Viral, Bacterial, Protozoal Disease of Animals

BACTERIAL, VIRAL, FUNGAL AND PARASITIC DISEASES
INTRODUCTION
An infectious disease is a disease which is transmitted with or without actual

contact. Infectious agents are living agents like bacteria, viruses, rickettsiae, fungal and
parasitic agents. They can enter the body of various species of domestic animals through
different routes and cause diseases. An etiological agent can cause a syndrome or
multiple syndromes. Many a times, a syndrome or a disease can be caused by multiple
agents. The diseases also can have various managemental practices and environmental
factors acting as precipitating or predisposing factors.
An infectious disease can be peracute, acute, subacute, chronic and subclinical.

These diseases cause enormous economic loss to the dairy, sheep, goat, swine and poultry
industry. The economic loss can be due to heavy mortality, decreased milk, meat, egg and
wool production and many a time it can reach astronomical proportions. The Veterinary
profession has made a major contribution in developing reliable diagnostic techniques
and effective control procedures for many of the diseases of domestic animals and also of
zoonotic diseases.
The animal husbandry activities contribute significantly to the National economy

and these activities varies from place to place. In our country, most of the animal
holdings are marginal as compared to large animal holdings in developed countries. In
addition, the ecological factors play a role in the transmission and control of animal
diseases. Hence, there is urgency in developing and implementing the monitoring and
surveillance of disease programmes of our country. In addition, developing proper and
rapid diagnostic tests to the field veterinarians is a must for quick diagnosis and effective
implementation of preventive and control measures.
For reducing the economic loss, good and effective animal husbandry activities;
proper diagnosis and treatment; and effective preventive and control measures are
required. The therapeutic measures have undergone a magnanimous and innovative
developments leading to the development of a large number of antibacterial agents from
penicillin to fluoroquinolones. Due to these developments, choosing a proper
antibacterial agent(s) against a particular disease is of paramount importance and this
depends upon:
1. The type of etiological agent(s) involved.

2. The characteristics of the clinical manifestation of the disease.
3. The susceptibility/resistance of a particular agent to an antibacterial agent.
4. The pharmacokinetics of the antibacterial agent used.
In addition, the following points are also important and should be considered:
1. As far as possible a single antibacterial agent should be used.
2. The antibacterial agent to which the causative agent is highly susceptible should be
used.
3. Whenever combination of drug is used, either bactericidal or bacteriostatic drugs
should be used.
4. Whenever an antibacterial agent is administered parenterally and locally, then the same
agent should be used as much as possible.
5. If good response is not obtained after 2-3 days of treatment then the next best drug
should be used.
6. The recommended dose, route of administration and schedule should be adhered to.
7. The proper selection of an antibacterial agent during the advanced stage of gestation
and neonatal period is very essential.
For the prevention and control of infectious diseases good and cheap vaccines are
needed. A deadly disease like Rinderpest has been eradicated from our country due to the
excellent work done by Rinderpest eradication scheme launched by the Ministry of
Agriculture, Government of India in 1954. Availability of a very good vaccine played a
key role in this project. Even though, vaccines are available for many diseases, it is still a
long way to go in developing effective vaccines for many other diseases.
The above facts clearly indicate that, still many problems have to be identified and
proper planning and effective implementation of research activities is required for the
development of proper diagnostic, therapeutic, preventive and control measures of many
infectious diseases of domestic animals and poultry. Future fruitful areas of research on
the above aspects will improve the productivity which in turn will improve the financial
status of the farmers and the national economy in particular.
Questions:
1. How infectious diseases will cause economic loss?
2. Define antibacterial agents and how they are classified?
3. Why one should know the pharmacokinetics of antibacterial agents.
4. Why bacteriostatic and bactericidal drugs should not be used simultaneously?
5. What do you mean by prevention and control of infectious diseases? What are the
different strategies employed for the prevention and control of infectious diseases of
domestic animals and poultry?
I. BACTERIAL DISEASES
1. ANTHRAX
(Neradi roga, Splenic fever, Charbon, Milzbrand)
Anthrax is an acute to peracute infectious disease of all domestic animals and

human beings, caused by Bacillus anthracis and is characterized by septicaemia and
sudden death with the exudation of dark tarry coloured and unclotted blood from the
natural orifices.
Etiology:
It is caused by Bacillus anthracis which is a Gram positive, rectangle shaped
bacterium measuring about 4-8 µm x 1-1.5 µm in breadth. It is a non-motile spore
forming organism. It can occur in singles, pairs or chains and is encapsulated.
Under aerobic conditions it forms spores. Commonly the spores survive for 3-4
years and in laboratory conditions it had survived for 70 years. Heat fixation and staining
may not kill the spores. The spores are very resistant. High carbon dioxide level and
putrefaction of the carcass inhibits the sporulation.
Epidemiology:
a) Occurrence: Anthrax is world wide in its distribution. The incidence of anthrax varies
with the type of soil and climate. It is many a time restricted to a particular area where it
is endemic and such areas are known as “Anthrax belts”.
Cattle and sheep are very susceptible to anthrax and horses, deers and bisons are
quite susceptible. Human beings and swine are less susceptible. The disease is almost
invariably fatal except in swine. Dogs, cats and rats are quite resistant.
b) Transmission: Spores can be picked up by the animals directly from the soil or from
fodder grown on infected soil from contaminated bone meal or protein concentrates or
from infected excreta, blood or other material. Water can be contaminated by the effluent
from tanneries, infected carcasses and by flooding and the deposition of anthrax infected
soil. The organisms enter the body commonly by ingestion of contaminated feed and
water. It can be also by inhalation, but this is not a common route compared to human
beings. In humans, the condition known as 'wool sorter's disease’ occurs as a result of
inhalation of spores.
It can also be transmitted by biting flies like Stomoxys, Tabanus and other insects.
These will act as mechanical vectors and at the site of bite there will be a swelling. The
spores can he transmitted from one county to another through animal by products like
meat, wool, hide, fertilizers, bone meal etc.
Pathogenesis:
Upon ingestion or inhalation, the organisms go to the regional lymph nodes and
multiply. Later on through the lymphatics they get into the blood and cause septicaemia.
The bacilli then invade all the body tissues and organs
There are two theories for the cause of death:
1. Log jam theory: In olden days, it was felt that the masses of bacteria blocked the
capillaries which resulted in anoxia of cells leading to death.
2. Toxins: Recently it has been shown that, the organism produces potent toxins which
affects the central nervous system (CNS) and cause oedema and tissue damage leading to
shock and acute renal failure. The details of the toxins are:
English worker Factor I Factor II Factor III

USA workers Oedema factor Protective antigen Lethal factor
The organism produces fibrinolysin which liquefies the fibrin. Hence clotting of
blood will not occur in anthrax. Rigor mortis also do not occur in anthrax where the
exact reason is not known.
Clinical findings:
Incubation period is probably 1-2 weeks
1. Cattle and sheep: Anthrax occurs in two forms:
a) Peracute form: Sudden death without any clinical signs is usually seen. In some
animals fever, tremors, dyspnoea and congestion of the mucosa are seen. Within 1-2
hours there will be collapse, convulsions and death. Oozing of unclotted, tarry coloured
blood from the natural orifices will be seen at the terminal stages and is very
characteristic of this disease.
b) Acute form: Very high fever (107oF), anorexia, marked depression, rapid deep pulse,
congestion and haemorrhages on the mucosae are seen. Heart and respiratory rates are
increased and pregnant cows can abort. There will be marked reduction in milk yield and
the milk may be blood stained or deep yellow in colour. The oedematous swellings occur
in the throat, sternum, flank and perineum. If the gastrointestinal (G.I) tract is involved,
diarrhoea and dysentery can be seen. Death usually takes place within 4 hours.
2) Pigs: The disease is either acute or subacute in nature. Many of the signs are very
similar to cattle. In addition petechial haemorrhages on the skin, the swollen lymph nodes
of the neck, oedema of the pharynx and neck are seen.
3) Horses: Similar to cattle:
Necropsy findings:
The rigor mortis is absent and bloat and putrefaction will be very fast. Petechial
haemorrhages on the serosa, mucosa and even ecchymotic haemorrhages through out the
body and tissues are seen. Unclotted tarry coloured blood in blood vessels and heart and
blood stained serous fluid in the body cavities. Spleen is enlarged too much which is soft
and liquefied, is a very characteristic finding. Gelatinous material is present in the
subcutaneous tissue. Local lymph nodes are enlarged.
Diagnosis:
1. History of sudden death and oozing of unclotted tarry blood from the natural orifices
is suggestive of anthrax. In veterinary field, one of the diseases to be kept in mind is
anthrax when there is sudden death of the animal
2. Demonstration of B. anthracis: Blood from the ear vein of a suspected case and tip of
the ear or a piece of spleen from a carcass is to be collected. When blood is collected, it
should not be exposed to air and only a small quantity is to be collected to prevent the
formation of spores and contamination of the area. Instead of this, pricking the ear vein
and making 2 or 3 blood smears and submitting to a laboratory is best. Fluid from the
oedematous swellings can be collected and smears are made. Methylene blue or Gram’s
staining is performed to demonstrate many bacilli in each field.
3. Blood can be cultured in blood agar plate or gelatin tube for demonstrating the cultural
characteristics.
4. Biological tests: the suspected material is injected, subcutaneously or applied to the
scarified area of guinea pig or mice and within 48 hours they will die, with visible
lesions. The organisms also can be demonstrated.
5. Serological tests: (a) Ascoli's test: It is a precipitation test. Here a small piece of ear,
or flesh from a carcass suspected for anthrax is minced and boiled in water for 2-5
minutes. After cooling it, it is centrifuged. Then a small quantity of the supernatant is
placed in a test tube and later layered with antisera. At the junction there will be
formation of white ring in positive cases.
(b) Indirect micro-agglutination test: 93-98% of the eases will be positive to this test.
(c) Agar gel precipitation test is also used.
Differential diagnosis:
Due to sudden death it should be differentiated from:
1. Lightning stroke: This condition will have the history of lightning and electrical
storms and there will be singeing of the hairs.
2. Peracute black quarter: Look for the crepitating swellings in neighboring animals.
3. Acute leptospirosis: Check for the haemoglobinuria.
4. Peracurte haemorrhagic septicaemia: In HS, blood smear examination will reveal
bipolar organisms and where as in anthrax many rectangular bacilli in chains will be
found.
5. Peracute lead poisoning and hypomagnesaemic tetany: These diseases will be
characterized by CNS signs.
6. Snake bite: Here there will be history of snake bite, fang marks at the site of bite and
local swellings.
7. Acute bloat: Do blood smear examination and presence of B. anthracis will
differentiate it from acute bloat.
Treatment:
The following treatment is given to the animals suffering from anthrax:
1. To overcome the etiological agent, administer any one of the following antibiotics:
a)Penicillin: During the olden days penicillin was considered as the drug of choice for
anthrax. It is administered @ 10,000- 20,000 IU/Kg body weight, i/m, once or twice a
day for 5-7 days. However, recent studies have indicated that penicillin alone can cure
only 52.59% of the cases suffering from anthrax.
b)Penicilin-streptomycin combination: like Vetopen or Dicrysticin @ 1-2 large
doses/cow, i/m, for 3-5 days is found to be very effective now a days and the survival rate
can be 100% if used early. Hence, it is better to administer strepto-pen combination
rather than penicillin or streptomycin-alone.
c) Oxytetracycline (OTC) can be used @ 5-10 mg/kg body weight, i/v or i/m for 3-5
days. However, recent studies indicated that the survival rate is only 41.5%.
2. To overcome the pyrexia, administer antipyretics like analgin @ 40 mg/kg body

weight, i/m.
3. To prevent the effect of histamine, administer antihistamines like Avil or chloril @
10-20 ml/cow, i/m.
4. High doses of corticosteroids like beta or dexamethasone @ 0.5-2.0 mg/kg body
weight i/v, i/m may be useful.
Prevention and Control:

1. Isolate the infected animals and treat them.
2. Strict quarantine measures should be adopted.
3. Manure, bedding and other contaminated material should be burnt.
4. Carcasses confirmed as anthrax should not be opened and should be disposed off by
burning or burial. For burial dig a deep pit and layer with 6-12" of limestone (Calcium
carbonate). Then place the carcasse and layer again with 6" of lime stone and close the
pit with lot of soil. The purpose of adding limestone is to prevent the spore formation.
The mechanism involved is: lime stone reacts with the putrefied carcasse and releases
CO2, which inhibits the spore formation.
5. Disinfect the area thoroughly with 10% formaline or 5% Sodium hydroxide or 5%
lysol or 3% per-acetic acid.
6. Vaccinate the healthy animals with Anthrax spore vaccine (Institute of Animal Health
and Veterinary Biologicals, Bangalore, IAH & VB). This vaccine contains live spores of
an uncapsulated avirulent strain of B. anthracis in 50% glycerol-saline. The dose for
cattle, buffaloes is 1 ml.,, sheep and goats is 0.2 ml, for camel is 2 ml and for elephants is
3 ml, s/c. The duration of immunity is one year and hence, administer the vaccine
annually. Discard the left over vaccine properly (burial/burning).
Questions:
1 Define the following:
a) Anthrax belt
b) Woolsorter's disease
c) McFaydean's reaction
2. Describe the clinical signs of Anthrax and how will you diagnose Anthrax?
3. What are the diseases to be considered under differential diagnosis of Anthrax & why?
4. Why necropsy is not conducted in carcasses suspected of Anthrax?
5. Why penicillin and streptomycin combination is considered as the drug of choice in
treating Anthrax?
6. List out the preventive and control measures of Anthrax.
2. PASTEURELLOSIS
Pasteurellae occur in many animal diseases as primary or secondary causes and the
nomenclature of these diseases has been indefinite and confusing. However the
following diseases have been identified:
1. Haemorrhagic septicaemia or septicaemic pasteurellosis of mainly cattle and
buffaloes
2. Pneumonic pasteurellosis of cattle.
3. Pasteurellosis of swine.
4. Pasteurellosis of sheep and goats.
(a) HAEMORRHAGIC SEPTICAEMIA

