and
edema. Many animals recover; however, some may die if not treated.
Figure 14.
Anemia and jaundice seen in Babesiosis.

Diagnosis: History and clinical findings may provide a presumptive diagnosis of

babesiosis. However, Giemsa-stained blood or organ smears by light microscopy
is essential to confirm the diagnosis. The most commonly used tests are ELISA, PCR
and a DNA probe, which can detect specific parasitemias at very low levels of
infection [44].

Treatment and prevention: Babesiosis can be treated using diminazene aceturate

(3-5 mg/kg), phenemidine diisethionate (8-13 mg/kg), imidocarb dipropionate (1-
3 mg/kg), and amicarbalide diisethionate (5–10 mg/kg) [43, 44]. Supportive
treatment such as blood transfusions (4liters of whole blood per 250 kg of body
weight), fluids, hematinics, and prophylactic antibiotics are important [43]. The
disease can be prevented by effective quarantine of the susceptible animals so
as not allow the introduction of the vector ticks. The control of ticks by dipping or
spraying animals at risk with recommended acaricides is paramount.

d.2 Coccidiosis
Coccidiosis is an enteric protozoan disease of goats caused by the
genus Eimeria. Coccidia go through a complex life cycle in the intestinal cells of
animals. Large number of eggs called oocysts are being produced in the intestine
and passed in the feces. The intestinal cells can be damaged as a result of growth
and multiplication of the coccidia in the intestinal epithelial cell thereby causing
diarrhea and other signs of the disease.

Etiology: Coccidiosis in goats is caused by several species of Eimeria, but E.

arloingi and E. ninakohlyakimovae are known to be pathogenic. All the
goat Eimeria spp are considered host specific and do not transfer infection from
goats to sheep. In most cases, concurrent coccidial and helminthic infections can
occur especially in animals on extensive management system [45].

Clinical signs: In most cases, clinical coccidiosis occurs between 5 and 8 weeks
of age. Most goat kids have subclinical infection. In acute or sub-acute infections,
the usual signs are pasty feces, dirty tails, stary coat, loss of weight, dehydration
and inappetence. More severe acute cases show mucoid or bloody diarrhea,
possible tenesmus, dullness, anorexia, weakness and anemia. Severe problems
lead to rapid onset of diarrhea, often with blood, tenesmus, and signs of
abdominal pain, lethargy, recumbences, and death. In chronic infections, there
is delayed puberty, debilitation, poor appetite, loss of weight and liver failure
especially in milking goats.

Diagnosis: Diagnosis can be based on history, age of kids, clinical signs especially
of severe diarrhea, fecal examination and postmortem findings. Acute
coccidiosis can be diagnosed by direct examination of feces but in chronic
coccidiosis that have very low oocysts number are seen in feces (Figure 15, Table
1), direct examination of feces may not be adequate [46].

Figure 15.
Slide showing coccidiosis in goats.
Treatment and prevention: Sulfadimidine (sulfamethazine) injection (10–
50 mg/kg) for five consecutive days is found effective. Vetcotrim bolus (10-
30 m/kg Per Os once daily for 3 days) has a good result. Decoquinate (Deccox,
0.5 mg/kg) and Monensin 13-20grams/ton of feed can be used in non-lactating
goats. Diclazuril (1 mg/kg, PO, once) and toltrazuril (20 mg/kg, PO, once) have
been used successfully; doses may need to be repeated. A metabolite of
toltrazuril, ponazuril (10 mg/kg, PO, once) reduced oocyst counts when used
experimentally in goat kids. Ensure good nutrition program, Improved good
hygiene in the house, minimize predisposing factors, avoid crowded pens and
pastures, Feed and water troughs should be raised off the ground to prevent fecal
contamination.

d.3 Theileriosis
Theileriosis is caused by Theileria spp. a genus comprising tick-borne transmitted
protozoa of the family Theileridae, order Piroplasmida, subclass Piroplasmia,
Phylum Apicomplexa. Theileria species affect domestic and wild ruminants,
especially in Africa, Europe, Australia, and Asia [47].

Etiology: Theileriosis in sheep and goats is usually caused by T.

lestoquardi (formerly T. hirci), T. uilenbergi or T. luwenshuni. Morbidity and
mortality rates of up to 65% (T. luwenshuni) and 75% (T. uilenbergi) have been seen
in susceptible animals introduced into endemic areas. Affected animals show
sustained fever and anemia.

