UNIT 1: DISEASES CAUSED BY INTERNAL PARASITES

FASCIOLIASIS (Liver fluke disease)

Fascioliasis is the disease caused by the infestation of liver flukes of the genus Fasciola.

Cause Fasciola hepatica and Fasciola gigantica.

Hosts Final host

All domestic animals, principally cattle, buffalo, sheep and goats. Intermediate host: Snail of the genus
Lymnea.

Lifecycle and transmission Adult Fasciola live in the bile ducts producing eggs that are excreted with the
feces. Hatching occurs only in moist conditions to produce miracidium, the first larval stage. Miracidia
must find and invade the tissues of a suitable host snail within 24 to 30 hrs. After several cycles of
asexual multiplication, the flukes leave the snail as cercaria. These attach to the herbage and transform
into metacercaria by secreting a tough protective cyst wall.

When metacercaria are ingested by the final host, immature flukes emerge from the metacercaria in the
intestine and migrate across the peritoneal cavity. The young flukes migrate through the hepatic tissue
for about 5 – 6 weeks, growing from 0.1 to 10 mm. After entering the bile ducts, they more than double
in size before egg laying starts about 10 – 12 wks after infestation. Adult cattle and sheep may remain
carriers for many years because of the longevity of the adult flukes.

Clinical findings

Acute fascioliasis: Acute fascioliasis is rare and is restricted to sheep. It is usually seen in the summer
and autumn. The clinical signs are:

 Sudden death, which may be accompanied by the passage of blood stained discharges from the
nostrils and anus, confusing with anthrax.
 Dullness
 Weakness Lack of appetite
 Paleness and edema of mucous membranes and conjunctiva
 Pain on palpation over the area of liver
 Death usually occurs within a period of 2 – 3 wks.

Chronic fascioliasis: This is the most common type of fascioliasis which is found in all types of animals of
all ages. Symptoms start appearing only after the immature flukes in the liver parenchyma become quite
mature.

 Anaemia – mucous membranes become pale.

 Rough skin coat.
 Bottle jaw condition
  The course of the disease is often as long as 2 – 3 months in those which die; many survive but
may remain in poor condition for longer periods.
 In cattle, most common symptoms are chronic diarrhea, fall in milk production and loss of
weight especially if lactating.

Diagnosis

On the basis of clinical findings:-

 Observation of eggs in fecal examination.

 Post mortem examination in acute cases.

Treatment

1. Triclabendazole (against all stages of fluke; drug of choice in acute outbreak)

 Sheep: 10 mg/kg body weight orally
 Cattle: 12 mg/kg body weight orally
 Higher doses for F. gigantica in buffalo.
2. Albendazole:
 Sheep: 7.5 mg/kg body weight orally
 Cattle: 10 mg/kg body weight orally
3. Nitroxynil (T.N. Fascionix 34% inj)
 10 mg/kg body weight SC against adult flukes.
 15 mg/kg body weight SC for immature flukes.
4. Oxyclozanide: 10 – 15 mg/kg body weight orally against adults.
5. Rafoxanide: 7.5 mg/kg body weight orally

Control

1. Biological control: Duck rearing

2. Mechnical: Manual picking of snail and destroying them.
3. Chemical: Use of CuSO4.
4. Prophylactic treatment of animals.
5. Management: Restriction from grazing on flooded pasture.

AMPHISTOMIASIS (Stomach fluke disease)

Amphistomiasis is a disease condition cause by flukes belonging to the family paramphistomatidae.

Important paramphistomes Paramphistomum sp, Cotylophoron sp, Calicophoron sp, Ceylonocotyle sp,
Gigantocotyle sp, Gastrothylax sp, Fischoedirus sp.

Final host

Ruminants Intermediate host: Water snails of the genus Planorbis.

Transmission and life cycle Similar to F. hepatica, except that the intermediate hosts are planorbid snails
and the immature flukes migrate along the duodenum through the abomasum to reach the rumen and
reticulum. The period required for maturation varies from 6 wks to 4 months.

Clinical findings

 Mature flukes in the fore stomach of the animals normally cause little harm, although loss of
weight, anaemia, a rough dry coat and drop in production are seen.
 When large numbers of immature flukes are migrating in the duodenum, there is severe
enteritis, which causes persistent foetid diarrhea accompanied by weakness, depression,
dehydration and anorexia.
 There may be bottle jaw condition and pale mucous membranes.
 Animals become very thirsty and drink frequently.
 Death usually occurs 15 – 20 days after the first signs appear.

Diagnosis

1. Clinical signs
2. Fecal examination: Observation of immature flukes or eggs in feces.
3. Post mortem examination

Treatment

1. 2 doses of Oxyclozanide @ 18.7 mg/kg body weight 2 days apart against immature
paramphistomes in cattle.
2. Hexachlorophen @ 7.5 mg/kg body weight in cattle for 3 days mixed with vegetable oil.
3. Niclosamide: Good activity against immature flukes.
 Cattle: 160 mg/kg body weight as a single dose or as 2 doses 3 days apart in cattle.
 Sheep: 100 mg/kg body weight

Control

 Biological control: Duck rearing

 Mechnical: Drainage of swamp, removal of snail through fishing net.
 Chemical: Use of CuSO4.
 Prophylactic treatment of animals.
 Management: Restriction from grazing on flooded pasture.

ROUND WORMS OF RUMINANTS

Round worms belong to the phylum nematoda of the invertebrate animals. Both free living and parasitic
forms of the parasite occur. Some of the parasitic round worms cause disease in animals and humans.
The adult parasites occur mostly in the gastrointestinal tract and also in various other sites in the body,
such as the lungs, blood, eyes and kidney. In the alimentary tract, the round worms either suck blood
being attached to the mucous membrane or absorb nutrients from the food of animals. Some of the
parasites also cause injury to the mucous membrane by tearing the host's tissues with their toothed
mouth parts. In general young animals are more susceptible to round worms and mature animals are
more resistant to round worm infection. Round worms are often grouped as large or small round worms
depending on their mature body size.

Large round worms of ruminants

The large round worms of livestock and poultry belong to the Ascarididae family. These are host specific,
a certain parasite occurring only in specific hosts. Toxocara vitulorum is the large round worm that
occurs in the small intestine of cattle and buffaloes. Young calves are mostly affected by the parasite,
while adults are usually resistant.

Signs

 Diarrhoea and emaciation are important signs.

 Rough body coat, stunted growth, anaemia and steatorrhoea (passage of abnormally increased
amounts of fat in the feces) are additional signs.

Diagnosis

 On the basis of clinical signs, observation of eggs in feces, observation of parasites in PM

examination.

Treatment

 Piperazine hydrate @ 250 mg/kg body weight orally.

 Pyrental @ 250 mg per calf.
 Levamisole @ 7.5 mg/kg body weight orally.

Small round worms of ruminants

Various genera and species of smaller round worms occur in different sites of the alimentary canal of
ruminants. The common small round worms of ruminants are:

Parasite genus Site of occurrence Haemonchus (Wire worm), Ostertegia Abomasum Trichostrongylus
Abomasum and small intestine Cooperia, Nematodirus, Bunostomum (Hook worm) Small intestine
Oesophagostomum (Nodule worm) Large intestine

Parasitic gastroenteritis in ruminants

Parasitic gastroenteritis is caused by round worms often known as scour worms or hair worms
(Trichostrongylus, Ostertagia, Cooperia and Nematodirus). These often occur together in the alimentary
tract (mostly small intestine and abomasum) of ruminants to cause the disease. Other alimentary
nematodes such as Oesophagostomum and Bunostomum may also cause parasitic gastroenteritis.
Young animals are most susceptible, while adults are less affected.

Signs
1. Cattle:-
 They pass soft feces in the beginning which later becomes very thin and dark green to yellow in
colour.
 The calves lose weight rapidly.
 They develop long and dry hair coat.
 The mucous membranes become pale and dry.
 There may be sub-mandibular edema.
 They become dehydrated with sinking of eyes in the terminal stages.
 In the terminal stages the calves become weak and emaciated and die.
2. Sheep and goats
 Diarrhea
 Loss of weight
 Dehydration
 Death

Diagnosis

Diagnosis is based on the combination of clinical signs and information on age of the animal, season of
the year, grazing history and fecal examination.

Treatment

1. Albendazole: (TN: Albomar, Analgon, Wormar) Cattle: 7.5 mg/kg Sheep: 5 mg/kg Goat: 10 mg/kg
orally
2. Fenbendazole: 5 mg/kg body weight (TN: Panfugal, Fenomar, Panacure)
3. Levamisole: (TN Almizole, Kalmisole) Cattle and sheep: 7.5 mg/kg Goat: 12 mg/kg orally
4. Ivermectin: 0.2 mg/kg by SC route (TN: Endact, Mectin)

Control

 Preventive treatment of animals.

 Avoiding grazing on contaminated pasture.

Haemonchosis in ruminants

Cause

 Haemonchus contortus in sheep and goats

 Haemonchus placei in cattle

Clinical findings

 There is bloody diarrhoea and severe anaemia, due to which the animals lose weight, become
very weak, recumbent and die consequently.
 There may be subcutaneous edema particularly under the lower jaw and the ventral abdomen.
Diagnosis and treatment

 Same as for parasitic gastroenteritis.

Oesophagostomosis in ruminants (Nodule worm disease)

Cause

 Oesophagostomum radiatum in cattle

 O. clumbianum, O. venulosum and O. asperum in sheep and goats.

Clinical findings

 In sheep there is severe persistent diarrhoea containing excess amounts of mucous and
occasionally blood, rapid loss of weight and humped back.
 Young calves may show anorexia, persistent dark green diarrhoea, emaciation and anaemia.

Treatment

1. Piperazine hydrate @ 300 mg/kg body weight orally.

2. Others similar to parasitic gastrogenteritis.

COMMON ROUNDWORMS OF PIGS

Oesophagostomosis

Cause

O. dentatum and O. quadrispinulatum.

Clinical findings

 There is diarrhoea in weaners and growers and slow growth.

 Pregnant sows show anorexia, become very thin, and following farrowing, milk production is
reduced with effects on litter performance.

Diagnosis

 On the basis of clinical signs and observation of nodules in the intestine at postmortem
examination.

Treatment

 Piperazine hydrate @ 285 mg/kg body weight orally.

 Ivermectin @ 0.3 mg/kg by SC route.

Ascariasis

Cause
Ascaris suum

Clinical findings

 Young pigs are mainly affected.

 There is poor growth, diarrhoea and decreased resistance to other diseases.
 There may be coughing and pneumonia while larvae are passing through the lungs.

Diagnosis

 On the basis of clinical signs, observation of eggs in feces, observation of parasites in PM

examination.

Treatment

 Ivermectin @ 0.3 mg/kg body weight by SC route.

 Fenbendazole @ 5 mg/kg body weight orally.
 Piperazine @ 250 mg/kg body weight.

COMMON ROUND WORMS OF POULTRY

Ascariasis

Cause

 Ascaridia galli
 These are grayish, threadlike and measure 6 to 12 cm in length in fully mature state. They occur
in the small intestine, mostly in the duodenum, in bunches.

Signs

 Retardation of growth
 Loss of weight
 Lack of appetite
 Reduced egg production
 Sometimes diarrhoea and anaemia may be observed
 There may be death of some birds.

Diagnosis

 On the basis of observation of eggs in feces, observation of parasites in PM examination.

Treatment

1. Piperazine @ 50 – 100 mg/bird or as 0.1 – 0.2% in water.

Examples: Piperazine liquid (45% piperazine hydrate) (Glaxo): 50 – 75 ml/100 birds

Piperazine hexahydrate (46%) (Wockhardt):

Below 6 wks (100 birds): 30 ml/3 – 5 litres of water

Above 6 wks (100 birds): 60 ml/5 – 10 litres of water

GID

Gid is a clinical condition in cattle, sheep and goats caused by the intermediate stage of the tapeworm
Taenia multiceps. Sheep and goats are most commonly affected than cattle.

Transmission, life cycle and pathogenesis

Adult Taenia multiceps live in the intestine of the dog, where they lay eggs that pass out along with the
feces. The intermediate hosts are affected when they feed on pasture contaminated by dog feces. The
eggs hatch to release an embryo, which penetrates the wall of the alimentary tract and is conveyed by
the blood to the central nervous system. In the central nervous system, it develops over a period of 6
months to form a cyst measuring up to 5 cm in diameter. In the cyst there are a number of larvae.

The final host dog is affected when it feeds on meat of affected intermediate host where the larvae
develop into adult forms in the intestine.

Signs

 The signs of gid depend on the site and size of the cyst.
 Animals with cyst in the brain show disorders of gait and stance, often with turning the head
towards the affected side, walking in circles towards the same side, and showing a one-sided
blindness in the opposite side.
 Other signs include excitement, incoordination and lying down on the ground (prostration).
 In some cases the animal keeps the head high and walks in a straight direction.
 When the spinal cord is affected, partial paralysis develops slowly.
 The cyst may cause a local softening of the skull, which if detectable, helps in diagnosis.

Diagnosis

 Symptoms, detection of coenurus in the skull.

Treatment

2. The only satisfactory treatment is surgical removal of the cyst. Treatment is possible only if the
cyst is located superficially. Aspiration of fluid through the softened skull bones can be done but
recurrence is common. Complete cyst, if located superficially can be removed surgically under
general anesthesia.
3. A C-shaped incision is given at the site of the cyst and the cyst is removed as a whole as far as
possible. The skin incision is closed with non-absorbable sutures and broad spectrum antibiotics
are recommended for seven days.
COCCIDIOSIS

Coccidiosis is a disease of mammals and birds caused by protozoa belonging to the genera Eimeria and
Isospora, and is characterized by the infection of the intestines and diarrhoea.

Cause

 Cattle: Eimeria zuernii, E. bovis, E. ellipsoidalis

 Sheep: Eimeria ovinoidalis, E. crandallis
 Goat: E. arloingi
 Pigs: Isospora suis, Eimeria debliecki

Transmission and pathogenesis

Coccidiosis is transmitted between animals by the ingestion of oocysts from the environment especially
in an unhealthy environment.

The ingested oocysts develop into vegetative form in the intestine where they penetrate the intestinal
epithelial cells. Multiplication of coccidia causes destruction of epithelial cells, which may be so severe
as to cause severe haemorrhage and anaemia. Inflammation of the intestinal epithelium also occurs.

Susceptibility

Young animals are more susceptible to coccidiosis and adults are more resistant. Calves under 1 year,
lambs under 6 months and a few weeks old piglets are more often affected.

Symptoms

In Calves

 In calves with milder infection there is foul smelling diarrhea without blood.
 In heavy infection, there is severe blood stained diarrhea accompanied by straining.
 Anaemia, weakness and dyspnoea occur due to loss of blood.
 Finally dehydration, emaciation and death may occur.

In Lambs and kids

 Lambs are more susceptible than kids.

 Heavy infection in lambs causes severe diarrhea, which sometimes contains blood.
 Growth rate is poor and there is gradual onset of weakness, inappetance, milk fever and
recumbency.
 Finally death may occur due to emaciation, anaemia and dehydration.

Piglets

 Anorexia and depression are common.

 I. suis causes severe enteritis in young piglets aged 1 – 2 weeks, causing diarrhea.
  Piglets lose weight.
 Vomiting may occur.
 The entire litters may be affected, and the case fatality rate may reach 20%.

Fowl Cause

 E. tenella (Caecal coccidiosis)

 E. necatrix
 E. acervulina
 E. maxima
 E. brunette
 E. mitis
 E. preacox.

Symptoms

 Disease occurs mostly in chicks aged 4 – 8 weeks.

 Depression, loss of appetite, drooping wings, huddling together.
 Soft feces or diarrhoea often containing blood.
 Reduction in growth.
 Mortality may be heavy.
 There is reduction in egg production in layers.

Diagnosis

 In the basis of history and clinical signs.

 Fecal examination: Presence of oocysts in the feces.
 PM examination:
a) In case of caecal coccidiosis caeca may be filled with blood tinged contents and caecal wall
shows patchy or diffuse haemorrhage.
b) In case of intestinal coccidiosis haemorrhagic pin point spots are seen in various parts of
small intestine.
c) Occasionally there may be haemorrhagic enteritis with blood tinged contents in the small
intestine.
d) In chronic cases white pinpoint to pinhead sized foci occur in the small intestine.

Treatment

Cattle, sheep and goat

1. Amprolium @ 10 mg/kg body weight orally for 5 days.

2. Sulfadimidine @ 140 mg/kg body weight orally for 3 days.

Pigs
 1. Amprolium @ 10 mg/kg body weight orally for 5 days.
2. Amprolium 25% @ 10 kg/tone of sow's feed from 1 week before farrowing to 3 weeks after
farrowing as prevention.

Poultry

1. Amprolium @ 125 gm/tone of feed i.e. amprolium, amprosol pw @ 30 gm/50 litres of drinking
water for 5 – 7 days.
2. Sulfachloropyrazine Na (TN ESB3 pw) @ 1 gm/ litre of drinking water for 3 days.
3. Sulfaquinoxaline + Amprolium (TN Coxiquin forte, Duocoxin) @ 1 gm/2 lit of drinking water for
5 days.
4. Sulfaquinoxaline + Diaveridine (TN Supercox) @ 1 gm/ lit of drinking water for 3 days, plain
water for 2 days and medicated water at half the dose rate for further 2 days.

Control

 Sanitation management
 Chemoprophylaxis

BABESIOSIS (Red water disease)

Babesiosis is a haemoprotozoan disease of domestic animals characterized by fever, anaemia and

haemoglobinuria and can be fatal.

Etiology

Cattle, buffalo

Babesia bigemina, B. bovis, B. divergens, B. major

Sheep, Goat

B. motasi, B. ovis Pig B. trautmanni

Transmission

Babesiosis is transmitted from an infected animal to a healthy animal by the bite of an infected tick.
Different genera and species of ticks are responsible for transmission of babesiosis in different animals.

Susceptiblility

Exotic and crossbred cattle are more susceptible than indigenous ones.

Signs

 Acute onset of high fever (104 - 106°F), anorexia, depression, weakness, cessation of
rumination, and a fall in milk yield.
 Haemoglobinuria – reddish brown urine.
  The mucous membrane of the conjunctiva are first congested, which soon become very pale,
which later become jaundiced.
 Diarrhoea is common.
 Respiratory and pulse rates are increased.
 Pregnant cattle may abort.
 Sometimes convulsions may occur.
 If untreated, death commonly occurs in a few days.

Diagnosis

 On the basis of clinical symptoms – haemoglobinuria is a typical feature.

 Clinical pathology – low RBC count, low PCV, low haemoglobin level.
 Examination of blood smear – blood from peripheral vessels is used to prepare smears and
stained with Giemsa stain and observed under the microscope for intraerythrocytic parasites.

Treatment

1. Diminazine aceturate (TN Berenil) @ 4 mg/kg body weight by IM or SC route.

2. Imidocarb dihydrochloride @ 1 mg/kg body weight by IM or SC route.

Supportive treatment

1. Antipyretic for the control of fever.

2. Glucose saline for dehydration.
3. Liver extract, vitamin B complex and iron orally or parenterally to correct anaemia.
4. Whole blood therapy to correct severe anaemia.

Control

Control of tick population and vaccination.

THEILERIOSIS

Theileriosis is a tick transmitted disease of cattle, sheep and goats caused by different species of the
genus Theileria, and is characterized by high fever, swelling of lymph nodes and anaemia.

Cause

 Theileria annulata – Cattle

 Theileria ovis – Sheep
 Theileria hirci – Sheep and goat

Susceptibility

All age groups of exotic cattle and crossbred are susceptible. Young are relatively more susceptible than
old ones.
Transmission

Transmission of theileriosis takes place during feeding of blood by an appropriate infected intermediate
host, the tick.

Clinical findings

 High rise of temperature (104.9 – 106.7°F) accompanied by dullness, anorexia, reduced milk
yield, nasal and ocular discharges, dyspnoea and swelling of superficial lymph nodes.
 Later on diarrhoea may be present.
 In some cases there may be emaciation and coma followed by death.
 Haemolytic anaemia in terminal stages and often icterus.
 Petechial haemorrhage may be seen on conjunctiva, under the tongue and vulva.
 Weakness, prostration and death.
 The disease runs a course of about a month and mortality is 90 – 95%.

Diagnosis

 On the basis of clinical findings.

 In the basis of clinical pathology: In RBC, these are predominantly rod shaped. Round, oval and
ring (annular) shaped forms also occur.
 Serological tests

Treatment

1. Buparvaquone @ 2.5 mg/kg body weight by IM route. TN Butalex inj @ 1ml/20 kg body weight
by IM.
2. Oxytetracycline @ 20 mg/kg body weight IM 72 hours apart.

Supportive therapy

1. Antipyretic, B – complex vitamins and glucose saline should be used.

Control

 Control of tick population

 Chemoprophylaxis: Chlortetracycline @ 16 mg/kg body weight orally for 8 days.
 Immunoprophylaxis: Rakshavac – T.