(Gantalu bene/ baavu/roga, H.S., Septicaemic Pasteurellosis, Barbone)
It is a septicaemic disease of mainly cattle and buffaloes caused by Pasteurella

multocida type I or B and is characterized by high morbidity and mortality rates, high
fever, swellings on the ventral aspect of the throat, neck and brisket causing dyspnoea.
Etiology:
It is caused by Past. multocida type I and B. It is a Gram negative small coccoid
rod measuring about 0.6 µm in length x 0.25-0.5 µm in breadth. They are known as
bipolar organisms because both the poles take up the stain and the part between the poles
will not take stain when stained by Gram's, methylene blue, leishman's and wright’s
stains. The organism can be destroyed by 0.5% phenol.
Epidemiology:
a) Occurrence: Very common disease in Southern Asia, Southern Europe including
USSR, Northern and central east Africa. Also recorded in USA. The animals susceptible
are: Buffaloes ++++, Cattle +++, Pigs ++, Horses + and sheep and goat - variable. Yaks
and camel are also susceptible.
It is a very common disease in many states of India. Dutta et al. (1990) collected
the data of HS for 13 years period of 1974-1986 from the Animal disease Surveillance
Bulletins issued monthly by the Animal Husbandry wing of the Ministry of Agriculture,
Government of India and analysed the data by employing various statistical methods.
During this period the morbidity and mortality rates due to HS were 6.40 and 6.28 per
lakh bovine population taking the first and second position as compared to other four
epizootic diseases namely FMD, RP, Anthrax and BQ. The disease was responsible for
an overall proportional mortality of 58.77% of the aggregate bovine mortalities due to 5
major epizootic diseases and has occupied the first place among these diseases.
However, the overall occurrence of HS had shown a declining trend on long term basis.
Gujarat, H.P., Kamataka, Manipur, Meghalaya, Rajasthan, Tripura, Arunachal
Pradesh and Chandigarh were classified as "high risk areas", where as A.P., Assam,
Maharashtra, Nagaland and Sikkim were classified as “medium risk areas" and Andaman,
Lakshadweep and Mizoram had the 'disease free' status of HS. The time series analysis
indicated that the occurrence of the disease was maximum during rainy season (July to
September) and it has clear cut seasonal pattern.
Any age group and breed can be affected. The organisms are already present in
the animal and due to stress or precipitating factors, the animals come down with the
disease and an outbreak occurs later on. The factors are:
1. Sudden change in weather: hot weather suddenly changing to chilly weather due to
sudden heavy down pour during the onset of monsoon rains leading to stress on
the animals. Stress is generally characterized by the release of nor-adrenaline
which will stimulate the release of ACTH. ACTH in turn will stimulate the
release of corticosteroids which will suppress the immune system and making the
organisms to vegetate, multiply and produce the disease.
2. Transportation of animals for long distances without proper feed and water.
3. Heavy work
4. Heavy worm infestation
5. Starvation
6. Viral infections like para-influenza (PI-3) and IBR.
b) Transmission: Past. multocida is a natural inhabitant of tonsils and nasopharynx. They

are mostly transmitted by ingestion of contaminated feed and water; and also by
inhalation. The animals which have come down with HS immediately after the onset of
monsoon rains will be a source of infection to other animals and results in outbreak.
Pathogenesis:
Upon ingestion or inhalation, the organisms get into the blood causing
septicaemia. Later on it can localize in respiratory and G.I tracts thus resulting in
inflammation, which is characterized by the accumulation of lot of fibrin in the lungs and
thoracic cavity. The organisms can liberate some unidentified toxins.
Clinical findings:
In per acute form, sudden death with oozing of reddish coloured discharge from
the natural orifices may be seen. I such cases usually the blood will clot.
In acute form, High fever (106-107°F), profuse salivation and petechiae on
mucosa initially and later on oedematous swelling of throat, ventral aspect of neck and
brisket occurs. These, are hot and painful. Respiration rate is increased, grunting sounds
may be heard initially, followed by marked dyspnoea due to pressure exerted by the
oedematous fluid on pharynx/larynx and trachea. So protrusion of tongue with open
mouth breathing will be seen in advanced stages. Finally the animal collapses and dies.
The course of the disease can be 24 hours to 5 days.
Necropsy findings:
Petechiae on the serosa, mucosa, epicardium and endocardium are seen. All the
lymph nodes are swollen and haemorrhagic. Subcutaneous oedema characterized by the
accumulation of gelatinous material particularly in the throat, neck and brisket.
Fibrinous broncho-pneumonia is also seen. The inter-lobular septae are thickened,
widened with serous fluid giving the appearance of marbling. The pleura and pleural
cavity contains lot of fibrin and serous fluid.
Diagnosis:
1. Symptomatic diagnosis can be made whenever the animals are presented with high
fever, oedematous swelling of the throat, neck and brisket and dyspnoea. In addition,
seasonal occurrence of this disease helps in tentatively diagnosing it as HS.
2. Demonstration of the causative agent:

a) The sample to be submitted from a live animal is blood. The blood smear is made and
stained with commonly used staining techniques observed for the presence of bipolar
organisms. In the initial stages of this disease, the organisms may not be readily
demonstrated and the exact reason is not known. Many veterinarians are of the opinion
that since the organisms are readily demonstrated from advanced cases, the septicaemia
may be seen during the terminal stages of this disease. Saliva and oedema fluid may also
reveal the organisms. From putrefied carcasses, collect a long bone for demonstrating the
organisms from the bone marrow.
b) Scarify the abdomen of the rabbit and apply the suspected blood. Within 24-48 hours
the rabbit will die and the characteristic lesions are seen. Here presence of haemorrhagic
tracheitis is almost a pathognomonic lesion
3. Serological tests: Many serological tests like haemagglutination test (HAT),
haemagglutination inhibition test(HI), Standard tube agglutination test (STAT),
Complement fixation test (CFT) and Mouse protection test have been used. Now a days
PCR assay for the rapid diagnosis of HS has been used.
Differential Diagnosis:
It should be differentiated from:
1. Anthrax: Sudden death with dark tarry coloured unclotted blood from the natural
orifices is very characteristic of anthrax. Anthrax can be confirmed by blood smear
examination where in Gram positive, long square ended bacilli in long chains are present.
However, blood smears suspected for HS will reveal Gram negative bipolar organisms.
2. Black Quarter: If sudden death is seen, then examine the neighboring animals for the
presence of crepitating swellings in the heavy muscles. BQ can be confirmed by
performing muscle biopsy where in the muscle smear upon Gram’s stain will reveal
plenty of Gram positive bacilli.
3. Contagious bovine pleuro pneumonia: It can be confirmed by culturing and CFT.
4. Viral diseases
Treatment:
Treatment is effective mostly in initial stages of HS in buffaloes. The following
treatment is commonly used:
1. To overcome the etiological agent, use any one of the following:
a) Sulphadimidine @ 130-150 mg/kg body weight, i/v, for 3-5 days, if necessary
administer the injectable first intravenously and then maintain with subcutaneous
injection or administer sulphadimidine tablets orally.
b) Strepto-penicillin: 1-large doses, i/m, for 5 days.
c) Sulpha-trimethoprim combination @ 15-30 mg/kg body weight i/m, i/v, for 5 days
and also can be maintained with oral preparations.
d) Tetracyclines @ 10-20 mg/kg body weight i/v or i./m for 5 days.
e) Fluoroquinolones: Recently pefloxacin @ 2 mg/kg body weight, i/v daily for 3-4
days appears to be very effective. Even efforts have been done to use Enrofloxacin
or Ciprofloxacin @ 2.5-5.0 mg/kg body weight, b.i.d., for 5 days.
f) Recent study of Veterinary College, Bidar indicated a sensitivity pattern of
Gentamicin (100%), Ofloxacin (92%), and Ceftriaxone, Streptomycin and
Sulfafurazole as 77%.
2. To reduce the fever, administer analgin @ 40 mg/kg or esgipyrine-N @ 10-20 ml/cow,
i/m or Diclofenac sodium @ 1 mg/kg, i/m.
3. To prevent the effect of histamine administer antihistamines like Avil or chloral, 10-20
ml/cow, i/m.
4. If necessary administer corticosteroids.
5. Administration of diuretics like frusemide (lasix) @ 3-5 mg/kg or acetezolamide (500-
1500 mg/cow) may help m reducing the lung oedema and swellings at the throat and
neck. Since, the gelatinous material is more, it may not be very useful.

2. Use good hygienic measures especially using of 0.5-1.0% phenol or 2-4% Sodium
carbonate (washing soda) as a disinfectant
3. Vaccinate all healthy animals by using any one of the following vaccines
a) HS broth vaccine (IAH & VB): It is a formalinized culture of Past. multocida (P
52) in nutrient broth. Dose is 5-10 ml, s/c.
b) HS alum precipitated vaccine (IAH & VB): The organisms are killed by formaline
and precipitated by alum. Dose is 5-10 ml, s/c.
c) HS oil adjuvant vaccine (Indian Veterinary Research Institute, Izatnagar; IVRI):
Organisms are killed with formaline and blended with oil of paraffin and lanolin.
Dose for cattle and buffaloes is 3 ml and for pigs and sheep 2 ml, s/c.
d) HS vaccine (Bharatiya Agro Industries Foundation, BAIF and Indian
Immunologicals (II): The dose is 2 ml s/c.
e) HS & BQ vaccine (BAIF & II): The dose is 4 ml s/c.
Note:
1. Calves are usually vaccinated when they are 5-6 months of age. If the vaccination is
done when they are 2-3 months of age then it should be repeated when they are 6 months
of age. Other wise they can come down with the disease.
2. In an outbreak of HS, even after vaccination of healthy animals, some animals will
come down with the disease which may be due to the animals being in incubation period.
Hence, the owners should be informed prior to the vaccination, to avoid unnecessary
complications.
3. Since the duration of immunity is for 6-8 months, vaccinate the animals every year
before the onset of monsoon rains. If necessary repeat the vaccination once in 6 months.
Levamisole @ 3 mg/kg body weight potentiates the immune response of the HS
vaccine when used along with the vaccine or after few days after the vaccination.
(b) BOVINE RESPIRATORY DISEASE (BRD)

It is a disease of cattle characterized by acute respiratory disease of uncertain
diagnosis. It is common in feed lot cattle especially calves of North America causing
severe economic toss. In feedlots, the morbidity rate will range from 15-45% of cattle
within 3 weeks after arrival and the population mortality rate varies from 1-5%.
It appears to have multiple etiology like Past. haemolytica. IBR virus, PI-3 virus,
bovine virus diarrhoea (BVD) virus, bovine respiratory syncytial virus, Mycoplasma
bovis and Mycoplasma dispar. In addition, several environmental and managemental
factors are also involved.
The clinical findings include unexpected death, dyspnoea, coughing, nasal
discharge, varying degree of depression, inappetance or anorexia, a fever ranging from
104-106°F, evidence of pneumonia on auscultation of the lungs and a variable response
to treatment.
Many antibacterials have been used for the treatment of this condition like OTC @
10 mg/kg body weight i/m; Procaine penicillin G @ 30,000-45,000 IU/kg body weight,
i/m; Trimethoprim - Sulfedoxine @ 15-20 mg/kg body weight, i/m and Tilmicosin. @ 10
mg/kg body weight, s/c for at least 3 days.
The control of outbreaks of acute BRD depends on minimising the effects of the
risk factors, enhancing immunity by the judicious use of vaccines and mass medication.
Pasteurella bacterins and respiratory viral vaccines have been used extensively either
single or in combination.
Mass medication of feedlot cattle upon arrival can be either administration of OTC
@ 20 mg/kg body weight, i/m to each animal or administration of chlortetracycline in the
feed @ 1,2, 4 gms per head daily for 2 weeks after arrival of feedlot cattle.
(c) PNEUMONIC PASTEURELLOSIS OF CATTLE

(Shipping fever, Pneumonia)
It is a disease of cattle usually associated with infection by Past. haemolytica
biotype A serotype 1 (also biotype T) and occasionally Past. multocida. Shipping fever is
an entity within the BRD complex and is characterized by acute bronchopneumonia with
toxaemia and fibrinous pleuritis.
It is a common disease of cattle in Europe, the UK and North America. It
commonly occurs in feedlot calves. The morbidity may reach 35%, the case fatality rate
may range from 5-10% and the population mortality rate may vary from 0.75-1.0%. Thus
it is a major cause of economic loss in the feedlot industry.
It commonly occurs in young cattle of 6 months to 2 years of age but all age
groups are susceptible. Stress of transportation of calves by truck appears to play a major
role in the occurrence of this disease. In addition, mixing of calves from different sources
at auction markets may also play an important role in the occurrence of this disease,
Management factors like poor ventilation and overcrowding are also involved.
The clinical signs of pneumonic pasteurellosis are fever of 104-106°F, anorexia,
depression, loud breath sounds and dyspnoea. Upon auscultation, crackling sounds and
pleuritic friction rubs can be heard. The course of the disease is 2-4 days.
Necropsy findings include various stages of acute bronchopneumonia and
fibrinous deposition in the thoracic cavity, fibrin strands and adhesions.
Treatment is similar to BRD. Animals in early stage of the disease responds well
within 24 hours to commonly used antibacterial agents.
Successful control begins with the adoption of good management techniques when
the calves are still on the range, the judicious use of efficacious vaccines and care in
handling and transportation of cattle. The vaccines have been administered by aerosol
route, s/c and i/m routes.
Use of long acting OTC or sulphamezathine upon arrival of feedlots or
administering sulphamezathine @ 150 mg/kg body weight on first day and then 75 mg/kg
body weight for another 5-10 days in feed or water can be used as chaemo prophylaxis.
(d) PASTEURELLOSIS OF SHEEP AND GOATS

Pasteurellosis in sheep and goats is caused by Past. haemolytica. It can be
pneumonic pasteurellosis which is the most common form seen in all age groups. Other
forms are septicaemic pasteurellosis in very young lambs and systemic pasteurellosis in
weaned lambs and mastitis in ewes.
There are two biotypes of Past. haemolytica and further divided into serotypes.
Among biotype A. serotype A2 is the most prevalent serotype isolated. The other biotype
isolated is T with serotypes T3, T4, T10 and T15.
Past. haemolytica is a normal inhabitant of the upper respiratory tract of sheep.
Colonization of nasopharynx and the tonsil occurs very shortly following birth probably
from the ewe and carriage persists through adult life.
i) Pneumonic pasteurellosis:
It causes economic losses in sheep in most parts of the world especially in UK,
USA, Holland and New Zealand and India. It occurs in all age groups and at all times of
the year. Outbreaks are common in late spring and early summer. Outbreaks often start
with sudden deaths in lambs from the septicaemic pasteurellosis and progress to
pneumonic pasteurellosis in the ewes and also in the lambs as they get old. Attack rates
upto 40% and a population mortality upto 5% may occur. A mortality rate of 20% has
been recorded in goats.
Outbreaks in flocks at pasture are frequently associated with changes in climate or
management and this is similar to the disease in cattle. Poorly ventilated barns; exposure
to bad weather, transport and malnutrition are associated with severe outbreak of this
disease. In range sheep, confinement for shearing, mating or supplementary feeding may
precipitate an outbreak and severe parasitism or rain and wind chill may also increase
susceptibility.
It is probable that disease is also predisposed by viral infections of the respiratory
tract like PI-3 virus and Adenovirus.
ii) Septicaemic pasteurellosis:

It is a disease of young lambs from 2 days to 2 months of age but most commonly
seen at 2-3 weeks. Past haemolytica biotype A causes this disease. Commonly young
lambs with this condition and pneumonic pasteurellosis in older lambs are seen
concurrently.
iii) Systemic Pasteurellosis:

It is associated with Past. haemolytica biotype B predominantly in weaned lambs
from 5-12 months of age. Stress plays an important role in the occurrence of this disease.
iv) Mastitis:
Past. haemolytica is a major cause of mastitis in ewes in Britain. Various typed
and untyped strains within biotype A are isolated and serotype A2 is most common.
Clinical findings:
Sudden death without clinical signs occurs in pneumonic pasteurellosis. It may
continue throughout the outbreak in lambs but in older lambs respiratory diseases can be
seen. As it progresses, nasal discharge, couching, slight froth at the mouth and dyspnoea.
Affected sheep have fever from 105-107°F and are depressed and anorectic. In more
chronic cases respiratory sounds are very audible. Death may occur as soon as 12 hours
but the course in most cases is about 3 days. Recovered sheep will have chronic
pneumonia and poor thrift and hence should be culled.
In systemic pasteurellosis, the course is often less than 6 hours and affected sheep
are found dead. Affected sheep are dull, prostrated and may have a frothy bloody nasal
discharge in the terminal stages.
Necropsy findings:
Petechial and ecchymotic haemorrhages are present throughout the body. In
pneumonic pasteurellosis, a greenish gelatinous exudate over the pericardium and large
quantities of straw coloured pleural exudate are characteristic findings. The lungs are
enlarged, oedematous and haemorrhagic.
In systemic pasteurellosis, the subcutaneous haemorrhages over the neck and
thorax are common. The trachea and bronchi contain blood stained froth, the lungs are
oedematous with subpleural ecchymosis without pneumonia. The tonsils and pharyngeal
lymph nodes are enlarged and there is ulceration and necrotic ulcers on the tips of the
folds of the abomasal mucosa.
Diagnosis:
For culturing and isolation and identification of the bacteria, the tracheo-bronchial
aspiration, tonsils, lungs and liver and mucosal lesions of the pharynx and oesophagus are
the best source of the organisms.
Treatment:
Treatment is similar to the ones used for HS. Long acting OTC @ 20 mg/kg body
weight, i/m is the drug of choice. Penicillin also can be used. Combination of Amoxicillin
and clavulanic acid is found to be effective. Medication of the water supplies with
chlortetracycline for 7-10 days may be beneficial.
Control measures are similar to the ones used in cattle. Attempts have been made
to produce an effective vaccine by using various biotypes and serotypes. It has been
shown to provide protection to newly born lambs when the pregnant ewes were
vaccinated. Also vaccinating the young lambs have been under study. However, the
development of an effective vaccine has proved elusive.
Recent exposure to an episode in a goat farm indicated that 2-4% Sodium
carbonate (washing soda) as a disinfectant and use of Slpha-trimethoprim combination
was highly beneficial.
(e) AVIAN PASTEURELLOSIS