Clinical signs: The clinical signs of theileriosis in goats infected with T.

lestoquardi are similar to other forms of theileriosis, which include anorexia, slight
oculo-nasal discharges, fever, salivation, enlargement of superficial lymphnodes,
weight loss, respiratory distress (Figure 16, Table 1), edema of the lungs, anemia,
icterus and diarrhea, death may occur due to asphyxia. Abortions may also be
seen. In most cases, experimental infection of sheep and goats with T.
annulata resulted in only mild to moderate clinical signs of fever and
lymphadenopathy [48].
Figure 16.
Respiratory distress and loss of weight.

Diagnosis: Theileriosis can be diagnosed on Giemsa-stained thin smears from

blood or lymph node biopsies. At necropsy, impression smears can also be used
to detect schizonts from many internal organs of infected animals such as the
liver, spleen, lymph nodes and lungs. Other diagnostics tools like antigen- specific
ELISAs and PCR are often used in diagnosis and can identify Theileria in the blood
of both carriers and clinical cases. Some tests can differentiate the species
of Theileria, while others are specific for the genus [48].

Treatment and prevention: Infected goats can be treated with antiparasitic drugs
like Buparvaquone (2.5 mg/kg) is very effective in the early stage of the disease.
Use of Oxytetracycline 10 mg/kg is found helpful. Antidiuretics and anti-
inflammatory drugs may also be used when there is evidence of pulmonary
edema. In advanced stage of the disease, treatment is less effective especially
where there is extensive destruction of lymphoid and hematopoietic tissues [49].
Control of ticks by spraying or dipping of animals with acaracides is the most
successful method used for the prevention of theileriosis, but this needs to be
applied at regular intervals to be effective. Pyrethroid compounds are often used
where animals are exposed to tickborne diseases.

d.4 Cowdriosis
Cowdriosis (Heartwater) is regarded as the most important infectious,
noncontagious, tickborne rickettsial disease of ruminants that is clinically
characterized by diarrhea, fever, hydropericardium, hydrothorax and edema of
lung and brain. The disease is seen only in areas infested by ticks of the
genus Amblyomma.

Etiology and transmission: The disease is caused by a pleomorphic

ricketssia Ehrlichia ruminantium which is an obligate intracellular parasite
previously known as Cowdria ruminantium.. Under natural conditions, E
ruminantium is transmitted by Amblyomma ticks. Transmission occur mainly
transstadially, but transovarial transmission rarely occurs.

Clinical signs: The incubation period of Heartwater in goats and sheep is 1–

5 weeks and the course of acute disease takes 3–6 days. The clinical signs are
dramatic in the peracute and acute forms. In peracute cases, animals may die
suddenly without any premonitory signs; other animals developed dyspnea and
intense convulsion. In the acute form, there is pale mucous membrane, anorexia
and depression (Figure 17, Table 1). Other signs of hyperesthesia, nystagmus,
chewing movements and a high-stepping stiff gait may be noticed. Terminally,
prostration with bouts of opisthotonus, circling or galloping movement, and
stiffening of the limbs, intermittent diarhea and convulsions are also seen.
Subacute form is less pronounced, but there may be prolonged fever, mild
incoordination and coughing. Nervous signs are inconsistent.

Figure 17.
Anorexia and depression.
Diagnosis: presumptive diagnosis is based on clinical, epidemiological and
pathological features; E.ruminantium colonies can be identifiable in the brain or
intima of blood vessels on staining with Giemsa or methylene blue; Molecular
methods like real-time PCR has an advantage of being less time consuming and
free of cross contamination; Serological tests such as indirect fluorescent antibody
tests, enzyme linked immunosorbent assays (ELISA) and Western blot are used for
definitive diagnosis.

Treatment and prevention: Sulfonamides and tetracyclines can be used in the

early stage of the disease, when it advances the prognosis may be poor.
Oxytetracycline 20%long acting at 10 mg/kg/day may be helpful or doxycycline
at 2 mg/kg/day will be effective, if administered early in the course of heartwater
infection. Diazepam may be required to control convulsions. Dexamethasone
injection will be serve as supportive care, although the rationale behind its
effectiveness is much more controversial. Control of tick infestation is a good
preventive measure in some instances but may be difficult and expensive to
maintain in others. In areas of endemicity, the use of dips against ticks of domestic
animals is highly recommended. Affected animals must be confined in a quiet
and cool areas that is devoid of any other disturbances because, any stimulation
can cause a convulsion and abrupt death. Vaccination can be helpful in the
prevention and control of cowdriosis.

d.5 Anaplasmosis
Anaplasmosis is a tickborne obligate intraerythrocytic bacteria of the
order Rickettsiales, family Anaplasmataceae, genus Anaplasma, that infect red
blood cells, causing fever and anemia.