UNIT 2. DISEASES CAUSED BY EXTERNAL PARASITES

LICE

Lice can be classified under the following two types based on their feeding habit:-

 Sucking lice Biting lice Hematopinus sp: Cattle, Pigs, Equines

 Bovicola (Damalina) sp: Cattle, Sheep, Goat, Equines
  Lignonathus sp: Cattle, Sheep, Goat, Dog
 Felicola sp: Cat
 Solenoptes sp:Cattle
 Trichodectes sp: Dog
 Heterodoxus sp: Dog

All of the lice of domestic fowls are of biting type and the most important ones of these are Liperus,
Cuclotogaster and Menacanthus.

The sucking lice have piercing mouthparts with the help of which they suck blood. The biting lice have
mouthparts adapted for biting and chewing. In mammals they ingest the outer layers of the hair, skin
scales, and blood scabs. The bird lice also feed on skin scales and scabs and can also digest keratin. So
they also feed on feathers.

Signs

 Lice cause irritation of the skin (itching), causing the animals to become restless and they
scratch, rub and lick themselves.
 There may be loss of milk production.
 There is usually pityriasis (shedding of bran like scales from the skin).
 Wool and hides become damaged.
 In heavy infestation anaemia may be caused.
 Usually the young and weak ones suffer heavy infestation.
 In heavy infestation there may be drop in egg production in poultry.

Diagnosis

 Detection of lice in the body.

Treatment

1. Deltamethrin (T.N. Butox) @ 1 ml per litre of water for dip or spray.

2. Cypermethrin 10% (T.N. Cyperin 100, Notix ) @ 1 ml per litre of water for dip or spray.
3. Ivermectin inj. (T.N. Mectin, Endact): 0.2% SC for sheep, goat and cattle and 0.3% SC for pig.

Chemical and herbal shampoos and body sprays are also available for pet animals. These should be used
as recommended by the manufacturer.

TICKS

There are two types of ticks – hard ticks and soft ticks, differentiated on the basis of the presence or
absence of a rigid chitinous scutum. The scutum covers the entire dorsal surface of the adult male of
hard ticks; in the adult female and in the larva and nymph it covers only a small area. The soft ticks lack a
scutum.

The important genera of ticks that occur in animals and birds are:-
  Hard ticks Soft ticks Ixodes, Haemaphysalis, Dermacenter, Amblyomma, Boophilus,
Hyalomma, Rhipicephalus Argas (the fowl tick), Otobius, Ornithodoros

Pathogenesis and clinical symptoms

 Tick infestation cause irritation to the skin due to which the animals scratch and rub
themselves. Due to this there may be dermatitis.
 They suck blood, and in heavy infestation can cause anaemia.
 The lesions caused by the toothed mouthparts during feeding cause cutaneous injury which
may become infected and predispose to maggot wound.
 There may be loss of wool.

Different genera and species of ticks transmit the protozoan and rickettsial diseases as babesiosis,
theileriosis and anaplasmosis. Some ticks found in Australia and South Africa produce toxins responsible
for tick paralysis.

Diagnosis

 Detection of ticks on the animal body.

Treatment and control

1. Butox @ 2ml/litre of water for spray or dipping.

2. Others same as for lice.

MITES

Mites cause various forms of the condition generally known as mange. The mites, like ticks are obligate
parasites but differ in some respects. The mites spend their entire life cycle from eggs to adult, on the
host while ticks are only temporary parasites. Mites are of two types: burrowing and non-burrowing
mites.

Burrowing mites: The most important burrowing mites are the Sarcoptes and Demodex.

Sarcoptes scabiei is the only species of the genus occurring in a wide range of mammals including man.
The disease in man is generally known as scabies. The adults feed on the succulent layer of epidermis.
The female mites penetrate deep in the epidermis causing tunnels, which run in various directions. The
mites are found at the ends of these tunnels where they lay eggs. Larvae that hatch from the eggs crawl
out and may infect other animals or may become adults on the same animal burrowing into new places.
Males live only superficially.

Demodex is of importance in dogs though other domestic animals may also be affected. Demodex lives
on hair follicles and sebaceous glands.

Non-burrowing mites: Of the non-burrowing mites the most important is the sucking mite Psoroptes.
Psoroptes lives on tissue fluids. The parasite is of greater importance in sheep in which it causes sheep
scab. Psoroptes does not burrow into the epidermis but only pierces through to suck fluid. During this
process inflammation may be caused with the exudation of lymph, which dries into a crust under which
are found the mites.

Symptoms

 Animals scratch themselves or even bite at the place due to itching.

 Red papules and vesicles form at the infected area. These are soon covered by crusts formed by
drying of lymph.
 Skin becomes thickened and wrinkled.
 Due to lack of blood supply hair and wool may fall off.
 In birds, the mites generally affect the legs of older fowls and turkeys. Formation of scales and
crusts affect the bending of joints and therefore become lame.

Diagnosis

 History of itching and clinical signs.

 Recovery of mites from skin scrapings digested with 10% warm KOH solution.

Treatment

1. Butox @ 4 ml/litre of water for spray or dipping.

2. Others same as for lice.

LEECHES

Leeches belong to the group Hirudinea of the phylum Annelida of the animal kingdom. The leeches that
attack livestock and man may be divided into two groups – fresh water leech and land leech.

a) Fresh water leech These live mainly in ponds, slow moving streams, ditches, flooded paddy fields,
tanks etc. These are moderately sized animals but both the length and diameter depends on the
amount of blood ingested and the time lapsed from the last feeding. The digestive system is
specially adapted to storing a large amount of blood which is digested over a considerable period of
time. When a host animal enters such shallow waters, either for drinking water or to feed on aquatic
vegetation, or for wallowing, the leeches smell the host and swim to attach on them. The most
common species is Hirudinaria granulose.
b) Land leech These are comparatively smaller and are confined to the damp hilly areas. They are
especially abundant during the rainy season and for sometime after that. They climb up on the grass
leaves, stalks and leaves of bushes and when an animal passes from near they drop on to them. The
common genus is Haemadipsa with several species and subspecies. Being small in size each
individual does not suck much blood. But it is possible that a number of leeches may attach to a host
at the same time.

Pathogenesis and clinical symptoms

The leeches attack the livestock to feed on blood. They have a set of three teeth in their oral opening.
Using them they pierce the skin of the animal. Once attached, they break the blood vessels to suck
blood. To prevent clotting of the blood the leeches produce an anticoagulant called hirudin. Once the
leeches have fed and gorged, they drop off the host. But due to the presence of hirudin, the wounds
keep on bleeding for some time.

Most of the damage is done to the loss of blood, which if repeated frequently and by a large number of
leeches, may result in anaemia and emaciation. However, most of the animals tolerate the attack well.
In some cases the open wound takes some time in healing but may be subjected to secondary infection.
A leech will attack any part of the body. It becomes especially troublesome if it gets attached to the
nasal passage, pharynx or larynx thus causing suffocation due to edema and blocking the passage with
their body and free blood. In rare cases, the eyes are attacked causing temporary or permanent
blindness.

Treatment This consists of removal of leech from the host. A leech should not be forcibly pulled from
the body since it is likely that the teeth may remain in the wound and may cause a sore. The simplest
way to remove the leech is to sprinkle it with common salt. Similarly, a saline solution, diluted vinegar,
tartaric acid (10%), or diluted chloroform may be used. When the leech is lodged deeper in the body,
like the nasal passage, irritating the nasal passage with the liquids mentioned above will dislodge it.
Similarly, the inhalation of turpentine or steaming barley is also effective. Local application of tincture of
iodine or spirit on the punctured skin should also be followed.

UNIT 3. BACTERIAL DISEASES OF LIVESTOCK

HAEMORRHAGIC SEPTICAEMIA (HS)

Synonym: Pasteurellosis, Shipping fever

Etiology

Pasteurella multocida. It is a Gram-negative coccus bacterium that takes characteristic bipolar staining
with Leishman’s stain.

Susceptibility

 Cattle and buffaloes are the most susceptible hosts. Young growing cattle within the age group
of 6 months to 2 yrs are most often affected. Sheep, goat and swine are rarely affected.

Transmission

 Through ingestion of contaminated food and water.

 Droplet infection may occur specially in animals kept in crowded barns.
 Wet and chilly weather or exhaustion due to heavy work favors the transmission of the disease.
 Morbidity and case fatality rates Both morbidity and case fatality rates vary between 50 and
100%.
Clinical findings

1. Cattle and buffalo

 Sudden onset of high fever (104 – 107°F) with concurrent shivering.
 It is followed by profuse salivation, lachrymation, submucosal petechiation, conjunctivitis,
severe depression and nasal discharge.
 There is sharp drop in milk production.
 Abdominal pain, severe diarrhoea or dysentery.
 Rapid respiration.
 Death usually occurs in 24 hours.

In less acute cases there is rise in body temperature and subcutaneous edema in the head, neck, dewlap
and brisket region. The edematous swellings are hot and painful. There is difficult respiration. Death
usually occurs within 20 – 24 hrs.

2. Sheep and goat

 The animals show high rise of temperature, depression, salivation, lachrymation and
mucopurulent nasal discharge. Death occurs in 24 – 48 hrs. Lameness may appear as a result
of bursitis or arthritis.
3. Pig
 Dullness and depression with profuse nasal discharge. Temperature ranges from 104 –
107°F. Disease usually occurs secondary to enzootic pneumonia virus infection.

Diagnosis

 On the basis of clinical findings.

 Identification of the organism:
a) Blood smear stained with Leishman’s stain show bipolar staining microorganisms.
b) Blood or nasal swab may be used for culture of the organisms. Blood agar and brilliant
green agar media are the suitable media.
 Animal inoculation test

Treatment

1. Treatment with one of the following antibacterial/antibiotics should be followed.

 Sulfadimidine sodium @ 150 mg/kg b. wt. IM for 3 – 5 days.
 Oxytetracycline @ 10 mg/kg b. wt. IM or IV for 3 days; or @ 20 mg/kg b. wt. IM as long
acting drug.
 Ampicillin @ 10 mg /kg b. wt. IM or IV for 3 days. d. Penicillin @ 20,000 – 30,000 IU/kg b.
wt. for 3 days.
2. Anti-inflammatory drug such as Dexamethasone inj. (4mg/ml) @ 2 – 5 ml IM or IV daily.
3. Antipyretic drug against fever.

Control Vaccination
1. HS vaccine (Alum precipitated): In animals above 3 months of age. It should not be used in pregnant
animals within the last 2 months of gestation. Immunity period is 6 months. It should be used before
monsoon ever year.
2. Cattle and buffalo: 5 ml SC; Calf, sheep, goat, pig: 3 ml SC route
3. HS, BQ combined vaccine: Same as HS vaccine.

BLACK QUARTER (BQ)

Synonym: Black Leg

It is an acute infectious disease of cattle characterized by the inflammation of muscles, severe toxaemia,
and high mortality. There is crepitation and serohaemorrhagic swelling in the heavy muscles like the
gluteal muscles.

Etiology

Black quarter is caused by Clostridium chauvoei, a Gram-positive, rod-shaped, spore forming bacteria.
Spores are very much resistant to altered environmental stress, heat, desiccation and disinfectants.
Spores can withstand boiling temperature and persist in the soil for many years.

Susceptibility BQ is a predominant disease of cattle but traumatic BQ may also be seen in other animals.
BQ most commonly occurs in cattle of 6 months to 2 years old and may also occur in buffalo, sheep and
goat and rarely in pigs and horse. BQ mostly occurs in the summer season and following heavy rainfall.

Transmission

 Through feed contaminated by soil and faeces.

 Contamination of wound by the spores and during parturition.

Clinical findings

1. Cattle and buffalo

 High fever (106 – 108°F) accompanied by severe depression, complete anorexia, ruminal
stasis and accelerated pulse rate (100 – 120/min). However, in some cases there may
not be fever.
 Marked lameness with swelling of upper part of the limbs or shoulder, chest, neck or
flank.
 Swelling is hot and painful in early stages but soon becomes cold and painless.
Crepitating sound can be felt on palpation over the swollen area.
 Skin over the swelling is discolored, hard and dry.
 There is also labored breathing.
 Animal dies within 12 – 36 hrs and mortality is usually 100%.
2. Sheep
  High fever, anorexia and depression.
 Stiffness of joint; lameness is not a constant feature but in positive cases is severe.
 Swelling being due to edema, no crepitation sound is heard.
 Discoloration of skin may be present.
 Necrosis and gangrene do not occur.
 Rams are more susceptible than ewes.

Diagnosis

 On the basis of clinical findings as high fever, lameness, crepitating sound and higher mortality.
 PM findings
a) Swelling cuts like a rubber sponge and body fluids rich in gas bubbles exude from the cut
surfaces of the swelling.
b) Metallic sheen in the muscle.
c) Affected muscles are deep red to black in colour and contain numerous gas pockets.
d) Muscles are dry at the center and have odour of rancid butter.
 Laboratory findings
a) Microscopic examination of smear from affected tissues or fluids of swelling reveals Gram-
positive rods with sub-terminal spores.
b) Cultural tests: Anaerobic culture from heart blood, peritoneal fluid, and affected muscle
grows within 23 hrs. Observation of Gram-positive rod shaped organisms.
c) Biological test
d) Serological tests

Differential diagnosis

 Anthrax: Unclotted, dark tarry blood bleeding form natural orifices; no swelling and crepitating
sound.
 Bacillary haemoglobinuria: No crepitating sound; bloody diarrhoea; bloat.

Treatment

1. Antibiotic treatment
a) Drug of choice is penicillin. Penicillin @ 5,000 - 10,000 IU/kg b. wt. for 3 – 5 days. It is
better to give crystalline penicillin (Benzyl penicillin Na/K) initially by intravenous route
followed by procaine penicillin through intramuscular route. i.e. For large animal: 20
– 40 lakhs IU; For small animal: 4 – 5 lakhs IU
b) Tetracycline can also be used @ 5 mg /kg b. wt. IM or IV bid for 3 – 5 days.
1. Analgesics and anti-inflammatory drugs should be used to relieve pain.
a) Esgipyrine N: Large animals: 2 – 4 ampoules IM; Small animals: 1 ampoule.
b) Proxyvet MP: Large animals: 15 – 20 ml; Small animals: 5 – 10 ml IM.

Control
  Carcass should be buried deep and soil contamination should be avoided.
 Animals should be kept far from contaminated areas.
 Dead animals should not be skinned.

Immunization

 Passive immunity: Inoculation of immune serum. Prophylactic dose: 15 ml for cattle and 10 ml
for sheep. It provides protection for 2 wks.
 Active immunity
i. BQ vaccine: In animals above 3 months of age. It should not be used in pregnant animals
within the last 2 months of gestation. Immunity period is 12 months. It should be used
before monsoon ever year. Cattle and buffalo: 5 ml SC; Calf, sheep, goat, pig: 3 ml SC
route
ii. HS, BQ combined vaccine: Same as BQ vaccine.

ANTHRAX

Synonym: Splenic Fever, Wool Sorter’s Disease (Man)

It is an acute or peracute infectious disease of human beings and animals characterized by sudden
death, black tarry exudates oozing from natural orifices of dead animals.

Etiology

It is caused by Bacillus anthracis, a straight, very large rod-shaped, sporebearing Gram positive bacteria.
The spores can thrive in the soil for 10 – 20 years.

Susceptibility

No mammal has got absolute immunity against anthrax. The most susceptible animals are cattle and
sheep. Goats, horses and pigs are less susceptible.

Transmission

 Most of the animals are infected while grazing in the areas that have experienced anthrax.
 Spores are transmitted through consumption of contaminated water, hay, foodstuffs of animal
origin like bone meal, blood meal.
 Transmission is also possible by inhalation of spores and through the skin.

Clinical findings

Incubation period ranges from 1 – 2 weeks (2 – 10 days). In cattle, sheep and goat two forms of the
disease appear:

1. Peracute disease
 Sudden death of animals without any previous symptoms may be seen.
  Fever (107°F), muscle tremor, mucosal congestion and collapse of the animal may be seen.
Duration is 1 – 2 hrs.
 Terminally there is convulsion and bloody discharge (black, tarry) from natural orifices.
2. Acute
 The acute form runs a course of about 48 hours. Acute form of the disease is found in cattle,
sheep, goat, pig and horse.
 High fever (107°F), severe depression, anorexia and ruminal stasis.
 Rapid and deep respiration.
 The mucosae are congested and haemorrhagic.
 Rapid pulse rate.
 Diarrhoea or dysentery is usually present.
 In milking cows the yield is very much reduced and may be blood-stained or deep yellow in
colour.
 Pregnant cows may abort.
 Edematous swelling of tongue, throat, sternum, perineum and flank.

Pigs

 Disease occurs in acute and sub-acute form.

 There is fever, dullness, anorexia and a characteristic inflammatory swelling of throat and
face.
 The swellings are hot but not painful and may cause obstruction to swallowing and
respiration.
 Petechial haemorrhage in the skin.
 There may be diarrhoea.
 Death usually occurs in 2 – 3 days.

Diagnosis

 On the basis of history and clinical symptoms.

 Laboratory examination
a) Examination of blood and edema fluid for bacteria reveals short chains like that of
Streptococcus.
b) Serological test (Ascoli’s precipitation test): Tissue extract (exudates) from spleen, kidney is
taken in 0.5 ml volume and mixed with 0.5 ml of hyperimmune serum of anthrax. Where
precipitate forms, it indicates a positive result.
c) Biological test: Inoculation of exudates from affected animal into rabbit, guinea pig kills the
test animal after 24 hrs. Spleenomegaly also occurs.
 PM examination
a) Spleenomegaly. Liver, kidney, and lymph nodes are congested and enlarged.
b) Blood fails to clot and becomes darker in colour than normal.
c) Tympany in dead animals.
d) Rigor mortis is absent in dead animals.
Note: Where death due to anthrax is suspected, PM examination should never be done.

Treatment

1. Drug of choice is penicillin. However, Oxytetracycline, Streptomycin, Chloramphenicol,

Ciprofloxacin and Erythromycin can also be used.
2. Procaine penicillin @ 20,000 IU/kg b. wt. IM twice daily.
3. Streptomycin @ 8 – 10 gm/day in two divided doses by IM route.
4. Oxytetracycline @ 5 mg/kg b. wt. IM.

Control

 Vaccination with Anthrax spore vaccine: 1 ml SC for all aged and sized animals. Immunity is for 1
year. Annual vaccination for three successive years is recommended in the outbreak area.
 Proper disposal of dead animals and bedding materials.
 Premises should be disinfected with 1 – 2 % NaOH and 2 – 5% phenol.
 Mass awareness and extension activity.

TETANUS

Synonym: Locked jaw

It is a non-contagious, non-febrile, highly fatal sporadic infectious disease of all domestic animals caused
by Clostridium tetani.

Etiology

Clostridium tetani are Gram-positive, straight, slender rods with rounded ends. These form a terminal
spore and give the appearance of drumstick.

Transmission

The organisms gain access into the body during parturition, handling of fetus, placenta and prolapse.
Transmission may also take place through contamination of an open wound. Neonatal animals may get
infection through contaminated umbilicus.

Clinical findings

The incubation period varies between 3 days and 4 weeks. Clinical findings are similar in all animal
species.

 Initially there is increase in muscle stiffness accompanied by muscle tremor.

 There is spasm of jaw muscles with restriction of jaw movements, protrusion of the third eyelid,
stiffness of the hind limbs causing an unsteady gait, and the tail is held out stiffly especially when
backing or turning.
 Marked erection of the ear.
 Exaggerated response to normal stimuli.
  The animal may continue to eat and drink in the early stages but mastication is soon prevented
due to locked jaw.
 If food or water is taken, attempts at swallowing are followed by regurgitation from the nose.
 Constipation is usual and the urine is retained.
 In cattle, particularly young animals, bloat is an early sign but is not usually severe and is
accompanied by strong, frequent rumen contractions.
 As the disease progresses muscular spasm increases and the animal adopts a 'sawhorse'
posture.
 Tail is immovable and raised.
 There is great difficulty in walking and the animal is inclined to fall.
 Opisthotonus is marked, the hind limbs are stuck out stiffly behind and the forelegs forward.
 The convulsions are at first only stimulated by sound or touch but soon occur spontaneously.
 The course of the disease and the prognosis vary both between and within species. The duration
of a fatal illness in horses and cattle is usually 5 – 10 days but sheep usually die on about the
third or fourth day.

Diagnosis

 On the basis of clinical signs and symptoms.

 Lab culture in anaerobic media and by smear preparation of exudates from wound site.

Treatment

The principle of treatment is based on:

1. Destruction of tetanus organism.

2. Neutralization of the circulating toxin.
3. Relaxation of the muscles to prevent asphyxiation.
4. Prevention of dehydration.
5. Penicillin is the drug of choice and should be given in massive doses.
 22,000 IU/kg body weight 3 – 4 times daily for 3 – 5 days, preferably by IV route.
6. Neutralization of toxin by tetanus antitoxin. LA: 1500 – 3000 IU by SC route single dose; SA:
250 IU by SC route single dose.
7. C. Relaxation of muscles by using muscle relaxant. Chlorpromazine (Largactil – 2.5% and 5%): 1
mg/kg b. wt. IM 3 – 4 times until recovery.
8. To prevent dehydration, intravenous rehydrating agents as dextrose/rintose saline can be used.
9. Rehydration and feeding using stomach-tube may also be followed. The feed should be soft and
moist.