(Fowl cholera)
It is a contagious disease of domestic and wild-birds caused by Past. multocida

and characterized by septicaemia in acute conditions and localized infection in chronic
condition.
Etiology:
It is caused by Past. multocida and its morphological features are similar to the
one which causes HS.
Epidemiology:
a) Occurrence: Fowl cholera has been recorded throughout the world in domestic fowls,
game birds and small feral birds (sparrows, crows, starlings). Turkeys are more
susceptible when compared to domestic fowls. Birds reaching sexual maturity (16 weeks
and above) are more susceptible when compared to the chicks.
b) Transmission: The organisms enter the birds by ingestion of contaminated feed and
water. The faeces and saliva contains the organisms. Transmission also can occur through
contact.
Pathogenesis:
The organisms enter through the pharynx or upper respiratory mucosa and gets
into the circulation. It causes septicaemia and the exact toxin is unknown. Then it
localizes in various visceral organs viz., liver, intestines (duodenum), heart, joints,
pneumatic bones, combs, wattles, eye and surrounding structures and causes
inflammatory changes.
Clinical findings:
Incubation period is 4-9 days. The disease can be peracute, acute or chronic.
1. Peracute: The birds may die within few hours without showing any signs.
2. Acute: Fever, anorexia, ruffled feathers, mucous discharge from the mouth, diarrhoea
(may be blood stained), increased respiratory rate, dyspnoea, discharge from the nostrils,
cyanotic combs and wattles can be seen.
3. Chronic: The wattles, sinuses, leg or wing joints, foot pads and sternal bursae are
swollen and oedematous. The eye and surrounding structures are swollen. Some birds
may exhibit torticollis due to ear infection.
Necropsy findings:
Petechial or ecchymotic haemorrhages are seen on serosa and mucosa in acute
cases and also on epicardium, endocardium and intestine (duodenum). Congestion in
various visceral organs. Pneumonic changes in the lungs. Ovaries of the laying hens are
commonly affected. Mature follicles often appear flaccid and thecal blood vessels are less
evident. Yolk material from the ruptured follicle may be found in the peritoneal cavity.
In chronic form the caseous or serofibrinous material is seen in the sinuses,
pneumatic bones, joints and abdominal cavity. Many small necrotic foci are present in
the liver.
Diagnosis:
Based on the clinical signs and necropsy findings the disease can be tentatively
diagnosed as fowl cholera. It can be confirmed by isolation and identification of the
organisms by collecting the nasal discharge, saliva, faeces and blood from live birds and
bone marrow, heart blood and liver from carcasses. The organisms can be demonstrated
by the routinely used staining techniques.
Serological tests like Rapid whole blood agglutination test, Rapid serum plate
agglutination test and Agar gel immuno diffusion test have been used but are of limited
value.
Fowl cholera should be differentiated from pullorum disease, fowl typhoid and
paratyphoid. Pullorum disease occurs in 2-3 week old chicks and most of them die
Ovules arc shrunkened. In fowl typhoid 1-3 months old chickens are affected and most
of them will die. Whereas fowl paratyphoid occurs within 2 weeks of age and most of
them will die. These diseases can be confirmed by necroscopy findings and culturing
and isolation and identification of the causative agents.
Treatment:
Administer sulphaquinoxaline @ 0.01-0.05% in drinking water or 0.05-0.1% in
mash for 5-7 days. Antibiotics like chloramphenicol @ 20 mg/kg, i/m; oxytetracycline
@ 40 mg/kg, i/m and Chlortetracycline @ 500 gm/ton of feed can be used. Hostacycline
or Terramycin poultry formula with antigerm 77 @ 1 teaspoonful per 4.5 litres of water
can be used.

Good management practices with good sanitation should be followed. Formaline
killed vaccine, bacterins and live attenuated vaccine have been administered orally,
drinking water and i/m also. Fowl cholera vaccine (FVRI) 1 ml, s/c at 8 weaks of age can
be used.
Questions:
1. Why Haemorrhagic septicaemia occurs, commonly immediately after the onset of
monsoon rains?
2. Why blood is commonly used for the diagnosis of H.S.?
3. Why long bone is submitted from the putrefied carcasse suspected of H.S.?
4. Why advanced cases of H.S. usually will not respond to treatment?
5. What type of vaccines is available for prevention and control of H.S.?
6. Why pneumonic pasteurellosis is known as shipping fever of cattle?
7. Write short notes on:
a) Clinical signs of H.S.
b) Clinical signs of Pasteurellosis of sheep and goats,
c) Necropsy findings of H.S. and Pasteurellosis of sheep and goat.
d) Treatment of H.S.
8. How will you diagnose fowl cholera?
9. How will you control fowl cholera?
3. CLOSTRIDIAL DISEASES
(i) BLACK QUARTER
(Chappe roga/bene, Black leg, Emphysematous gangrene, Symptomatic anthrax)
It is an infectious disease of cattle, buffaloes and sheep caused by Clostridium

chauvoei and is characterized by high fever, emphysematous sero-haemorrhagic swelling
of the heavy muscles and lameness.
Etiology:
It is caused by Clostridium chauvoei. It is a Gram positive bacilli, measuring about
3-8 µm in length. X 0.6 µm in breadth. It occurs singly or in short chains. It is motile by
means of peritrichous flagella, anaerobic and non-capsule forming organism. It forms
spores which are present in the sub-terminal or terminal region of the organism which
gives a 'pea shaped' appearance to the organism. The spores are highly resistant to the
environmental conditions, disinfectants and persist in the soil for many years as it is a
‘soil borne’ organism..
False black leg is caused by Cl. septicum. Mixed infections with Cl. chauvoei and
Cl. septicum can occur but the significance of CL. septicum as a cause of disease is
debated.
Epidemiology:
a) Occurrence: BQ occurs in many countries of the world every year and causes severe
economic loss. It is a very important disease in India as it is recorded in almost all states.
Cattle and sheep are commonly affected. Cattle in the age group of 6 months to 2
years and rapidly growing on a high plane of nutrition are highly susceptible. Sheep of
any age group can be affected.
BQ commonly occurs every year immediately after the onset of monsoon rains,
where there will be sudden change in the weather condition which will act as a stress, on
the body. It causes severe economic loss to the farmers as it occurs every year and kills
good number of animals.
b) Transmission: It is a soil borne infection but the portal of entry of the organisms into
the body is in dispute. However, it may be through the alimentary mucosa after ingestion
of contaminated feed and water in cattle and through the wounds in sheep due to
shearing, docking and lambing.
Pathogenesis:
Upon ingestion, the organisms go to the intestine and then gets into the blood and
localizes in heavy muscles especially of the hind quarters and shoulders. There organisms
lie dormant and only during stress the spores develop into vegetative forms. Then
multiply and produce the disease. The stress may be sudden change in weather which
occurs immediately after the onset of monsoon rains and also transportation of the
animals for long distances.
The organisms in the muscle liberate toxins which may produce – (1) loss of
phagocytic activity of the neutrophils; (2) damage the endothelium of the capillaries
leading to oedema and (3) necrosis of muscles. A11 these changes produces necrotizing
myositis where in there will be waxy or hyaline degeneration of muscles. The organisms
ferment sugars and produce gas. This gives the smell of rancid butter. The hydrogen
sulphide reacts with iron and forms Iron sulphide which gives dark colour to the muscles.
From the affected muscles the organisms can get into the blood and can localize in
lungs, liver, heart, kidneys and spleen and can produce gas, oedema and necrosis.
Clinical findings:
Incubation period is 2-5 days. In peracute form the animal may die suddenly
without showing any signs. There can be oozing of blood tinged fluid or blood from the
natural orifices which will coagulate immediately.
Commonly the acute form is seen. There will be very high fever (106-108°F),
depression, anorexia, decreased milk production and dullness. Then there will be acute
lameness. In the heavy muscles, there will be swelling which will be hot and painful in
the beginning and soon becomes cold and painless. Oedema occurs and emphysematous
or crepitating sounds can occur upon palpation of this region. Later on such lesions can
be seen in the base of the tongue, heart muscle, diaphragm, psoas muscle, brisket and
udder. It can be generalized where in the entire body can be affected. The affected skin
will be discoloured and soon becomes dry and cracked. Later on sloughing of skin and
muscles can occur. The course of the disease can be 12-36 hours and also can be 3-5
days. During the final stages the animal will be recumbent, and then coma and death
occurs.
In sheep, acute lameness in one or several limbs is noticed. Oedema and
crepitation cannot be felt before death. High fever, anorexia and depression are also seen
and death occurs very quickly.
Necropsy findings:
The carcasse lies on the ground with the affected hind limbs stuck out stiffly.
Bloating and putrefaction occurs quickly. Incision of the affected muscle mass reveals the
presence of dark, discoloured, swollen tissue with a rancid odour, a metallic sheen on the
cut surface and an excess of thin sero-sanguinous fluid containing bubbles of gas. All the
body cavities contain excess fluid which is blood stained.
Diagnosis:
(1) By history of occurrence of BQ immediately after the onset of monsoon rains and by
signs of high fever, lameness and crepitating swellings of the heavy muscles, one can
diagnose it tentatively as BQ.
(2) By necropsy findings of characteristic lesions one can diagnose it as BQ.
(3) Isolation of the causative agent:
a) Do muscle biopsy, then make a smear, air dry it, heat fix it and perform Gram's
staining. If plenty of Gram positive bacilli are present then it is BQ.
b) For culturing, collect the heart blood and aspirate the fluid from muscle tissue by
using Pasteur pipette and sections of muscle immediately after death.
c) Inject the suspected material s/c into a guinea pig and within 14-30 hours it will
die.
(4) Serological tests like Fluorescent antibody test (FAT) and Enzyme linked
immunosorbent assay (ELISA) are used for diagnosis of BQ. Recently double immuno
diffusion and counter immuno electrophoresis have been used to demonstrate the toxins
in the exudates of muscles.
In peracute BQ there will be sudden death and this should be differentiated from:
1. Anthrax - blood smear examination will reveal the Gram positive bacilli in chains and
no organisms will be seen in BQ.
2. Lightning stroke – history of lightning and singeing marks will be seen.
3. Bacillary haemoglobinuria is characterized by Anaemia and passing of coffee
decoction coloured urine, which are not seen in BQ.
4. Lactation tetany - tetany and convulsions are characteristics of this condition.
5. Acute lead poisoning is characterized by CNS signs like bellowing, circling, head
pushing and blindness and these are not seen in BQ.
Treatment:
The following treatment is usually followed in BQ:
1. To eliminate the etiological agent administer penicillin which is the drug of choice @
10,000-20,000 IU/kg body weight, i/v (crystalline penicillin) and penicillin i/m for 3-5
days.
Initial stages of BQ will respond well and moderate to advanced cases may not
respond well, inject penicillin to the lesion if it is localized.
Tetracyclines and ampicillin also can be used i/v.
Metronidazole which is effective against anaerobes can also be administered along
with penicillin @ 5-10 mg/kg body weight, i/v. It is available as flagyl, anaerid,
aristogyl (100 ml vial containing 5 mg of metronidazole/ml and 5% dextrose) and
unimezol (540 ml sachet containing 2 mg of metronidazole/ml and 5% dextrose).
Some field Veterinarians, will make incisions in the affected area to create aerobic
condition so that worsening of the condition is prevented.
2. To prevent the effect of histamines administer antihistamines.
3. To reduce the pyrexia, administer analgin.
4. To overcome the toxemia, administer dexamethasone @ 0.5-2.0 mg/kg body weight
i/v.

1. Good hygienic measures should be followed.
2. Isolate infected animals and treat them.
3. Vaccinate the healthy animals with any one of the following vaccines:
(a) BQ vaccine (IAH & VB): It is a formaline killed vaccine containing Cl.
chauvoei and Cl. septicum. The dose for cattle and buffaloes is 5-10 ml and for
calves, sheep and goats is 2-3 ml, s/c. Vaccinate the animals before the onset of
monsoon rains.
(b) BQ vaccine (BAIF): It is a formaline killed, aluminum precipitated vaccine
and the dose is 2 ml s/c.
(c) Combined BQ & HS vaccine (BAIF): The dose is 4 ml, s/c.
(d) Raksha HS + BQ vaccine (II) : The dose is 3 ml, s/c.
The above vaccines can be administered to calves 6 months and above of age and
repeated annually. In endemic areas it can be repeated once in 6 months.
The immunity does not develop for 14 days after vaccination and animals in
incubation period may die within this period even after vaccination.
Recent studies indicated that levamisole when administered along with BQ
vaccine potentated the immune response.
4. To prevent the soil contamination, it is better to burn or bury the carcasses.
(ii) BRAXY
(Bradsot, Bradapest, Cling)
Braxy is an acute infectious disease of sheep caused by Cl. septicum and is

characterized by sudden onset, high fever, abdominal pain and short duration of illness.
Etiology:
It is caused by Cl. septicum a Gram positive rod measuring 2-10 µm in length and
0.4-1.1 µm in breadth with rounded ends.
Epidemiology:
a) Occurrence: This disease has been recorded in UK, Europe, Southern Australia and
rarely in North America. It commonly occurs in weaner and yearling sheep.
b) Transmission: It is a soil borne disease and the organisms enters the animal through
ingestion of spores.
Pathogenesis:
Upon ingestion the organisms go to the abomasum and get localized. The
organisms produce alpha, beta, gamma and delta toxins which cause severe abomasitis
and absorption of toxins leads to toxaemia which results in high mortality.
Clinical findings:
Sudden onset of death of lambs without premonitory signs can occur. In other
lambs, there will be high fever (107oF) depression, complete anorexia and distension of
the abdomen with abdominal pain. Recumbency and coma are followed by death within
a few hours of the onset of clinical signs.
Necropsy findings:
Autolysis is rapid. Localized area of congestion, oedema, necrosis and ulcers are
seen in the abomasum. Excessive amounts of straw coloured fluid in the pericardium and
serosanguinous fluid in the abdominal cavity. There may be few sub-epicardial
haemorrhages.
Diagnosis:
Very difficult to diagnose this disease on clinical signs and the best way of
diagnosis is by culturing and isolation of Cl. septicum from the abomasal wall and heart
blood collected within an hour of death.
Braxy should be differentiated from infectious necrotic hepatitis. This can be done
by the presence of liver lesions in infectious necrotic hepatitis and this is absent in braxy.
Treatment:
There is no satisfactory treatment for braxy however penicillin and hyperimmune
serum may be tried.

Vaccinate the lambs with formaline killed whole culture of Cl. septicum s/c, twice
at an interval of 2-3 weeks. This is the best way to prevent and control this disease. Refer
for details of vaccine given under BQ.
(iii) MALIGNANT OEDEMA

(Gas gangrene, Big head)
Malignant oedema is an acute rapidly fatal wound infection of all the species of
domestic animals caused by the bacilli of the genus Clostridium, characterized by the
inflammation at the site of infection and fever.
Etiology:
Cl. septicum, Cl. chauvoei. Cl. perfringens. Cl. sordelli and Cl. novyi have all been
isolated from lesions.
Epidemiology:
a) Occurrence: All the species of domestic animals and all age groups are affected. The
disease is distributed throughout the world. The infection is usually soil borne and is
sporadic.
b) Transmission: The portals of entry of the organisms are through the surgical or
accidental wounds. Needles without proper aseptic precautions when used for i/m
injections also can transmit the bacilli. Crows after eating the infected carrion, can
transmit the organisms to the eyes of weak sheep.
Pathogenesis:
The exotoxins produced in the wounds will cause extensive oedema and necrosis
which will end in gangrene. The potent toxin are absorbed and causes toxaemia and
death.
Clinical findings:
Clinical signs appear rapidly after infection. At the site of primary infection a
swelling develops, which will pit on pressure, the skin darkens and tense. High fever
(106-107°F), depression, weakness, muscle tremors, stiffness or lameness and foul
smelling discharges from the wounds are-noticed. Death occurs in 24-48 hours.
In rams it is known as 'swelled head' because oedema of the head occurs and then
spreads to the neck.
Necropsy findings:
Usually gangrene of the skin with oedema of the subcutaneous and inter-muscular
connective tissue around the site of infection is noticed. The oedema fluid is serous or
gelatinous material; blood stained and contains bubbles of gas in infection due to all the
organisms except Cl. novyi infections. Subserous haemorrhages and accumulation of
serosanguinous fluid in body cavities are common.
Diagnosis:
Diagnosis is mainly on clinical signs and culturing and isolation of the organisms.
Treatment:
High doses of crystalline penicillin i/v, 3 or 4 times a day is beneficial. Administer
Esgipyrin-N or Diclofenac sodium twice a day, i/m. Open the swelling with a surgical
incision, remove the oedema fluid and irrigate with hydrogen peroxide.
In Bidar few cases were successfully treated high dose of Fortified procaine
penicillin and Diclofenac sodium.