Etiology and transmission: Anaplasma ovis may cause mild to severe disease in
sheep, goats and deer which is typically transmitted by ticks or biting flies. Up to
17 different tick vector species (including Dermacentor, Rhipicephalus, Ixodes,
Hyalomma, and Argas) have been reported to transmit Anaplasma spp.
Iatrogenic transmission can occur when instruments are re-used without proper
sanitation, including instruments used for dehorning, ear tagging, castrating, and
vaccinating. In utero transmission has also been reported.

Clinical signs: Anaplasmosis is usually subclinical or less severe in young animals, it

is severe and often fatal in older. Anaplasmosis is characterized by progressive
anemia due to extravascular destruction of erythrocytes. Macrocytic anemia
with circulating reticulocytes may be present late in the disease [50]. Animals with
peracute infections succumb within a few hours of the onset of clinical signs.
Acutely infected animals lose condition rapidly. Incoordination, loss of appetite,
dyspnea, and a rapid pulse are usually evident in the late stages. The urine may
be brown, but, contrary to babesiosis, with no hemoglobinuria. Mucous
membranes appear pale and yellowish. There is abortion, hematologic
parameters gradually return to normal after convalescence.

Diagnosis: Diagnosis based on clinical features, hematological changes, blood

smears, and serologic testing. Microscopic examination of Giemsa-stained thin
and thick blood films (Figure 18, Table 1) is critical to distinguish anaplasmosis from
babesiosis and other conditions that result in anemia and jaundice, such as
leptospirosis and theileriosis. Serological tests like ELISA, complement fixation, or
card agglutination tests has been used to identify chronically infected carriers but
with doubtful degree of accuracy. Nucleic acid-based detection methods can
be used, but carrier level of infections may not be detected [50].

Figure 18.
Slide showing anaplsma spp.

Treatment and prevention: Oxytetracycline has been reported to reduce severity

of the disease. The use of imidocarb has been shown to be very effective in the
treatment of anaplasmosis. Good sanitary methods such as cleaning of
stalls/pens regularly can help to reduce contamination. Avoid re-using of needles
and disinfect medical equipments when use. Treatment with an effective
acaricides to kill ticks may help to reduce the incidence of anaplasmosis.
E. Viral diseases of goats
e.1 Peste des petits ruminants (goat plaque)
Peste des petits ruminants is an acute, highly contagious transboundry viral
disease primarily affecting goats and less commonly in sheep associated with
high morbidity and mortality caused by PPR virus of the genus morbilliirus and
family paramoviridae that closely resembles rinderpest virus.

Etiology and transmission: is caused by a PPR virus of the genus Morbillivirus of the
family paramoviridae (sub family Paramixovirinae) under the
order Mononegavirales which is related to but distinct from Rinderpest virus of
cattle. The PPRV is genetically grouped into four genotypes (lineages) [51], based
on the Fusion (F) and Nucleoprotein (N) gene sequences. Lineages I and II
circulate mainly in West Africa, lineage III is mostly in Eastern part of Africa, while
lineage IV is generally found in Asia, but has now spread to the African continent
and become the most prevalent of all the lineages [52]. The disease is transmitted
by infected aerosols in situation of close contact of animals and confinement
seems to favor outreaks. Fomites like bedding, feed and water troughs also help
in the transmission of PPR.

Clinical signs: In acute form, goats typically display an abrupt rise in temperature
to 40–41°C. Within a few days, infected animals develop oculo-nasal discharges
(Figure 19, Table 1), thirst, anorexia, depression and leukopenia [3].

Figure 19.Purulent oculo-nasal discharges.

Conjunctival mucous membranes may be congested, followed by serous and
mucopurulent exudates. Affected animal develop necrotic oral erosions that
produce a fetid smell. There is profuse diarrhea which develops within 2 to 3 days
and is accompanied by abdominal pain, tachypnea, loss of weight and severe
dehydration. There may be abortion 5 to 10 days after the onset of fever. The
incubation period is usually 4-5 days.