BRUCELLOSIS

Synonym: Bang’s disease, Contagious abortion, Undulant fever (Man)

It is an acute or chronic contagious disease of domestic animals characterized by abortion in late
pregnancy often with retention of placenta.

Etiology

 Brucella are small Gram-negative rod shaped bacteria.

 Brucella abortus: Cattle, swine, sheep, horse and dog.
 Brucella militensis: Goat
 Brucella ovis: Sheep
 Brucella suis: Swine
 Brucella canis: Dog

Transmission

 Sources of infection are aborted foetus, fetal membranes and discharges from the uterus,
infected milk and semen in males.
 Transmission usually takes place by the ingestion of contaminated feed and water.
 Infection may also occur through intact or injured skin and conjunctiva.
 Transmission may also occur during copulation.
 Contaminated hands of milker may also transmit the disease.

Symptoms

1. Cattle
 Abortion usually takes place from 6 months onwards. Retention of placenta and metritis
usually occur after abortion.
 There is grayish white mucoid or mucopurulent discharges form the vagina.
 There may be swelling of the bursa of the joints of limbs known as hygroma or bursitis.
 In the bull, there is epididymitis and orchitis, which is painful.
 Bulls lose sexual desire and remain infertile if both testes are involved.
2. Pigs
 Abortion usually takes place between 2nd and 3rd months.
 If there is birth of live piglets, they are usually weak.
 Sterility/infertility, orchitis and lameness are seen in a boar.
3. Sheep and goat
 Abortion and sterility are principal signs.
 Orchitis and lameness due to arthritis and synovitis may be seen.

Diagnosis

 Isolation of organisms from lungs of aborted foetus, uterine exudate, vaginal discharge, milk,
abscesses of testes and epididymis.
 Brucella milk ring test (BMRT): Milk is taken in a test tube to which hematoxyline stained antigen
is added @ 1 drop of antigen to 1 ml of milk. The mixture is incubated for 30 – 60 minutes at
 37°C. In positive cases white milk with blue cream layer forms. In negative cases, blue milk with
white cream forms.
 Serological tests can also be performed.

Treatment

1. There is no known treatment that can cure Brucellosis completely. Tetracycline, streptomycin can
reduce severity to some extent but cannot cure the disease.

Control

 Test and slaughter.

 Isolation of positive testing animals.
 Cases of abortion should be handled with care.
 Contaminated surroundings should be disinfected.
 Strict quarantine measures should be followed.
 Vaccination: Strain 19 Brucella vaccine. Animals should be vaccinated at 3 months of age @ 5ml
by SC route. Vaccination at adult stage may show some reaction and abortion may result in
pregnant animals.

MASTITIS

Mastitis denotes the inflammation of the udder irrespective of the cause. It is characterized by physical,
chemical and microbial changes in the glandular tissue of the udder. Changes in the milk include change
of colour, change of consistency and presence of abnormally large number of leucocytes.

Etiology

A large number of microorganisms can cause mastitis. The microorganisms may be bacteria, fungi,
mycoplasma and virus.

Bacteria : Streptococcus, Staphylococcus, Corynebacterium, Mycobacterium, E. coli, Brucella,

Pseudomonas, Klebsiella sp. Fungus : Trichosporon, Candidia, Aspergillus, Cryptococcus. Virus :
Vesicular stomatitis virus, Infectious rhinotrachetis virus etc.

Susceptibility

High yielding dairy cows are the most susceptible animals. Exotic and crossbred cows are more affected
than indigenous ones. Infection rate is more in later lactations than first lactation.

Transmission

Transmission mostly occurs through the teat canal. Some of the bacteria that can cause mastitis are
naturally present in the udder, which can cause the disease when resistance is low.

Clinical findings
The disease may have peracute, acute, sub-acute or chronic form.

1. Peracute mastitis: It is the most serious form of the disease. There is high fever (106 – 107°F),
anorexia and difficulty in respiration. The udder is excessively swollen and extremely painful. There
may be cessation of milk secretion and milk may be stained with blood.
2. Acute mastitis: Udder becomes swollen and yellow or brown fluids with flakes or clots may replace
the milk. Infection may be localized to only one quarter or the entire udder may be involved.
Infection may cause the udder to be non-functional or recovery may be achieved by judicial
treatment.
3. Sub-acute mastitis: There are variable changes in milk but practically no changes in the udder
tissues. Culture of milk will show presence of pathogenic bacteria.
4. Chronic mastitis: It is the terminal stage of the disease. Udder becomes hard due to fibrosis. The
quarters may become thickened, firm, nodular and sometimes atrophic. The milk may appear
yellowish fluid or white with clots or flakes.

Diagnosis

 On the basis of clinical symptoms.

 Laboratory tests
1. California Mastitis Test (CMT): In this test plastic paddle with four chambers is used. Milk
from different quarters is taken separately in each chamber. Equal amount of CMT reagent
is added to the milk and rotated and the reaction observed immediately. Formation of
greenish blue gel or precipitate denotes positive case.
2. White side test: In this test 5 drops of milk and two drops of 4% NaOH solution are taken on
a glass plate. It is then mixed with a glass rod for 20 – 25 seconds. In acute cases the mixture
becomes thick and viscid and chronic cases white flakes are formed.
3. Cultural tests can also be performed so as to identify the bacteria and antibiotic sensitivity
test carried out to select the appropriate antibiotic for treatment.

Treatment

1. Antibiotics can be used parenterally or through the intramammary route.

a) Intramammary preparations: Different combinations of antibiotics or single antibiotic
intramammary preparations are available.
 Pendistrin SH: Used 12 hourly (b.i.d.) for 6 or more infusions.
 Tilox, Ampiclox (Ampicillin + Cloxacillin): Used 24 hourly for 3 infusions.
 Mastiwok (Cefoperazone 250 mg): Single dose
b) Parenteral
 Gentamicin (Gentabiotic) @ 4.4 – 6.6 mg/kg IM for 3 – 5 days.
 Ampicillin (Bacipen) @ 2 – 5 mg/kg IM or IV for 3 – 5 days.
 Amoxycillin + Cloxacillin (Moxel): 10 mg/kg IM or IV for 3 – 5 days.
 Ampicillin + Cloxacillin (Kloxamp, Inclox): 6 – 10 mg/kg IM for 3 – 5 days.
2. Anti-inflammatory drugs
 a) Proxyvet MP (Meloxicam + Paracetamol): Inj. 20 – 30 ml IM; Bolus: 2 – 4 bolus daily.
b) Oxalgin NP (Nimesulide + Paracetamol): 1 – 2 bolus daily.
3. Milking should be done completely. Use of oxytocin @ 10 – 20 IU may be necessary when there is
incomplete milking. 4. Use of saline solutions is helpful to improve the condition and should be used
@ 2 – 5 bottles per day in alternate days.

FOOT ROT

Synonym: Infectious pododermatitis, Foul foot

It is an infectious disease of animals characterized by inflammation, necrosis and ulceration of

interdigital space resulting into lameness. Cattle, sheep, goat and pigs are more susceptible.

Etiology

Spherophorus necrophorus (Fusiformis necrophorus), a large rod shaped, Gram negative bacterium.

Transmission

The bacteria commonly enter the foot via a cut or injury by nails, stones etc. Wet and muddy conditions
influence the entry of the bacteria through the break in the foot. Penetration of skin by larvae of
Strongyloides papilosus may set up route of infection for the bacteria.

Clinical findings

 Fever (103 – 104 °F), anorexia and loss of body weight.

 There is inflammation, necrosis and ulceration skin of the interdigital space. The lesion has a
characteristic odour.
 Affected animals may kick on the ground and are unwilling to move. Lameness is the most
important sign.
 Lactating animals may give less milk.
 In sheep, the horns may be affected.
 Swollen feet and legs.

Diagnosis

 Diagnosis may be made on the basis of clinical symptoms and rapid spread of the disease as an
outbreak.
 Isolation of the bacteria through bacterial culture may be done to identify the bacteria.

Treatment

1. Parenteral treatment: Any of the following antimicrobials can be used.

 Sulphadimidine @ 150 – 200 mg/kg body weight IV.
 Procaine Penicillin G @ 22,000 IU/kg body weight IM.
 Ampicillin @ 10 mg/kg body weight IM or IV.
  Oxytetracycline @ 10 mg/kg body weight IV.
 Ceftiofur @ 1 – 2 mg/kg body weight IM.
2. Local treatment
Scrubbing of the foot and removing all necrotic tissue and local dressing with antibiotic ointment or
5% copper sulphate under a pad or bandage. Foot bath containing 5% copper sulphate or 10%
formalin are also recommended.

Control

 Pens and yards should be clean and dry.

 Sharp objects should be removed from yards and pasture.
 Infected animals should be isolated from the rest of the flock.
 Foot bath should be kept on the doorway.

PNEUMONIA

The inflammation of lungs is called pneumonia.

Cause

Pneumonia can be caused by a number of agents as bacteria, viruses, fungi, parasites and other non-
biological irritants such as dust, smoke, hot and cold air etc.

Clinical findings

 Rapid shallow breathing is an important sign of early pneumonia.

 Dyspnoea (difficult respiration) occurs in the later stages.
 There may be polypnea (increased respiration rate).
 Coughing is another important sign.
 There may be nasal discharge.
 There may be abnormal breath sounds on auscultation.
 There is usually fever in pneumonia caused by bacteria and viruses.

Treatment

1. Treatment consists of removal of the cause. In case of bacterial pneumonia antibiotics and NSAID
(Non Steroid Anti Inflammatory Drug) should be used. The choice of antibiotic depends on the
tentative diagnosis of the causative agent. In general, broad spectrum antibiotics such as ampicillin,
cloxacillin, streptopenicillin, tetracyclines, enrofloxacin, cotrimoxazole etc can be used.
2. There are a number of bacteria that can cause pneumonia. However, only the bacteria that have
lungs as their principal target organs are considered here.

Contagious bovine pleuropneumonia (CBPP)

It is a contagious septicaemic disease of cattle and buffaloes characterized by fever, cough and
pneumonia.
Etiology

Mycoplasma mycoides var. mycoides.

Transmission

Transmission occurs by inhalation of infective droplets from diseased animals. The organisms are also
present in urine and placenta and transmission can also occur by their inhalation. Recovered carrier
animals are potential source of infection.

Clinical signs

 There is sudden onset of fever (105° F), reduction in milk yield, anorexia and cessation of
rumination.
 There is severe depression and the animal is unwilling to move.
 The animal coughs after exercise.
 The animal stands with the elbows outwards, arched back and extended head.
 Respiration is shallow, rapid and accompanied by expiratory grunt.
 Pain is evident on percussion of the chest.

Diagnosis

Diagnosis is based on combination of clinical findings and serological tests.

Treatment

1. Sulfadimidine is of some value.

2. Streptomycin, Chloramphenicol and Oxytetracycline are somewhat effective.
3. Tylosin tartrate is more effective than others. Dose: 2 – 5 mg/kg body wt. bid.

Control

 Slaughter of all affected and carrier animals.

 Strict quarantine measures should be followed.
 Vaccination (live vaccine): All available vaccines are live vaccines prepared from organisms of
reduce virulence only in the areas where the disease is present. The vaccines have some side
effects as arthritis and myocarditis. Vaccination is done in animals above 2 months of age.

Contagious caprine pleuropneumonia (CCPP)

It is a highly fatal contagious disease of goats caused by Mycoplasma mycoides var. caprae and is very
much similar to contagious bovine pleuropneumonia. Transmission occurs by inhalation.

Clinical findings

 Morbidity rate is 100% and case fatality rate varies from 60 – 100%.
 There are dry and painful cough, dyspnoea and nasal discharge.
  There are fever (104.5 – 106 °F), anorexia, dullness and depression.
 The animals lie down a lot but can stand and walk. The diseased animals lag behind others.
 In the terminal stages mouth breathing, protrusion of tongue, frothy salivation are observed and
death occurs in two or more days.

Diagnosis

 Similar to CBPP.

Treatment

1. Oxytetracycline: 15 mg/kg body wt. IM.

2. Tylosin tartrate: 10 mg/kg body wt. IM along with cotrimoxazole orally for 5 – 7 days.

Control

 Strict quarantine measure should be followed.

 Removal of affected animals.
 Vaccination: Live vaccines are available which should be used according to manufacturer's
recommendation.

ENTEROTOXAEMIA

Enterotoxaemia is a group of acute, often-fatal disease resulting from the absorption of exotoxin
produced in the intestine by various types of the bacterium Clostridium perfringens.

Etiology

Clostridium perfringens are Gram-positive rods and can form spores that can live in the soil for several
years. There are six different types of the bacterium: A, B, C, D, E and F, of which type F is least common
and not as important as others.

Transmission and susceptibility

Mostly young animals are affected when they are a few days or weeks old. The organisms are naturally
found in the alimentary tract of adult animals. In the young ones disease occurs after the spores of
bacteria are ingested during suckling where the teats have been contaminated by the bacteria.
Enterotoxaemia caused by Clostridium perfringens type A

1. Cattle, Sheep, Goats and Foals

 There is an acute onset of severe depression, intense jaundice, anaemia, haemoglobinuria,
dyspnoea and severe abdominal pain.
 Temperature ranges from normal to 106°F.
 The disease is highly fatal, most of the affected animals die within 12 hrs after the onset of
illness. Occasional animals survive for several days.

Enterotoxaemia caused by Clostridium perfringens type B

  The bacteria cause lamb dysentery. Ocasionally foals and calves are also affected.
 The disease is characterized by severe dysentery, abdominal pain, spasms and aimless
wandering.
 In peracute cases there is sudden death without any signs.

Enterotoxaemia caused by Clostridium perfringens type C

 The disease is also called struck and affects sheep, goat and cattle.
 The clinical signs include abdominal pain, weakness, depression, failure to suckle and
haemorrhagic diarrhoea.

Enterotoxaemia caused by Clostridium perfringens type D

The disease is called pulpy kidney disease and is most common in lambs; calves and goats are
occasionally affected.

1. Lambs
 Duration of illness is very short, often less than two hours and never more than 12 hours.
Animals may be found dead without any previous signs.
 In closely observed flocks depression, yawning may be seen.
 Affected lambs may jump in the air, fall to the ground, go into convulsion and die within few
minutes.
2. Calves
 In peracute cases death without previous symptoms occurs.
 In acute cases in calves there is sudden onset of bellowing, mania and convulsions before
death occurs in 1 – 2 hours.
 In subacute cases the calves become quiet, docile, appear to be blind and do not drink.
Recovery usually occurs in 2 – 3 days.
3. Goats
 Diarrhoea is the main symptom and there is severe abdominal pain, convulsions and death
occurs in 4 – 8 hrs.

Enterotoxaemia caused by Clostridium perfringens type E

 Clostridium perfringens type E is a rare cause of enterotoxaemia in calves and lambs. The
disease is similar to that caused by type C.

Enterotoxaemia caused by Clostridium perfringens type F

 Clostridium perfringens type F causes diarrhoea in calves and lambs. It is not a fatal disease.

Diagnosis

 Diagnosis of enterotoxaemia caused by different types of Clostridium perfringens can be

made on the basis of history and clinical symptoms and incidence of death in very short
 period. Smears prepared from intestinal contents are observed under the microscope for
identification of bacteria. Bacteriological culture and serological tests are also performed for
confirmation.

Treatment

 Type specific hyperimmune antiserum and vaccinations are available for treatment or
prevention.
 Type A and D antiserum are only preventive.
 Type B antiserum may treat enterotoxaemia in calves caused by type B and C of the
bacteria, but in other species death usually occurs before treatment can be initiated.
 Oral or parenteral administration of penicillin may reduce the number of bacteria in the
intestine and thereby reducing the amount of toxin produced.
 Different kinds of vaccines are also available which should be used according to
manufacturer’s instructions.

STRANGLES

It is an acute infectious disease of horses characterized by catarrhal inflammation of upper respiratory

tract and abscess formation in the adjacent lymph nodes.

Etiology

It is caused by Streptococcus equi, a Gram-positive, coccobacillus, capsulated bacterium.

Susceptibility

Horses, donkeys and mules are the species affected. Horses are more susceptible than donkeys and
mules. The disease can occur at any age but young horses aged 6 – 36 months are most susceptible.

Symptoms

 The disease develops suddenly with sudden anorexia, fever (103 – 105°F), depression and
unwillingness to move.
 There is serous nasal discharge which rapidly becomes mucopurulent and more in amount.
 There is severe pharyngitis, laryngitis and rhinitis.
 Pharyngitis may be so sever that the animal is unable to swallow and attempts to swallow food
and water is often followed by regurgitation through the nostrils.
 A soft moist cough is present, which causes pain. The head may be extended to relieve pain.
 Affected lymph nodes become hot, swollen and painful and abscess develops in the lymph
nodes of the throat region. The abscesses rupture in about 10 days discharging thick creamy
yellow pus.
 Complications occur due to abscess formation in other organs such as liver, spleen and visceral
lymph nodes. Spread of organisms to lungs causes pneumonia due to which death may occur.
Diagnosis

 Symptoms of upper tract infection with purulent nasal discharge and enlargement of the lymph
nodes of the throat regions are diagnostic of strangles.
 Detection of bacteria in culture of nasal swabs and discharges from abscess can be done to
demonstrate bacteria.
 There is increase in the number of neutrophils in the blood.

Treatment

1. Procaine penicillin G @ 22,000 IU/kg b. wt. IM every 12 hours or potassium or sodium penicillin
G @ 22,000 IU/kg b. wt. IM every 6 hours.
2. Tetracycline @ 6.6 mg/kg b. wt. IV every 12 – 24 hours.
3. Sulfonamide – trimethoprim combination @ 15 – 30 mg/kg, orally or intravenously every 12
hours.
4. Provide warm shelter for horses to prevent from wet and cold weather.

Control or Vaccination

 Autogenous vaccine:- 1 ml SC, 3 injections each at 10 days interval and then repeat annually.
 Inactivated vaccine:- 2 ml SC, 3 injections each at 10 days interval and then repeat annually.

GLANDERS

Synonym: Farcy

It is a contagious disease of equines occuring either in acute or chronic form characterized by nodules
or ulcers in the respiratory tract and on the skin.

Etiology

Glanders is caused by Actinobacillus mallei (Pseudomonas mallei), a Gramnegative rod-shaped

bacterium.

Susceptibility

Horses, mules and donkeys are the species usually affected. Man is susceptible and the infection is
usually fatal.

Transmission

Transmission mostly occurs by the ingestion of food and water contaminated by nasal discharge or
sputum. Transmission by inhalation and from skin lesions is possible but rare.

Clinical findings
 1. Acute form
 There is high fever, cough and nasal discharge.
 Ulcers appear in the nasal mucosa and spread rapidly.
 Nodules form on the skin of lower limbs and abdomen.
 There is dyspnoea due to swelling of nasal mucosa.
 Death occurs in a few days due to septicemia.
2. Chronic form
 Horses usually develop the chronic form of the disease.
 There is intermittent fever, chronic cough and laboured respiration.
 Nodules form on the nasal mucosa, which soon become ulcerated causing nose bleeding.
 There is enlargement of sub-maxillary lymph nodes, which soon ulcerate, discharging pus.
 The skin form of the disease is characterized by the appearance of subcutaneous nodules,
which soon ulcerate discharging pus.
 On healing, the ulcers are replaced by star shaped scar.

Diagnosis

 Clinical signs are diagnostic of the disease.

 Mallein test: 0.1 ml mallein is injected intra-dermally into lower eyelid with tuberculin syringe.
The test is read at about 48 hours. A positive case shows marked edema of the eyelid causing
severe purulent conjunctivitis.

Treatment

1. Sulfadimidine @ 30ml/50 kg of 33% solution IM on first day followed by 15 ml daily.

2. Trimethoprim and sulfonamides @ 15 – 30 mg/kg b. wt. orally, IM or IV can also be used. E.g.
Biotrim 1 ml/30 kg b. wt.

Control

 Isolation of diseased animal.

 Separate feeders should be used for each animal.

UNIT 4: VIRAL DISEASES OF LIVESTOCK

RABIES

It is an acute viral disease of all warm blooded animals characterized by signs of abnormal behaviour,
nervous disturbances, impairment of consciousness, ascending paralysis and death.

Cause

Rabies is caused by RNA virus belonging to the genus Lyssavirus and the family Rhabdoviridae.

Susceptibility
All warm blooded animals are susceptible to rabies. Animals of all ages are affected.

Transmission

The rabies virus is present in the saliva of the affected animals and transmission commonly occurs by
the bite of rabid animals. Transmission may also occur by contamination of an open wound by infective
saliva.

Symptoms

Incubation period varies from 2 weeks to several months, usually 15 – 60 days.

