Diagnosis & Treatment of Different Diseases in Sheep & Goat 

India is blessed with the most fabulous livestock wealth in the world. Animal husbandry and livestock production is the backbone of the Indian agriculture and plays an important role in the rural economy by providing employments, livelihood and food security to the rural population.

Sheep and goat are the most important livestock in arid, semi-arid and mountainous regions where crop and dairy farming are not economically feasible. These are the principal livestock contributing to the livelihood of a 70- 80% of small & marginal farmers and landless labourers. (Acharya, 1982 : Kurup, 2004). About 13.8% & 27.8% of the total livestock contributed by Sheep & Goat. (DAHD, 2019). The goat population, i.e. 148.88 million showing an increase of 10.1 per cent over the previous census. The total number of sheep in the country is 74.26 million in 2019, an increase of 14.1 per cent over the previous census.

According to 20^th livestock census, 2019

Animals ( category)	Population (in millions) 2012	Population (in millions) 2019	% Growth
Cattle	190.90	192.49	0.83
Buffalo	108.70	109.85	1.06
Sheep	65.07	74.26	14.13
Goats	135.17	148.88	10.14
Pigs	10.29	9.06	-12.03
Poultry	729.2	851.81	16.80

(Department of Animal Husbandry and Dairying, 2019)

About Goats and Sheep:

 Goats and sheep are small ruminants, herbivorous animals. Goats and sheep will graze grass and browse forbs (weeds and wild flowers) and brush closer than other herbivores and thus require more intense grazing management. Goats tend to browse vegetation of higher quality than do cattle.

Sheep are fairly selective feeders, preferring grasses/pastures and forbs; goats, on the other hand, are mainly browsers, preferring shrubs and forbs.

Goats and sheep “sort” grain mixes, selectively choosing preferred ingredients, and therefore should be fed pelletized or textured feeds. Goats like to eat with their heads up and will select portions with higher nutrient content. Goat and sheep husbandry play an important role in rural economy.

Both the animals have been popularly described as Mortgage lifters of India.

The practice of clinical veterinary medicine consists of two major facets: the making of a diagnosis and the provision of treatment and control measures.

For treatment and control to be of optimum value the diagnosis must be as accurate as possible; thus, the diagnosis is the crux of all medical problems.

A diagnosis is the identification of the disease affecting the animal, and to be complete should include three parts:

1. Identification of the clinical manifestation of that abnormality produced by the causative agent– classification of the animal’s illness
2. Abnormality of structure or function (the disease) produced by the causative agent
3. The above two then usually allow identification of the specific cause of the illness.

The illness should be classified as precisely as possible and should, ideally, include the animal species (and if possible more detail), the causative agent, and the predominant body system affected.

Physical Examination of animal: On the basis of Appearance, Behaviour, Physical condition, Skin coat, Posture, Gait, Any discharges

Posture: Abnormal posture is not necessarily indicative of disease, but when associated with other signs it may indicate the site and severity of a disease process. Sheep that are blind, as in early pregnancy toxemia are immobile are stand with the head up and have an expression of extreme alertness. When the animal is recumbent there also may be abnormalities of posture.

Posture is typically elevated with the animal at rest in a comfortable position and unrestrained.

Examination of all body parts like head, neck, thorax, abdomen, limb, tail, joints, tendon, ligaments etc, should be made to elicit the structural abnormalities concerning the posture.

Dorsal bending of spinal column- Kyphosis Ventral bending – Lordosis

Lateral bending – Scoliosis from standpoint of posture.

Spotting of sick animals

Sl. no.	Parameter	Healthy animal		Sick animal
		Sheep	Goat
1.	Look of animal	Alert		Dull
2.	Head	Raised		Bent downwards
3.	Eyes	Wide open, bright		Dull with white deposition at the corners
4.	Conjunctival m.m.	Normal		Pale or congested
5.	Nose	No discharge		Slimy discharge
6.	Movement	Active		Sluggish, lameness
7.	Response	Quick		Slow
8.	Feces	Normal		Hard / loose, mucus/blood-stained, discolouration, dysentry
9.	Pulse (/min)	70-90	70-90	Increased
10.	Body temperature ( o F)	102.4	103.8	Increased
11.	Respiration (/min)	12-30	12-30	Increased, difficult
12.	Grazing	Normal		Abnormal
13.	Rumination	Regular		Irregular
14.	Feed and water intake	Normal		Reduced
15.	Udder	Normal		May be swollen
16.	Skin	Healthy		Infected, external parasites

Posture based diseases in Sheep & Goat

1. Pregnancy Toxaemia

 This disease is also known as: Lambing paralysis, Twin lamb disease, Twining kid diseases, Twinning Disease, Pregnancy ketosis, Sleepy sickness, Ante partum paralysis. This is a highly fatal metabolic disease.

Causes: Common disease of ewes in the last 6 weeks of pregnancy and immediately after lambing. During late pregnancy, the ewe has a very high energy requirement to provide for her own needs and the growth of the lamb or lambs she is carrying. If the energy requirement is not met by feed intake, the ewe will break down her own body tissues. Negative energy balance & females carrying multiple foetuses are more prone. If the rate at which the ewe breaks down her tissues is too rapid, toxic wastes from the breakdown process accumulate and pregnancy toxaemia occurs.