Good hygienic measures are followed during shearing, docking, castration and
lambing. Vaccinate the animals with formalinized bacterin. ET vaccine (BAIF)/ Bovilis
MCV (Intervet, 50 ml vials)) is a pentavalent vaccine containing Cl. perfringens type B,
C, D; Cl. septicum and Cl. oedematiens adsorbed on Aluminium hydroxide gel and the
dose is 2 ml, s/c. Pregnant ewes are vaccinated 15 days prior to lambing. The primary
vaccination is done at 4-6 weeks of age in lambs born to vaccinated ewes and secondary
vaccination is done every 6 months. The primary vaccination is done within 1 week of
age in lambs born to unvaccinated ewes and secondary vaccination is done every 6
months. This will give protection against pulpy kidney disease, Struck, Lamb dysentery,
Black disease, Braxy and Malignant oedema.
(iv) TETANUS
(Danurvayu, Locked Jaw)
It is a highly fatal infectious disease of all domestic animals caused by the

neurotoxins of Clostridium tetani and it is characterized by hyperaesthesia, tetany and
convulsions.
Etiology:
It is caused by Cl. tetani which is a Gram positive long slender rod measuring
about 2-5 µm x 0.5 µm. The spores are about 2-3 times the diameter of the cell and are
situated terminally giving the ‘drum stick’ appearance. The organisms are having round
ends and can occur in singles or in chains. Some strains have been identified but all are
antigenically almost similar.
In gelatin slab culture, the colonies appear like 'fir tree' growth i.e., the growth is
good at the bottom of the tube and poor growth near the top. These characteristics are due
to the anaerobic nature of the organisms. The spores are resistant to the environmental
conditions and can persist in the soil for years.
Epidemiology:
a) Occurrence: Tetanus occurs in all farm animals of the world. Commonly it occurs as a
sporadic disease but occasionally it can occur as an outbreak in young cattle, young pigs
and lambs. Mortality rate is 80%. Horses are highly susceptible followed by sheep, cattle
and pig. Carnivores are rarely affected. Human beings are susceptible. Birds are resistant.
The organisms are commonly found in the soil and faeces of man and animals especially
those of horses.
b) Transmission: The organisms enter the body through the wounds:
1. Horses — punctured wounds of the hooves.
2. Cattle — wounds of the genital tract at the time of parturition.
3. Sheep — wounds of castration, docking and shearing.
4. Pig — wounds of castration.
Pathogenesis:
The organisms go to the deeper part of the wound and multiply when there is
lowering of the local tissue oxygen tension. They produce 3 types of toxins:
1. Tetanospasmin is the neurotoxin which is responsible for the disease.
2. Tetanolysin is the haemolysin.
3. Fibrinolysin.
The neurotoxin gets into the peripheral nerve and migrate through the nerve into
the spinal cord and then to the brain. It does not produce any lesion. The mechanism of
action of the toxin is not clearly understood. It may potentiate the normal sensory stimuli
leading to the convulsions and tetany. The death is due to asphyxia which is due to
fixation of the muscles of respiration.
Clinical findings:
Incubation period is 1-3 weeks and some times it can be several months. In sheep,
the clinical signs can be seen between 3-10 days after shearing or docking. In all animal
species, the clinical findings are almost similar.
Initially the locked jaw appearance i.e., difficulty to open the mouth occur which
will come in the way of ingestion of feed and water. There will be drooling of saliva. The
animal stands with tail raised, erected ears, dilated nostrils and retraction of the eyelids.
Prolapse of the third eyelid is an important early sign seen commonly in horses. The
animal moves with difficulty. Constipation and retention of urine can occur due to
inability of the animal to have posture of defaecation and micturition. Tetany occurs and
as it progresses the animal adopts a saw horse appearance. In the beginning temperature,
heart and respiratory rates are normal. In young animal bloat can occur due to strong and
frequent contractions of the rumen.
The animal stands and walks with difficulty. The animal then falls down and once
it is down, mostly it will not get up. Due to light, sound or other stimuli, the animal
becomes hyperaesthetic and tetany and convulsions will occur. This will be repeated very
often. Excessive sweating occurs. Opisthotonus is marked, the hind limbs are stuck out
stiffly behind and fore limbs forwards. During tetany or convulsion the animal may die
due to asphyxiation. At this stage, the temperature will be very high (108 - 110°F) which
is due to convulsions.
In horses and cattle, the course of the disease is 5-10 days and in sheep and other
animals it is 3-4 days. Those animals which survive, the convalescent period will be long
and will recover from the disease, but the number is very low.
Necropsy findings:
No gross or histopathological lesions are seen in tetanus.
Diagnosis:
1) By history of occurrence of wound few days to few weeks before the onset of clinical
signs.
2) By clinical signs of hyperaesthesia, convulsions and prolapse of the third eyelid.
3) Serological test like Radioimmuno assay (RIA), ELISA etc, have been used for the
diagnosis of tetanus.
Tetanus should be differentiated from:
a) Hypocalcaemic tetany (eclampsia) in mare - it is confined to the lactating mares and
administration of calcium will cure the condition.
b) Acute laminitis in horses - no convulsions,
c) Cerebrospinal meningitis - hypersensitivity to sound and movement is not seen.
d) Lactation tetany of cattle - prolapse of the third eyelid and bloat are absent.
e) Enzootic muscular dystrophy of lambs - no tetany.
f) Enterotoxaemia - sudden death of well fed and well grown young calves.
Treatment:
There are three main principles of treatment viz., eliminating the causative agent,
neutralizing the toxins-and to relax the muscle tetany so as to avoid asphyxiation.
1) To overcome the etiological agent and to prevent the further release of the toxins
administer penicillin @ 20,000-40,000 IU/kg body weight, i/m. If the wound is present,
inject penicillin around and into the wound.
2) To neutralize the toxin, administer Anti tetanus serum (ATS) @ 3 lakh IU/horse, i/v,
s/c, or i/m, at 12 hours intervals, 3 times. It is available as ATS (Bengal immunity) in
various strengths of 750, 1500, 5000, 10,000 and 50,000 IU/ampoule.
It is better to administer ATS into and around the wound and after allowing for
sometime then only the wound should be cleaned with hydrogen peroxide.
Once the clinical signs are seen, ATS may not be very effective.
3) To overcome tetany and convulsions, any one of the following can be used to relax the
muscles:
a) Chloral hydrate -1-2 ounce, i/v.
b) Magnesium sulphate -10% solution, 200-300 ml, i/v, s/c.
c) Administering of ataractic drugs like Chlorpromazine (largactil) may be useful @ 0.88
mg/kg, i/v or 2.2 mg/kg i/m.
Since no lesions are produced in the brain, if the muscle relaxants are given
properly along with good nursing care then one can save the life of the animal.
4) Keep the animal in a darkroom with abundant space. Then:
a) Avoid sound
b) Give good bedding
c) Give enema repeatedly
d) Pass the catheter and remove the urine repeatedly.
e) Pass the stomach tube and feed the animal repeatedly.
f) If necessary, do tracheotomy.

1) Proper sterilization of surgical instruments is very essential.
2) Before performing surgery, administer ATS (1500-3000 IU),
3) Vaccinate the animals with Tetanus toxoid (which is nothing but formaline inactivated
tetanus toxin), 5-10 ml, i/m, repeat after 6-8 weeks and give once more after one year. If
necessary repeat every year. Vaccinating the pregnant ewes in the last 2 or 3 weeks of
pregnancy will prevent tetanus in the new born lambs.
(v) ENTEROTOXAEMIA
The term enterotoxaemia is used because the organisms in the intestine multiplies
and produce toxins which will be absorbed into the circulation resulting in toxaemia. The
disease is due to the toxins.
Etiology:
It is caused by Cl. perfringens. It is a Gram positive rod measuring about 4-8
µm by 0.8-1.5 µm. The ends are square. They are non-motile. The spores are sub-
terminally or centrally located. The organisms are commonly seen in soil and alimentary
tract of normal animals. The mechanism which makes them pathogenic and produce the
disease is not clearly under stood.
Epidemiology:
a) Occurrence: Enterotoxaemia is worldwide in its distribution.
The diseases caused by Cl. perfringens are:
1) Lamb dysentery: It is caused by Cl. perfringens type B and occurs in young lambs
upto 3 weeks of age. The incidence may reach 20-30% and the case fatality rate may
approach 100%. Some lambs may die without any clinical signs. Some may have severe
abdominal pain, recumbency, failure to suckle, passing of brown fluidy faeces sometimes
containing blood; then coma and death. within 24 hours.
2) Struck: it is caused by Cl. perfringens type C. It is a disease of adult sheep which will
die suddenly without signs. Some may have abdominal pain and convulsions before
death.
3) Entero-toxaemia in calves: It is caused by Cl. perfrigens type B and C. Commonly

calves of 7-10 days of age are affected and also upto 10 weeks of age can be affected.
The clinical signs exhibited are diarrhoea, dysentery, acute abdominal pain, violent
bellowing and aimless running. Later on tetany and opisthotonus are seen. The course
of the disease can vary from few hours to few days.
4) Haemorrhagic enterotoxaemia of piglets: It is caused by Cl. perfringens type C and

the piglets of upto 7 days of age are most commonly affected. Susceptibility to disease
and its severity decreases with age. Case fatality rate is high and mortally rate can be
80% in severe outbreaks. Affected piglets are dull, depressed and can have diarrhea,
dysentery and reddening of the anus. The course can be less than 24 hours.
5) Enterotoxaemia of foals: It is caused by an unknown type Cl. perfringens and Cl.

perfringens type B and C and the foals in the first week of life are commonly affected.
Depression, severe abdominal pain, diarrhoea, mild dysentery in the early stages and later
on subnormal temperature and death within few hours.
Pathogenesis:
The organisms in the intestine produce various toxins like alpha, beta and epsilon.
Most important one is beta toxin, which causes haemorrhagic enteritis and also ulcer in
the intestines. The alpha toxin can cause haemolysis and tissue necrosis.
Necropsy findings:
Haemorrhagic enteritis with ulcers which may be 2.5 cms in diameter and
penetrate almost to the serosa. The lesions are commonly seen in the ileum.
Subendocardial and subepicardial haemorrhages and excess of serous fluid in the
peritoneal cavity.
Diagnosis:
Diagnosis is usually done by:
1. Demonstrating lot of Gram positive bacilli in the intestinal contents. '
2. Mouse inoculation test - details are given in pulpy kidney disease.
3. ELISA has been used to detect the toxins in the intestinal tract and antitoxins in the
sera of recovered animals.
4. Attempts are being made to study the nucleotide sequence and to develop a
Polymerase Chain Reaction (PCR) test.
It should be differentiated from, Colibacillosis, Salmonellosis, Transmissible
gastro-enteritis and Actinobacillus equuli and this can be mostly done by culturing of
suspected materials.
Treatment:
1) To neutralize the toxin administer the hyper immunised serum @ 25-50 ml/animal, s/c
or i/v.
2) Administer a broad spectrum antibacterial agent like tetracycline or sulphonamide
orally and parenterally.
3) Administer the universal antidote orally to prevent the further absorption of the toxins
and even neutralization of the toxins. It contains:
Activated charcoal 2 parts (Adsorption of the toxin)
Magnesium oxide 1 part (Neutralises excess acidity)
Kaolin 1 part (Astringent action)
Tannic acid 1 part (Precipitation and neutralization of the toxins)
Dosage: 30-100 gm., b.i.d., orally for 2 days.

Vaccination is done by using type specific toxoid or bacteria, s/c. Usually pregnant
ewes, sows, cows and mares will be vaccinated twice. The first dose is adminstered 6
weeks before parturition and the second dose will be given 2 weeks before parturition.
ET vaccine (BAIF) and Bovilis MCV (Intervet) is a pentavalent vaccine
containing Cl. perfringens type B, C, D and Cl. septicum and Cl. oedematiens. The
details are given under malignant oedema.
(vi) PULPY KIDNEY DISEASE
It is an acute toxaemia of ruminants especially sheep caused by Clostridium

perfringens type D and is characterised by diarrhoea, convulsions, paralysis and sudden
death.
Etiology:
It is caused by Cl. perfringens type D and its morphological characteristics are
similar to this group.
Epidemiology:
a) Occurrence: It occurs throughout the world. Morbidity rate can be upto 10% and the
case fatality rate can reach 100%. It is recorded in lambs, adult sheep, goats, calves and
rarely adult cattle, deer and domestic camels. Most common in lambs between 3-10
weeks of age. Single lambs are more susceptible than twins.
It is also known as "over eating disease" because ingestion of lush rapidly growing
pasture, young cereal crops and heavy gain feeding will cause the disease. Increased
incidence has been also noticed after dosing with phenothiazine. Fast growing animals on
high plane of nutrition are highly susceptible.
b) Transmission: It is not a contagious disease since the organisms are normally present
in the intestine.
Pathogenesis:
Due to changes in the environment of the intestines, the organisms migrate from
the large intestine to duodenum and jejunum. They multiply and produce epsilon toxin
which causes profuse mucoid diarrhoea. Also it increases the permeability of the
intestinal mucosa. They will also stimulate the CNS in the beginning and depresses the
CNS later on. In this disease hyperglycaemia is noticed and the exact reason for this is
not clearly understood. According to Worthington et al. (1979), it may be due to the
rapidly developing brain oedema releasing catecholamines which will activate Adenyl
cyclase which in turn produce cAMP. Increased levels of cAMP causes glycogenolysis
leading to more formation of glucose which results in hyperglycaemia. In goats,
haemorrhagic enterocolitis has been recorded.
Clinical findings:
Lambs may die without showing any slinical signs. Others may show dullness,
depression, yawning, facial movements and anorexia. Later on severe clonic convulsions
with frothing at the mouth occurs. Animals which survive for few hours show green
pasty diarrhoea, staggering, recumbency, opisthotonus and severe clonic convulsions.
In calves, similar signs may be seen but the CNS signs like bellowing, maniacal
behaviour, convulsions etc., are predominantly seen.
In goats peracute, acute and chronic forms of this disease occurs. In peracute
cases, fever (I05°F), severe abdominal pain, dysentery and death in 4-36 hours. In acute
cases, diarrhoea, abdominal pain with death or recovery in 2-4 days may occur. In
chronic cases, anorexia, intermittent severe diarrhoea and sometimes dysentery for
several weeks may be noticed.
Necropsy findings:
Petechiae in the epi and endocardium. Slightly excess amount of serous fluid in
the pericardial sac. Patchy congestion of the abomasal and intestinal mucosae. The
characteristic finding is soft, pulpy kidneys.
In goats, there is acute fibrinonecrotic and haemorrhagic entero-colitis.
Diagnosis:
1) Estimating the blood glucose level which will be elevated and may be 150-200 mg/dl.
2) Glucose test of urine will be positive
3) Mouse inoculation test: For this test, submit 3-4 feet of terminal ileum and also
caecum and colon contents under freezing conditions or add a drop of chloroform per 10
ml of sample.
To one group of mice or rabbits the filtrate of the intestinal contents (0.2-0.5 ml) is
injected i/v. If the filtrates contains toxin, these animals will die in few minutes to hours.
Take 2 ml of the intestinal filtrate in a test tube and add 1 ml of antiserum
containing known antitoxins to Cl perfringens type D. Incubate for 1 hour at 37oC. Then
the mixture is injected i/v to mice. If the mice survives then it is positive for pulpy kidney
disease, because the toxin present in the filtrate is neutralized by the antitoxin present in
the serum.
4) Smears of ingesta from several places of small intestine when stained with Gram's
stain will be having plenty of short, fat Gram positive rods from the ET carcasses. .
5) Serological tests like Agar gel precipitation test (AGPT), RIA and FAT can be used.
Recently ELISA and counter immuno electrophoresis are used.
This disease should be differentiated from, acute pasteurellosis, hypocalcaemia
with hypomagnesaemia, anthrax, rinderpest and blue tongue.
Treatment:
The treatment of ET is many times not effective due to the acute nature of this
disease. However, the following therapeutic measures may be beneficial in prolonged
cases:
1) To neutralize the toxins administer antiserum @ 25-50 ml, i/v or s/c and is the best
way to treat, if available.
2) To prevent the further absorption of the toxin and even to neutralize the toxins
administer universal antidote orally.
3) To eliminate the organism from the g.i. tract administer broad spectrum antibacterial
agents like tetracyclines, sulphonamides. Chloramphenicol, orally and parenterally.
Metronidazole can be used @ 7 mg/kg body weight orally and parenterally.
4) To overcome the toxaemia administer dexamethasone and also plenty of balanced
electrolyte solution i/v.
5) To prevent the effect of histamine administer Avil.
Prevention and Control -