1. Dogs: Two types of syndromes are noted in dogs – furious form and dumb form; however it is not
always possible to distinguish between the two.
(a) Furious form
 There is change in behaviour of the dog and it does not obey its master.
 It shows unusual violence and frenzy behaviour due to which the dog develops an urge to
bite and run away.
 It remains in unusual alert condition.
 The dog snaps or bites imaginary objects and may show fly catching stance.
 The dog bites any object near to it.
 The dog may hide in the dark due to photophobia.
 There is a change in the sound of the bark.
 In the end, the dog will lose its ability to bark, the lower jaw will hang, the tongue
protrudes and the head drops down. The dog will develop dyspnoea, ascending paralysis,
coma and death. Death occurs in 3 – 4 days after the onset of symptoms. In any case
death occurs in 10 days.
(b) Dumb form: This form is also known as the paralytic form.
 There is paralysis of lower jaw, tongue, larynx and hind quarters.
 The dogs are not capable of biting.
 Dogs produce unusual sound known as “howl”.
 There is hanging of jaw and the dog is unable to close the mouth.
 The condition may be confused with choke – a condition of esophageal obstruction.
 There is constant salivation.
 In the terminal stages the dogs show progressive weakness and paralysis due to which the
dog staggers and falls.
 Ultimately there is coma and death.
2. Cattle
 The animal is alert and hypersensitive to sounds and movement.
 The animal may attack other animals and inanimate objects.
 There is excessive bellowing and the sound is hoarse.
 Increased sexual excitement in both sexes.
 There is variable appetite.
  There is twitching of ears and tremors muzzle.
 The animals cannot swallow due to paralysis of pharyngeal muscles.
 There are signs of choke.
 Death occurs in 1 – 6 days, within 24 – 48 hours in severe cases.
3. Pigs
 Clinical findings in pigs are extremely variable.
 Pigs may show excitement and become furious or become dull and in coordinated.
 There is twitching of nose, rapid chewing movements, excessive salivation and convulsion.
 Affected pigs may walk backwards.
 In terminal stages there is paralysis and death occurs in 12 – 48 hours after the onset of
symptoms.
4. Goats
 Symptoms are more or less similar to cattle. They show aggression and bleat continuously.

Diagnosis

 Diagnosis is done on the basis of clinical symptoms. A suspected dog must be isolated for
at least 10 days. If rabid, it will die in that time.
 In rabies laboratory, smear of brain tissue (hippocampus) of suspected animal is made and
is observed under the microscope for the presence of special lesions called negri bodies.
Presence of negri bodies indicates positive case of rabies.

Treatment

There is no specific treatment of clinical rabies. Treatment should not be attempted after clinical signs
are evident. The site of wound should be washed with running water and soap. Alkali prevents
multiplication of rabies virus. So sodium bicarbonate or caustic soda may be used. Tincture of iodine
may also be used. The wound should not be sutured within 24 hours of bite but only after 48 hours.

Control

Regular vaccination of dogs is recommended in endemic areas. Different vaccines with different
methods of preparation are available and should be used according to the manufacturer’s
recommendation.

 Pre-exposure use: 1 ml SC or IM at 3 months of age or above.

 Post-exposure use: A course of 6 injections at 0, 3, 7, 14 and 28 days should be given. Immunity
is for 2 years; however it is better to give annual vaccination in endemic areas.

RINDERPEST

Synonym: Cattle plague

Rinderpest is an acute or subacute highly contagious viral disease of cattle, buffalo, sheep, goat and pigs
characterized by fever, necrotic stomatitis, gastroenteritis, diarrhea, dehydration and destruction of
lymphocytes.

Cause

Rinderpest is caused by RNA virus of the genus morbillivirus and the family Paramyxoviridae.

Susceptibility

Young and purebred exotic cattle are more susceptible to the virus than crossbred and indigenous
breeds. Goat, sheep and pigs are more resistant to infection than cattle and buffaloes and only mild
form of the disease occurs in them. Wildlife is often affected during outbreak and infection usually
spreads in them from infected cattle.

Morbidity and mortality

In highly susceptible populations, the morbidity and mortality rates are approximately 100% and 50%
(25 – 90%) respectively. In endemic areas, most of the cattle population has some degree of immunity
and case fatality rate rarely exceeds 30%.

Transmission: Close contact between infected and non-infected animals is usually necessary for spread
of the disease. The virus is excreted by infected animals in urine, faeces, oral, nasal and eye discharges,
milk, sweat and vaginal discharges. Healthy animals become infected by the ingestion of contaminated
food and water and by inhalation of aerosol.

Clinical findings

 In acute cases the incubation period is usually 6 – 9 days.

 In the first stage of the disease there is high fever (105 – 107°F). During this stage there is
anorexia, fall in milk yield, dryness of muzzle, lachrymation and staring body coat. In this period,
the faeces are hard and covered by mucus and streaks of blood.
 After 2 – 3 days of fever, there is inflammation of oral, nasal and conjunctival mucosa. There is
profuse blood-stained salivation. The nasal and lachrymal discharges soon become
mucopurulent.
 Grey colored necrotic lesions 1 – 5 cm in diameter, develop on the inside of the lip, adjacent
gums, on cheek mucosa and on the surface of the tongue. Later on they become general in the
mouth. Similar lesions are common on nasal, vulval and vaginal mucosae and pregnant cattle
may abort.
 Thereafter there is erosion of the necrotic material leaving raw, red areas with sharp edges and
these may coalesce to form shallow ulcers.
 There is severe foul smelling watery diarrhea (shooting diarrhea) containing mucous, blood and
fragments of necrotic epithelium.
  In the final stages the animals become very much emaciated and dehydrated. There is
dyspnoea, prostration and the body temperature falls below normal due to which death usually
occurs in a period of 24 hrs.

In endemic areas, both sub-acute form and cutaneous (skin) form occur with lower morbidity and
mortality rates. In the sub-acute form, there is mild temperature, anorexia, salivation but not dysentery.
In the skin form small pustules develop on the neck, over the withers, inside the thighs and on the
scrotum. Most affected animals recover and immunity is life long.

In sheep, goats and Asian pigs symptoms and lesion are similar to cattle but appear in a mild form.

Diagnosis

 A provisional diagnosis of rinderpest is based on history of outbreak, clinical findings, gross

lesions, and morbidity rate and post mortem lesions. Partial confirmatory diagnosis can be
achieved by total WBC count which becomes less than 4000/ml of blood.
 For confirmatory diagnosis various serological tests for antibody detection should be done. E.g.
Agar gel diffusion test, compliment fixation test, virus neutralization test, ELISA test.
1. PM findings
 The carcass is dehydrated, emaciated and soiled with fetid faeces.
 Small necrotic areas are seen on the oral mucosa and separation of these necrotic materials
leaves ulcers with red colour. Similar lesions occur in pharynx, upper esophagus and abomasum,
particularly in the pyloric region.
 The mesenteric lymph nodes are swollen, hemorrhagic and necrotic.
 Colon mucosa presents characteristic red colored zebra stripping.

Treatment

Treatment is ineffective with any drugs. Antibiotics are largely used to control secondary bacterial and
protozoal diseases.

Control

1. Prevention of movement of animals and its products from endemic/epidemic areas by strict
quarantine measures should be followed.
2. In endemic areas controls can be achieved by annual vaccination. The principal vaccine used
against rinderpest throughout the world is “Tissue culture Rinderpest vaccine”. It is generally
available in small ampoules which after reconstitution/dilution are used @ 1ml/animal by SC
route. Immunity is for several years but annual vaccination is recommended in endemic areas for
3 – 4 years.

FOOT AND MOUTH DISEASE (FMD)

FMD is an acute febrile highly contagious disease of cloven footed (even toed) animals characterized by
vesicle formation in the epithelium of buccal cavity (oral cavity), tongue, nares, muzzle, feet, teats and
udder.

Cause

It is caused by RNA virus belonging to genus Apthovirus and Picornaviridae family. There are seven
major serotypes of the virus. They are O, A, C, SAT-1, SAT-2, SAT-3 and Asia-1. These are antigenically
different to each other and cross-immunity between them does not occur.

Susceptibility

Cattle are the most susceptible species. Buffalo, sheep, goat, pig and deer are susceptible to infection.

Morbidity and mortality

The morbidity rate in FMD outbreaks can reach 100% with virulent virus and highly susceptible animals.
However, the case-fatality rate is generally very low, about 2% in adults and 20% in young ones.

Transmission

The disease spreads at an extremely rapid rate through direct contact with the infected animals. All the
secretions and excretions – urine, milk, faeces and saliva remain infective. The vesicles also contain a
large number of viruses and are infective. Infection occurs by the ingestion or inhalation. Cattle may also
remain as a carrier following recovery after infection.

Clinical findings

The incubation period varies between 1 – 7 days.

 At the onset of the disease, there is high fever (104 – 106°F), reduction in milk production,
severe depression and anorexia.
 The period of fever is followed by appearance of characteristic vesicle in the oral mucosa,
interdigital space, udder etc.
 At this stage temperature falls down and there is profuse salivation and lameness. The saliva
hangs in long strings and there is frequent smacking of lips.
 The vesicles rupture within 24 hours leaving ulcers on the surface.
 Finally the mucosal surface is covered with grey fibrinous covering which turns yellow or brown
and the epithelium is restored so that the animal starts eating again.
 Due to the presence of vesicle at the interdigital space the animals are lame and rupture of
these vesicles cause painful swelling of the lower part of feet.
 Secondary bacterial infection may cause loss of hooves, mastitis in dairy cows and pregnant
cattle may abort.
 Young animal may suffer heavy mortality even without typical vesicular lesion in mouth and
feet. Death is due to gastroenteritis and degeneration of heart muscles.
  After recovery the animal shows panting, anemia, overgrowth of hair and diabetes mellitus.
 In sheep, goat and pigs the disease is often mild. Large vesicles occur in the snout and feet of the
pigs. Adult sheep show symptom of fever, nasal discharge, salivation, lameness and in these
three species lesions are more marked in the feet than in mouth.

Diagnosis

Diagnosis is based on history, clinical symptoms and serological tests.

Treatment

There is no specific treatment for FMD. Symptomatic treatment may be followed. Antiseptic mouth
wash with potassium permanganate, sodium carbonate, boric acid, and glycerin may be applied over
mouth lesions. Antibiotics may be applied to prevent secondary bacterial infection.

Control

 Prevention of movement of animals and animal products form enzootic areas should be
followed with strict quarantine measures.
 Vaccination should be followed regularly:
a) Raksha FMD vaccine [Indian Immunologicals]:
 Large animal: 3 ml Small animal: 1 ml by SC route. Initial vaccination 4 months Booster
vaccination 2 – 4 months later Revaccination Every 6 months thereafter
b) Raksha Triovac [Indian Immunologicals]: Against FMD, HS and BQ
 Cattle and buffaloes : 3 ml Initial vaccination 4 months of age Booster vaccination 9
months later Revaccination Annual

PESTE DES PETITS RUMINANTS (PPR)

Synonym: Pseudorinder pest; Goat plague; Kata

It is a sub-acute or acute, highly contagious disease of small ruminants having resemblance to rinderpest
and characterized by fever, anorexia, stomatitis, gastroenteritis and pneumonitis.

Cause

PPR is caused by the virus belonging to the genus morbillivirus and the family Paramyxoviridae. It is
closely related to rinderpest virus.

Susceptibility

PPR occurs mostly in goats and less often in sheep. Kids over four months and under one years of age
are most susceptible to the disease.

Morbidity and mortality

Morbidity rate ranges from 50 – 90%. Case fatality rates are 55 – 85% in goats and less than 10% in
sheep.

Transmission

Close contact with an infected animal or contaminated material is required for the spread of the
disease. Large amount of the virus are present in all body excretions and secretions, especially in
diarrheic faeces. Infection is mainly by inhalation but can also occur through the conjunctiva and oral
mucosa.

Clinical findings

The disease occurs in acute or sub-acute forms. The acute form is seen mainly in goats and is similar to
rinderpest in cattle except that severe respiratory distress is often present in PPR.

1. Acute form
 It is characterized by high fever (above 104°F) accompanied by dullness, anorexia, rough
body coat, sneezing and serous discharge from the eyes and nostrils.
 The ocular and nasal discharges later on dry up matting the eye lids and partially occluding
the external nares.
 After one or two days of fever necrotic lesions develop in the mouth and extend over the
entire oral mucosa.
 Profuse mucoid and blood tinged diarrhea develop in 3 – 4 days after onset of fever.
 Dyspnoea and coughing occur later. The respiratory signs become worse when there is a
secondary bacterial pneumonia.
 Death usually occurs within one week of the onset of illness.
2. Sub-acute forms are common in sheep but they also occur in goats. The signs and lesions are less
severe and a few animals may die within 2 weeks, but most of them recover.

Diagnosis

 It is based on history and clinical findings.

 On blood examination there is leucopenia (reduction of leukocytes), haemoconcentration,
hyponatremia (reduction in blood sodium) and hypocalcemia.
 Confirmatory diagnosis requires serological tests.

PM lesions

 Carcass is severely dehydrated, hindquarters soiled with fluidy feces and crusts of exudates are
present around the eyes, nose and lips.
 Areas of erosion, necrosis and ulceration are present in the oral mucosa, pharynx and upper
oesophagus.
 Hemorrhagic ulceration is marked in ileo-cecal region, colon and rectum where they produce
typical 'zebra stripes'.
 There is pneumonia, mucopurulent exudate in the nasal passage up to the trachea.
Treatment

There is no treatment against PPR. Supportive treatment includes fluid therapy for dehydration and
antibiotics to prevent secondary bacterial infections. Lesions around the eyes, nostrils and mouth should
be cleaned and good nursing provided.

Control

 Strict sanitation and hygiene measures should be followed in a flock.

 Proper quarantine measures should be followed.
 Vaccination: Tissue Culture Vaccine @ 1ml SC at 3 months of age or above.

SWINE FEVER

Synonym: Hog cholera

It is a highly contagious disease occurring in acute, chronic or inapparent form in pigs of all ages
characterized by rapid and sudden onset, fever and hemorrhage in the skin and internal organs.

Cause

Swine fever is caused by a virus belonging to the genus Pestivirus and family Togaviridae.

Occurrence

Among the domestic animals, only the pigs are naturally infected. All breeds and ages are susceptible.

Morbidity and mortality

The disease usually occurs in epidemics, often with morbidity of 100% and mortality rate nearly 100%
when infected by a highly virulent virus. However, inapparent form of the disease may be caused by
virus of low virulence.

Transmission

The disease may be transmitted directly or indirectly. Direct transmission occurs by inhalation or
ingestion of contaminated food and water. The virus is present in urine, ocular and nasal discharges.
Indirect transmission through flies and mosquitoes, breeding and feeding appliances/equipments, boots
and vehicles may also occur. In pregnant sows the virus can cross the placenta and infect the foetus
leading to still birth or abnormal piglets dying soon after birth.

Clinical findings

1. Per acute form: This form occurs mostly in young pigs which die within 24 hours after a high rise of
temperature 106 – 107°F and sometimes with red coloured patches in the non-hairy part of the
skin.
2. Acute form: It is the most common form of the disease.
  There is high rise of temperature up to 107°F.
 Animals show dullness, depression, anorexia, vomiting, constipation followed by diarrhea,
dehydration and loss of body weight.
 There is hyperemia of skin with purple colouration of snout, ears, abdomen, inner sides of
legs and necrotic lesion occur on the tip of the ear, tail, lips and vulva.
 There is mucopurulent to purulent discharge from the eyes and eyelids may glue together.
 Nervous signs such as circling, incoordination, muscle tremor and convulsion also occur.
 Death usually occurs in 5 – 7 days after onset of illness.
 Reproductive disorders in sows such as mummified fetus, abortion, abnormal piglets may be
seen.
3. Chronic form: In chronic form, morbidity is 90% and mortality is 60 – 70%. The signs are chronic
diarrhea, pneumonia, depression, anorexia, persistent mild fever, skin lesion such as loss of hair,
dermatitis, blotching of ears and finally deep purple coloration of the abdominal skin.

Diagnosis

It is based on history, clinical manifestation, PM lesions and serum test. The characteristics PM lesions
are presence of button ulcers in the caecum or colon, turkey eggs appearance of kidney.

Treatment

There is no specific treatment for swine fever. Hyper immune serum in the early stages of disease may
reduce mortality rate and should be applied 50 – 150 ml/ animal IM or SC.

Control

 Slaughter of infected animals and the dead body should be buried or burnt.
 Disinfection of the premises should be followed during an outbreak.
 Garbage should be properly cooked before feeding.
 Vaccination: Swine fever vaccine (Lapinized – live): 1 ml SC. It provides immunity for one year.

CANINE DISTEMPER

Synonym: Hard pad disease

It is a highly acute, contagious disease of dogs characterized by biphasic fever, ocular and nasal catarrah
(excessive secretion of mucous membranes), skin lesions, gastroenteritis, broncho-pneumonia and
nervous signs.

Cause

It is caused by RNA virus belonging to the genus morbillivirus and family Paramyxoviridae.

Susceptibility
All members of the canine family e.g. Dog, fox, jackal, wolf, etc are susceptible. Exotic breeds of dogs
are most susceptible than indigenous breeds. Dogs of all ages are affected but young ones between 3 –
6 months are most susceptible and mortality rate in them is also high.

Transmission

Transmission mainly occurs by inhalation. The virus is present in all secretion and excretion of the body.
Transmission through ingestion of contaminated water and food is also possible.

Symptoms

 The dog is dull and depressed and is indifferent to its surrounding for a day or two in the initial
phase of the disease.
 There is a high rise of temperature (103 – 104°F). In this stage the nose will become dry and hot
and eyes become congested.
 The animals become markedly depressed and anorectic.
 The temperature usually comes down in 3 – 4 days and remains normal till 11 – 12 days after
which the temperature rises again (diphasic fever).
 The second rise of temperature is accompanied by rhinitis, conjunctivitis, gastroenteritis and
bronchopneumonia.

There may be variation in the clinical manifestations depending on severity and the system involved. In
general, the systems involved and the manifestations are:

(a) Pulmonary form: It is more prevalent than digestive form. It is characterized by oculonasal
discharge pharyngitis and bronchitis. Bronchopneumonia is a constant feature.
(b) Digestive form: Loss of appetite, vomiting abdominal pain and loose faeces with or without
blood.
(c) Ocular form: Swollen eyelids, congestion of conjunctiva and purulent discharge from the eyes.
(d) Nervous form: Restlessness, excitement, chewing movement, excessive salivation and
convulsion. The dog may show epileptic fits/seizures (the dog falls down on its side and performs
running movement). Later on there is ascending paralysis. During seizures, there may be
involuntary defecation and urination.
(e) Cutaneous form: There is appearance of vesicle and pustules in the skin of abdomen and thigh.
The skin of foot pad and nose become hard due to hyper keratosis.

Diagnosis

Diagnosis is based on characteristic clinical symptoms, history of immunization and laboratory tests.

Treatment

1. There is no specific treatment for canine distemper. Anticanine distemper serum may be given to
save the life of the patient. It should be given @ 1 – 5 ml/kg body weight by IV, IM or SC route as
soon as possible. In severe cases 5 – 10 ml/kg body weight can also be given.
 2. Other symptomatic treatments may be tried such as broad spectrum antibiotics, neurovitamins
and anticonvulsants.
 Neurovitamins: Neurobion/Neuroxin @ 2 – 3 ml IM for 1 week.
 Anticonvulsant: Chlorpromazine HCl @ 5mg/kg b. wt. orally or 1 – 2 mg/ kg b. wt. IM or IV.
3. Vaccination
 Candur – DHL (Hoechst India Ltd.): It provides immunity against canine distemper, canine
hepatitis and leptospirosis. It is given 2 ml by SC or IM at 7 – 9 weeks of age. Repeat at 12
– 14 weeks of age and then annually.
 Canilep – DHL: It provides immunity against canine distemper, hepatitis, leptospirosis and
Parvovirus. It is given 2ml by SC at 6 – 8 weeks of age. Repeat at 12 weeks of age and then
annually.

UNIT 5. BACTERIAL DISEASES OF POULTRY

PULLORUM DISEASE

Synonym: Bacillary White Diarrhoea

Pullorum is a disease that usually occurs in an acute, systemic form in chicks and poults characterized by
white diarrhoea and high mortality, but is more often localized and chronic in case of adults,
characterized by sub-optimal production.

Etiology

Salmonella pullorum, a Gram negative, rod shaped bacterium.

Hosts

Chicken and turkeys are the most important hosts. Quails, ducks, guinea fowl, pheasants, sparrows,
pigeons and some other birds can suffer from the disease.

Transmission of the disease occurs in the following ways:

a. Vertical transmission:- A carrier hen lays infected eggs which when hatched produces an infected
chick.
b. Horizontal transmission: Infection through consumption of contaminated feed and water, by
inhalation and in the incubator from hatched diseased chicks to other healthy chicks.

Morbidity and mortality

Chicks die between 2 – 7 days of age if they have infection during hatching. If they get infection after
hatching, they show symptoms about 10 days post infection, up to the age of 3 weeks. Maximum
mortality usually occurs in the 2nd week after hatching and it declines rapidly in the 3rd and 4th weeks
and may stop in 5th week of age. Mortality may vary from no losses to 100% in serious outbreaks.
Morbidity is often much higher than mortality.
Symptoms

Young chicks

 Very poor hatchability; dead-in-shell chicks.