Symptoms: The initial signs are dullness and loss of appetite and affected sheep lagging behind the mob when driven. Later the ewe will stand alone, appear dopey and will not move when approached. If driven the ewe will appear blind, stumble and go down. A goat and sheep may adopt a posture keeping the head in elevated direction with erect ears as if listening higher sound. Star -gazing posture may be noted. The ewe will eventually sink into a coma and die within 5-7 days.

Diagnosis: Based on history of pregnancy, inadequate amount of grain feeding.

Detection of ketone bodies in urine and blood glucose below 25 mg/dl.

Differential Diagnosis: Milk fever and louping ill.

On post mortem, the liver is generally tan to yellow in colour and is quite soft and there is often plenty of fat on the carcass.

Treatment: Trenbolone acetate 30 mg once daily through I/M route can be improve appetite.

Mild cases: treated with hand feeding of grains and administrating oral propylene glycol (60 ml) orally twice a day.

Severe cases: 200 ml of 5% Dextrose through I/V route along with 40 IU of insulin SC.

Animals with recumbency should be treated with antibiotics, 25 mg dexamethasone, 3 litre 5% Dextrose with bicarbonate.

Advanced cases; may require an emergency caesarean section (administering 15-20 mg of dexamethasone I/V).

Prevention-Ewes and does should be placed under such diets so that they do not become over fat.Minimum change of feeds should be made during advanced pregnancy.Concentrate feeding @ 0.25 kg/d/head (10% protein) – last 2 wks. Care should be taken to avoid over stress and fasting during late gestation.Vitamin A rich feed during gestation period. Deworming should be done induction of pregnancy. Adequate water should be provided to the animal. Animal should be kept away from sun and hot.

2.  Milk fever 

Also known as: Parturient hypocalcaemia, Parturient apoplexy, Parturient paresis.

Causes:

 Disturbance of metabolism: decrease se in calcium intake under conditions of increased calcium requirements (late gestation). Low serum calcium concentration.

Ewes: in late pregnancy with multiple fetuses and lactating ewes (early lactation).

Young sheep – up to one year old and goat may also suffer.

Symptoms: By acute-onset hypocalcemia and rapid development of hyperexcitability and ataxia, progressing to depression, recumbency, coma, and death. When recumbent, does are in a sternal frog-lying position, with the hind legs extended behind. Goat muscle tremors are more commonly seen than in sheep.

Diagnosis: is based on the history and clinical signs.

Differential diagnosis: Pregnancy toxemia in ewes and does.

Treatment: initiated immediately, usually administered as calcium borogluconate I/V (50–150 ml of a 23% solution). Calcium- containing products that also contain phosphorus and magnesium, as well as dextrose, likely have additional therapeutic value.

Oral or SC administration of a calcium solution helps to prevent relapse.

During treatment, the heart should be monitored, and therapy slowed or stopped if arrhythmias occur.

Prevention:

 Avoid physical stresses on sheep & goat in the last month of pregnancy.

Avoid grazing late pregnant or lactating ewes on lush pasture or cereal crops.

Keep calcium and magnesium solution on hand while handling pregnant or lactating ewes.

Supply a mix of 2 parts stock salt to 1 part stock lime next to the drinking water source for the mob during the last two weeks of pregnancy and early lactation.

3.  White Muscle Disease

 Also known as: Stiff Lamb Disease, Nutritional Muscular Dystrophy

Causes: deficiency of selenium and/or vitamin

Selenium and vitamin E also play key roles in the animal’s normal immune response. Suboptimal levels of these nutrients impair the animal’s ability to control oxidative reactions in the cells, which can result in extensive muscles necrosis.

WMD is most commonly found in newborns or fast growing animals (3 days to 6 month of age). Skeletal muscles, cardiac muscles and diaphragm are affected.

Symptoms: mild stiffness to obvious pain upon walking, to an inability to stand.

Abnormal posture with abducted front leg and scapulae protruding over the line of withers.

When the disease affects the heart, the animal shows signs similar to pneumonia, including difficult breathing, a frothy nasal discharge (may be blood stained), and fever. The heart and respiratory rates are elevated and often irregular. Death may occur as a result of the effects of myopathy.

Diagnosis: history and clinical signs & laboratory finding

Differential diagnosis: Enterotoxemia

Treatment: Parenteral administration of combination of sodium selenite /alpha- tocopherol preparation- treatment of choice in acute phase of NMD.

If animal not respond in 24 hrs- retreated again. The concentrations of selenium (per ml) vary greatly with each product, and excessive or repeated injections of selenium can result in selenium toxicity and possibly death.

Prevention:

 Deficiencies occur when animals are fed poor- quality hay or straw or lack access to pasture.Feed supplementation with Se is a desirable approach to control.