Diagnosis: History and clinical features give a presumptive diagnosis in endemic

regions. The virus can also be detected in acute cases from various swabs and
blood samples, using PCR and ELISA.

Treatment and prevention: PPRV infection has no specific treatment. Mortality can
be reduced by supportive care, including the administration of Antibiotics such
as chloramphenicol, penicillin, and streptomycin, inflammatory agents, as well as
nutritional support. State and federal veterinarians should be notified if PPRV is
suspected. Sheep and goats can be protected against PPR by immunization with
rinderpest vaccines or by the simultaneous administration of PPR hyper immune
bovine serum and virulent PPRV [52]. Premises should be decontaminated, and
the area quarantined. Movement restrictions can also aid in the prevention of the
disease.

e.2 Goat pox

The sheep pox virus (SPV) and goatpox virus (GPV) are serious acute, often fatal
febrile contagious viral skin diseases of sheep and goats caused by the members
of the Poxviridae, genus Capripoxvirus which is characterized by widespread skin
eruptions. They are believed to be closely related antigenically and
physicochemically, which are able to infect both sheep and goats.

Etiology and transmission: Sheep pox and goat pox is caused by the infection of
sheep pox virus (SPV) or goat pox virus (GPV), closely related members of the
genus Capripox virus in the family Poxviridae. SPV is mainly thought to affect
sheep and GPV primarily to affect goats, but some isolates can cause mild to
serious disease in both species. (CFSPH). Transmission is by direct contact, while
indirect transmission by contaminated implements, vehicles or products such as
litter or fodder. Indirect transmission by mechanical vectors like insects is also
possible. Transmission by inhalation is important. SPV and GPV are shed in saliva,
nasal and conjunctival secretions.
Clinical signs: Sheep pox and goat pox appear similar, with clinical signs that
typically include: Fever, red spots that become blisters (Figure 20, Table 1) on the
muzzle, eyelids, ears, udder or in severe cases all over the body [53]. Lesions can
develop internally causing breathing difficulties, depression, lethargy, reluctant to
feed, oculo-nasal discharges or swollen eyelids and enlarged superficial
lymphnode.

Figure 20.
Clinical manifestation of capripoxvirus.

Diagnosis:Capripoxviruses, their antigens and nucleic acids can be detected in

skin lesions (e.g. biopsies, scrapings, vesicular fluid, scabs); oral, nasal and ocular
secretions; blood; lymph node aspirates; and tissue samples from external or
internal lesions collected at necropsy PCR can identify viral RNA directly in tissue
samples, blood and secretions. Other tests to detect capripoxvirus antigens
include enzyme-linked immunosorbent assays (ELISAs), immunostaining methods
and agar gel immunodiffusion (AGID).

Treatment and prevention: There is no specific treatment for sheep pox or goat
pox, but supportive treatment may reduce morbidity and other complications.
Newly introduced animals should be quarantined. Other biosecurity measures,
such as prevention of contact with other herds and disinfection of fomites are also
helpful. Stringent cleaning and disinfection of farms and equipment, animal and
vehicle movement controls within infected areas, Vaccination may be
considered in the area where the disease is endemic.
e.3 Caprine arthritis encephalitis (CAE)
Is a viral disease of goats caused by a lentivirus called caprine arthritis encephalitis
virus, which is an enveloped, single-stranded RNA in the family Retroviridae. The
disease is found worldwide [54]. There are several genetically distinct isolates of
the virus that differ in virulence.

Etiology and transmission: Caprine arthritis encephalitis virus is an enveloped,

single-stranded RNA lentivirus in the family Retroviridae. There are several
genetically distinct isolates of the virus that differ in virulence. Cross-species
transmission is possible via feeding of colostrum or milk from infected goats.
Therefore, the ovine and caprine lentiviruses are commonly referred to as small
ruminant lentiviruses [55].

Clinical signs: the most common sign is polysynovitis-arthritis which includes joint
swelling (Figure 21, Table 1) and lameness of varying severity. There is Stiffness,
abnormal gait and posture, loss of weight and depression. In goats which develop
the neurological form of the disease, show ataxia, incoordination, hypertonia and
hyperreflexia are also common. The goat has increased difficulty standing and
eventually is unable to stand [56]. Lameness may be sudden.

Figure 21.
Joint swelling seen in CAE.