 Death shortly after hatching without any marked symptoms.
 Huddling near the heat source, loss of appetite, white diarrhoea.
 In sub-acute form lameness associated with swollen hock joints may be seen in growing birds
and result in poor growth rates.

Adults

 Few birds show sub-optimal production.

Lesions

Young chicks

 The newly hatched chicks which die of the disease may not show any gross lesion, except
congested lungs. Some of them may show haemorrhagic streaks on normally yellowish liver.
 The chicks which die later may show grayish necrotic spots in the liver, grayish necrotic nodules
in the lungs and heart, catarrhal enteritis, presence of semisolid yellowish material (cheesy
material) in the ceca.
 Unabsorbed and coagulated egg yolk may be present in the peritoneum.

Adult birds

 Adult birds have abnormal ovary with cystic, misshapen and discolored ova (brownish or
greenish).
 There may be haemorrhage and atrophy of ovary.
 Occasionally there is arthritis of hock joint, pericarditis and peritonitis.

Diagnosis

 On the basis of history, clinical signs and PM lesions.

 Identification after isolation of bacteria following bacterial culture.
 Serological tests: Rapid plate agglutination test is usually done.

Treatment

Treatment does not prevent the birds from becoming carriers. The treatment of birds is therefore
questionable. For treatment Furazolidone, Trimethoprim and Sulphadiazine combination are good.

1. Antibacterials
 Furazolidone: 500 gm/tonne of feed as prophylaxis; 1 – 2 kg/tonne of feed as curative for 14
days.
  Furaltadone [Furasol, Fural]: 0.5 gm/liter of drinking water for chicks; 1 gm/ liter of drinking
water for growers and layers.
 Sulfadiazine + Trimethoprim combination: Biotrim @ 1 ml/2 – 4 liters of drinking water for 3
days
 Woktrin pw. @ 1 gm/liter of drinking water for 3 days.
2. Multivitamins should be provided to reduce stress Vimeral liquid @ 5 ml, 7.5 ml and 10 ml for 100
chicks, growers and layers respectively.

Prevention and control

 Incubation of eggs from affected birds should be avoided.

 Chicks should be obtained form breeder flock known and tested to be free from the disease.
 The positive reactors should be immediately removed from the farm and destroyed.
 Disinfection of fumigation of incubator and eggs must be routinely done.
 Maintenance of hygiene in the farm.

FOWL TYPHOID

It is an acute or chronic septicaemic disease which mainly affects adult birds and sometimes chicks
under unhygienic conditions.

Etiology

The causative agent of fowl typhoid is Salmonella gallinarum, Gram negative bacterium. It has similar
antigens to S. pullorum. Thus antigen of one can cross agglutinate another.

Hosts

The disease mainly affects chickens and turkeys. Ducks, pheasants, peacocks, guinea fowls and a few
other birds are also known to suffer from the disease. Disease may be seen at any age but it is more
common in birds of about 3 – 6 months of age.
Transmission

Salmonella gallinarum may be found in 10 – 50% eggs laid by a carrier hen. Feed and water play an
important role in the spread of the disease. The disease also affects newly hatched chicks but in this
case mortality continues up to the age of maturity. On contaminated premises not exposed to sunlight
the organisms may survive from 3 – 8 months. It dies in 24 hours on exposure to sunlight.

Mortality

Mortality may be moderate or very high, depending on virulence of the bacteria.

Clinical signs
  Acute outbreak occurs in younger chicks in growers which show signs like that of pullorum
disease characterized by somnolence, loss of appetite, water to yellow mucoid diarrhoea that
adheres to the vent, and ruffled feathers.
 Death of birds takes place from second day and declines by about 5th day and usually stops by
about 8 months.
 There is decreased growth in birds that survive the infection.
 In growing and mature fowls there are sudden drop in feed consumption, droopy wings and
ruffled feathers, pale heads and shrunken combs.
 In chronic cases symptoms may not be seen. However, birds may show paleness of comb and
wattle, mucous membranes of eyelids and oral cavity, continuous loss of condition, and chronic
yellow diarrhoea which adhere to the feathers around the vent.

Lesions

Young chickens

 In peracute cases, few or no gross lesions are observed.

 In prolonged cases, the gross lesions are swelling and redness of liver, spleen, and kidneys.
 Swollen copper coloured liver is usually observed.
 As in case of pullorum disease grayish necrotic spots may be seen in liver, lungs, heart and
gizzard.

Adult chickens

 Grayish, white necrotic foci in the liver and myocardium.

 Pericarditis and peritonitis from ruptured ova.
 Haemorrhagic, mishshapen and discoloured ova.
 There is catarrhal type of enteritis.

Diagnosis

The methods of diagnosis are similar as described for pullorum disease. The antigens of S. pullorum and
S. gallinarum are similar. Thus antigens of one can crossagglutinate another. It may be difficult to
differentiate the condition from pullorum disease. The following differences are seen:

Pullorum (Fowl typhoid)

S.NO. Pullorum S.No. Fowl Typhoid

1 Chicks are mostly affected.
2 Diarrhoea, whitish is a constant symptom.
3 Liver is of normal colour.
4 Ova are abnormal.
5 Ferments dextrose with gas formation.
6 Bacteria do not ferment dulcitol and maltose.
7 Bacteria turn litmus milk acid.
1 Adults are mostly affected.
2 Diarrhoea is not constant, feces is yellowish.
3 Liver is of copper colour.
4 Ova are not usually affected.
5 Ferments dextrose without gases.
6 Bacteria ferment dulcitol and maltose.
7 Bacteria turn litmus milk alkaline.
Treatment and control measures

 Treatment and control measures are similar to pullorum disease.

CHRONIC RESPIRATORY DISEASE (CRD)

It is a chronic disease of fowls affecting the respiratory system characterized by respiratory noise, cough,
nasal discharge, and frequently sinusitis in turkeys.

Etiology

It is caused by Mycoplasma gallisepticum, a Gram negative bacterium.

Hosts

CRD affects different bird species, most importantly chickens and turkeys. It affects all ages of the fowl,
but is most common in young birds of 4 – 10 weeks of age. In older birds the disease usually occurs after
first being infected by another bacterium, Escherichia coli and some respiratory viruses.

Transmission

Transmission mainly occurs by inhalation and through eggs. It spreads relatively slowly to other birds.
CRD is common in flocks raised under bad management such as poor ventilation, over crowding,
inadequate and unbalanced feeding etc.

Morbidity and mortality

Morbidity and mortality are higher especially during cold months and in young birds than in older birds.
However, it is negligible when not complicated by other diseases.

Symptoms

 The most characteristic signs are seen in adult birds and the disease starts with sneezing,
coughing, respiratory distress and respiratory noise.
 Feed consumption is reduced and birds lose weight.
 In laying flocks egg production declines to as much as 50%.

Lesions

 The most important pathological lesion is cloudy appearance of one or more air sacs. In
complicated cases the air sacs contain caseous (cheesy) material.
 Excess mucous in nasal passages, trachea, bronchi and air sacs.
 Trachea and conjunctiva may be congested.
 In cases complicated by E. coli there is fibrinous pericarditis and perihepatitis.

Diagnosis
  On the basis of history, symptoms and PM lesions.
 Isolation and identification of bacteria.
 Serological tests.

Treatment

Antibiotics such as Tylosin, Tetracyclines, Tiamulin, and Enrofloxacin can be used. However, the drug of
choice is Tylosin.

1. Tylosin tartrate (TN Tylosin, Tylan): 1 gm/liter of drinking water for 3 – 5 days. 2
2. Chlortetracycline/Oxytetracycline powder: 1 – 2 gm/liter of drinking water.
3. Tiamulin: 0.025 % in drinking water for 3 days; e.g. Tiamutin @ 55 gm/100 liters of drinking water
for 3 days.

Prevention and control

 Incubation of eggs from affected birds should be avoided.

 Disinfection of fumigation of incubator and eggs must be routinely done.
 Maintenance of hygiene in the farm.

COLIBACILLOSIS

Bacteria of the species Escherichia coli are normal inhabitants of the digestive tract of mammals and
birds. These are opportunistic bacteria that cause secondary infection in all types of immunosuppressive
diseases of enteric infection such as IBD, mycotoxicity, ND and CRD. E. coli infections include
colisepticaemia, yolk sac infection, salpingits, egg peritonitis, air sac disease and coligranuloma (Hjarre's
disease) in poultry, caused entirely or partly by the bacteria. These conditions can be conventionally
grouped together under colibacillosis. E. coli are Gram negative, flagellated rod shaped bacteria.

1. Colisepticaemia

It is a disease of chicks generally of 5 – 10 weeks of age. Broilers are most susceptible. Mortality can
reach 5%, occasionally more, with morbidity reaching up to 50%. Predisposing factors may include other
respiratory infections (CRD), other diseases as coccidiosis or respiratory virus infections or poor
nutrition.

Symptoms

The first signs are decreased feed consumption and depression. Later on there is watery diarrhoea
(which causes pasting of vent, feathers), dyspnoea, sneezing, respiratory noise, dehydration, emaciation
and death.

Lesions

 The most important lesion is fibrinous pericarditis (resembling plastic sheet) with milky fluid in
the pericardium.
  Air sac membranes are cloudy in appearance and may become thicker.
 Fibrinous perihepatitis with dark liver.
 Liver, spleen, lungs and kidneys are dark and congested.

Diagnosis

 Disease in growing birds with lesions of fibrinous pericarditis and perihepatitis.

 Bacterial culture – direct culture form the heart, liver, lungs and air sacs.
2. Omphalitis (Yolk sac infection, Mushy chick disease)

It is the most common cause of heavy mortality in chicks during the first week after hatching. Affected
chicks are weak and retarded in growth, anorectic and have inflammed navel. Mortality is generally 5 –
10% but may reach 100%.

Transmission

 Contaminated feed and water.

 Hatchery borne infection – during hatching period, unhygienic condition in hatchery from
contaminated egg shell.
 No or very less vertical transmission.

Lesions

 Yolk sacs appear distended and contain foul smelling, yellow or brown curdled yolk.
 Septicaemic carcass with subcutaneous blood vessels engorged and dilated; congested lungs
and liver; dark and swollen kidneys.
 There may be pericarditis and perihepatitis.
 Adhesions between the skin, abdominal wall and underlying yolk sac may be seen.
3. Egg peritonitis

Adult layers are generally affected with this condition. Flock egg peritonitis outbreaks are often linked to
cannibalism and vent pecking. Mortality is negligible, 1% in a month.

Lesions

 Yellowish fibrinous or fibrinopurulent material is present in the abdominal cavity with

inflammation and distortion of the ovaries and salpingitis.

Treatment

1. Many different antibiotics and other drugs have been used for treatment.
 Cephalexin (Lixen pw, Cephalexin) Treatment: 20 gm/ 500 chicks, 200 growers and 100 layers
for 3 – 5 days. Prevention of early chick mortality: 20 gm/1,000 chicks for 3 – 5 days.
 Enrofloxacin (Meriquin, Enrocin, Enrox) 1 ml/1 – 2 liters of drinking water for 3 – 5 days.
 Neomycin + Doxycycline (Bidox N, Neodox forte) 1 gm/ 5 liters of drinking water for 5 days.
Stress and early chick mortality: 1 gm/10 liters of drinking water.
  Colistin sulphate (Colistin pw.) 200 gm/ ton of feed or as 2 gm/15 – 20 liters of water for 75 –
100 birds for 3 – days.
 Chloramphenicol (Neochlor pw.) 1 gm/5 liters of water on first day followed by half the dose for
3 – 5 days.
2. Vitamin C: Addition of 330 mg of vitamin C/kg feed during outbreak reduces mortality. It can also be
used in drinking water. E.g. C-Care 500 @ 10 gm/15 litres of drinking water.
3. Vitamin E and A to enhance immunity. Vitamin E: E-Care-Se @ 5 gm/200 birds through drinking
water. Vitamin A: Recovit, Vimeral etc.

UNIT 6. VIRAL DISEASES OF POULTRY

NEW CASTLE DISEASE (ND)

Synonym: Ranikhet Disease (RD)

It is a highly infectious disease of poultry and other birds characterized by respiratory and nervous signs,
lower production and high mortality.

Cause

ND is caused by an RNA virus belonging to Paramyxoviridae family. Numerous strains of the virus have
been identified. The strains of the virus are classified as velogenic, mesogenic and lentogenic, in order of
decreasing virulence.

Occurrence

ND occurs worldwide and apparently all birds are affected, with the most severe outbreaks seen in
domestic fowls and turkeys.

Transmission

The sick birds excrete the virus through feces and nasal secretion. The virus enters into the birds through
the digestive system through food and water or respiratory system through air. Pig, calf and man can
spread the disease. The disease can be spread by attendants, wild birds and fomites.

Mortality

In acute or velogenic strain infection, mortality may reach up to 90 – 100%, but if the temperature of the
environment is low it may go up to 55%. In milder forms it may vary from 5 – 10%.

Symptoms

Symptoms differ somewhat on the basis of velogenic, mesogenic or lentogenic strain of virus being the
cause.

1. Velogenic strain
 Sudden death.
  The typical symptoms are dullness and depression, respiratory noise, gasping with outstretched
neck, nasal discharge and greenish watery diarrhea.
 Sometimes in nervous form of the disease, there may be torticollis (twisting of the neck),
incoordination or even paralysis.
 In laying birds there is loss of egg production in addition to the above symptoms.
2. Mesogenic strain
 It is milder form of the disease and is less severe.
 Mortality is variable and ranges from 5 – 15%.
 Respiratory distress, greenish diarrhea, marked loss of egg production and nervous symptoms
characterized by paralysis of wings and legs, torticollis are the typical features observed.
3. Lentogenic strain
 It is mild form of the disease that occurs with mild respiratory symptoms and rapid
reduction of egg production.
 Mortality in adult birds may be negligible but in young chicks it may reach 5%.
 The disease may be asymptomatic and its existence recognized only by serological tests.

Lesions

 Pinpoint hemorrhages are found at the tips of proventricular glands and submucosa of gizzard.
 The cecal tonsils are necrotic and hemorrhagic.
 Enteritis with ulcers in the intestine, which can sometimes be seen without opening the
intestine. The ulcers are hemorrhagic and generally with necrotic surface.
 In laying birds, the ova are congested and there may be salpingitis (inflammation of the oviduct),
leading to ova in the peritoneum.
 There may be additional lesions in the respiratory tract such as trachetis, air sacculitis and
conjunctivitis.
 In infection by lentogenic strain, the lesions may not be clear. Respiratory lesions may be
intensified by secondary infection such as Mycoplasma.

Diagnosis

 Diagnosis is based on history, clinical signs and PM lesions.

 Serological tests are necessary for confirmatory diagnosis.

Treatment

There is no effective treatment for ND. Antibiotics may be used to prevent secondary infection caused
by bacteria, and vitamins and electrolytes should be used as supportive therapy.

Prevention and control

Four types of vaccines are available for prevention: F strain, B strain, R2b and Lasota.
  F and B strain vaccines are given as a drop instilled into the nostrils or eyes of one day old chicks
or at 3 – 7 days old chicks. This vaccine can protect birds up to 15 weeks of age; hence broilers
may need only this vaccine.
 Lasota vaccine alone and lasota combined with IB vaccines are available. Lasota vaccine alone
can be given in 4 – 10 days old chicks by intranasal or intraocular route; in 5 – 6 weeks old chicks
in drinking water and again in 15 – 16 weeks old birds in drinking water.
 R2b vaccine is injected @ 0.5 ml/bird by SC or IM route at the age of 8 – 13 weeks.

INFECTIOUS BURSAL DISEASE (IBD)

Synonym: Gumboro disease

IBD is an acute highly contagious viral disease of young chickens of the age group of 3 – 6 weeks that
causes variable mortality and immunosupression.

Cause

IBD is caused by an RNA virus belonging to Birnaviridae family.

Occurrence

Chickens aged between 3 – 6 weeks are most susceptible to IBD, although birds from 1 – 20 weeks of
age have been reported to be affected.

Transmission

The disease spreads rapidly because of its highly contagious nature. The virus is shed in feces of affected
birds and transmission occurs due to contamination of feed and water. Attendants, visitors and fomites
can also help in the spread of the disease. Recovered birds do not become carrier and it is not
transmitted through eggs.

Morbidity and mortality

Morbidity rates range from 10 – 90% and sometimes reach 100%. Mortality reaches a peak and reduces
within a week. It is usually less than 10% but can reach 30% or more. Thereafter recovery is rapid.

Symptoms

 The birds suffer from whitish or watery diarrhea, and sit quietly with closed eyes and ruffled
feathers.
 There are anorexia, depression and occasionally trembling.
 Body temperature rises at about 48 hours after infection and drops below normal sometime
before death.
 Pecking of vent is one of the earliest and common signs.

Lesions
  The bursa of Fabricius first becomes enlarged, but atrophies within 3 – 8 days after infection.
 The bursa may contain mucopurulent exudates and hemorrhagic spots may be present in the
mucosal surface of the bursa.
 The kidneys become pale and the ureters may be dilated with urates.
 The liver may be swollen and pale.
 Hemorrhage is common in muscle especially of breast, thigh, leg and wing muscle. Occasionally
haemorrhage is seen in the proventricular mucosa just near the junction with gizzard.

Diagnosis

 Diagnosis is based on the age of affected birds and gross lesions.

 Serological tests are employed for confirmation.

Treatment

1. There is no specific treatment for IBD and antibiotics are used to prevent secondary bacterial
infection. Vitamin C, E and electrolytes are given as supportive therapy.
 Vitamin E: E-Care-Se @ 5 gm/100 birds in drinking water.
 Electrocare @ 1 gm/2 litres of drinking water.

Prevention and control

Both killed and live vaccine vaccines are available against IBD. However, live vaccines are extensively
used. There are 3 strains of live vaccines. They are: Mild attenuated (Lukert strain), Intermediate
(Georgia strain) and Hot strain.

Vaccination schedule

1. First : 11 – 13 days age – Intermediate strain

2. Second : 24 – 26 days age – Hot strain
3. Third : 36 – 40 days age – Hot strain

The reconstituted vaccines are given as one drop by intranasal or intraocular route or in drinking water.

Control

 All dead birds must be disposed through burning or by deep burial.

 The floor wall and all other surfaces should be disinfected with suitable chemicals.

INFECTIOUS BRONCHITIS (IB)

Infectious bronchitis is a highly infectious viral disease of poultry which causes respiratory symptoms
and decline in weight gain or drop in egg production with deterioration of egg quality.

Cause

It is caused by an RNA virus belonging to Coronaviridae family.

Occurrence

The disease can occur in any season but cold weather is more favourable for the spread of the disease. It
affects only poultry and of any age but young chicks of 1 – 4 weeks of age are most severely affected. It
may affect birds up to 6 ½ months.

Transmission

Transmission of IB occurs mainly by inhalation of infective droplets and also by contaminated feed and
water. The virus is shed in the respiratory discharge and feces.

Mortality

Mortality is usually around 10 – 25% in young chicks in uncomplicated cases. In cases of secondary
infection, mortality may be from 50 – 100%. Mortality is negligible in birds above 6 weeks of age.

Symptoms

 Small chicks show signs of sneezing, coughing, gasping, respiratory noise, watery eyes, general
weakness and depression. The birds tend to huddle near the heat source.
 Adult birds show sudden reduction in egg production to as low as 50%. The egg quality also
deteriorates.
 Egg shell can become thin, weak, misshapen and rough.
 The albumin can be thin and watery.
 The yolk may have blood spots.
 Mild sneezing, respiratory noise and coughing may be seen in some layers.
 In growing birds, in addition to respiratory signs, there is reduction in weight gain. Many mild
outbreaks in broiler and layers manifest only as reduction in weight gain or egg production.

Lesions

 There is excess mucous, catarrhal or caseous in the respiratory tract, i.e. from nasal cavity to the
bronchioles.
 The two bronchi may show caseous plugs just at the point of entry into the lungs.
 The lungs are congested; there are trachetis, air sacculitis and reddening of trachea.
 In laying hens, the oviduct may show ruptured ova and fluid in the abdominal cavity.
 In the nephrogenic form, the kidneys are swollen and pale, and the tubules and ureters become
distended due to deposition of urates. The urates may be deposited throughout the body as in
the case of gout.

Diagnosis

 It is diagnosed on the basis of history, clinical signs and post mortem lesions.
 Serological tests should be done for confirmation.

Treatment
There is no specific treatment for IB.

Prevention and control

Vaccination is done with attenuated virus by aerosol spray, intranasal or intraocular in one day or 6 days
old chicks or in drinking water for older birds. Vaccination to one day old chicks is done only when there
is a likely challenge, otherwise vaccination is usually done at 3 – 5 weeks of age and the booster
vaccination followed at 13 – 15 weeks of age. IBH 120 is the commonly used vaccine.

MAREK'S DISEASE (MD)

It is an acute infectious disease of domestic fowls characterized by the enlargement of one or more of
the peripheral nerves.

Cause

It is caused by a DNA virus belonging to Herpesviridae family. There are different strains of the virus
which can be grouped under two main pathogenic types i.e. classical strain and acute strain.

Occurrence

MD is principally a disease of poultry. The disease occurs in all age groups of poultry but most commonly
occurs in young birds between 2 – 5 months of age.