4.  Polioencephalomalacia

 Also known as: Cerebrocortical necrosis

 Caused by: deficiency of Thiamine

In goat: disease is occurs due to under intensive management condition, fed more grain concentrate feed.

PEM: Softening of the gray matter of the cerebral cortex , also known as cortical necrosis.

PEM caused by imbalance of the production or destruction of thiamine.

Symptoms:           Excitability, uncoordinated staggering or the appearance of being drunk (ataxia), possible diarrhea, and muscle tremors & expression of neurological abnormalities.

Acute neurological dysfunction; excitability elevation of head (Opistotonos) while standing staring off into space (Stargazing posture), aim less wondering, circling, ataxia.

Treatment: Thiamine is treatment of choice

Dose: 10 mg/kg bwt. Repeated every six hours for 24 hours

Prevention : Increased roughages feeding.

Avoidance of moldy feeds. In herd : supplementation of the grain ration with thiamine mononitrate. Maximum tolerable dietary sulphur level for ruminants is 0.5% when the diet contain at least 40 % forage. ( NRC 2005).

5.  Enterotoxemia

 Also known as: Pulpy Kidney Disease, Over eating disease

Frequently severe disease of sheep and goats of all ages.

Causes: Caused by two strains of bacteria called Clostridium perfringens –strains are termed types C and D. Bacteria : normally found in low numbers in the GIT of all sheep and goats.

Clinical signs: Animals may abruptly go off of feed and become lethargic.

Affected animals may show signs of stomach pain, such as kicking at their belly, repeatedly laying down and getting up, laying on their sides, panting, and crying out. Diarrhea may develop; in some cases, there is blood visible in the loose stool.Animals may lose the ability to stand, lay on their sides, and extend their legs, with their head and neck extended back over their withers.

This posture is caused by the effects of the toxins on the brain.

Death commonly occurs within minutes to hours after this sign is seen.

Treatment:

 Severe cases- may not be successful. Death is usually sudden. Mild cases with analgesics, probiotics, antibiotics, anti-toxin, oral electrolyte solutions.

Prevention:

 Vaccination of females (in late gestation) and offspring and good feeding management.

6.  Enzootic ataxia

 Also known as:  Swayback

 Causes: Disease occurs due to Copper deficiency in lambs and kid goats.

Swayback refers : congenital form of the disease

Enzootic ataxia: if it is develops after birth.

Ewe: 2nd half of pregnancy leads to abnormal maturation & subsequent degeneration of neurons and myelin in the developing foetus and lamb   postnatally.   Lesions   occur   in the cerebrum, brainstem & spinal cord in the congenital form. Only in the brainstem and spinal cord in cases with a postnatal onset. Kids may be unable to rise or may walk with severe in coordination. Symmetrical paresis and ataxia are usually observed first in hind limb. Periodic spasmodic contractions of hind limb & overstretching of the tarsal joints. Affected kids may adopt a straddle-legged posture and collapse from weakness after standing a few minutes.

Diagnosis:           Determined by physical examination, laboratory tests, necropsy lesions, and review of local copper status.

Treatment: Copper glycinate, parenterally to kids as an single total dose of 60 mg (Seaman & Hartley, 1981).

Prevention:

 Cu & MO ratio in the overall diet should be kept between 5:1 to 10.( Rankins et.al., 2002).

Oral copper sulphate in drinking water @ 1.5 g/head/week during pregnancy.

7.  GID

 Also known as: Coenurus cerebralis , Sturdy, Staggers.

Metacestodal infection of ungulates, esp. sheep & goat.

Caused: by Coenurus cerebralis which is the larval stage of Taenia multiceps. It primarily causes a focal encephalopathy. In goat, metacestode development occurs primarily in the CNS, also in skeletal musculature and the heart as well.

Clinical signs: neurological form of disease may show a variety of signs. Infected animals developed nervous signs in the head tilt, unilateral blindness, circling, loss of balance. Goat may hold its head in upward directions as if looking at the sky (star -gazing posture).

Some animals show forward walking with the head held high and a hypermetric gait followed by head pressing against obstacles instead of circling, grinding of teeth.

Diagnosis: based on clinical findings.

Differential diagnosis: PEM, Listeriosis, CAE, cerebral hematoma, rabies.

Treatment:

 No known, consistently effective anthelmentics therapies for elimination of the metacestode in clinically affected animals. ( Sharma and Chauhan, 2006)

PRAZIQUANTEL @ 100 mg/kg orally , more reliable effective (Verster and Tustin 1990).

Surgical removal of cyst from infected area.

Control: Reducing stray dog population, restricting the feeding of small ruminant’s carcasses and offal to dogs & ensuring strict, regular treatment of dogs kept with livestock for control of mature tapeworms.

8. Caprine Arthritis Encephalitis (CAE):

First recognized in the early 1970s, CAE has emerged as a significant and costly disease of

Causes: Infected with lentivirus genus of the family retroviridae. Arthritis is most clinical presentation in animals. Caprine arthritis and encephalitis (CAE) virus infection is manifested clinically as poly synovitis-arthritis in adult goats and less commonly as progressive paresis (leukoencephalomyelitis) in kids. CAE virus can be transmitted vertically and horizontally.