1. Overeating should be prevented.
2. Vaccinate the animals with any one of the following :
a) Enterotoxaemia vaccine (IVRI): it is a formaline killed vaccine. The dose is 2.5 ml, s/c
and the preferred site may be on the ventral aspect of the base of the tail; twice at an
interval of 2 weeks. The duration of immunity is 6-8 months. Hence is has to be repeated
once in every 6 months.
b) ET vaccine (BAIF) and Bovilis MCV contains Cl. perfringens type C and D with an
adjuvant and the details are given under malignant oedema.
c) Bovilis ETV (Intervet) – 100 ml vial and used for the prevention of pulpy kidney
disease. The dose is 2 ml, and the route is s/c. The schedule is similar to that of Bovilis
MCV.
(vii) BACILLARY HAEMOGLOBINURIA
(Red water disease)
It is an acute, highly fatal toxaemia of cattle and sheep caused by Clostridium

haemolyticum and is characterized by high fever, jaundice, haemoglobinuria and necrotic
infarcts in the liver.
Etiology:
Cl. haemolyticum causes this disease and its morphological characteristics are
similar to Cl. chauvoei. It is a soil borne anaerobe.
Epidemiology:
a) Occurrence: Recorded in many countries of the world. It is mainly a disease of cattle
but rarely it can occur in sheep and pigs.
b) Transmission: Most probably by ingestion of contaminated feed and water the
organisms enters the animal.
Pathogenesis:
Upon ingestion the organisms go to the intestine and then into the liver. Due to
certain conditions like migrating liver flukes and invasion of the liver by Cysticercus
tenuicollis which cause the anaerobic condition of the liver, the organisms multiply and
produce two types of toxins namely:
1. Haemolysin which causes lysis of the RBCs leading to haemoglobinuria and jaundice.
2. Necrotizing toxin is responsible for the formation of the thrombus in the sub-terminal
branch of portal vein leading to large anaemic infarct which is the most characteristic
lesion.
Clinical findings:
Fever (103-106°F), depression, weakness, anorexia, jaundice and passing of coffee
decoction coloured urine. Later on signs of anaemia will be seen. Severe dyspnoea is
noticed before death. The course of the disease is 12 hours to 4 days.
Necropsy findings:
Petechial or diffused haemorrhages in subcutaneous tissues, yellow colouring of
the serous and mucous membranes and excessive amount of serous fluid in the cavities
are seen. Anaemic infarcts in the liver which may be one or more in number with a
diameter of 5-20 cms. are very characteristic.
Diagnosis:
Bacillary haemoglobinuria can be diagnosed on clinical signs, lesions and
culturing of material from infarcts, heart blood and many other organs immediately after
death.
Treatment:
1. Administer high-doses of penicillin or tetracyclines to overcome the etiological agent.
2. Blood is transfused to overcome anaemia and also haematinics may be administered.

Vaccinate the animals with formalin killed whole culture of Cl. haemolyticum
adsorbed on Aluminium hydroxide.
(viii) BOTULISM
It rapidly fatal, motor paralysis caused by the toxin of Cl. botulinum and is
characterized by flaccid paralysis.
Etiology:
It is caused by the toxins of Cl. botulinum type A, B, C, D and E. The spores are
extremely resistant. The toxin also survives for long periods.
The organisms may be also found in the intestinal tract of healthy animals. If they
die, in the carcasse they multiply and elaborate toxinsand will be source of infection. In
human beings the source of infection is canned, processed or raw fish or fish products.
Epidemiology:
a) Occurrence: Botulism has been recorded in many countries of the world and in all the
species of domestic animals including domestic birds and wild birds. Human beings are
also affected.
It is most common birds. Cattle, sheep and horses are susceptible, but and cats
appears to be resistant.
b) Transmission: Source of infection in animals is almost always carrion which include
domestic animals, wild animals and birds. Also decaying vegetable material plays an
important role. In these conditions, the organisms multiply and elaborate the toxins.
Animals having pica will ingest such materials containing the toxins. Pica commonly
occurs as a result of deficiency of phosphorous in most of the animals and in sheep it is
due to deficiency of protein or net energy.
Pathogenesis:
Upon ingestion, the toxins gets into the intestine and then into the blood. The toxin
blocks the release of acetylcholine at the myoneural junction which leads to motor
paralysis. Flaccid paralysis develops and the animals die of asphyxia. No gross or histo-
pathological lesions are produced.
Clinical findings:
Cattle and horses: Incubation period is 3-17 days. Paralysis of the hind limbs
occurs and then it spreads towards the neck. Initially convulsions of entire limb can
occur. Drooling of saliva, hanging of tongue from the mouth, in co-ordination, stumbling,
knuckling and finally the animal dies due to respiratory paralysis.
Sheep: Similar to cattle but the flaccid paralysis is seen at the final stages of disease.
Birds: The signs can be seen within few hours to one or two days after the ingestion.
Drowsiness, weakness and impairment of flying or walking are the initial signs. Later on
paralysis of limbs, neck and wings occurs. The paralysis of the neck is characterized by
drooping of the neck and hence the term 'limberneck' is given. The death of the birds is
due to respiratory distress and in water birds it is due to drowning.
Necropsy findings:
Gross or histological lesions are absent in botulism.
Diagnosis:
Diagnosis of botulism can be done by clinical signs and analyzing the carrion and
feed for toxins. Culturing of feed can be done. Mouse protection test and modified CFT
also can be used. Animal inoculation test also can be performed by injecting the
suspected material (serum, intestinal content or putrefied material) intra peritoneally to
mice. Paralysis and death of the mice within 1-2 days means positive for botulism.
Treatment:
Treatment may not be useful. Purgatives may be given to remove the toxins from
the g.i. tract and CNS stimulants may be useful.

1) Set right the pica, by supplementing minerals or proteins.
2) Proper disposal of carrion or carcasses, either by burning or burial.
3) Proper disposal of decaying vegetables and grasses and contaminated hay or silage.
4) Toxoids may be used for vaccination.
Questions:
1. Why crepitation of heavy muscles occurs in Black quarter?
2. Why Penicillin is the drug of choice for treating BQ ?
3. Why vaccination against BQ should be done before the onset of monsoon rains?
4. Why anti-tetanus serum should be administered before the surgical operations?
5. What is the difference between anti-tetanus serum and tetanus toxoid ?
6. Why pulpy kidney disease is also known as over-eating disease?
7. Why intestinal loop with intestinal contents should be submitted from a carcase
suspected of pulpy kidney disease or enterotoxaemia?
8. Why Sodium bicarbonate is used in cases having haemoglobinuria?
9. Why proper disposal of carcasse is indicated in botulism?
10. Why flaccid paralysis occurs in botulism?
a) Clinical signs of BQ.
b) Clinical signs of Tetanus
c) Lamb dysentery
d) Universal antidote
e) Enterotoxaemia
f) Treatment of tetanus.
12. Give the important necropsy findings of
a) Lamb dysentery
b) BQ
c) Pulpy kidney disease
d) Bacillary haemoglobinuria.
4. DISEASES OF THE UDDER
(i) MASTITIS
Mastitis means inflammation of the mammary gland caused by varieties of

bacteria and fungi and is characterized by physical, chemical and bacteriological changes
in the milk and by pathological changes in the milk and glandular tissue.
The term mastitis is derived from Greek word - Mastos means breast, Itis means
inflammation. It is a disease complex resulting from interplay; between infectious agents
and managemental practices and environmental factors.
The most important changes in the milk includes discolouration, the presence of
clots and the presence of large number of leucocytes.
Etiology:
Mastitis is caused by many bacteria, fungi and viruses. They are:
1.Bacteria: Innumerable genera and species of bacteria cause mastitis. The
predominant organism is Staphylococcus aureus followed closely by Streptococcus
agalactiae. The other bacteria causing mastitis in cows and buffaloes are E. coli, Str.
uberis. Str. dysgalactiae. Str. zooepidemicus, Str. faecalis, Str. pyogenes. Campylobacter
jejuni, Haemophilus somnus. Str. pneumoniae, Corynebacterium pyogenes. Cor.
ulcerans, Klebsiella Spp., Enterobacter aerogenes, Mycobacterium bovis; M. lacticola.
M. fonuitum. Bacillus cereus, Pasteurella multocida, Pseudomonas pyocyaneus.
Bacteroides fundibuliformes, Serratia marcescens, Mycoplasma bovis, M. canadensis, M.
bovigenitalium. Acholeplasma laidlawi, Nocardia asteroides, N. farcinicus, Leptospira
interrogans serovar pomona and L. interrogans hardjo.
2. Fungi and Yeast: Fungal agents like Trichophyton Spp., Aspergillus fumigatus, A.
nidulus and Pichia Spp.
Yeasts like Candida Spp., Cryptococcus neoformans, Saccharomyces Spp,
Algae like Prototheca trispora and P. zopfii.
3. Viruses: Viruses causing IBR, BVD, FMD, cow pox, pseudo cowpox, and ulcerative
mammilitis does not play major role in producing mastitis and they may pre-dispose the
cow to bacterial mastitis.
Epidemiology:
a) Occurrence: Mastitis occurs through out the world. It is a very common disease
causing problems to the dairy industry in both the developed and developing countries of
the world. It is a common disease of the high milking cows like exotic and cross breeds.
In other species of domestic animals it is not so common. In buffaloes the incidence of
mastitis is not so high when compared with the high milking cows.
The incidence is high in cows from 3rd lactation and above wherein optimum milk
production occurs. Lot of work has been done on bovine mastitis without much
significant break through in developing a suitable vaccine for mastitis.
It causes severe economic loss to dairy industry. According to 1962 report the
economic loss due to mastitis in India is 53 crores. Now it may be about 6000 crores per
year. According to previous reports in USA the annual loss is about 1.3 billion dollars
probably due to 100-250 dollar/cow/year loss. The economic loss may be due to:
1) Decrease in milk production - 15% of the milk produced by the cow in its life or one
entire lactation.
2) Due to mortality - In coliform mastitis the mortality is 20% and in Cory. pyogenes it is
50%.
3) Discarding of milk during mastitis and its therapy.
4) Cost of treatment.
5) Diseases transmitted to suckling calves.
6) It also comes in the way of milk trading from one country to another country as milk
meant for human consumption may not be of standards prescribed by the World Trade
Organization.
b) Transmission: The organism can enter the udder through various routes.
l. By milkers hands: This is the common mode of transmission wherein a person after
milking a cow with mastitis gets contaminated with bacteria. Then without washing the
hands properly and without dipping in antiseptic solution this person will milk the cow
without having mastitis. In doing so the organisms from the mastitis cow will be
introduced into the teat orifice of other animals.
2. Trauma or injury to the teat: Injury to teats and udder may be due to physical agents
like wires, fencing, sharp objects and rough surface. In addition, it can be due to viruses
like FMD virus and cow pox virus which can affect the teats and udder causing lesions.
These lesions may break open resulting in raw surface which can be contaminated very
easily. Injury also can occur while milking the cows by using milking machine where in
there may be excessive stripping, removal of the teat cups too violently and abnormality
in teat cup liners.
3. Intramammary infusions: This is the common mode of transmission of fungi because
the fungi are resistant to commonly used antibiotics as intramammary infusion i.e., the
intramammary infusions are contaminated with fungi. Hence, when this is infused the
fungi are also getting inside the mammary gland later on producing the fungal mastitis.
4. Haematogenous: The common example is tuberculous mastitis where in the organism
from the lesions gets into the blood and then localizes in the udder producing mastitis.
5. Inhalation: The organism like Mycoplasma enters the animals through inhalation and
gets into respiratory tract. Then they enter the blood and through circulation localizes in
the udder.
6. Infected suckling calves.
Pathological changes:
The organisms to produce pathological changes in the udder, they overcome the
various defense mechanisms of the udder. There are two types of defense mechanisms in
the udder. They are:
1. Non specific mechanisms:
i) Teat sphincter: Commonly in the aged cows and also in high milk producing cows
after milking, the teat sphincter cannot close the teat canal properly, which makes the
organism to enter the teat canal easily. However in buffaloes this is not the case, because
the teat sphincter closes the teat canal after milking. That is why the incidence of mastitis
is less in buffaloes when compared to cows.
ii) Milk: In high milking cows, the flushing action of milk will make the organisms to be
thrown out of the teat canal.
iii) Lactenins: are substances present in the milk. They are:
a) Lysozymes: They are found in neutrophils, fluids and tissues. The enzymes kills the
gram positive bacteria by splitting the acylaminopolysaccharide and for killing the Gram
negative bacteria, it needs the binding of the complement to the bacteria, In normal milk
1.5 IU of lysozyme/ml is present. In mastitis the level of lysozyme is increased
(subclinical: 100 IU/ml, chronic: 500 IU/ml, acute: 1000 IU/ml).
b) Lactoferrin: This is an iron binding protein present in the milk. It binds to the iron
and forms a complex and makes the iron not available for the growth and multiplication
of bacteria, like Mycobacterium tuberculosis, E.coli, and Pasteurella multocida.
However, E. coli produces enterochelin and Mycobacterium tuberculosis produces
Mycobactin which are iron chelating substances so that iron is freed from this complex
and utilized for their growth and multiplication.
c) Peroxidase system: This system oxidises thiocyanate and this oxidised thiocyanate is
highly inhibitory to bacterial multiplication.
2. Specific immunity:
a) Humoral immune response: The milk and colostrum of cow contains good amount
of immunoglobulins (Igs). The majority of Igs in the milk are of IgG class and the
amount of IgA is low. But the incidence of mastitis is very high in cows and the exact
reason for this is not known and it may be due to the presence of small quantity of IgA
which is actually involved in local protection.
The incidence of mastitis in other species of domestic animals like bitch and swine
is low which may be due to the presence of good quantity of IgA and IgG in milk,
b) Cell mediated immune response: The presence of macrophages, T and B
lymphocytes has been recorded in the milk, but its significance is not clearly understood.
Whenever acute inflammation of the mammary gland occurs, there is massive infiltration
of neutrophils. These neutrophils are called milk neutrophils. The phagocytizing and
killing power of milk neutrophils is low when compared with the blood neutrophils. This
may be due to glycogen content of the milk neutrophils is 38% less than that of glycogen
content of blood neutrophils and also the lysosomal content is less.
Pathogenesis:
The development of mastitis occurs in three stages and they are:
1. Invasion: It is the stage wherein the organisms pass from the teat orifice into the teat
canal.
2. Infection: In this stage the organisms multiply rapidly and invade the mammary tissue
rapidly.
3. Inflammation: Various types of inflammation like peracute, acute, sub-acute, chronic
and chronic granulomatous can occur.
a) Peracute and Acute Mastitis: Here congestion and oedema occurs first, then there
will be massive infiltration of neutrophils and accumulation of lot of fibrin occurs.
After sometime the neutrophils dies and releases lot of proteolytic and hydrolytic
enzymes which act upon the cells and destroys them. The inflammatory mediators are
also absorbed. The by products of cellular destruction are absorbed into the blood and
then into the circulation, resulting in toxaemia. Also toxaemia may be due to the release
of endotoxins by E. coli in the udder and then getting absorbed into the circulation. The
effects of endotoxins are:
1) They act on neutrophils and releases pyrogens which will stimulate the synthesis of
Prostaglandin E (PGE) in the hypothalamus. Then PGE will stimulate the posterior
hypothalamus which is having the heat conserving centre, resulting in high fever for a
short period. Later on the temperature drops down to subnormal leading to death of the
animal.
2) Endotoxins activates the alternate pathway of complement. The fractions of
complement C3a, C5a, C567 are known as anaphylotoxins which will act on platelets and
may be on mast cells, resulting in the release of histamine which will initiate the
inflammation.
3) Endotoxins can suppress the myocardium.
4) Endotoxins can damage the liver
The enzymes of neutrophils acts on the milk and spoils it and these contents may
combine with fibrin and form floccules, flakes or clots. If proper treatment is given in
early stages and then scavenger cells will remove the cellular debris and then
regeneration of cells occur.
b) Chronic mastitis: Usually it occurs as sequelae to acute mastitis. Here lot of
mononuclear cells infiltrate the affected part and then fibrous tissue replaces the damaged
cells. The udder becomes shrunkened and hard and milk production will be drastically
reduced.
c) Chronic granulomatous mastitis:
The etiological agents involved in this type of mastitis are Stap. aureus,
Mvcobacterium bovis and Myco. tuberculosis. Here lot of mononuclear cells infiltrate the
area, the macrophages fuse together to become epithelioid cells and giant cells are also
seen. Around these, monocytes and lymphocytes are present. The lesion may be
encapsulated with fibrous tissue. The udder is hard, shrunkened and nodules can be felt
upon palpation. This type of inflammation is called "Botryomycosis' wherein it is
characterized by the presence of sulphur granules and upon crushing in between the two
slides Gram positive cocci in the form of bunch of grapes can be demonstrated upon
Gram's staining.
d) Gangrenous mastitis : The cause is Stap. aureus. Here due to thrombus formation the
blood supply to the necrotic part of udder is reduced resulting in putrefaction, the affected
part becomes blue or black in colour and sloughing of the part occurs.
Classification of Mastitis and Clinical findings:
1. Depending on severity and duration the following types can occur:
a) Peracute mastitis: Both the systemic signs and local signs are seen in peracute
mastitis
Etiology: Stap. aureus, E. coli, Coryne. pyogenes, Klebsiella spp.,etc.
Systemic signs: Sudden in onset, high fever (105-107°F), marked depression, complete
anorexia, sudden drop in milk production, atony of the rumen, rapid pulse and respiratory
rates, weakness and sunken eyes. As it progresses the animal is unable to stand and will
be recumbent and can have a classical posture of milk fever. The temperature suddenly
drops and will be subnormal, which is indicated by cold extremities. Finally there will be
coma and death.
Local signs: It may or may not be seen. If seen, there will be marked increase in the size
of the affected part of the udder. Here one or more quarters can be affected. The udder
will be warm and painful to touch and will be hard. The secretions can be watery or
blood tinged. The course of the disease is very short and may be 6-24 hours.
b) Acute mastitis:
Etiology: The organisms which cause peracute mastitis, can also cause acute mastitis and
in addition, the other organisms like Strep. agalactiae. Mycoplasma mycoides,
Pseudomonas spp., etc., and fungi can also cause the same.
Both systemic and local signs are seen.
Systemic signs: Marked systemic signs may or may not be seen. If seen it will be almost
similar to that of peracute mastitis.
Local signs: Similar to peracute mastitis. Initially the secretions can be watery and blood
tinged, later on it may be yellowish and pus like. The supramammaiy lymph nodes are
enlarged. Slight to severe udder oedema may occur.
The peracute and acute mastitis are commonly seen immediately after parturition.
In both cases the udder is hard. This is due to massive infiltration of neutrophils, fibrin
and fluid. The course of the disease is 3-5 days.
c) Subacute mastitis:
Etiology: Staph. aureus, Strep. agalactiae, Strep, dysgalactiae etc.
The systemic signs are not seen and the local signs are less marked.
d) Subclinical mastitis:
Etiology: Similar to subacute mastitis.
In this type of mastitis both the systemic and local signs are absent. This type of
mastitis can be only detected by certain laboratory tests like California mastitis test
(CMT), Wisconsin mastitis test, white side test, leucocyte count, Mastrip test, etc.
e) Chronic mastitis and chronic granulomatous mastitis:
Etiology: Stap. aureus - Botryomycosis, Mycobacterium bovis, Nocardia asteroides
and Cryptococcus neoformans and others
Systemic signs - Absent.
Local signs: Decrease in size of udder and the udder will be hard and upon palpation
nodules can be felt. Milk may contain few clots.
f) Gangrenous mastitis:
Etiology: It is caused by Stap. aureus.
Systemic signs: Moderate fever, decrease in milk production.
Local signs: One or more quarters may be affected. Due to thrombosis of veins there will
be local congestion and oedema initially. Later on the skin of the affected part of udder
becomes blue in colour. Serosanguinous fluid will dribble from this part drop by drop, the
skin sloughs off and the affected part of udder also will slough off bit by bit. Then it will
be complicated with maggots and foul smelling discharge come from this part. Finally the
entire affected part will be sloughed off. The course of this condition is 1-2 weeks.
2. Depending on Etiology:
i) Streptococcal mastitis by Strep. agalactiae: This organism is an obligatory parasite.
It can cause acute, subclinical and chronic mastitis in cows, ewes and does. Most
important cause of mastitis in these animals. The organisms are located in teat canal and
teat cistern. Hence the treatment is very successful because the drug will easily reach to
these sites and effective concentration of the drug will be there. Drugs like penicillin,
cloxacillin, cephalosporins, OTC etc., are used.
ii) Mastitis due to Streptococci other than Strep. agalactiae: Strep. uberis, Strep.
dysgalactiae, Strep, zooepidemicus mostly cause subclinical and chronic mastitis and
rarely acute mastitis.
iii) Mastitis due to Stap. aureus: It causes all the types of mastitis. Organisms are
located in the deeper parts of udder like acini, interstitial space and hence the treatment is
very difficult. The cure rate may be 60-80% in lactating cows with clinical cases when
treated with ampicillin-cloxacillin combination, penicillin-streptomycin combination,
novobiocin, tetracyclines and cephalosporins. Commonly it is advocated to treat such
cases during dry period.
iv) Coliform mastitis: It is a soil borne infection and it occurs when the hygienic
conditions are poor. It is also known as "Environmental mastitis” because the bacteria
are transmitted from the environment to the cow rather than cow to cow transmission.
E. coli after localizing in udder produce endotoxins hence not only mastitis but
also toxaemia is seen. Here peracute or acute mastitis occurs and there can be 20%
mortality. The case fatality rate may reach 80%. If proper treatment is given early the
recovery will be good. Peracute form is most common in recently calved cows. Chronic
and subclinical cases also have been recorded. Drugs like enrofloxacin, ciprofloxacin,
colistin sulphate, chloramphenicol, gentamicin, amoxycillin, trimethoprim and sulpha
combination and cephalothin can be used.
One of the important preventive measures is replacing saw dust or shavings used
for bedding with straw or sand.
(v) Mastitis due to Corynobacterium (Actinomyces) pyogenes:
It is known as 'summer mastitis' in UK because it is commonly recorded during
summer. This organism causes peracute mastitis which will be purulent in nature. The
secretion will be pus like and foul smelling. Abscesses develop in the affected part of the
udder and will ripen and break open discharging pus, leading to destruction of the
quarter. It can cause mortality rate of 50%. Usually after recovery the milk production
will not come back to normal. Hence such cows should be culled.
Treatment involves administering of sulphadimidine or OTC parenterally
vi) Tuberculous mastitis: Mycobacterium bovis upon inhalation or ingestion will form a
primary foci and due to secondary dissemination will get into blood. Through circulation
it will localize in the udder and cause granulomatous inflammation. The affected part of
udder is hard and shrunken and nodules can be felt upon palpation. The abnormal milk
comes at the end stage of milking. When such milk is collected in a test tube and allowed
to stand for 5 minutes, fine floccules will settle to the bottom of the tube and amber
coloured fluid will be at the top. The diagnosis is by culturing of milk and by tuberculin
testing.
The affected animals are usually not treated and are culled, as these animals are a
source of infection to other animals and human being.
vii) Leptospiral mastitis: L. interrogans pomona, L. interrogans hardjo causes mastitis,