Transmission

MD is transmitted by direct contact through feed, water and fomites. The most common mode of
infection is by inhalation of infective particles. Vertical transmission does not occur. Feather follicle cells
are the most common sources of infection.

Mortality

In classical MD, mortality is lower and may be around 10 – 30%. In acute MD mortality varies from 25 –
60%. Sometimes both types of disease may be seen in the same flock.

Symptoms

1. Classical MD
 There is paralysis of one or both legs or wings.
 There is incoordination; one leg is held forward and the other backwards.
 If cervical nerves are affected torticollis (twisting of neck) may be seen.
2. Acute MD
 There is partial or complete paralysis of wings or legs.
 The affected birds appear dull and depressed.
 Many birds die without showing any previous symptoms.
 There is respiratory distress if the heart is involved.
 In both the forms the birds gradually lose weight and become emaciated.
Lesions

1. Classical MD
 There is enlargement of one or more nerves; the most commonly affected nerves are sciatic
nerves of leg, brachial nerves of wings, and vagus nerves along the neck.
 The enlargement of nerves is slight to as much as 3 or 4 times the normal. The nerves become
rounded instead of normally flat; they lose their characteristic striations and may appear grayish
instead of glistening white.
 Occasionally tumors occur in gonads, lungs, kidney, heart and liver.
2. Acute MD
 There is enlargement with tumors in gonads, liver, spleen, lungs, muscles, heart, kidneys,
proventriculus and intestine in decreasing order of frequency.
 Sometimes tumorous nodules develop in the skin, especially in the feather follicles. The nodules
may be up to one centimeter in diameter.
 Enlargement of mesentery and bursa of Fabricius is common.
 There is also involvement of nerve as in classical MD, but to a lower extent.

Diagnosis

 Classical MD can be diagnosed on the basis of symptoms of lameness or paralysis and presence
of nerve lesions. Acute MD can be diagnosed by the presence of tumors in internal organs. 
Serological tests should be done for confirmation.  It is necessary to differentiate MD from
Avian Leucosis Complex (ALC).
 Variables MD ALC
 Age generally affected

2 – 5 months (mostly 2 – 2.5 months)

3 – 8 months

Mortality

10 – 60% Rarely above 5% Nerves Affected Not affected Bursa of Fabricius Shows diffuse enlargement
Has nodular tumors Paralysis Frequently seen Not specific Ovary Frequently affected Rarely affected
Follicles and skin Affected Not affected Feather Affected Not affected

Treatment

There is no specific treatment for MD.

Prevention

The most commonly used vaccine is HVT – 126. The reconstituted vaccine is used @ 0.2 ml SC in one day
or 10 days old chicks.

FOWL POX
 It is a slow spreading viral disease of poultry and other birds characterized by the development of
nodular skin lesions on the unfeathered parts of the body (cutaneous form) or fibrino-necrotic lesions in
the mucous membranes of the upper respiratory tract, mouth and oesophagus (diphtheritic form).

Cause

It is caused by a DNA virus belonging to Poxviridae family.

Occurrence

It occurs in domestic fowl, pigeons, turkey and canary. It occurs in birds of any age but is more common
at 5 – 12 months of age.

Transmission

Infection through intact skin or mucous membrane does not occur. It occurs by infection of wound of
wattles, comb, and skin due to fighting or pecking or through abrasions of the mucosa of mouth. Blood
sucking insects may also transmit the disease.

Morbidity and mortality

Morbidity varies from a few birds being infected to the entire flock if a virulent virus is present and no
control measures are taken. Birds affected with cutaneous form are more likely to recover than those
with diphtheritic form involving the respiratory tract. Flock mortality is usually low, but in severe cases it
may be as high as 50%.

Symptoms and lesions

Disease may occur in one of the two forms – cutaneous or diphtheritic or both in case of chickens. In
case of turkeys, oculonasal form may also be seen. Signs vary depending on the susceptibility of the
host, virulence of the virus, distribution of the lesions, and other factors.

 Cutaneous form: In this form small nodules form on the hairless parts of the body, such as
combs, wattles, eyelids and skin of face. The nodules are first grayish yellow which later
become brownish and finally blackish. Other parts of the body are less frequently affected.
After about 1 week scale formation takes place. Mortality is low in this form.
 Diphtheritic form: Yellowish cheese like materials get deposited on the mucosa of the mouth,
oesophagus or trachea with mild or severe respiratory signs when lesions occur in the trachea.
It causes more mortality due to obstructed breathing and secondary infection. It is usually
around 25%.
 Oculonasal form: There is conjunctivitis and cheesy material accumulates under the eyelids.
The eyelids stick together and may cause blindness. Sometimes infection may spread to the
nasal cavity and cause its swelling. Mortality is mostly due to blindness and starvation as a
result of inability to find the feeder.

Diagnosis
  On the basis of lesions
 Serological tests
 Biological tests

Treatment

There is no specific treatment for fowl pox.

Prevention

Two types of live vaccines are available. Vaccines should not be used in a flock affected with other
diseases or in generally poor condition. Vaccination is done by wing web method to 4 week old chicken
and to pullets about 1 – 2 months before egg production is expected to start. Attenuated fowl pox
vaccine can be used on chicks as early as 1 day of age.

UNIT 7. FUNGAL DISEASES OF LIVESTOCK AND POULTRY

RINGWORM

Ringworm is a contagious infection of the keratin layer of the skin, hair, feathers or nails by the
dermatophyte fungi.

Cause

Ringworm is caused by a group of fungi, commonly referred to as dermatophytes. Trichophyton and

Microsporum are the two genera of fungi causing ringworm in animals. The genus of fungi causing
ringworm in humans is Epidermophyton. There are many species of fungi affecting different animal
species, but there is no rigid host specificity. Man may be infected from animals.

Occurrence

Ringworm occurs in all animal species in all countries but is more common in crowded areas. High
incidence in winter with spontaneous recovery in spring is common, but outbreaks also occur during the
summer season. High humidity is favorable for multiplication of the fungus.

Transmission

Direct contact with infected animals is the common method for the spread of the disease, but indirect
contact with fomites is probably more important.

Zoonotic importance

Ringworm of animal origin can affect man. About 80% of human ringworm in rural areas occurs as a
result of contact with infected animals.

Clinical findings

1. Cattle
  The typical lesion is a heavy, gray-white crust raised above the skin. The lesions are roughly 3 cm
in diameter.
 In the early stages the surface below the crust is moist.
 In older lesions the scab becomes detached and only alopecia may be visible.
 Lesions are most commonly found on the neck, head and perineum, but may occur over the
whole body, particularly in calves.
 Itching does not occur and secondary bacterial invasion is uncommon.
2. Pigs
 Lesions have a ring of inflammation surrounding a scabby, alopecic center.
 Superficial, dry, brown crusts cover the affected area and are raised only at the edges.
 Most lesions occur on the back and sides. Spontaneous recovery does not occur in adult pigs.
3. Sheep and goat
 Lesions mostly occur on the head and are round with bald patches and grayish crust.
 Lesions usually disappear in 4 – 5 weeks.
 Similar lesions occur in goats but are generally distributed all over the body.

Diagnosis

The diagnosis of ringworm is done on the basis of characteristic lesions and demonstration of causative
fungi by direct microscopic examination of skin scrapings or by cultural methods.

 Microscopic examination of skin scraping: Skin scrapings should be taken only after cleaning the
lesion with ether or alcohol. The materials are soaked in 10% solution of KOH or NaOH and
examined under the microscope by putting coverslips over them. The fungal elements (hyphae)
are observed. Round or polyhedral spores can also be observed.

Treatment

1. Local application: The crusts should be removed by scraping or brushing. The medicine should be
rubbed vigorously. Suitable topical applications include Whitfield’s ointment, Salicylic acid (2 – 10%),
Benzoic acid 2 – 6%, Phenol 4 – 5%, Iodine 2 – 5%, Miconazole 2% cream or solution, Cotrimazole 1%
cream or solution.
2. Systemic antifungal agents: Griseofulvin can be used orally, but is contraindicated in pregnancy.
 Horse: 100 mg/kg body weight for 20 days.
 Calf: 10 – 16 mg/kg body weight for 14 – 50 days.
 Dog and cat: 7 – 20 mg/kg body weight

MYCOTOXICOSIS

Mycotoxicosis refers to any of the different toxic conditions caused by the ingestion of toxins produced
by various fungi. There are different mycotoxins produced by different genera and species of fungi. A
particular mycotoxin may be produced by one or more different fungi and a single species of fungi may
also produce different mycotoxins. However, not all fungi are toxin producers. Mycotoxins Produced by
Most common Aflatoxin Aspergillus flavus and Aspergillus parasiticus. Ochratoxin Aspergillus ochraceus.
Less common mycotoxins Rubratoxin Penicillum rubrum and Penicillum perpurgenum Fusariotoxin
Fusarium species T2 toxin Fusarium species Stachybotrystoxin Stachybotryx atra Tremorgan toxin
Penicillum cyclopodium and Aspergillus flavus.

Growth of fungi

Fungi grow in the feed if they have more than 14 % moisture, and if there is insufficient ventilation in the
store room. Maize, rice, wheat, groundnut cake, cotton seed cake, molasses etc are suitable substrates
for the growth of fungi.

Mycotoxicosis in poultry

Cause

Mycotoxicosis is caused by ingestion of feed contaminated by toxins produced by different fungi.

Symptoms

Mostly the name of the disease caused by the mycotoxin is given after the name of the particular toxin.
The symptoms of different mycotoxins may differ slightly, but more of the symptoms are common to all
mycotoxins. In general the effects of mycotoxins are: 1. Immunosupression: Due to immunosupression,
there is failure of vaccines and increased susceptibility to secondary diseases such as CRD, Colibacillosis
etc.

1. Disturbance in Calcium and Vitamin D3 metabolism: Due to this the bones become fragile and there
is abnormal shell formation.
2. Poor protein and fat metabolism: Due to this, there is reduction of growth, reduction in egg
production, small sized eggs, ascites, fluid in pericardium etc.
3. Reduced tissue strength: Due to this, there is increased chances of bruising and erosion of gizzard.

Some other symptoms specific to certain toxins are anemia, swelling of vent or prolapse of cloaca
(usually Fusariotoxicosis), presence of yellow cheesy plaques on the palate, incoordination of body and
convulsions (T2 toxicosis), necrotic patches in buccal cavity and tip of tongue (Stachybotrystoxicosis).

Lesions

 The most prominent lesion in mycotoxicosis is a fragile liver. The liver is congested, necrotic and
has fatty change and is enlarged.
 In most mycotoxicosis the kidneys are pale and necrotic, enlarged and there may be visceral
gout later on.
 Hemorrhages in different organs may be seen and is the result of a combination of different
toxins.

Other lesions specific to different toxins are

 Atrophy of bursa and wasting of muscles.

  Cystic dilatation in the oviduct.
 Necrosis in the corners of mouth, margin of tongue, palate.
 Necrotic areas in buccal cavity.

Diagnosis

The disease which has similar symptoms and lesion is suspected as mycotoxicosis when:

 No other agent of the cause of the disease is suspected.

 Disease transmission will not be possible.
 There is a history of change in feed.
 There is no effect of antibiotic therapy or vitamin supplementation.
 Body growth is subnormal.
 The disease develops during or after rainy season.

Confirmatory diagnosis requires the detection of toxins in feed in toxicological labs. At least 4 kg feed
stuff should be sent to the lab, preserved at 4°C. However, it is a time taking process and is not practical.

Treatment and prevention

There is no specific treatment of the disease after the disease has developed. However, it can be
prevented by following methods:

1. Moisture content in feed should be below 10% and proper ventilation should be provided in the
storage room.
2. To prevent the growth of fungi during the rainy season the following chemicals can be used –
 CuSO4 @ 250 gm/ton of feed
 Gention violet @ 276 gm/ton of feed
 Propionic acid @ 1200 gm/ton of feed.
3. Toxin binders may be used in feed so that the toxins may not be absorbed form the gut:
 UTPP-S: @ 2.5 kg/ton of feed if moisture = 14 – 15 %.
 UTPP-S: @ 5 kg/ton of feed if moisture = 15 – 16.5 %.
 UTPP-S: @ 10 kg/ton of feed if moisture = 16.5 – 18 %.

Supportive therapy Liver tonic should be fed to enhance the function of liver. Example:

 Brotone or Tefroli @ 5 ml/10 ml/20 ml for 100 chicks, growers and layers
 Livfit vet granules @ 2 kg ton of feed.

Mycotoxicosis in farm animals

Cause

Mycotoxicosis is caused by ingestion of feed contaminated by aflatoxins produced by Aspergillus flavus

and Aspergillus parasiticus.
Clinical findings

 Anorexia, depression, bloody diarrhoea, emaciation, ascites, anemia and jaundice are the
common signs.
 There is decreased growth rate and in milking animals there is reduction in milk production.
 Nervous signs like incoordination, circling, convulsions and blindness may be seen in cattle.
 Sometimes tenesmus (unsuccessful effort to defecate and urinate) and rectal prolapse may be
seen.

Diagnosis

It is done on the basis of history of feeding with contaminated feed, clinical signs and characteristic
lesions in the gastrointestinal tract.

PM lesions

 The liver is enlarged; there is haemorrhage and fatty degeneration of liver.

 There is enlargement of spleen, pancreas, kidneys and bile duct.
 There are hemorrhages throughout the gastrointestinal tract, most extensively in the stomach,
abomasum, colon and rectum.

Treatment

There is no specific treatment to mycotoxicosis but the effects of aflatoxins can be minimized by:

 Adding more protein and methionine in the feed.

 Adding liver preparation in the feed.
 Exposing the feeds in sunlight for 2 – 3 days.
 Reducing moisture level of feed.

Control

To prevent the growth of fungi, antifungal agents like propionic acid, sodium propionate can be used @
2 – 8 kg/ton of feed

ASPERGILLOSIS

Aspergillosis in poultry Synonym: Brooder pneumonia

It is a mycotic disease that mainly affects the respiratory system but sometimes infection may spread to
other visceral organs.

Cause

The main cause of aspergillosis is the fungus Aspergillus fumigatus. But other species may also be
involved in the development of the disease.
Occurrence

The disease develops in the brooder stage in chicks, quails, turkeys and other birds. It is mostly seen in
the chicks below 10 days of age but may affect birds up to 10 weeks of age.

Transmission

Infection is generally by the inhalation of spores. The spores are released from moldy litter, feed or nest
boxes. It is widely prevalent in the post-monsoon season. The disease often originates from infected
eggs, where the embryos get infected through contaminated egg shell.

Symptoms

 The clinical symptoms depend on the site of infection.

 In the respiratory system, the infection leads to the symptoms as dyspnoea, depression, and
open mouth breathing (gasping).
 Other symptoms are loss of appetite, emaciation, increased thirst, decreased growth rate,
conjunctivitis, blindness and occasionally CNS symptoms such as torticollis.

Lesions

 Lungs show almost uniform sized, raised pin-head sized, yellowish nodules.
 The air sacs become thick and cloudy, showing yellowish plaques.
 Necrotic foci may occasionally be seen in the liver, spleen, kidneys, proventriculus and other
organs.

Diagnosis

It is done on the basis of the following:

 Disease prevalence at brooding period among chicks.

 Clinical signs and postmortem lesions.
 Micriscopic observation of fungal hyphae in samples taken from the lesions.
 Isolation and identification of fungus through culture.

Treatment

1. Similar to mycotoxicosis.
2. Hamycin @ 10 ml/ liter of drinking water for 10 – 15 days.

Prevention and control

 Similar to mycotoxicosis.

Aspergillosis in farm animals

Aspergillosis is a disease primarily of the respiratory tract, producing characteristic granulomatous
lesions.

Cause

Aspergillus fumigatus are not highly pathogenic and may not produce any clinical signs. But due to the
presence of some predisposing factors, they may produce clinical signs. The factors may be prolonged
use of antibiotics, prolonged use of corticosteroid, exposure to radiation, neoplastic disease,
malnutrition and tuberculosis.

Transmission

The infection spreads through the inhalation and ingestion of Aspergillus spores developed in damp feed
or straw. Direct transmission from one animal to another or animal to man has not been recorded.

Clinical signs

In cattle, the infection may be symptomless. In general, the main types of manifestations observed in
animals and man are:

1. Pulmonary form: There is pneumonia characterized by high rise of temperature followed by

subnormal temperature, accelerated shallow breathing, respiratory noise, mucopurulent nasal
discharge, sneezing and cough.
2. Abortive form: It is the most common form in older cows, mare and ewes. Abortion usually
occurs in 6 – 8 months of pregnancy.
3. Other signs are foetid diarrhoea and conjunctivitis.

Diagnosis

Diagnosis is difficult when the animal is alive. A chronic disease with respiratory signs and without
response to antibiotic therapy can be suspected for aspergillosis. The following post mortem lesions are
helpful for diagnosis:

 Fibrinous pneumonia with blood tinged fluid in the pleural cavity, multiple granulomas with
necrotic centers in the lungs.
 Yellowish necrotic cotyledons with leathery appearance of placenta, and ringworm like lesions in
the foetal skin are suggestive of mycotic abortion.
 Fungal hyphae can be observed on direct examination of smear of cotyledons, fetal stomach and
skin.

Treatment

1. No effective treatment is available for aspergillosis.

Control

 Moldy feed and straw should not be fed to the animals.

  Sanitation and good management practices should be followed to control fungal growth.

UNIT 8. METABOLIC DISEASES

MILK FEVER

Synonym: Parturient paresis, Hypocalcemia

It is a disease of cattle, sheep and goats occurring around the time of parturition due to hypocalcemia
and characterized by weakness, recumbency and ultimately shock and death.

Cause

Low concentration of calcium in the blood is the basic cause of milk fever. The normal level of calcium in
blood is about 10 mg/100 ml blood. One or more of the following factors may act to lower the
concentration of calcium in the blood:

1. Imbalance between calcium output in the colostrums and calcium absorption from the intestine
and bone.
2. Lower levels of parathyroid hormone and vitamin D.
3. Excessive calcitonin level in blood.
4. Acidosis and diarrhea.
5. Feeding more than 100 gm of calcium daily during the dry period.

Occurrence

1. Cattle: The disease occurs most commonly in high producing adult lactating dairy cattle. It is most
common in 3rd to 7th parturition. The Jersey breeds are most susceptible than others. In cattle milk
fever occurs at 3 main stages in the lactation cycle:
 Prepartum: Last few days of pregnancy and during parturition.
 Most cases occur within the first 48 hours after calving to about 10 days of parturition.
 Occasional cases occur 6 – 8 weeks after parturition.
2. Sheep and goats: Ewes suffer from milk fever particularly in the period from 6 weeks before to 10
weeks after lambing. It commonly occurs in outbreaks in groups of ewes exposed to forced exercise,
long distance transport, sudden deprivation of food, and grazing on oxalate containing plants or
green cereal crops. Milking goats become affected mostly in the 4 – 6 years age group.

Clinical findings

1. Cattle: Three stages of milk fever in cattle are commonly recognized and described:

Stage I: In this stage the cow is still standing and there is a brief stage of excitement and tetany
(involuntary muscular contraction) of head and limbs. The animal does not move and eat. There may be
slight shaking of head, protrusion of tongue and grinding of teeth. Hind limbs become rigid and the
animal is prone to fall down. Rectal temperature is usually normal to slightly above normal.
Stage II: In this stage the animal sits on the sternum. The animal is less conscious and the head usually
rests on the flank (S – shaped posture). The animal is unable to stand. The skin and extremities are cool,
muzzle becomes dry and the rectal temperature is subnormal (97 – 101°F). Mucous membranes of the
eye also turn dry with dilated pupil. The pupilary reflex is completely absent and eyes are unable to
blink. The arterial pulse is weak and the venous pressure is low, making it difficult to raise the jugular
veins. There is marked decrease in the intensity of heart sounds but increase in pulse rate (about 80
beats per minute). Ruminal stasis and secondary bloat are common and constipation is characteristic.
Skeletal muscles become flaccid with depression of pain sensation.

Stage III: The third stage is lateral recumbency. There is complete relaxation of muscles. Temperature
becomes more depressed and the heart sounds are completely inaudible and pulse rate may go up to
120 bpm. It may be impossible to raise the jugular veins. Bloat is usual. Without treatment the animal
may die due to cardiovascular failure.

2. Sheep and goats: The disease in ewes is similar to that in cattle. The early signs include unusual gait
and tremors of shoulders followed by recumbency. The characteristic posture is sternal recumbency
with legs under the body or stretched out behind. Ruminal movements are absent, the head is
rested on the ground and the respiratory rate is increased. Venous blood pressure is low and pulse
impalpable. Death often occurs in 6 – 12 hours if treatment is not administered.

Diagnosis

 On the basis of history and clinical symptoms.

 Serum calcium levels are reduced to below 8 mg/dl, usually below 5mg/dl.

Treatment

Treatment should be initiated as soon as possible. Complications of milk fever occur when cows have
been in sternal recumbency for more than 4 hours.