Vertical transmission: Dam to kid via virus contaminated colostrum and milk.

Horizontal transmission: direct or close contact with infected animals.

Symptoms: Carpal joints are most frequently involved. Progressive weight loss can occur as the sole clinical manifestation of CAE virus infection. A kid or lamb unable to extend the knee due to swelling of the carpal joint.

Permanent kneeling due to ankylosis of the carpi in a goat with advanced CAE arthritis

Diagnosis: based on history, clinical signs, Postmortem examination

Treatment: No specific treatments for any of the clinical syndromes associated with CAE virus infection.

Mild cases: providing regular, correct hoof trimming, provinding easily accessible feed and water. Use of additional comfortable bedding, Administration of NSAIDs such as phenylbutazone or aspirin.

Control:

 At farm level: 3 main areas. To raise CAE free kids by implementing kid rearing technique.

Culling or separating diseased and seropositive animals from healthy seronegative animals. Periodic serological testing of the herd.

9.  Tetanus

 Well known Clostridial disease of humans and animals.

Causative agents: Clostridium tetani

 In goat via-disbudding, dehorning, castration, tattoing, hoof trimming, puncture wound etc.Goats maintained in barns currently or previously used for horse may be increased risk of disease.

Clinical signs: early sign include anxious expression, stiff gait and mild bloat. One week- old kid within four days of disbudding- main clinical sign. Adult doe- several months after dystocia. Affected goat adopt a characteristic base-wide, or “sawhorse” stance and ears and tail become stiff. Reluctance to move and difficulty opining in mouth. Over a time goat become permanent recumbent with rigid extension of all limbs and opisthotonos.

 Diagnosis: clinical findings

Treatment: systemic penicillin inhibits additional bacterial proliferation and toxin release.

Supportive care

Control:

Prevented by a combination of improved hygiene and immune-prophylaxis.

All wound should be cleaned promplty and thoroughly.

Disbudding, castration should be accompanied by injection of 150-250 units of antitoxin.

Adults -500-750 units of antitoxin dystocia & wound treating. Routine vaccination –herd health program.

10. Rickets:

Rickets is skeletal disorder of young, growing animal, characterized by decreased concentration of calcium and phosphorus in the organic matrices of cartilage and bone.Present in young, growing animals.

Causes: Absolute deficiency of vitamin D and phosphorus.

Chronic cases- either calcium or P in the face of adequate vitamin D.

Clinical findings:

 Stiff gait, a tendency to remain recumbent, a bowing deformity of the forelimbs, swollen

carpi, enlargement of costo-chondral junctions, a lesion known as rachitic rosary.

Bowing deformity of the forelimb due to carpal epiphysitis associated with excessive calcium feeding.Bowing deformity of the forelimb due to carpal epiphysitis associated with excessive calcium feeding.

Loosening of the shoulder blade attachments and dropped withers have been identified.

Diagnosis: History, clinical signs, laboratory findings, radio graphical finding.

Treatment: all lambs and ewes are treated with a parenteral supplement of vitamin D3.

Prevention:

 

Examination of housing and access to sunlight (Increase production of vitamin D3 Precursors). Nutrient analysis of ration. Supplementation of vitamin D during gestation period so new born can receive enough vitamin D from their Dams to prevent early rickets if the ewes have adequate vitamin D status.

11. Foot rot

 Also known as: foot scald, Interdigital dermatitis, benign foot rot.

Caused by: Dichelobacter nodosus, fusobacterium necrophorum

Foot scald, foot abscesses are most common in temperate regions occurs in the spring and early summer in association with warm temperature& heavy rain fall.

Clinical finding: Mild lameness in foot scald. Swelling of the interdigital epidermis.

In foot rot, lameness can be quite pronounced when there is necrotic under running of the horn. Severely affected animal may walk on their carpi.

Swelling of inter digital epidermis & separation of hoof at the skin –horn junction.

Diagnosis: Clinical signs are highly suggestive diagnosis of the disease. The disease can be confirmed by demonstration of B. nodosus in pus smears and scrapings taken from the edge of the lesions. The smears can be stained by Gram’s method or by dilute carol fuchsin. The bacteria stain faintly by Gram’s method but in carol fuchsin, they appear as large Gram- negative rods with terminal enlargement at one or both ends.

Footrot should be differentiated from other causes of lameness such as traumatic injury, necrobacillosis, dermatophilosis (strawberry footrot), bluetongue, parasitic dermatitis, arthritis, foot and mouth disease and vesicular stomatitis.

Treatment and Control:

 A single heavy dose of penicillin-streptomycin (containing 70,000 IU penicillin and 70 mg/kg streptomycin) given intramuscularly can be effective in the treatment of the disease.

A follow-up treatment may be required if the response after the initial injection is not satisfactory.

Chloramphenicol, tetracycline, erythromycin, tylosin, clindamycin, nitrofurazole parenteral and topical preparations can also be used in the treatment of the disease.