wherein characteristic feature is presence of blood or blood clots in the milk. No other
clinical signs are seen. Such cases are treated with streptomycin parenterally and
intramammarily.
vii) Mastitis due to Nocardia asteroides: The entry of organisms into the udder is
through the contaminated intramammary infusions. It causes chronic granulomatous
inflammation.
Novobiocin 500 mg, Nitrofurazone 0.2% are used intramammarily for such cases.
ix) Mastitis due to Mycoplasma: Mycoplasma agalactiae var bovis causes acute mastitis
in high milking cows. All the quarters are affected. The secretion will be colostrum like
or soft cheese like or yellow coloured strand like. When it is allowed to stand in a test
tube, the floccules will settle at the bottom of tube and turbid whey coloured fluid at the
top will be found. As the damage is great, they produce small quantity of milk after
recovery. Hence such cows should be culled.
Such cases of mastitis are treated with Tylosin or OTC @ 5-10 mg/kg body
weight, i/m. Also these drugs can be administered intramammarily.
x) Mastitis due to Pseudomonas: Pseudomonas aeruginosa causes acute mastitis. The
milk may be bluish or greenish tinged. The affected quarter will have a bread-
butter/shaggy appearance. It is very difficult to treat. However drugs like gentamicin or
carbenicillin and other third and fourth generation cephalosporins can be used
parenterally and intramammarily.
xi) Fungal Mastitis: The fungi enter the udder as contaminants of intramammary
infusions. Usually it occurs after the bacterial mastitis because for the treatment of
bacterial mastitis various antibacterial agents are used creating a sterile condition in udder
which is good for the fungi. The fungi rapidly multiply and produces acute mastitis. The
organisms can be demonstrated in the milk.
Any one of the following drugs can be used for the treatment of fungal mastitis:
a) Mycostatin vaginal oblet (Nystatin) can be used. Crush one oblet and mix with 60-80
ml of distilled water and infuse intramammarily.
b) Sodium iodide i/v or Potassium iodide orally can be used.
d) Miconazale @ 100 mg/quarter can be used intramammarily.
Diagnosis of Mastitis:
Mastitis can be diagnosed by the physical examination of the udder, examination
of the milk and culturing of milk.
A) Physical examination of the udder:
1. Size : Enlarged and hard indicates acute mastitis.
Shrunken and hard indicates chronic mastitis.
2. Shape: Stand behind the animal and observe for the change in shape. The swollen or
shrunkened quarters can be easily recognized.
3. Consistency: Similar to size. Hard to touch and painful udder means acute to peracute
mastitis and if there is no pain and nodules are felt upon palpation it is chronic mastitis.
4. Observation of supra-mammary lymph nodes: If they are enlarged, it may be
peracute or acute mastitis or tuberculous or mycoplasmal mastitis. In mycoplasmal
mastitis all quarters are affected.
B. Examination of the milk:
a) Physical examination of the milk:
i) Colour: Normal milk is white in colour or white milk with a yellow tinge. Reddish
tinge and blood clots indicates haemogalactia. When the milk is allowed to stand and
amber coloured fluid at the top indicates tuberculous mastitis and turbid whey indicates
mycoplasmal mastitis. Bluish or greenish tinge indicates pseudomonas infection.
The abnormal milk comes at the beginning of the milking in all types of mastitis
except in tuberculous mastitis wherein abnormal milk comes at the end stage of milking.
ii) Odour: Putrid odour is present in corynebacterium infection which is due to
Peptococcus asacharolyticus or Micrococcus indolicus which will be always associated
with corynebacterium.
iii) Consistency: Watery - acute and peracute mastitis
Thick pasty - Purulent mastitis
Colostrum like or soft cheese like - mycoplasmal mastitis
iv) Presence of flakes or clots can be detected by stripping the milk on the strip cup
having wire mesh with black background or on the palm of the hand. The flakes or clots
will be sticking to the wire mesh or palm of the hand.
b) Chemical examination of milk:
I) pH of milk: Normal pH : 6.4 - 6.8
Mastitis : 7.4 and above
Methods:
(1) Using pH paper : This is not so accurate.
(2) Bromothymol blue test :
Method: Take 1 ml of 0.13% bromothymol blue solution in a test tube and add 5 ml
of milk and mix well.
Results: Yellow colour - Normal
Green to greenish blue colour - Mastitis
(3) Indicator paper method: This method was developed by Suryanarayana Rao et al.
(1981) at National Dairy Research Institute, Bangalore. Here the filter paper is cut into
strips and dipped in bromothymol blue solution and air dried.
Similar method has been employed by National Dairy Development Board
(NDDB) and collaborated with Dabur Ayurvet Ltd., and commercially released as
Mastrip for milk examination.
Method: Clean the udder with water and dry it. Discard the first few strippings of
milk. Then place a drop of milk on the strip of Mastrip and within 30
seconds compare the colour with the colour chart.
Results: Yellow - Normal
Greenish yellow - Subclinical Mastitis
Green - Advanced Subclinical Mastitis
Blue - Clinical Mastitis
This test is advocated for detecting the subclinical mastitis. The results of this test
agrees with CMT by 95%
4) Bromocresol purple test:
Method: Take 0.5 ml of 0.9% bromocresol purple solution in a test tube and add
9.5 ml of milk and mix the contents.
Results: Pale greyish to purple colour indicates normal and deep purple colour
indicates abnormal milk.
ii) Chloride Test:
Method: Take 1 ml of milk in a test tube and add 5 ml of silver nitrate and then 2
drops of potassium chromate and mix the contents.
Results: Brownish red colour - Normal
Yellow colour - Mastitis
Normal content of chloride in. milk is 0.08 – 0.14 gm% but in mastitis its level is
increased.
iii) Catalase test:
Method: Place a drop of milk on a slide and then put a drop of Hydrogen peroxide
in Methylene blue on this drop and immediately place a coverslip.
Result: If air bubbles accumulate on the under surface of the coverslip having a
blue background then it is positive.
In mastitis, milk contains lot of neutrophils. These neutrophils contain an
enzyme called catalase which acts on Hydrogen peroxide and release oxygen
which will accumulate in the form of air bubbles.
iv) White side test:
This test was developed by Murphy and Hansen in 1941.
Method: Place 5 drops of milk on a glass-slide and then add 2 drops of 4%
Sodium hydroxide. By using a stick, mix the contents for half a
minute.
Results: No change in the milk - Normal.
If the contents become thick, viscid and strand like material comes along
with the stick when it is slowly moved away from the contents then it is
positive for acute mastitis.
If the contents become watery with flakes, then it indicates chronic
mastitis.
v) California Mastitis Test:

(a) Original :This test was developed by Schalm and Noorlander in 1957.
Method: Take 3-5 ml of milk in the cup of CMT paddle then add 3-5 ml of CMT
reagent. Mix the contents by making rotatory movements of the paddle 30
seconds but not more than 60 seconds.
Results:
No change - Normal
Traces - No distinct wave, tiny lumps are seen.
+ - Thickening and definite wave. Does not adhere to the
. bottom of the cup
++ - Marked thickening and adhere to the bottom of cup.
+++ - Too much thickening which will appear like a ball.
Mechanism: The anionic detergent present in the CMT react with DNA present in
the leukocyte which is responsible for thickening of contents.
Because the anionic detergent, trietholamine sulfonate, present in the CMT
reagent is not readily available in our country, the CMT reagent is modified and used as
modified CMT by:
b) Pandit and Mehta-(1969) – Since the original ingredient trietholamine sulfonate was
not available in our country the same has to be imported and this will increase the
cost. Hence, these authors modified this test by using the ingredients available in
our country and compared the results with that of original CMT. Add- 3 grams of
sodium lauryl sulfate in 100 ml distilled water. Heat to 50°C to dissolve and then
adjust the pH to 8. Then add 2 ml of 0.5% of bromocresol purple solution.
c) Sharma and Rajani (1969): It contains:
Sodium hydroxide - 1.50gms
Teepol - 0.50gms
Bromothymol blue - 0.01gms
Distilled water - 100.00 ml
Any one of the above reagents can be used to perform the test which is very
similar to that of the CMT test. The results almost agree with the CMT test.
CMT test can be used for milk from individual quarters, all the 4 quarters,
individual cows and herd bulk tank.
In Michigan mastitis test, Wisconsin mastitis test and Lye mastitis test the
principle is similar to that of CMI.
vi) NAGase Test: It is based on the measurement of cell associated enzyme (N-acetyl-p-
D-giucosaminidase) in the milk. Large number of samples can be handled. It requires an
average automatic cell counter. It is the most accurate of the indirect tests. But the
method is laborious.
vii) Hotis test:
Method: Take 0.5 ml of 0.5% Bromocresol purple reagent in a test tube. Then
autoclave the tubes. Then collect milk directly into the tubs (9.5 ml).
Incubate at 37°C for 18 hours. After incubation examine the tube.
Results: If bright canary yellow coloured colonies are adhering to the tube wall and
bottom, then it is positive for Strep. agalactiae. The mechanism involved is
that the organisms ferment the lactose in the milk to form lactic acid. This
lactic acid reacts with bromocresol purple to give this colour to tits
colonies.
viii) Electrical conductivity: It is based on the increase in sodium and chloride ions and
the consequent increase in electrical conductivity, which occurs in mastitic milk. It
identifies clinical mastitis accurately but the accuracy with subclinical infections is only
50%. Automated analyzers are available for this purpose for individual milk samples and
also while machine milking.
C) Microscopic Examination of Milk:
i) Staining of the milk smear:
Routinely used staining techniques like Giemsa, Wright's and Leishman's of
blood smear cannot be used for milk smears as milk contains lot of fat globules. Hence
Newman's stain and Newman-Lampart stains are used. They contain:
Contents Newman's stain Newman Lampart stain
Methylene blue 1.0 gm 1.12 gm
95% Ethyl alcohol 60.0 ml 54.00 ml
Tetrachloroethane - 40.00 ml
Xylene 40.0 ml -
Glacial acetic acid 6.0 ml 6.00 ml
Method:
1) Centrifuge the milk and discard the supernatant.
2) Mix the sediment and put a drop on the glass slide and make a smear with another
slide or with a stick.
3) Air dry the smear. Avoid heating over the spirit lamp or Bunsen burner as cracks
will appear.
4) Pour any one of the above stain and allow for 5 minutes.
5) Wash in water, air dry and observe under the oil immersion lens.
Results:
Leukocytes, epithelial cells, tissue macrophages, bacteria and yeast (egg shaped
and budding, strongyle ova like) can be easily identified.
The advantages of this staining technique when compared with commonly used
stains are:
1. It fixes the smear.
2. It removes the fat.
3. It not only stains the bacteria but also fungi and leukocytes.
ii) Counting of milk leukocytes: Bulk milk cell count (BMCC) and individual cow cell
count (ICCC) can be carried out by a direct microscopic examination of stained smears
on a glass slide or electronic somatic cell counter. BMCC can be used as a screening test.
Method:
1. Take a glass slide and draw a circle of 5.59 mm radius which will give an area of 1
sq.cm.
2. Mix the milk sample slowly and dip the platinum loop (4 mm) in the milk sample
and withdraw the loop, place the loop on the circle and spread it over the entire
circle. Air dry it and do Newman-Lampart staining of the smear. Observe under the
oil immersion lens and count the number of cells in a field. Repeat the procedure
and count the number of cells in 10 fields. Total them up and divide by 10 to get
the average number of cells/field.
Total leukocytes/ml of milk = Average no. of cells counted x 5.00,000
Results:
Average No. per field Classification
0-3 Negative
3-6 +
6-8 ++
Above 8 +++
If milk contains one million and above cells per ml of milk, then it is significant.
D) Culturing of milk:
Culturing of milk is done to isolate the bacteria present in milk and also to know
the type of mastitis in cow. It also helps in proper treatment and control measures. Before
collecting the milk, the teat and teat orifice should be swabbed with spirit. Then discard
the first 2 or 3 strippings and then collect the milk in a sterilised screw cap test tube and
immediately submit it to the laboratory. Bacterial cell counts/ml of milk and culturing for
individual isolation of the bacteria and antibiotic sensitivity assay can be performed.
The following media are commonly used:
1. Edward’s medium
2. Sodium azide. crystal violet, blood agar - in these streptococci will grow and
others are inhibited.
3. Salt agar medium.
4. Glycine tellurite agar - only streptococci will grow.
Treatment:
a) Peracute mastitis: The following therapeutic measures are undertaken for the cows
suffering from peracute mastitis:
1. To overcome the etiological agent, administer the antibacterial agent both parenterally
and intramammarily.
i) Parenteral treatment: The following points should be kept in mind while administering
the antibacterial agent parenterally:
1) Try to perform culturing and antibiotic sensitivity assay and use the agent to which the
bacterium is highly sensitive.
2) Try to administer the same antibacterial agent parenterally as well as intramammarily.
3) Choose the agent which will have good distribution in the udder after parenteral and
intra-mammary administration. For this purpose use the Table 1.
4) When the combination of drugs is used, do not mix bacteriostatic with bactericidal
drugs.
5) Antibiotics must be able to penetrate the leucocytes in sufficient concentration to be
effective.
Table 1. Classification of antibacterial drugs according to their potential distribution
throughout the udder after parenteral and intramammary administration.
Sl. Name of the drug Administered Administered
No. Parenterally intramammarily
G M P G M P
1. Sulphanilamide + - - + - -
2. Other sulphas - + - + - -
3. Erythromycin + - - + - -
4. Oleandomycin + - - + - -
5. Tylosin + - - + - -
6. Spiramycin + - - + - -
7. Lincomycin + - - + - -
8. Clindamycin + - - + - -
9. Penethamate + - - + - -
10. Chloramphenicol + - - + - -
11. Trimethoprim + - - ± - -
12. Tiamulin + - - ± - -
13. Nitrofurans - - - + - -
14. Ampicillin - + - + - -
15. Amoxycillin - + - + - -
16. Hetacillin - - - + - -
17. Cephalexin - - - + - -
18. Novobiocin - + - + - -
19. Penicillin G - + - - + -
20. Cloxacillin - + - - + -
21. Cephalosporins - + - - - -
22. Tetracyclines - + - - + -
23. Streptomycin - - + - - +
24. Neomycin - - + - - +
25. Kanamycin - - + - - +
26. Gentamicin - - + - - +
27. Polymyxin - - + - - +
NOTE: G = Good distribution, M = Moderate distribution & P = Poor distribution.
ii) Intramammary infusions:
1) Antibacterial agents: Two types of preparations viz., commercially available
ointments (oily) and aqueous preparations can be used imtramammarily. The
commercially available intramammary infusions in India are given in Table 2.
Table 2. Intramammarv infusions available in India
a) Pendistrin ointment (Sarabhai) 7.5 ml tubes
Pencillin G Potassium 1, 00, 000 IU
Streptomycin sulphate 75 mg
b) Pendistrin-SH ointment (Sarabhai) 6,00 ml tubes

Procaine penicillin G 1,00,000 IU
Streptomycin 100 mg
Sulphamerazine 500 mg
Hydrocortisone acetate 29 mg
c) Broacil mastitis ointment (IDPI,)

Ampicillin 75 mg
Griseofulvin 35 mg
Prednisolone 3 mg
d) Mastalone ointment (Pfizer) 10.00 ml tube
Oxytetracycline hcl 200 mg
Oleandomycin 100 mg
Neomycin sulphate 100 mg
Prednisolone 5 mg
e) Terramycin Animal formula for Mastitis (Pfizer) 14.2 gm tube

Each gram contains 30 mg of Oxytetracycline hcl
f) Chlortetracychne HCl ointment (Cyanamid) 7.0 gm syringe
Contains 420 mg of Chlortetracycline hcl
g) Nefuran intramammary 3.0 gm tube
Nitrfurazone 150 mg
Furazolidone 150 mg
h) Alciclox (Vet) Inframammary (Alembic)

Cloxampicillin Intramammary (BAIF)
Tilox Inframammary (Wockhardt)
Vetclox plus intramammary (Sarabhai)
Ampicillin 75 mg
Cloxacillin 200 mg
i) Floclox-D infusion (Ranbaxy) Disposable syringe
Cloxacillin benzathine 500 mg
j) Floclox-L infusion (Ranbaxy) Disposable syringe

Cloxacillin Sodium 200 mg
k) Pivipol solution (Ar-Ex Lab) 100 ml bottle

Povidone iodine 1%
l) Rifijet intramammary (Intercare) Disposable syringe

Rifamycin 500 mg
m)Vetimast intramammary (Hindustan Ciba-Geigy)
Contains Cephacetril sodium equivalent to 235 mg
Cephacetrile in 10 gm of suspension
n) Mammitel (Intas Pharmaceuticals) 10 gms syringe
Colistin sulphate 50,000 IU
Cloxacillin sodium 200 mg
o) Cobactan (Intervet) 8 gm syringe

Cefquinone 75 mg
(4th generation cephalosporin effective against
Streptococci, Staphylococci, E. coli
Once in 12 hours for 3 times)
p) Amilox (Pranov Agro) Similar to Cobactan
Local application:
Mastilep (Dabur Ayurvet Ltd.,) 125 gm tube
After cleaning the udder with water it was dried with a towel or paper napkin and
then Mastilep applied locally to the udder and massaged, twice a day. One tube is used
for 5-6 applications. It is used alone in subclinical mastitis and used as above along with
other antibacterial agents intramammarily for clinical mastitis. Mastilep produces
antibacterial antiinflammatory, analgesic, anti histaminic and immuno modulatory
effects.
Technique of administering intramammary preparation :

a) Commercial preparation (oily):
1. Remove the secretions of the udder by milking.
2. Fix the nozzle to the tube after removing the cap and plastic covering.
3. Apply spirit or tincture of iodine to the teat orifice.
4. Remove the cap of the nozzle and introduce the nozzle through the teat orifice into the
teat canal.
5. Squeeze the tube so that the contents will get through the nozzle into the teat canal.
Full insertion of the conventional mastitis tube cannula can result in temporary
dilation of the teat sphincter muscle and the keratin plug that normally occludes the teat
duct is sometimes removed allowing entry of bacteria.
b) Aqueous preparation:
1. Put 18 gauge needle through the hole of the pendistrin nozzle.
2. Insert the nozzle into the teat canal and fix the needle to the syringe, then the
preparation is infused by pushing the piston.
3. The dose of the aqueous preparation is given in the Table 3 and the amount of distilled
water or 5% dextrose used/quarter varies from 50-500 ml.
Usually the preparation is infused once a day for 3-5 days. If the response is poor
after 2-3 days, then switch over to another antibacterial agent.
Table 3. Antibacterial agents used as Intrarmammary infusions either in
distilled water or 5% Dextrose
Sl.No Antibacterial agent Dose per quarter

.
01. Penicillin 1-5 lakh IU
02. Streptomycin 0.50-1.00 gm
03. Penicillin-streptomycin 2.50-5.00 ml
04. Ampicillin 0.25-0.50 gm
05. Chloramphenicol 0.25-0.50 gm
06. Tetracyclines 0.50-1.00 gm
07. Erythromycin 0.30-0.50 gm
08. Neomycin 0.50 gm
09. Cloxacillin 0.50 gm
10. Carbenicillin 1.00 gm
11. Spiramycin 0.25 gm
12. Lincomycin 0.20-0.40 gm
13. Gentamicin 0.08-0.30 gm
14. Amoxycillin 0.25-0.50 gm
15. Tylosin 0.50-1.00 gm
16. Novobiocin 0.25 gm
17. Tiamulin 0.50 gm
18. Enrofloxacin 0.20-0.40 gm
19. Ciprofloxacin 0.20-0.40 gm
Note: The dose is fixed by the clinician depending on the severity and also
By considering the existing acts and regulations defined by the
concerned agencies.
Table 4. Advantages and disadvantages of commercially available (oily) an
aqueous intramammary infusions
Sl. Sl.
Advantages Disadvantages
No. No.
Oily Preparation
01. Readily available and 01. Dose is fixed
easily administered
02. Slightly non irritating 02. Slightly costlier

03. Effect may be slightly for a more 03. Few preparations are available
period than acqueous in India
Aqueous Preparation
01. Dose can be adjusted according 01 Effect may be for slightly
to severity shorter duration
02. If prepared with 5% Dextrose 02 Time consuming
much more effective
03. Cheap
04. Will be easily diffusing and can
reach the deeper parts of udder
05. Any antibacterial agents can
be used
2) Use of 5% dextrose intramammarily: Recent studies have indicated that

administration of antibacterial agent in 5% dextrose is much more beneficial than the
agent administered in distilled water. Because, this preparation is less irritating since
dextrose is a soothening agent. In addition, the glycogen content of milk neutrophil is
38% less than blood neutrophils and by supplying the energy in the form of dextrose the
functions like phagocytising and killing of the bacteria by the milk neutrophils is
enhanced.
3) Use of Dimethyl sulfoxide (DMSO) intramammarily: Prepare 90 per cent solution

of DMSO by mixing 90 ml of DMSO in 10 ml distilled water. Administer 40 ml of this
into the quarter.
The use of this preparation increases the permeability of cells and tissues thus the
DMSO and any other antibiotic used along with DMSO can diffuse into the deeper parts
of the udder. DMSO is having bactericidal effect on E. coli. It produces anti-
inflammatory effect also.
4) Use of corticosteroids intramammarily: Any corticosteroid can be infused

intramammarily @ 1-3 ml/quarter. The corticosteroid stabilises the lysosomes and cell
wall so that the enzymes and the endotoxins are not released. Thus further toxaemia is
prevented. They produce anti-inflammatory effect and also overcome pain. Here these
drugs are administered directly to the site of infection. Hence the effect is fast and the
duration is short i.e., for 1-2 hours, because within this time the cortisones are absorbed
into the blood and carried through the circulation.
5) Removal of pus from the udder: Administer oxytocin 10-30 units i/v or i/m and
after few minutes milk the cow and remove the pus. If the pus is solid this method will
not be successful. Hence any one of the following enzymes can be used:
1. Trypsin @ 0.25 - 0.5 gm/quarter
2. Streptokinase - streptodornase @ 20,000 – 50,000 IU/quarter. This will cause
polymerization of DNA which is responsible for liquefaction of pus.
3. Hyalase (Rallis India) contains 1,500 IU of Hyaluronidase in each ampoule.
Administer 1-3 ml in 20-30 ml of distilled water /quarter.
Administer any one after diluting with distilled water intramammarily and allow
for 15 minutes to 1 hour. After this period massage the udder and milk the cow. Here the
solid pus becomes liquefied so that it can be removed easily.
6) Use of Immunoglobulins intramammarily: Recent studies indicated that 150 mg of

Immunoglobulins (Igs) along with antibiotic produce very good effect when compared
with Igs alone or antibiotic alone intramammarily.
2. To overcome toxaemia administer:
a) Corticosteroids like beta or dexamethasone @ 0.5-2.0 mg/kg body weight, i/v, i/m.
b) Administer 1-2 litres of 20% dextrose, i/v, to a cow. The following effects are
observed:
i. It produces osmotic diuresis so that more toxins are eliminated i.e., it keeps
the renal system patent.
ii. It supplies energy to the liver which will function better resulting in
increased detoxification.
iii. It over comes hypoglycemia which is seen in toxaemia.
iv. It helps to overcome udder oedema.
3. To overcome dehydration administer balanced electrolyte solution like Arolyte-M

and the amount depends on the degree of dehydration.
4. To reduce the fever the antipyretics like analgin @ 40 mg/kg, i/m or esgipyrin @ 10-
20 ml/cow, I/m.
5. To overcome the effect of histamines administer antihistamines like Avil @ 10-20

ml/cow, i/m.
6. To reduce the swelling of the udder apply Swellnil or Iodex ointment and massage
well. If necessary pack the udder with ice cubes for few minutes.
b) Acute mastitis: Treatment is similar to peracute mastitis. Here antibacterial agents are
administered for 1-2 days parenterally.
c) Subacute and chronic mastitis: Parenteral treatment is not given and only local
treatment with intramammary infusions for 3-5 days is used. Usually there will be
fibrosis of udder in chronic mastitis. There is no good treatment available in allopathy to
overcome this fibrosis. However, the following combination of Homoeopathic drugs may
be beneficial:
Echnesia 200x
Phytolac 200x
Apismal 200x
10-20 globules of each administered orally, b.i.d., for 2-3 weeks.
d) Subclinical mastitis: Treatment is usually given during the dry period. Commonly
200-300 mg of cloxacillin in 3% aluminium monostearate is infused into the udder.
Floclox-D can be given.
e) Chronic granulomatous mastitis: As the affected quarter(s) is almost destroyed, the

treatment will not be successful and such cows are culled if more number of quarters are
affected. If one quarter if affected, then drying off of such quarter is done .
If a quarter does not respond to treatment and is classified as incurable, the
affected animal should be isolated from the milking herd or the affected quarter may be
permanently dried off by producing a chemical mastitis. Methods of doing this, arranged
in descending order of severity, are infusions of:
3% Silver nitrate solution 30-60 ml.