Standard treatment: 100 – 200 gm of calcium borogluconate (8 – 10 gm of calcium) i.e. Cattle/buffalo :

400 – 800 ml of a 25% calcium borogluconate solution Sheep/goats : 25 – 50 ml IV, SC warmed to body
temperature.

If the animal is recumbent for a considerable period of time, there will be ruminal bloat resulting in
cardiac trouble and asphyxia. In such case administer antihistamine:

Avil inj. LA: 5 – 10 ml IM or Histal/Zeet: 3 – 5 ml; SA: 0.5 – 2 ml

Hypocalcaemia with concurrent hypomagnesemia Mild to moderate tetany and hyperesthesia persisting
beyond the first stage suggests concurrent hypomagnesemia. Tetanic convulsions, opisthotonus may be
present. The heart and respiratory rates are increased and the heart sounds are much louder than
normal. Without treatment death occurs during a convulsion.
Hypocalcaemia with concurrent hypophosphatemia The clinical findings are typical of milk fever, which
responds in all respects except that the cow is unable to stand after treatment.

GRASS TETANY

Synonyms: Hypomagnesemic tetany, Lactation tetany, Grass tetany, Wheat pasture poisoning

It is a metabolic disease of cattle, horse, buffalo, sheep and goat characterized by hyperesthesia,
incoordination, tetany and convulsion as a result of disturbed magnesium homeostasis.

Cause

A deficiency of magnesium in the blood is the principal cause of hypomagnesemic tetany. The normal
magnesium level is 2.33 mg/dl (1.7 – 3.0). A number of factors are capable of causing hypomagnesemia
in ruminants and a combination of these factors results in the occurrence of the disease. The factors are:

a) Dietary factor: A low level of Mg in diet is one of the factors. High potassium and nitrogen content in
feed lowers Mg absorption.
b) Pasture: Young green grasses are poor in Mg content than mature grass. Cereal grasses contain
lower Mg than legumes. Cool season grasses are generally lower in Mg content. Low Mg content of
soil and high K and N2 fertilizer application causes lower Mg level in pasture.
c) Lactation: Considerable quantity of Mg is excreted through milk and this may be a factor for reduced
Mg level in blood.
d) Ammonia formation: Excessive production of NH4+ in the rumen from protein rich diet prevents the
absorption of Mg.
e) Starvation f. Diarrhoea g. Prolonged transport of cows and ewes in late pregnancy.

Occurrence

Cattle in the first 2 months of lactation and at 4 – 7 years of age are most susceptible. In sheep it
generally occurs in ewes with twins after 1 – 4 months of lambing.

Clinical findings

1. Acute form
 Sudden cessation of grazing.
 Unusual alertness.
 Twitching of the muscles and ears.
 Severe hyperesthesia and slight disturbances causes continuous bellowing, staggering gait and
the animal falls down followed by clonic convulsions lasting for a minute. During the convulsive
episodes there are:
 Opisthotonus
 Nystagmus (rapid rhythmical movements of the eyes)
  Champing of jaws
 Frothing at the mouth
 Raised temperature (104 – 105°F) Heart sounds are increased and may be heard from a distance
 Death usually occurs within half to one hour.
2. Sub-acute form
 Onset is gradual.
 Slight inappetance.
 Vigorous limb movements.
 Throwing (retraction) of the head.
 Spasmodic urination and frequent defecation.
 Muscle tremor and tetany of hind limbs.
 Sudden movement, noise may cause initiation of violent convulsions.
3. Chronic form
 Animals may not show clinical signs and there may be sudden death.
 A few animals show vague syndromes including dullness, indifferent appetite and may develop
to sub-acute form.

Diagnosis

 On the basis of history, clinical symptoms and serum analysis (below 0.5 mg/dl of blood).

Treatment

Solution containing Ca and Mg salts should be administered IV followed by SC. E.g. Mifex, Magical,
Thiacal: 1 bottle or ½ bottle followed by 100 – 150 ml of 10% MgSO4 by SC route.

Control

 2% MgSO4 spray to pasture every 2 weeks during danger period.

 Addition of MgSO4 to water supply during risk period.

KETOSIS

Synonym: Acetonemia in cattle; Pregnancy toxemia in ewes

It is a metabolic disorder occurring as a result of impaired carbohydrate and fat metabolism.

Cause

A negative energy balance due to hypoglycemia (relative or absolute lack of carbohydrate) leading to
oxidation of fats, which in turn leads to the production of ketone bodies, is the cause of ketosis. The
factors that can produce ketosis are:

 Negative energy balance in the first few weeks of lactation in high producing cows
 Low insulin: glucagon ratio
 Insufficiency of Adrenaline, Cortisone, Thyroxine hormones
  Lack of exercise
 Hepatic insufficiency
 Loss of appetite
 Starvation
 Deficiency of coenzyme A
 Deficiency of cobalt, phosphorus
 Silage rich in butyric acid.

Occurrence

The disease occurs in goats during late pregnancy, where it is identical to ovine pregnancy toxemia and
also in lactating does, where it resembles bovine ketosis. 90% cases occur in the first 10 days of lactation
in bovine. In sheep it generally occurs in the last 6 weeks of pregnancy and in ewes carrying twins and
triplets.

Clinical findings

Bovine ketosis Acute form

Two major syndromes (form) of acute ketosis are described:

1. Wasting form
 There is gradual decrease in appetite over 2 – 4 days. The pattern of appetite loss is often
unusual in that the cow first refuses to eat grains, then silage but may continue to eat hay or
straw. Later on all food and water may be refused.
 There is rapid loss of body weight and cows have a woody appearance due to loss of
subcutaneous fat.
 The feces are dry and covered with mucous.
 Milk production is sharply decreased with reduction in SNF.
 The temperature, pulse and respiration rates are normal.
 The cow disinclines to move and eat.
 Ruminal movements may be decreased in amplitude and number.
 A characteristic odor of ketones is detectable on the breath and in milk.
2. Nervous form: The animal is in a state of delirium. The characteristic signs are:
 Walking in circles
 Head pushing or leaning into the feeding trays
 Blindness
 Aimless wandering
 Vigorous licking of the skin and inanimate objects, and depraved appetite
 Chewing movements with salivation
 The animal bellows on being pinched
 Moderate tremor and tetany may be present and there is usually an incoordinated gait
 The nervous signs last for one to two hours and may recur at 8 – 12 hours gap
 Very few affected animals die.
Sub clinical bovine ketosis

There is presence of ketone bodies in urine and blood in excess amounts but without any obvious
symptoms.

1. Ovine ketosis
 Separation from the group is the earliest sign.
 Blindness manifested by alert behavior but disinclination to move.
 Constipation is usual; the feces are dry and scanty.
 There is grinding of teeth.
 When forced to move it stumbles over objects and when an obstacle is encountered, presses its
head against the obstacle.
 In later stages tremors of the muscles of the head cause twitching of lips, champing of jaws and
salivation. There is convulsion after tremors and the ewe falls down.
 There is star gazing posture, incoordination and falling when attempted to walk.
 Fetal death occurs commonly and affected ewes commonly have difficulty in lambing.

Diagnosis

 On the basis of history, clinical findings and biochemical analysis.

Cattle/Sheep Normal (mg/dl) Ketosis (mg/dl) Blood glucose 40 – 50 20 – 40 Ketone bodies in blood Up
to 10 10 – 100 (50) Ketone bodies in urine Usually less than 10, may be up to 70 80 – 1300

Rothera’s test (for detection of ketone bodies in urine)

Composition of reagent Ammonium sulphate: 100 gm Ammonium carbonate: 50 gm Sodium

nitroprusside: 3 gm

Mixture of the above chemicals is taken up to half of a test tube. The suspected urine is slowly added to
form a layer on the top of the reagent. Without mixing, the tube is set aside for a few minutes. In
positive cases, potassium permanganate colour quickly appears. In field condition, milk can also be used.

Treatment

Cattle

A.
1. IV infusion of 500 ml of a 50% solution of glucose.
2. Oral administration of glycerol or glycerine Adult cattle: 100 gm bid for 2 –3 days Small cattle: 50 gm
bid for 2 – 3 days
B. Glucocorticoids
1. Dexamethasone or Betamethasone: 5 – 10 ml IM single dose. Occasionally another dose may be
required.
2. Prednisolone inj: 5 – 10 ml IM
C. Miscellaneous: Vitamin B12 and Cobalt therapy.

Sheep

1. Oral drenching of 160 ml of solution containing 45 gm of glucose, 8.5 gm common salt, 6.17 gm
glycerine and electrolytes every 4 – 8 hours.
2. 5 – 7 gm of glucose IV 6 – 8 times a day.
3. Propylene glycol or glycerine: 110 gm/day orally.

It may be necessary to terminate pregnancy and can be done by administration of 15 – 20 mg of

dexamethasone to induce abortion.

VISCERAL GOUT IN POULTRY

Gout in poultry is a condition where there is a deposition of uric acid or urates of sodium and calcium in
the visceral organs of poultry.

Cause

Many factors may result in gout in poultry such as:

 Excess of protein, especially protein of animal origin in the diet of poultry.

 Deficiency of vitamin A.
 Disease involving kidneys.
 Specific diseases such as IBD or IB in chicks.
 Nephrosis due to over medication with sulfonamides or other kinds of medicines.
 Fungal toxins in feed.

Lesions

 The kidneys are swollen, mottled and grayish in colour due to deposition of urates.
 The ureters are dilated with white, pasty material.
 In advanced cases whitish chalky deposits are also seen on the serous membranes and surfaces
of liver, heart etc.

Treatment, prevention and control

1. Supply plenty of water with electrolytes: Electrocare @ 1gm/2lt of drinking water or 1kg/tonne of
feed.
2. Removal of the possible cause.
3. Adequate supply of vitamin A: Vitablend WM Forte liquid @ 2 ml, 5 ml and 5 – 10 ml per 100 chicks,
growers/broilers and layers respectively.
4. In suspected fungal toxicity, the feed should be changed.
5. Goutex: 5 – 10 ml/100 broilers for 10 – 15 days; 20 ml/100 layers for 10 – 15 days.
 UNIT 9: DEFICIENCY DISEASES

RICKETS

Rickets is a chronic disease of young growing animals characterized by defective calcification of growing
bones.

Cause

Rickets is caused by an absolute or relative deficiency of any or a combination of calcium, phosphorus or

vitamin D in young growing animals.

Epidemiology

The prevalence of rickets is highest in piglets followed by puppies, lambs, kids and calves. It occurs
naturally in calves, lambs and kids mainly due to phosphorus and vitamin D deficiency. It occurs in
piglets in intensive fattening units where the effects of excessive phosphorus in diet are worsened by
deficiency of calcium and vitamin D.

Clinical findings

 Reduced growth.
 Bow-legged condition, usually forward and outward bending of limbs.
 Enlargement of the limb joints, especially of the forelimbs.
 There is stiffness of joints, lameness and tendency to lie down for long periods.
 Animals are very susceptible to fracture of bones.
 Arching of back.
 Eruption of teeth is delayed and the teeth are poorly calcified, causing pitting and wearing
rapidly. There is severe thickening and softness of jaw bones due to which, it may be impossible
to close the mouth, especially in calves and lambs. As a result the tongue protrudes and there is
drooling of saliva and difficulty in feeding.

Poultry

 There is reduced growth or no growth at all.

 Curving of beak, due to which there is a gap formation between the upper and lower beak.
 There are bone deformities like nodular swelling of costo-chondral junction of ribs; rib cage
becomes flattened, bending of legs and bone becomes soft and flexible.
 The birds try to sit on the hock joints.

Diagnosis

It depends on history of diet (such as deficiency of calcium, phosphorus and vitamin D), clinical
symptoms and X – ray report.

Treatment
Supplementing diets with calcium, phosphorus and vitamin D is the best treatment. E.g. bone meal,
dicalcium phosphate, limestone powder, oral calcium preparations, mineral mixtures etc.

1. Ascal/Ostocalcium/Merical [Contain calcium, phosphorus, vitamin D3 and vitamin B12]: LA: 50 ml,
SA: 20 ml and pet animals: 5 ml twice daily; Poultry: 20 – 60 ml/100 birds.
2. Dicirol [Contains vitamin D3]: 2 gm/ton of feed for all animals and birds.

VITAMIN DEFICIENCIES

Vitamin A deficiency

Deficiency signs

 Night blindness.
 Xeropthalmia (dry eye condition): Xeropthalmia with thickening and clouding of the cornea
occurs only in calf. In other species a thin serous mucoid discharge occurs from the eyes,
followed by corneal keratinization, clouding and sometimes ulceration and photophobia.
 The hair becomes rough and dry. There is presence of bran like deposits on the skin and multiple
cracks in the hooves.
 The animal becomes anorectic, weak and shows reduced growth.
 Reproductive efficiency may be decreased.
 There may be nervous symptoms like incoordination and blindness.
 There may be keratinization of epithelial cells of the digestive, respiratory, reproductive and
urogenital system.

Poultry

The symptoms include weakness, incoordination, retardation of body growth, ruffled feather, loss of
yellow colour of shank and abnormally large combs. The birds become susceptible to conjunctivitis, CRD,
coccidiosis and other infections.

Diagnosis

Diagnosis is based on history of diet and laboratory estimation of vitamin A in serum.

Treatment

1. Vitamin A [Vitamin A, Alvite – A] injection: LA: 12 ml, SA: 6 – 12 ml deep IM per week for 2 – 3
occasions.
2. Vitacept injection [contains vitamin A, D3 and E]: LA: 10 ml, SA: 5 ml IM twice a week.
3. Vitablend AD3: LA: 5 gm daily with feed.
4. For poultry: Vitablend WM forte/Vita – A solution @ 2, 5 and 5 – 10 ml/100 chicks, growers and
layers respectively with water for 10 days.

Vitamin D deficiency
Deficiency signs

1. Rickets in young animals.

2. Osteomalacia in adults: In this condition the bones become soft and flexible and can be bent easily.
The bones are very much susceptible to fracture.

Poultry

Deficiency symptoms of vitamin D in poultry are seen only after several weeks of deficiency. The
symptoms are stunted growth, weak bones, small rib cage, swollen joints and soft shelled eggs.

Treatment

Addition of vitamin D in feed: Dicirol @ 2 gm/ton of feed.

Vitamin E deficiency

Deficiency signs

1. Infertility in some animals.

2. Muscle degeneration
 White muscle disease in calves characterized by weakness and stiffness followed by paralysis
 Stiff lamb disease in lambs.
 Mulberry heart disease in pigs.
3. Crazy chick disease in poultry: The chicks appear to push its head under its breast. Other symptoms
of poultry are reduction in egg production and enlargement of hock joints.

Treatment

1. E – Care – Se injection: 1 ml/25 – 50 kg body weight IM for 2 – 3 occasions in alternate days.

2. E – Care – Se powder: 5 gm/200 chicks, layers and growers and for 50 broilers respectively.

Vitamin K deficiency

Deficiency signs

There is delay in blood clotting wherever there is any kind of injury and rupture of vessels.

Treatment

1. Kaysol forte : 50 gm/3000 birds for 5 – 7 days or,

2. Multisol K : 5 – 10 ml/100 birds for 5 – 7 days with drinking water.

Deficiency of water soluble vitamins

A number of water soluble vitamins can be prepared in the alimentary tract of animals, more commonly
in the ruminants. The microbes present in the alimentary tract are capable of synthesizing thiamin,
pantothenic acid, nicotinic acid, riboflavin, pyridoxine, biotin and folic acid. Therefore, deficiency of
these vitamins rarely occurs in adult ruminants. Deficiency is seen in non-ruminants and very young
stage of ruminants when the dietary supply is less.

Thiamin (B1) deficiency

Deficiency signs

 Loss of appetite, stunted growth and emaciation are the most common signs in most species,
especially in young age.
 In poultry the symptoms are seen due to polyneuritis. The characteristic symptoms are that the
chicks stand on their hocks and make a star gazing posture.

Treatment

Supply of vitamin B preparation in diet or by injection.

1. Neuroxin, Neurobion injection [contains vitamin B1, B6 and B12]: LA: 5 – 10 ml; SA: 1 – 2 ml IM
for 3 – 5 days
2. Ambiplex liquid : LA: 5 – 10 ml; SA: 1 – 5 ml Poultry : 5 – 10 ml/100 birds in drinking water for a
week.
3. Bivinal liquid: Poultry: 10 – 20 ml/100 birds Calves: 20 – 30 ml/animal Adult cow/buffalo: 40 –
60 ml

Riboflavin (B2) deficiency

Deficiency signs

 Dermatitis; excessive salivation; diarrhea; corneal opacity; photophobia; muscular weakness;

anaemia; redness around the mouth; sudden death.
 Poultry: Curled toe paralysis, due to which birds walk on hock joints. There is also diarrhea.

Treatment

1. Ambiplex/Albiplex liq.: Poultry : 5 – 10 ml/100 birds Large animals : 5 – 10 ml/animal Small

animals : 1 – 5 ml/animal

Niacin or Nicotinic acid deficiency

Deficiency signs

 Deficiency is very rare in animals.

 Pellagra in man, characterized by oral lesions.
 In animals signs are anorexia, black tongue (in dog, characterized by fiery tongue with blue
patches), diarrhea, dehydration, weakness.
 In poultry enlargement of hock joints, inflammation of mouth, diarrhea and poor feathering.

Treatment
B–complex preparations such as Ambiplex, Albiplex etc.

Pyridoxine (B6) deficiency

Deficiency signs

 Chicks: Stunted growth, incoordinated movement, aimless running with jerking type of
movement, convulsions of legs and wings.
 Adult birds: Loss of appetite, drop in egg production, reduced hatchability.
 Other animals: Anemia, anorexia, poor growth, alopecia, dermatitis.

Treatment

Neuroxin, Neurobion inj for animals. Vitamin B complex preparation for poultry.

Pantothenic acid deficiency

Deficiency signs

 Chicken: Stunted growth, ruffled feather, and formation of scab at commisures of mouth and
eyes, dermatitis.
 Pig: Anorexia, reduced weight gain, dermatitis, dark brown exudates around the eyes, patchy
alopecia and diarrhea and incoordination with characteristic goosestepping gait.

Treatment

B – complex vitamin preparations containing pantothenic acid.

Folic acid deficiency

Deficiency signs

Deficiency is rare in animals and birds. In poultry reduced growth, poor feathering, feather
depigmentation and anemia are seen. In other animals glossitis and anaemia are common signs.

Treatment

B – complex vitamin preparations containing folic acid.

Biotin deficiency

Deficiency signs

 Pigs: Lameness associated with cracking of hooves and dermatitis.

 Poultry: Deficiency is rare in poultry and whenever occurs, symptoms like dermatitis, paralysis
and increased number of dead embryos in hatching eggs is seen.

Treatment
B – complex vitamin preparations containing biotin.

Choline deficiency

Deficiency signs

 Chicken: Fatty liver condition, paralysis.

 Other animals: Anorexia, slow growth, weakness, ataxia and difficulty in respiration.

Treatment

Choline chloride (Cholimix @ 100 gm/tone of feed).

Cyanocobalamin (B12) deficiency

Deficiency occurs due to deficiency of cobalt in diet.

Deficiency signs

 Anaemia, reduced growth, poor appetite.

 Chicken: Slow growth, poor appetite, increased embryonic death.

Treatment

Vitamin B-complex preparations. Cobalt preparations should also be given, e.g. CoFeCu.

Ascorbic acid (Vitamin C)

Deficiency symptoms are not seen in farm animals and birds. In man deficiency causes scurvy
(characterized by inflammation of oral cavity e.g. mouth, lips, tongue, gums associated with bleeding).
Deficiency may cause infertility in cattle and increased susceptibility to infection.

MINERAL DEFICIENCY

Calcium deficiency

Primary deficiency is due to a lack of calcium in the diet, but is uncommon. Secondary deficiency due to
low calcium intake with high phosphorus is more common.

Deficiency signs

It is sporadic in nature and is not common where feeding is adequate. Symptoms are non-specific and
more marked in young animals than adults.

 In young animals there is slow growth and poor development of incisors, delayed eruption of
permanent teeth and abnormal wear of permanent teeth.
  In adult animals symptoms are nonspecific. Inappetance, stiffness, tendency of the bones to
fracture, disinclination to stand, difficult parturition, reduction in milk production and reduced
fertility are the common signs.
 In presence of secondary factors, calcium deficiency may lead to rickets, osteomalacia or
osteodystrophy fibrosa (replacement of bones by cells of fibrous tissue).

Diagnosis

Histological study of bones or bone ash analysis.

Treatment

Oral or parenteral calcium supplementation should be given. Bone meal should be given through diet.
Calvin DS/Merical/Calcicare/Caldhan/Ascal/Ostocalcium vet @ 50 ml twice daily orally.

Phosphorus deficiency

Primary deficiency is due to lack of phosphorus in diet and secondary due to vitamin D deficiency.

Deficiency signs

Young animals grow slowly and develop rickets. In adult animal the following symptoms are seen:

 Reduced feed intake is the first sign.

 Slow growth, low milk yield, osteomalacia, reduced fertility characterized by anoestrus, irregular
estrus, and delayed sexual maturity.
 Pica i.e. eating of inedible materials likes bone, wood, clothing, soil etc.
 In high producing cattle, the animals are unable to stand but are bright and alert.