Regular hoof trimming is recommended and has been found to facilitate recovery of the treated animals.

Control is based on the prevention of the spread of the bacteria, maintaining good hygienic conditions in the herds and minimisation of predisposing factors.

Foot-baths containing 5 % copper sulphate, 10

% zinc sulphate and 5 – 10 % formalin are used in intensive production systems.

12. Bloat

 Bloat is over distension of the rumen- reticulum with gases of fermentation. When the animal grazes on lush young pasture, particularly if the pasture is wet. Some plants,

e.g. clover, lucerne and alfalfa are especially dangerous in causing bloat.

Choking due to foreign objects (esophageal obstruction) will also cause bloat by preventing gas release and causing accumulation of gas in the rumen.

Types (on basis of forms of gas): Primary or frothy bloat/nutritional Secondary or free-gas bloat

Symptoms: In all types of bloat abdominal distension is initially most prominent in the left para lumber fossa and may also involve

the entire left side of abdomen and the right ventral abdomen if severe.

Many cases of bloat are first recognized by finding animals dead at pasture.

Diagnosis: easily confirmed by physical examination.

The difficulty in the diagnosis of bloat comes when animals are found dead.

Treatment:

 Oil of turpentine is a common home remedy.Poloxalene (surfactant) @ of 100 mg/kg b.wt.

Trocharization of the rumen through the left paralumber fossa can be lifesaving in goats in the terminal stages of bloat.Goats/Sheep trocharized for relief of bloat should be placed on a 3-5 days course of broad- spectrum antibiotic therapy after the procedure.

Preventive measures:

 When goat/sheep are fed grains, Conc. mixture should not be too finely ground and should not be abruptly introduced into the ration.

Daily drenching of individual animals with oil before turn out.

Feeding the ionophores monensin or lasalocid to the animal.

Pature management: Sowing of grasses with legume. Using forage type high in condensed tannin. Strip grazing. Swathing and wilting Alfalfa for twenty-four hours before turning animals out onto pasture. (Radostitis et.al.2007)

Blue tongue (BT)

• This is acute infectious but not contagious disease of sheep characterized by fever, inflammation and ulceration of buccal mucosa and tongue.
• This disease mostly affects sheep and goat and cattle are very rarely affected.
• Blue tongue is endemic in India.
• It is basically a disease of sheep and young sheep within the age group of one year are more prone to infection.
• Suckling lambs are relatively resistant due to their acquired passive immunity through colostrum.
• The disease occurs mainly during the rainy season particularly in the months of October, November and December.

Causes

• It is caused by Arthropod-borne orbi virus in the family of Reoviridae.
• Biting insect of the genus of the Culicoides transmits the virus during the rainy season while blood sucking.
• Mosquitoes and other ectoparasites like sheep ked, Melophagus ovinusmay transmit the disease mechanically.
• The disease is more prevalent in late summer and early autumn which makes conducive environment for the multiplication of the vectors.
• Transmission through semen and placental route is possible.
• The virus is resistant to decomposition, desiccation and against antiseptic agents.

Clinical symptoms

• Fever
• Depressed attitude and off feed.
• Reddening and swelling of nose and oral mucosa,
• Profuse nasal and oral discharge,
• Inflammation and ulceration of lips, gums,  buccal mucosa and tongue,
• Cyanotic (bluish) appearance of tongue,
• Tilting of neck towards one side (wry neck)
• Lameness, reddening and swelling of coronary band of the limbs.
• Congestion of conjunctival mucous membranes and matting of eyelids,
• Foul smelling diarrhoea.
• Dyspnoea, snoring and Pneumonia may be observed.
• Death due to respiratory failure.

Suggested first aid

• Separation of sick animals should be made.
• Affected animals should be kept away from solar exposure.
• Adequate rest to the affected animal.
• Affected animals should be fed with porridge made of rice, ragi and kambu.
• Apply glycerin or animal fat on the ulcers.
• Immediate consultation should be made to the nearest qualified veterinary doctor for treatment.
• Animals should not be allowed for grazing.
• Ulcers in the mouth can be treated with saline water or dissolve 1g of

Potassium permanganate in 1 liter of water and wash the mouth 2 to 3 times a day with this solution.

• Contact your nearest Veterinary Assistant Surgeons for further advice regarding the antibiotic administration or symptomatic treatment to be given to the affected sheep.
• Contact nearest Veterinary Assistant Surgeons for ring vaccination in the event of outbreak of disease.

General prevention and control measures

• Proper Vaccination of animals with regular intervals.
• Vaccination schedule:

First  vaccination at	Next vaccination at	Month of vaccination	Dose
3 months of age	Once in a year

• Attempt should be made to control the vector (culicoides) population with fly repellants.
• Use of ectoparasiticides injections should be suggested in the areas more prone to vector population.
• Grazing of the animals should be avoided in areas where there is lot of vectors.
• Cattle may act as carrier. Viraemic stage remains in them for more than 5 weeks. So movements of cattle should be restricted.
• Importation of animals from the areas prevailing the disease should be avoided.
• Strict regulation is to be followed to prevent entry of diseased animals from endemic zones.
• The spread of the disease can be controlled by the use of insect repellents, external application of fly repellents and spraying of butox (1ml in 1 liter of water) in the breeding places of the insects.
• The sheep can be housed in insect proof sheds.
• Cloud of smoke with dried leaves / wood during 6 – 8 P.M. might help to keep off Culicoides from sheep sheds.