Diagnosis: Based on history and clinical manifestations. Serologic tests like agar
gel immunodiffusion test and ELISA are useful to determine herd CAEV status.
Treatment and prevention: There is no specific treatments currently exist, likewise
there is no vaccine but supportive care is indicated. To prevent spread of the
disease, infected animals are separated from non-infected goats, or culled [55].
Separating goat kids from infected goats, and feeding the kids with cow’s milk, or
pasteurized goat milk, will prevent infection [54]. Goats should also be quarantine
and tested for CAE virus before introducing to the herd.

e.4 Contagious ecthyma (orf)

Orf is one of the most widespread highly infectious viral diseases of mostly small
ruminants and sometimes other species, including wild animals. It occurs
worldwide and characterized by scabby and pustular lesions on the muzzle,
commissures of the lips and nostrils.

Etiology and transmission: is caused by Orf virus which is type species of the
genus Parapoxvirus of subfamily Chordopoxvirinae of family Poxviridae. Natural
transmission of disease occurs through direct or indirect contact with infected
animals particularly with dried crusts that falls on the pastures during grazing.

Clinical signs: The primary lesion develops on the lips, muzzle and may extend to
the mucosa of the oral cavity. Early in the infection, sores appear as blisters that
develop into crusty scabs (Figure 22, Table 1). Lesions can sometimes be found on
the feet and around the coronet, there is inappettance and loss of condition.
During the course of the disease, there is presence of a nodules with red
colorations in the center, a bluish white rings in the middle and peripheral
erythematous. The lesions may progress to form papules and extends through
vesicular and pustular stages to become encrusted. The Coalition of the
numerous discrete lesions produces a large scab that result in the proliferation of
dermal tissue that produces a verrucose mass beneath them [57].

Figure 22.
Crusty scab in Orf.
Diagnosis: is based on clinical features and histopathology of skin lesions,
transmission experiments and demonstration of a pox virus by electron
microscopy of skin biopsies of infected skin.

Treatment and prevention: Antibiotics such as penicillin, chloramphenicol and10%

Potassium permanganate solution is effective in case of lip lesions. In a situation
complicated with stomatitis or enteritis, parenteral administration of antibiotics in
conjunction with topical applications of salicylic acid ointment can give good
result. Live vaccines should be used cautiously to avoid contaminating
uninfected premises, and vaccinated animals should be separated from
unprotected ones.

F. Metabolic and nutritional diseases of goats

f.1 Peripaturient hypocalemia (milk fever)

Parturient paresis is a non-febrile metabolism disturbance of pregnant and
lactating ewes and does characterized by acute-onset of hypocalcemia, hyper
excitability, circulatory collapse, flaccid paralysis, depression, recumbency,
coma, and death.

Causes: Parturient paresis is as a result of decreased calcium intake on

circumstance of high demand for calcium particularly during late gestation. This
will result to low serum calcium concentration in pregnant animals with multiple
fetuses. As fetuses mature and their bones mineralize, they require increasing
amounts of calcium. Goats are required to mobilize stored calcium so as to
increase calcium absorption, to meet up with the requirement. Failure to meet up
with such calcium requirement especially during these periods put goats at
significantly high risk of this condition.

Clinical signs: In early hypocalcemia, the most commonly noted clinical signs are
lethargy and inappetence (Figure 23, Table 1), decreased body temperature, stiff
gait, ataxia, salivation, depressed rumen motility, mild bloat or constipation,
recumbency, weakened uterine contraction and if untreated, death.
Figure 23.
Lethargy and inappetence

Diagnosis: A working diagnosis is based on history and clinical signs. In outbreaks

occurring before parturition, pregnancy toxemia is the main differential diagnosis
[58]. Diagnosis can be confirmed by testing serum calcium concentration before
treatment. Urine ketone or serum beta-hydroxybutyrate concentrations should
always be evaluated at the same time. Tentatively, diagnosis of acute
hypocalcemia is aided by a rapid response to slow IV administration of calcium.