Diagnosis Histological study of bones or bone ash analysis.

Treatment

1. Tonophosphan or tonoricin injection: LA: 5 – 10 ml in acute cases and 2.5 – 5 ml in chronic cases
in alternate days till recovery.

SA: 3 ml in acute cases and 1 ml in chronic cases in alternate days till recovery.

Half of the above dose is administered IM or IV and rest by SC.

Iron deficiency

Primary deficiency in diet is the cause of iron deficiency. Secondary iron deficiency may be brought
about by blood sucking parasites or haemoprotozoan diseases. In animals deficiency may not usually
arise except in baby pigs raised on cemented floors without access to soil.

Clinical signs
  In piglets deficiency is more common in 3 weeks of age. There is slow growth, reduced feed
intake, mild diarrhea, lethargy, dyspnoea, anemia and sudden death.
 Anaemia is the principal sign in all animals.

Diagnosis

On the basis of history of diet and iron level in the feed. Hemoglobin level may be reduced below 8
mg/ml or less.

Treatment

1. Ferrous sulphate: 2 – 6 gm orally depending on body weight/day /animal.

2. Imferon: 10 ml for large animals and 1 ml for piglets IM in alternate days.
3. CoFeCu: 1 tablet daily orally.

Cobalt deficiency

Deficiency signs

There is no specific sign characteristic of cobalt deficiency. The signs of vitamin B12 deficiency are also
the signs of cobalt deficiency. Some of the nonspecific signs are loss of appetite, loss of body weight,
weakness, slow growth, reduced milk yield, decreased wool production, lachrymation, anemia and pica.

Diagnosis On the basis of history of diet, clinical signs, estimation of cobalt in soil, plants and blood.

Treatment

1. Cobalt sulphate Cattle and buffalo: 500 mg/animal daily by oral route. Calf/Sheep/Goat: 100 –
200 mg/animal daily by oral route.
2. CoFeCu: 1 tablet daily orally or vitamin B12 in diet or by parenteral injection.

Copper deficiency

Primary deficiency is due to low intake in diet and secondary deficiency is due to excess of molybdenum
or sulphur in diet.

Deficiency signs

Anaemia, diarrhea, bone weakness, stiffness of legs, depigmentation of hairs and wool, delayed estrus,
sudden death due to heart failure.

Diagnosis

History of diet, clinical signs, estimation of copper in soil.

Treatment

1. CuSO4 : LA: 2 – 4 gm daily orally; SA: 1.5 gm daily orally.

 2. Cofecu : 1 tablet daily orally

Iodine deficiency

Primary deficiency is due to low intake in diet and secondary deficiency is due to high intake of calcium
and goitrogenic plants like Brassica sp., white clover, cabbage etc.

Deficiency signs

 Goiter.
 Reduced milk production, leg weakness, increased death in young ones, increased gestation
length, alopecia at birth, facial edema, decreased libido in bulls.

Diagnosis

By the development of goiter, estimation of thyroxine level in blood.

Treatment Potassium iodide should be mixed in salt @ 200 mg/kg.

Sodium chloride deficiency

Dietary deficiency of sodium chloride is most likely to occur during lactation, hot climatic conditions, in
animals engaged in heavy work and in animals grazed in pasture containing low amount of sodium
chloride.

Deficiency signs

 Cattle: Frequent urination and polydipsia (frequent drinking of water), loss of appetite, loss of
weight, reduction of milk production, pica including licking of dirt and each others’ body coat,
drinking urine are the usual symptoms.
 Pigs: Anorexia, reduced water intake and reduced weight gain are the common signs.

Diagnosis

On the basis of clinical symptoms, history of feeding and analysis of salt in urine.

Treatment

Inclusion of salt in the ration @ 0.5%.

Zinc deficiency

Deficiency occurs due to low level in the diet or due to high amount of calcium, phytic acid and sulphur
in the diet.

Deficiency signs

 Animals have slow growth associated with reduced appetite.

  Skin disorders: A condition called “parakeratosis” is observed in pigs where circumscribed
erythema (reddening of skin due to congestion of skin) occurs on the skin. Alopecia is also
observed. Alopecia and general dermatitis occur around the head and neck in cattle. Loss of
wool, thickening of skin occur in sheep.
 Skeletal disorders: In young birds leg weakness and ataxia are seen. The long bones become
shorter, thicker and crooked. The joints become enlarged and rigid.
 Reproductive disorders: Sexual maturity of animal is delayed. Infertility in rams.

Diagnosis

Diagnosis depends on clinical symptoms, history of feeding and laboratory analysis of blood.

Treatment

1. 3 – 4 gm of Zinc sulphate or Zinc Carbonate in diet for cattle.

2. 200 mg Zinc sulphate or Zinc Carbonate in diet for pig, goat and sheep.

Manganese deficiency

Deficiency occurs due to low level in feed or due to high calcium or phosphorus in diet.

Deficiency signs

The usual symptoms are infertility such as delayed estrus, bone weakness due to which the animals may
have short legs and are reluctant to move.

Diagnosis

It depends on history of feeding, estimation of manganese in blood and clinical findings.

Treatment

1. 2 – 4 gm of MnSO4 in cattle feed daily.

2. 24 – 57 mg manganese/45 kg body weight for pigs.

Potassium deficiency

Deficiency is rare in farm animals.

Deficiency signs

Slow growth rate, anaemia, diarrhea, and weakness.

Diagnosis

It depends on clinical symptoms and history of diet.

Treatment

Addition of potassium chloride in diet.

Selenium deficiency

Deficiency of selenium occurs along with deficiency of vitamin E in the diet.

Deficiency symptoms

 Infertility in some animals.

 Muscle degeneration: White muscle disease in calves; stiff lamb disease in lambs and mulberry
heart disease in pigs.
 Crazy chick disease in poultry: The chicks appear to push its head under its breast. Other
symptoms of poultry are reduction in egg production and enlargement of hock joints.

Treatment

1. E – Care – se injection: 1 ml/25 – 50 kg body weight IM for 2 – 3 days in a week.

2. E – Care – se powder: 5 gm/200 chicks, layers and growers and for 50 broilers respectively.

For mineral deficiencies the following mineral mixtures can be used:

1. Agrimin forte/Chelated agrimin forte [vitamin + mineral mixture]: Mixing in feed @ 1% or

individual feeding @ 25 – 30 gm for large animals and 5 – 10 gm for small animals daily.
2. Nutrisacc powder [vitamin + mineral mixture + live yeast culture]: Individual feeding @ 100 gm
for large animals and 50 gm for small animals daily orally.
3. Minamil [vitamin + mineral mixture]: Mixing in feed @ 1% or individual feeding @ 20 – 25 gm
for large animals and 5 – 10 gm for small animals daily. Poultry: 2 – 5 kg/ton of feed.

UNIT 10. PUBLIC HEALTH

Zoonosis is defined as those diseases and infections which are naturally transmitted between vertebrate
animals and man.

The World Health Organization lists about 150 such zoonotic diseases. Zoonoses are responsible for
great economic losses particularly in animals, meat, milk and other foods and products of animal origin.
In addition, some of the zoonoses are fatal, such as anthrax and rabies, and some others are less severe
such as cowpox or may cause recurring symptoms such as brucellosis in humans.

Importance of zoonoses

Zoonotic diseases can be transmitted directly by contact with an animal (e.g., rabies, through a bite), via
a contaminated environment (e.g., anthrax) and via food (e.g., campylobacteriosis) or indirectly via
vectors, such as mosquitoes or ticks (e.g., West Nile fever and Lyme disease, respectively). The
organisms causing zoonoses include viruses, bacteria, fungi, protozoa and other parasites, with both
domestic and wild animals acting as reservoirs for these pathogens. The diseases they cause in humans
range from mild and self-limiting (e.g. most cases of toxoplasmosis) to fatal (e.g. Ebola haemorrhagic
fever). In the United Kingdom, food is thought to be the most common source of zoonotic diseases.

The importance of zoonotic diseases is well demonstrated by a survey of infectious organisms which
showed that, of the 1415 species known to be pathogenic to humans, 61% (868) are zoonotic. It is
perhaps worth noting that many of the zoonotic agents causing disease in humans cause little or no
obvious clinical disease in their animal hosts.

As population numbers continue to increase and new areas are opened up for food production, both
humans and their domestic animals are more frequently exposed to diseases as a result of encounters
with "wild" animals, thus increasing human exposure to once rare zoonotic infections. Increased
urbanisation allows faster spreading of any new disease between populations within an area, while air
travel enables a disease to be spread worldwide within a comparatively short space of time. The ever-
increasing trade in animals and animal products has also contributed to the spread of zoonotic diseases.

Pathogens that can be transmitted between different host species are of fundamental interest and
importance from conservation, public health and economic perspectives. Success in the prevention and
control of major zoonoses depends on the capability to mobilise resources in different sectors and on
coordination and intersectoral approaches, especially between national (or international) veterinary and
public health services.

It is essential to know the direction of transmission of these diseases i.e. whether they are transmitted
from animals to man or from man to animals. The following terminologies are used to describe the
reservoirs of such diseases.

a) Anthropozoonoses: These are diseases and infection transmitted from lower vertebrate animals
to man. E.g. Japanese encephalitis, rabies, plague, leptospirosis, hydatidosis etc.
b) Zooanthroponoses: These are infections transmitted from man to lower vertebrate animals. E.g.
staphylococcosis, human tuberculosis in cattle, streptococcosis, enterobacterial infections etc.
c) Amphixenosis: These are infections maintained in nature by both man and lower vertebrates
and may be transmitted in both directions. E.g. salmonellosis etc

Classification according to modes of transmission Zoonoses are also classified on the basis of the
lifecycle of the infecting organism such as:

1. Direct zoonoses: These are those zoonoses that are transmitted from an infected vertebrate host to
a susceptible vertebrate host by direct contact, by contact with a fomite, or by a mechanical vector.
The infective agent (causative agent) undergoes no essential developmental change during
transmission. E.g. Rabies, trichinosis and brucellosis.
2. Cyclozoonoses: These zoonoses require more than one vertebrate host, but no invertebrate host for
the completion of the causative agent’s development cycles. Most of the cyclozoonoses are cestode
infections. E.g. Human taeniasis, echinococcosis etc.
3. Metazoonoses: The metazoonoses are transmitted mechanically by invertebrate vectors. In the
invertebrate host, the agent may multiply or develop, or both before transmission to another
vertebrate host is possible. E.g. Japanese encephalitis, plague, schistosomiasis etc.
4. Saprozoonoses: The saprozoonoses are those infections which require a non-animal developmental
site or reservoir. Organic matter (including food), soil, and plants are considered to be non-animal.
E.g. various forms of larva migrants and some of the mycoses.

Milk Borne Diseases

Milk is an efficient vehicle for the transmission of many diseases and infections. It is also an excellent
medium for the growth and multiplication of the number of the bacteria and some protozoa. Milk
provides the essential nutrients for the growth of bacteria. Therefore, the quality of milk for human
consumption should be superior so as to prevent the transmission of the milk borne diseases. The
sources of infection or contamination of milk are:-

1. Dairy animals
2. The human handler
3. The environment such as vessels/utensils polluted water, flies, dust, etc.

Milk borne diseases

1. Infection of animals that can be transmitted to man:

a) Infections of primary importance: Tuberculosis, Brucellosis, Streptococcus, Staphylococcus,
Salmonellosis, Q-fever, etc.
b) Infection to lesser importance: Cow pox, Foot and mouth disease, Anthrax, Leptospirosis, tick
borne encephalitis.
2. Infections primary to man that can be transmitted through milk: Typhoid fever, paratyphoid fever,
shigellosis, cholera, Escherichia coli infection, Streptococcus, Staphylococcus, Diphtheria,
Tuberculosis, Enterovirus, Viral hepatitis.

Clean milk production

Clean milk is defined as the milk obtained from healthy dairy animals and which is free from any kinds of
microbial or non microbial contamination.

Some bacteria are normally present in the milk even under good milking practices. The sources of these
bacteria are the udder and the teat itself. The multiplication of these bacteria can reduce the quality of
milk. Therefore, the milk should be immediate cooled to below 10C after milking.

To reduce the contamination of milk by different micro-organisms and thus reduce the chances of
infection from milk borne disease the following things should be considered:

 Maintain the dairy animals in good health.  Maintain good hygiene and sanitation in the barn.  The
milker and other attendants should be clean, healthy and should have healthy habits.  All the vessels
that come in contact with milk should be clean and sterilized.  Milk for human consumption should be
pasteurized.

Meat Borne Diseases

Meat is defined as the flesh of animals that is used for human consumption. It is another excellent
medium where a number of organisms can grow rapidly. Therefore, to prevent transmission of disease
through meat, the quality of meat, the health of the meat producing animals and the sanitation of the
slaughter house should be given high importance.

The major diseases and infections that can be transmitted through unwholesome meat are:

1. Worms: Taenia solium, Taenia saginata, Trichinella spiralis

2. Bacterial diseases: Anthrax, Actinomycosis, Tuberculosis

To prevent transmission of disease through meat, meat inspection should be carried out. Animals that
are intended to be slaughtered for meat should be examined and the process is called ante-mortem
examination/inspection. After animals are slaughtered, the meat should again be examined and the
procedure is called postmortem examination. These examinations are carried out so that the animals
that are likely to transmit the different diseases to man could be identified. The meat from these
animals could be discarded.

The common conditions for rejection of meat/animal are:

a) In anti mortem examination: Emaciation, exhaustion, pregnancy, sheep pox, actinomycosis,

brucellosis, febrile conditions, diarrhoea and other diseases likely to make the meat unfit for
consumption.
b) In post-mortem examination: Cyst of Taenia, Echinococcus, liver fluke, abscess, Sarcocystis, parasitic
and nodular infection of lungs and liver, TB.

For the prevention of meat borne diseases, the animal should be slaughtered in a clean and healthy
environment in the slaughter house. Ante-mortem and post-mortem examination should be done for
each animal that is to be slaughtered or has been slaughtered. Other things that should be considered in
the slaughter house are:

a) The slaughter house should be located away from the residential areas.
b) The floors and walls of the slaughter house should be impervious/concrete.
c) The offal (other than muscle, brain, liver, tongue) should be properly disposed and should not be
mixed in the public sewage.
d) There should be independent, continuous and sufficient supply of water to the slaughter house.
e) The meat should be stored below 5°C after dressing is complete.
f) Meat should be transmitted in fly proof vans.
g) Other animals than those that are to be slaughtered should not be allowed to enter the slaughter
house.
Some important zoonoses

Viral zoonoses

SN Disease Agent

Reservoirs or hosts

Mode of transmission

Prevention and control

1. Rabies

Lyssa virus (Rbabdoviridae)

Canines, mongoose, vampire bats

Bite of infected animal and licks on open wound.

Vaccination of dogs, control of stray dogs.

2.

Japanese encephalities

Arbovirus (Flaviviridae)

Pig, cattle, buffalo and horses

Mosquito bite Control, isolation of infected animals.

3.

Avian influenza

Influenza virus (Orthomyxoviridae)

Poultry, turkey, other birds and pigs

Through contaminated feed and water, fomite, inhalation, Consumption of raw meat and eggs.

Test and slaughter of infected birds. Consumption of cooked meat and eggs only.

Bacterial zoonoses

SN Disease Agent

Reservoirs or hosts
Mode of transmission

Prevention and control

1. Tuberculosis

Mycobacterium bovis

Cattle and buffalo

By milk Test and slaughter of infected animals, avoiding contact with infected animals and not
consuming infected milk

2. Brucellosis

Brucella militensis B. abortus B. canis B. suis

Cattle, buffalo sheep, goat, horse, pig and dog

Contact with infected tissues, blood, urine, vaginal discharges, aborted fetus and placenta. Milk and milk
products, infected droplet.

Test and slaughter the infected animals Avoiding contact Consumption of pasteurized milk only.

3. Anthrax

Bacillus anthracis

Cattle, buffalo, sheep, goat, horse, pig

Inhalation of spores, contact with infected animals and soil

Avoid contact, vaccination of animals, proper disposal of dead animals

4. Leptospirosis

Leptospira interrrogans

Cattle, buffalo, sheep, goat, horse, pig and rodents

Direct contact with infected tissues, urine, droplets, infection

Treatment of infected animals and man. Good sanitation vaccination of population at risk

5. Plague

Yersinia pestis Rodents and Fleas

Bite of fleas rats fleas man pneumonic form can transmit from man to man
Control of fleas and rodents, treatment of infected man. Vaccination of population at risk.

6. Salmonellosis

Salmonella typhimurium

S. enteridis

Most mammals, poultry and man

Ingestion of meat and other products of animal origin. Contamination of food and water.

Vaccination of animals, meat hygiene and good sanitation

Protozoal zoonoses

SN Disease Agent

Reservoirs or hosts

Mode of transmission

Prevention and control

1. Leishmaniasis (Kala azar)

Leishmania donovani

Dogs, jackals, foxes, rodents and other mammals

Bite of sand fly Dog, rodent and sandfly control

Helmintho zoonoses

SN Disease Agent

Reservoirs or hosts

Mode of transmission

Prevention and control

1. Taeniasis
a) Taenia saginata
b) Taenia solium

Intermediate host: Cattle Final host: Man

Intermediate host: pig/man Final host: man

Consumption of under cooked meat of infected animals or food contamination by eggs

Treatment of affected animals, meat inspection and good sanitation of slaughter house

2. Hydatid disease

Echinococcus granulosis

Intra: ruminants and occasionally man Final host: dog

Contamination of human food and water with parasite eggs

Preventing dogs from eating raw meat and infected meat. Meat inspection and proper disposal of
infected meat/animals.

3. Trichinellosis

Tichinella spiralis

Most mammals, most importantly pigs

Ingestion of undercooked meat

Meat inspection, deep freezing and proper cooking of pork

Mycotic zoonosis

SN Disease Agent

Reservoirs or hosts

Mode of transmission

Prevention and control

1. Ringworm

Microsporuim spp. Trichophyton spp.

Cattle, buffalo, sheep, goat, pig, dog, cat

Direct or indirect contact with infected animals

Isolation and treatment of infected animals and good hygienic condition of barns.

UNIT 11. INTRODUCTION TO ARTIFICIAL INSEMINATION

Artificial insemination is the process of introducing the spermatozoa into the female reproductive tract
by artificial means. The technique may be employed in all domestic animals.

There are far more spermatozoa in an ejaculate than are need to fertilize one oocyte. Thus it is possible
to collect, dilute and store the semen from a sire and use this for inseminating many females. AI enables
rapid genetic improvement in a population on a wider scale than would be possible with natural
insemination.

Advantages of AI

1. AI greatly increases the utilization of superior sires. Marked increase in production can be achieved
in the herd using AI to proven sires. A large number of female animals can be bred to a sire than
compared to natural insemination.
2. The semen can be stored in frozen condition for many years after the bull is dead.
3. Semen can be used from bulls after they have been progeny tested.
4. The need to rear and feed a bull on the farm is removed.
5. Careful screening and monitoring of bulls at AI centers can control genital diseases.
6. Old and injured and heavy bulls can be utilized.
7. Quick transportation of semen to distant places can be done.

Disadvantages/limitations of AI

1. It requires well-trained operator and special equipment for semen collection, examination, dilution,
freezing and shipping.
2. It requires well-trained persons for insemination.
3. Improper cleaning and sterilization of instruments may lead to lower fertility.
4. There may be chances of genetic abnormalities in the wide spread of AI.
5. Intrauterine insemination of pregnant female may lead to abortion.

Artificial Insemination techniques

There are two insemination techniques:

1. Vaginal speculum method

2. Rectal palpation method
1. Vaginal speculum method :- In this method, vaginal speculum is made into use. This method is
relatively easier but requires different sized speculum for different sized animals and the speculum
should be 100 % sterilized.

Procedure

 First the speculum is sterilized and lubricated preferably with liquid paraffin.
 The vulval lips are dilated and the speculum is introduced into the vaginal passage.
 The speculum is opened inside the vagina and the cervix is located by using a torch light.
 Then the insemination pipette is introduced between the speculum and into the cervix.
  The pipette is inserted up to the half of the cervix and the semen deposited there.
 Lastly, the pipette and then the speculum are withdrawn.
2. Recto vaginal method

It is the most widely used technique and is simple and easy to operate. By this method, intrauterine
insemination is also possible.

Procedure

 A glove is first put on the hand that is to be inserted into the rectum. It is lubricated with soap
and water before inserting.
 The hand is then inserted into the rectum in the shape of cone.
 Any dung in the rectum region is removed.
 The cervix is located by the hand and held properly through the rectal folds.
 Care should be taken to avoid use of force when the animals is straining and to prevent
ballooning of rectum by suction of air.
 Then the exterior of the vulva is cleaned and the inseminating pipette is introduced into the
vagina, first in an upward and forward direction and then horizontally forward.
 The pipette is directed to the mouth of the cervix by the palm or fingers of the hand in the
rectum.
 The pipette is introduced into the cervix and the semen is deposited deep inside it at the
beginning of the body of the uterus.
 The semen should not be deposited deep into the horns.
 Then the pipette is withdrawn followed by the hand.