Peste-des-Petits Ruminants (PPR)

• It is an acute highly contagious viral disease of small ruminants characterized by fever, loss of appetite, stomatitis, gastroenteritis and pneumonitis.
• The disease is markedly evident in goat and sheep are less susceptible.

Causes

• The disease is caused by Moribillivirus of Paramyxoviridae family.
• Natural transmission occurs primarily through direct contact with infected sheep and goat.
• Transmission may take place through contaminated food, water, beddings and other appliances.
• Secretions and excretions are rich source of virus and spread of the disease take place through their contamination. Faeces are the main spreading agent and through it the disease may occur in epidemic proportion.
• The disease may spread in a flock through introduction of newly purchased sick animal from market.
• There is no carrier state in animals; the spread of the disease is possible through animals with subclinical infection.
• Ingestion of infected material is the main way of transmission but it may also take place through inhalation and contact with ocular secretions.
• The disease is not transmitted through insect vectors.
• Wild ruminants have been suspected to play a role in the spreading of this disease.

Clinical symptoms

• High rise of temperature (104 to 105 ˙F).
• The animal will show dull coat, dry muzzle and inappetance.
• There will be profuse serous nasal discharge accompanied by sneezing and coughing.
• The discharge may be crust like, hard and matt the nasal and ocular surroundings.
• Oral necrotic lesions noticed in lips, buccal mucosae, gums, dental palate & tongue, with malodour (halitosis).
• Congestion of conjunctival mucous membranes and matting of eye lids.
• Signs of pneumonia and animal may die due to respiratory distress.
• Diarrhoeic faeces may contain mucus and blood.
• Pregnant goat may abort.
• Most of the animals recover and death may occur in few of them.

Suggested first aid

• Separation of sick animals should be made.
• Adequate rest to the affected animal.
• Affected animals should be fed with porridge made of rice, ragi and kambu.
• Apply glycerin or animal fat on the ulcers.
• Immediate consultation should be made to the nearest qualified veterinary      doctor for antibiotic treatment.
• Animals should not be allowed for grazing.
• Ulcers in the mouth can be treated with saline water or dissolve 1g of Potassium permanganate in 1 liter of water and wash the mouth 2 to 3 times per day with this solution.
• Contact your nearest Veterinary Assistant Surgeons for further advice regarding the antibiotic administration or symptomatic treatment to be given to the affected animals.
• Contact nearest Veterinary Assistant Surgeons for ring vaccination in the event of outbreak of disease.

General control and prevention management

• Regular and proper vaccination of animals.
• Vaccination Schedule

First  vaccination at	Next vaccination at	Month of vaccination	Dose
3 months age	Once in a year

• Strict sanitation and hygienic measures are to be adopted in a flock. It is susceptible to most disinfectants, e.g. phenol, sodium hydroxide (2%).
• Restriction should be made for introduction of new animals in a flock especially in areas where the disease is prevalent.
• Sick animals bought from market should not be introduced without observation for a definite period.
• Sick animals should be segregated and treated with serum along with conservative management.
• Quarantine measures should be strictly attended in imported sheep and goat before introduction.

 Sheep pox

 

• • It is an acute to chronic viral disease of sheep and goats characterized by generalized pox lesions throughout the skin and mucous membranes.
  • All breeds of sheep and goats irrespective of age and sex are affected.
  • It is possible to infect goats with sheep pox virus and sheep with goat pox virus.
  • Sheep are naturally susceptible to sheep pox. Younger sheep are more susceptible over old ones.
  • Disease occurrence period is April- June.

Causes

• • It is caused by a member of the genus Capri pox virus, pox viridae family.
  • Cutaneous lesions (crust, nodules) resulting in aerosols, saliva, faeces, nasal secretions from sick animals for 1-2 months and dried scabs at ambient temperature may be the source for spread of virus.
  • Susceptible to highly alkaline or acid PH and virus remains viable for as long as six months.
  • Virus susceptible to 56˙c for 2 hrs and 65˙c for 30 minutes.
  • The usual mode of transmission is from direct contact with the infected animal.
  • Indirect transmission by contaminated litter, fodder, water and attendants may spread the virus through mechanical ways.
  • The virus may gain entrance through wound and abrasions.
  • The virus may present in skin papules. While the affected animals rub their body on other animals, the virus is passed directly to susceptible animals.
  • The biting insects (mechanical vectors) may inoculate the virus intradermaly or subcutaneously.
  • Aerosol or droplet infection is quite possible.
  • Dog, cat etc. may mechanically transport the virus to other places.
  • The virus may pass from infected mother to the foetus through placenta.