Treatment and prevention: Treatment is by IV administration of calcium

borogluconate 50–150 milliliters of a 23% solution, which will elicit rapid response.
Oral or subcutaneous administration of a calcium solution helps to prevent
relapse [58]. Other treatment of Calcium-containing products that also contain
phosphorus and magnesium, as well as dextrose, will have an additional
therapeutic effect. Prevention is by supplementing adequate dietary
requirement for calcium throughout gestation.

f.2 Pregnancy toxemia/ketosis

Is a metabolic often fatal disease that occurs in all parts of the world. It is most
prevalent in very fat does or does carrying multiple fetuses. This is a condition of
late pregnancy and early lactation most commonly occurring in the last month
of gestation.
Causes: is caused by in adequate nutrition or disturbance in carbohydrate or
sugar metabolism especially during last trimester of pregnancy in does. As the
pregnancy progresses, the need for energy in the body increases, at the same
time, the rumen capacity decreases as a result of fetal growth.

Clinical signs: Does with ketosis have poor appetite, lethargy and stress. They also
tend to separate from the herd, lag behind and become depressed. There is
abnormal gait and posture, apparent blindness with severe depression and
frequent urination. A classic symptom is sweet-smelling (ketotic) breath. Goats
may also grind their teeth and grunt, muscle tremors, opisthotonos, followed by
recumbency (Figure 24, Table 1), coma and death usually follows within a few
days.

Figure 24.
Goat with ketosis showing sternal recumbency.
Diagnosis: To determine pregnancy toxemia in a flock. Blood glucose monitor
should be used with a BHBA (beta-hydroxybutyrate) blood strip to test the glucose
level. Does with a reading of 0.8 mmol/L or higher can be classified positive for
pregnancy toxemia and should be treated accordingly.

Treatment and prevention: Administer a readily usable form of energy (especially

glucose) and get the doe eating on her own usually with the help of anabolic
steroids. Treatment is often ineffective if pregnancy toxemia is in advanced stages
[59]. Oral administration of propylene glycol 1o0ml/day for three consecutive
days may be helpful. Supplementation with calcium lactate may also be
suggested. Subcutaneous administration of protamine zinc insulin at 0.4 U/kg daily
may increase survival rate especially during the first half of pregnancy. Excessive
fat should be reduced and weight gains should be allowed only during the 6
weeks before kidding will reduce the incidence of ketosis. Give high-quality
forages in addition to supplements that are very palatable during the last 2
months of pregnancy. This allows does to receive adequate energy even though
rumen volume is decreased.

f.3 Lactic acidosis (grain overload)

Is a carbohydrate fermentation disorder of the rumen that usually affect goats of
all breeds and ages, as a result of feeding with large amount of highly
fermentable concentrates, underfeeding of effective fiber and poor
management practices.

Causes: occurs in goats that have been fed predominantly forage but abruptly
introduced to a large of amount of readily digestible carbohydrates especially
grain. It can be caused by abnormal feeding of an effective fiber and poor
management practices.

Clinical signs: In acute acidosis, there will be sudden death. Other signs include
an increased pulse and respiratory rates, decreased rumen motility, mild bloat,
staggering, abnormal posture (Figure 25, Table 1) and even coma [60]. Subacute
acidosis is difficult to recognize but occurs more frequently. Loss of appetite,
panting, diarrhea, dehydration, lack of rumination and signs of discomfort may
be noticed.

Figure 25.
Goat with grain overload.
Diagnosis: The diagnosis is obviously based on history and clinical findings. It can
also be confirmed by, a low rumen fluid pH (less than 5.5), and the absence of
live protozoa when rumen fluid is examined under the microscope.

Treatment and prevention: Treatment usually includes drenching with a solution of

sodium bicarbonate, Magnessium sulphate, administration of an antibiotic to
suppress the lactic acid-producing bacteria and a change in feeding practices.
Prevention involves slowly introducing concentrate feeds to allow the adaptation
of rumen microflora. Provision of a properly balanced diet and proper feed
management practices.

Conclusion
Animal diseases are global challenges that are considered as a major
impediment to livestock especially goat production. To establish an early warning
and proper implementation of strategic preventive measures in a country prone
to disease affliction, focus should be made on identifying principal epizootic
diseases that have a strong impact on the public health, social and economic
significance. This work clearly identified the commonest diseases ravaging goats
from infectious: bacteria, fungal, parasitic, protozoa, rickettsia and viral, to non-
infectious: metabolic disturbance/nutritional disorders and spells out the
treatment regimen and the preventive measures that will remedy the
predicament in goat production. It behooves on government, veterinarian, para-
veterinarians and practioners to co-opt this idea and move forward to design a
novel innovative policies and ideas that will help in the prevention, control and
eradication of the diseases.

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