Clinical symptoms

• • Skin papules appear in 2-5 days following temperature and first appear on the hairless parts of the skin.
  • Soon after development of papules rhinitis, conjunctivitis may be observed.
  • Papules like pock lesions appear in all the parts of the body, e.g., lips, cheeks, snout, nostril, face, ear, feet, thigh, abdomen, eye lid, neck, teat and udder.
  • The eyelids are swollen and they may completely cover the eye ball.
  • Mucopurulent discharges from eyes and nose.
  • Animals become weak, disoriented and eventually unable to stand.
  • The mucous membrane of the eyes, nose, lips, vulva and prepuce become necrotic.
  • Animals die due to the development of labored breathing as a result of broncho-pneumonia.
  • Animals that survive develop scab and shed over a period of 3-6 weeks, leaving a raw granulating area.

Suggested first aid

• • Isolation of infected herds and sick animals for at least 45 days after recovery.
  • Use of disinfectants like ether (20%), chloroform and formalin (1%), phenol (2%) to prevent the transmission of disease.
  • Strict sanitary measures are to be adopted.
  • Contact nearest Veterinary Assistant Surgeon for further treatment.

General control and preventive measures

• • Regular vaccination of animals.
  • Vaccine availability: IVPM, Ranipet, Vellore District, Tamilnadu – Sheep pox vaccine – Sheep thyroid attenuated live tissue culture vaccine – Available in 50 ml and 100 ml vials @ 60 paise per dose should be administered sub-cutaneously with the following vaccination schedule,
  • Recommended vaccination schedule:

First  vaccination at	Next vaccination at	Month of vaccination	Dose
3months of age	Yearly once	Feb-March	Adult – 5 ml S/c Kids – 2.5 ml S/c

• • Isolation of infected herds and sick animals for at least 45 days after recovery.
  • Quarantine before introduction into herds.
  • Use of disinfectants like ether (20%), chloroform and formalin (1%), phenol (2%) to prevent the transmission of disease.
  • Animal traffic from the infected areas is to be prevented.
  • Proper disposal of cadavers and products.
  • Strict sanitary measures are to be adopted.

Tetanus

 

• • It is a non-contagious, infectious disease of mammals caused by bacterial toxin characterized by spasmodic
    contraction of skeletal muscles.
  • Sheep and goat are more susceptible than cattle.

Causes

• • The disease is caused by bacteria known as Clostridium tetani which is remain in the intestine of the herbivorous animals as normal habitat.
  • The organism can be grown under strict anaerobic condition.
  • The spores are very much resistant and can persist in the soil even for years. The spores can be destroyed by boiling
    at 115˙C for 30 to 60 minutes.
  • Vegetative forms can be destroyed by heat and disinfectants but spores are highly resistant to many physical,
    chemical agents and common disinfectants.
  • Cl. Tetani spores require anaerobic conditions at the wound site for germination and liberate potent toxins.
  • Spores may continue to persist as dormant manner in tissues for many months until favourable conditions develop
    for their germination.
  • The organisms are very much resistant and therefore remain in the environment especially in the street dust,
    garden soil and animal manured soil in large number for a considerable period.
  • Organisms may continue to live in the faeces for a long period of time and thus remain as a potential source of
    infection to man and animals.
  • The organisms gain entrance through deep punctured wound contaminated with bacterial spores. Trauma and damage of the tissues caused by injection, dog bites, vaccination or chemical agents such as calcium salt, lactic acid
    or by infection with other bacteria may help in the initiation of the disease process.
  • Organisms may gain access during parturition and manual handling of the genitalia with contaminants, retention
    of placenta and prolapse, castration by open method, shearing, docking and vaccination may augment the transmission if, not attended properly.
  • Neo-natal animals may get the infection through contaminated umbilicus.
  • Deep wound in the feet during grazing, ploughing or transport, wound of oral mucosa, dental caries, wound due to surgical interference, wounds by a penetrating object e.g. nail etc. and contaminated by dirt may influence the
    disease transmission.

Clinical symptoms

• • Stiff gait and apathy to feed is the initial sign of the disease.
  • The initial signs consist of restricted movement, muscular stiffness and difficulty in walk, lack of coordination,
    unusual walking.
  • Stiffness of muscles of the limbs with extended back and neck arched, reporting sudden death.
  • Stiff gait spasm of mouth muscles results mouth become held tight, difficult to separate the jaws, ”lock-jaw”
    condition.
  •  Prolapse of the third eye lid, head drawn on one side or back ward, pump handle position of the tail, erection of the
    ears, immobility of the ears and characteristic “saw horse stance” are the features.
  • The rigidity of the facial muscles gives an anxious expression.
  • There is restriction of mastication and dribbling of saliva from the mouth.
  • Suppression of rumination and bloat are the important attributes.
  • Animal remains hypersensitive and over reaction to sudden noise or physical contact and reflex irritability is noted from the start of symptom.
  • Death usually occurs in 3-4 days.

General control and preventive measures

• • Proper vaccination at day old should be used. Giving two doses of vaccine at least four weeks apart. An annual
    booster dose is recommended.
  • Tetanus toxoid vaccines at the times of exposure of body tissues to environment prevent the disease occurrence.
  • Providing passive immunity to the lambs by giving ewes a booster vaccination, a few weeks before lambing commences.
  • Care of any local wound and make sure the wound is not contaminated by dirt.
  • Cleanliness and proper hygienic measures are to be adopted at the time of parturition and following parturition.
  • The animal should not be allowed to graze near barbed wire fencing.
  • Yards should be watered to decrease dust.
  • Open method of castration should be discouraged in the village level.
  • Proper care should be taken to handle the retention of placenta and prolapsed cases.
  • Sterile surgical instruments are to be used at the time of operation.
  • Wound should be drained with deep incision. The animal should be kept away from metallic and sharp objects.
  • Hygiene is essential while undertaking any husbandry or surgical procedure.
  • All out precautions should be taken during castration.

 

Orf

• Clinical symptoms
  • Appearance of nodular eruptions on the oral commisures, lips, mouth and nostrils and the lesions are followed by papules, vesicles, pustules and ulcers in 3 to 4 days.
  • Extensive lesions on the feet lead to lameness.
  • Mastitis may result in ewes with lesions on the udder.
  • Profuse salivation, lacrymation accompanied by nasal discharge.
  • Ewes nursing infected lambs may develop lesions on the udder.
  • In young lambs, the initial lesion may develop on the gum below the incisor teeth.

Suggested first aid

• • Affected animal should be segregated from the rest of the flock.
  • Strict hygienic and sanitary measures are to be adopted.
  • Contact nearest Veterinary Assistant Surgeon for treatment.

General control and preventive measures

• • Lambs should be vaccinated when one month old.
  • For better results, a second vaccination 2-3 months later is suggested.
  • Vaccines should be used cautiously to avoid contaminating uninfected premises and vaccinated animals should be segregated from unprotected stock until the scabs have fallen off.
  • Strict hygienic and sanitary measures are to be adopted.
  • Non immunized lambs should be vaccinated before entering infected feedlots.

 

Anthrax

• Symptoms
  • Sudden death within 48 hrs of illness of animal
  • Following death there is oozing of blood from the natural orifices.
  • Bloat may develop
  • Oedema may predominantly notice under the neck, brisket region, thorax, abdomen and flank.

Suggested first aid 

• • The dead animal body should not be opened.
  • Should have consultation with nearest qualified veterinary doctor.
  • This disease should be brought under the notice of the regulatory officials in case of an outbreak.
  • Care should be taken to destroy the dead body by deep burial with quick lime.

Prevention and control

• • Periodical and regular vaccination should be done.
  • Strict quarantine measures in anthrax prone areas.
  • Preventing the introduction of infected animals into disease free areas.
  • Care should be taken to destroy the dead body by deep burial with quick lime.
  • Persons handling the anthrax infected animals should adopt adequate sanitary measures.
  • The adjacent areas of the dead and infected animals should be thoroughly disinfected by 3% per acetic acid or 10% caustic soda or 10% formaline.
  • The fodder from infected pasture should be destroyed and not to be given to the other animals.

CONCLUSION:

Different disease condition has a specific posture which is helpful for diagnose a particular disease. So that proper treatment should be given to the animals.Clinician very much thorough about disease condition otherwise wrong diagnosis may happen.Disease in animals adversely affect the economics of production and in turn, profit.

Vaccination schedule for sheep:-

Disease

Age and booster doses

Route

Remarks

Foot and mouth disease

6-8 weeks;

repeat every 6-9 months

s/c or i/m depending on the vaccine

 

Hemorrhagic Septicaemia

3-4 months;

repeat annually

1 ml s/c

May/ June

Sheep pox

3 months

s/c

 

Tetanus

Tetanus toxoid

0.5 – 1 ml s/c or i/m

 

Anthrax

4-6 months; repeat annually

0.5 ml s/c at tail fold

In endemic areas only

Enterotoxaemia

3-4 months, repeat after 15 days and then annually.

2.5 ml s/c

First two doses before august

Vaccination schedule for goats:-

 

Disease	Age and booster doses	Route	Remarks
Foot and mouth disease	6-8 weeks, repeat every 6-9 months	s/c or i/m depending on the vaccine
Enterotoxaemia	3-4 months, repeat after 15 days and then annually.	2.5 ml s/c	First two doses before august
Hemorrhagic Septicaemia	3-4 months,, repeat annually	1ml s/c	May/June
Anthrax	4-6 months, repeat annually	0.5 ml s/c at tail fold	In endemic areas only
Tetanus	3-4 months, repeat at 6 months and then annually	0.5 – 1 ml s/c or i/m

Compiled  & Shared by- Team, LITD (Livestock Institute of Training & Development)

 Image-Courtesy-Google

 Reference-On Request.

VACCINES FOR LIVESTOCK & POULTRY IN INDIA

https://icar.org.in/sites/default/files/2022-06/Vaccines-for-Livestock-and-Poultry.pdf

CONTROL & MANAGEMENT OF IMPORTANT DISEASES OF SHEEP & GOAT