5% Copper sulphate solution 20 ml
1:500 Acriflavine solution 100-300 ml
1:2000 Acriflavine solution 300-500 ml
In addition, 30-60 ml of 10% formaline or 50-100 ml of 1:1000 Potassium

permanganate solutions has been used.
If a severe local reaction occurs, the quarter should be milked out and stripped
frequently until the reaction subsides. If no reaction occurs, the quarter is stripped out
10-14 days later. Sometimes, two infusions may be necessary.
.
f) Gangrenous mastitis: Parenteral treatment with a broad spectrum antibiotic is given
for several days. The affected quarter is treated as an open wound. If a quarter is affected,
it will be completely sloughed off. The remaining quarters will be alright and the
production of the milk will be good in these quarters. The clinician may have to fight
with the case for 3-4 weeks.
g) Fungal mastitis: The treatment is similar to the ones mentioned under this heading in
classification of mastitis according to etiology.

1. Good hygienic measures are very important as the disease is commonly seen in poor
hygienic conditions. This may be related to:
a) Keeping the cow clean.
b) Keeping the bam clean.
c) Proper disposal of excretions.
d) Applying of disinfectant solution to barn.
2. Regular testing of the udder and milk for mastitis and isolating and treating the
affected ones.
3. Using a proper milking order - milking the cows in first and second lactation first and
then the cows in other lactations and the affected cows last.
4. Teat dipping in antiseptic solution: This prevents the entry of the organisms into the
teat orifice and teat canal. This is done usually after milking. Any one of the following
can be used:
that is teat orifice is closed. It is removed after washing of the teats before milking.
5. Dry cow therapy: Here at the beginning of dry period the secretions are removed and
the antibacterial agent in the intramammary tube are infused, @ 1 tube per quarter. Only
once it is administered to all the quarters and left as such. Any antibiotic in an oily base
can be used but commonly cloxacillin has been used. The purpose of this is, the
organisms which have hidden in the udder during the dry period will be eliminated, so
that peracute and acute mastitis immediately after parturition will occur.
6. Polyethylene coil implantation: This coil is passed through teat orifice and implanted
in the teat cistern. The intramammary device (IMD) can be smooth or rough. Here the
coil is inserted into the teat cistern which causes irritation and good number of
neutrophils will infiltrate into this area. These neutrophils will eliminate any bacteria
getting into the cistern.
7. Vaccination: Different types of vaccines are used with various ways of administration
like i/m, s/c, intramammarily into or near the supra mammary lymph node and into the
udder tissue without much success. These methods have reduced the incidence and also
severity of disease, but did not give 100% protection.
Antibiotic Residues in Milk:

A serious consequence of the use of antibiotics/antibacterial agents in milk is their
effect on the manufacture of dairy products (reduced cheese yield, off flavour of butter
milk, diminished starter culture growth and invalidation of certain quality control tests)
and the development of sensitivity syndrome in human beings and also increased
resistance to antibiotics. In most of the countries the maximum intramammary dose of
antibiotics/antibacterial agents is limited by legislation and the presence of detectable
quantities of antibiotics in milk constitutes adulteration.
Veterinarians have the responsibilities of warning farmers of the need to with hold
milk and they should be aware of the with-holding times of each product, details of which
are usually required to be included on its label.
An approximate guide to the recommended periods for which milk should be with
held from sale after different methods of antibiotic/antibacterial agents are:
Udder infusion in a lactating cow : 72 hours

Parenteral injection, one only : 36 hours
Parenteral injection, series of : 72 hours
Antibiotics parenterally in long acting bases : 10 days
Intra uterine tablet : 72 hours
Dry cow intramammary infusion : To be administered at least 4 weeks before
calving and the milk with-held for at least 96 hours afterwards
(ii) HAEMOGALACTIA
Haemogalactia means passing of blood or blood clots in the milk. It can be
physiological or pathological.
Physiological haemogalactia occurs in high milking cows immediately after
parturition where in there will be severe congestion of the udder leading to seepage of
RBC's from the congested blood vessels into the milk. This condition will be there for
two or three days and after wards this will disappear on its own.
Pathological causes of haemogalactia are:
1. Trauma or injury to udder.
2. Acute or peracute mastitis,
3. Leptospiral mastitis.
4. Tumors of the mammary gland - rare.
In this condition, the milk will be light pink to dark chocolate - brown in colour. It
may or may not contain blood clots and such milk is unfit for human consumption.
Diagnosis: Haemogalactia can be diagnosed by clinical signs and by performing occult

blood test of milk, which is very similar to the test used for urine.
Treatment:
The following drugs have been used with variable results:
1. Calcium borogluconate @ 150-250 ml/cow, i/m, s/c and this will help in clotting.
2. Stadren, Clauden, Siocltrome, Semichrome, Styptochrome, @ 10 ml/cow, i/m, once a
day for 3-5 days.
3. Vitamin K (Menadione sodium bisulphite, 1 ml Amps) @ 10 ml/cow, i/m for 3 days.
Also as Vitamin K3 as Kapilin injection.
4. Administer n-butyl alcohol (6-7.5% solution) @ 30-60 ml/cow i/v, once or twice.
5.Administer 5 ml of formaline in 1 bottle of dextrose saline i/v to a cow. If it is not
possible one can administer 10-30 ml of 10% formaline solution orally.
6. Styplan tab - 10-20 tab/tow, b.i.d, orally for 3-5 days.
7. Ipec 6C 10 globules, b.i.e., orally for 3-5 days.
8. Mimosa pudica (muttidare muni) – handful of such leaves are taken and with water
crushed to have a paste and administered orally. This can be done for few days. It has
given good effect.
(iii) UDDER OEDEMA
Udder oedema is also known as caked udder. In this condition there will be
excessive accumulation of fluid in the interstitial tissue spaces of the udder and also sub
cutaneous tissue surrounding the udder. Commonly seen in high milk yielding cows, just
few days before parturition or immediately after parturition which is physiological in
nature. It can be also seen in pathological conditions like peracute and acute mastitis. The
exact mechanism involved is not understood. It may be due to severe congestion of udder
due to peracute or acute mastitis and seepage of fluids into the udder and subcutaneous
tissue. It may be also due to hypoproteinaemia.
Treatment:
1. Removal of the etiological agent - if it is due to peraeute or acute mastitis by using
antibacterial agents (broad spectrum).
2. To reduce the oedema, administer diuretics like Acetazolamide (Diamox) @ 500-1500
mg/cow, b.i.d, orally for 3 days. Also frusemide (Lasix 2 ml Amps ) 500 mg i/v, i/m once
a day or 250 mg twice a day can be used.
3. Apply iodex or swellnil ointment or Amrithmalam and massage the udder.
4. Apply magnesium sulphate-glycerine paste to the udder and tie with a cloth - it
withdraws the fluid,
5. Pack the udder with ice cubes or sprinkle cold water to udder.
6. Alternate application of hot and cold water along with mild exercise may be useful.
7. 200 mg of diethylistilboestrol in 10 ml sweet oil on first and 3rd day after calving may
be benificial.
(iv) HYPOGALACTIA AND AGALACTIA
Hypogalactia means decrease in milk production arid agalactia means no milk

production.
1. Psychological agalactia: It has been recorded in cows and buffaloes. Most commonly
seen in recently parturited animals, especially in buffaloes. Here there will be
psychological imbalance because of mourning of death of calf and it may be also due to
excitement.
This condition can be treated by using any one of the following drugs:
a) Administration of Ataractics like chlorpromazine (largactil, available as 25, 50 and 100
mg tablets) @ 250 mg/cow, b.i.d., orally, l-3 hours before milking for 3-7 days. This
drug brings about psychological balancing effect and makes the cow calm and quiet
so that oxytocin and prolactin will be released leading to let down of milk. It may also
stimulate the release of prolactin which increases the milk secretion. If
Chlorpromazine tablets are not available then one can use Neocal forte (Intas) tablets.
b) Administration of metaclopramide (Perinorm, Tomid, Maxeron, 2 ml amps) @ 10 ml/
cow i/m, for 3 days can also be used. It brings about the sedative effects and also may
stimulate the release of prolactin which will increase the milk production.
c) Use of placentrex (2 ml amp) @ 10 ml/cow, i/m for 3 days is also indicated.
2. Palaserlu: This condition has been recorded in Andhra Pradesh in buffaloes where in.
engorgement of teat occurs at the time of milking and the milk production is reduced.
It has been observed that presence of persistant corpus luteum (CL) leading to
oestrogen - progesterone imbalance which may cause improper release of oxytocin.
This can be treated either by enucleating of CL or by administering 0.5 ml stilbesterol
for 2 days.
3. In buffaloes where proper letdown of milk has not occurred, hypo or agalactia can
occur. It can be treated by administering oxytocin @ 10 – 20 IU per cow, i/m. Many
people raised their voice against such practice thinking that it is unethical.
4. Mineral and Vitamin mixtures if supplemented after parturition the milk production
may be improved.
5. Some cows and buffaloes will abort after 5th month of gestation and above and will
give less amount of milk. Such cases cannot be treated properly. Advice the owner to
wait for another lactation.
6. If proper development of the udder has not taken place then hypogalactia or agalactia
can occur. Such cases may respond to gonadotrophins, but treatment will not be
undertaken and such cows will be culled.
7. Allergic mammilitis: This condition has been recorded commonly immediately after
parturition in buffaloes and sometimes even in lactatitng buffaloes. Initially, this
condition was recorded in Andhra Pradesh and now even in few districts of Northern
Karnataka. In the beginning efforts have been made to isolate the causative agent by
culturing the milk samples and the results were negative. This lead to the belief that it
may be an allergic reaction to probably repeated exposure of streptococci and that’s why
the name ‘allergic mammilitis’ has been given. Recently, a herpes virus has been
identified by electron microscopic studies from such cases and now this condition may be
similar to the condition recorded as Bovine ulcerative mammilitis.
In this condition engorgement of the teats will occur resulting in improper letting
down of milk leading to hypo or agalactia. If not treated in the initial stages it may lead
to necrotic changes and sloughing off of the affected teat/teats can occur. Sometimes it
may end in death of the animal.
Treatment: The treatment will be effective in the initial stages of this condition and in
later stages the treatment may not be effective. The following treatment has been tried in
the field :
1. Antibacterial agents preferably the broad spectrum ones have been used for 3-5 days
parenterally as well as locally.
2. NSAIDS like Diclofenac sodium, Esgipyrin-N, Meloxicam can be used at the
prescribed rates.
3. Anti-histamines like Avil, Chloril etc, may be administered.
4. Corticosteroids like dexamethasone or prednisolone can be used.
5. Recently, anti-viral drug like Acyclovir ahs been tried orally and intramammarily with
moderate success.
Qestions:
1. How bovine mastitis causes economic loss affecting the dairy industry and the national
economy.
2. Why the incidence of mastitis is high in milking cows when compared to buffaloes?
3. Define subclinical mastitis and what is it's significance?
4. Why anthrax, lightning stroke and snake bite should be considered under the
differential diagnosis of bovine peracute mastitis?
5. What is the significance of antibiotic sensitivity assay in bovine mastitis?
6. Why treatment of bovine mastitis is difficult in the field conditions?
7. Why vaccines for bovine mastitis are not available for the field veterinarian?
8. Justify the statement that "teat dipping and dry cow therapy" are very essential for the
prevention and control of bovine mastitis.
9. Why intramammary infusions are commonly used for the treatment of bovine mastitis
10. Why chlorpromazine is used orally for the treatment of psychic hypogalactia in cows
and buffaloes?
a) Haemogalactia
b) Psychic hypogalactia
c) Udder oedema (dysfaberculous mastitis)
d) Fungal mastitis
f) Coliform mastitis
5. COLIBACILLOSIS
(i) NEONATAL DIARRHOEA COMPLEX
(Karugalalli bedi roga, Colibacillosis, Calf scours)
Diarrhoea is a clinical sign of a disease which can have many causes. In all
diarrhoeas, the physiological result is the failure to absorb fluids or secretions that are
increased into the intestine or both.
Etiology:
For many years Escherichia coli was considered as the primary pathogen in
diarrhoeic calves and the term colibacillosis has been in common use. Still now also it
can cause this disease in calves, piglets and lambs. However, now a days this disease in
calves appears to be a disease complex with multifactoral etiology and its interplay with
environmental factors and managemental practices.
A. Bacteria:
1. It is a Gram negative short rod, 1-3 µm x 0.5 µm, coccoid bipolar shaped to long
filamentous forms occurring in single or short chains. Usually motile with peritrichous
flagella but some are non motile. This organism is incriminated as major cause of
scours. Always the same serotype is not isolated from routine bacteriological procedures.
It is always present in the intestinal tract and can cause a secondary infection
following viral agents. K-99 and K-88 are the common serotypes isolated from calves
and piglets. E. coli has been divided into two groups namely enteropathogenic organisms
and septicaemic groups. Enteropathogenic organisms are not invasive but localized in
intestine especially in ileum and cause diarrhoea through the production of endotoxins.
Commonly 25% of the cases of calf diarrhoea could be due to E. coli but it can
reach 75%. The case fatality rate varies from 10-50%. Septicaemic serotypes have the
ability to pass the intestinal wall and invade the tissues and these usually do not cause
diarrhoea. They localize in the brain and joints and produce meningo-encephalitis and
arthritis respectively.
2. Salmonella: Commonly S. typhimurium and S. dublin occurs in 2-6 week old calves.
3. Cl. perfringens type B and C: There are several types like A, B, C and E and type C is
most common producing a necrotizing toxin. Changes in management and weather might
result in change in nursing habits of calves that could result in overloading on milk which
may result in atony or hypomotility of digestive tract which is ideal for the growth and
production of clostridial organisms and their toxins.
B. Viruses:
1. Reovirus like agent/Rota virus/Neonatal calf diarrhoea virus : Scours can occur within
hours after birth with an infection with reo virus, but when first introduced into a herd,
calves aged 30 days or older may be also affected.
2. Corona virus: Causes scours in calves of 5 days to 6 weeks of age.
3. Parvo virus: Usually produces diarrhoea during the first week after birth.
Experimentally calves develop diarrhoea 24-48 hours following inoculation.
4. BVD Virus: The cause of diarrhoea in neonatal calf and may become infected in utero
or postnatally.
C. Protozoa:
a) Coccidiosis: Affects young calves of 3 weeks and above of age. It can be a severe
problem when overcrowding and poor sanitation and stress occurs. Eimeria bovis and
E. zurnii are most predominant species isolated but others can also produce this
disease.
b) Cryptosporidia: They are intracellular protozoan parasites currently classified under
sub-phylum sporozoa and sub-class coccidia. They occur in intestinal tracts of mice,
rabbits, guineapigs, dogs, cats, humans, calves, reptiles and arthropods.
D. Chlamydia psittaci:
It is an obligate intracellular parasite of mucosal cells of abomasum and intestines.
E. Fungi:
Fungi like candida, mucor, absidia, aspergillus and phycomycetes can occur
following extensive antibiotic therapy.
F. Management and environmental factors:
Overcrowding, poor sanitation, damp pens, poor ventilation, sudden change in
weather and poor quality replacers play an important role in the onset of this disease.
G. Colostrum:
All new born animals are more susceptible to infection than their adult counter
parts. They are born agammaglobulinaemic and possess almost no resistance to infection
until after they have ingested colostrum and absorbed sufficient quantities of
lactoglobulins from the colostrum. The immune system of the new born animal is also
less mature than its adult counter part and does not respond as effectively to antigen as
does the older animal. In addition, the new born calf produces large quantities of
corticosteroids beginning 8-10 days before birth which will affect the cellular immune
mechanism.
Epidemiology:
a) Occurrence: One of the important disease of the new born calf and other neonates of
domestic animals causing severe economic loss as a result of high mortality rate.
Recorded in almost all the countries of the world.
b) Transmission: The portal of entry of organisms can be oral, naso-pharyngeal and
navel routes.
Pathogenesis:
The mechanism involved in diarrhoea can be:
1. Defective absorption of fluids
2. Increase in secretions
3. Increase or normal intestinal motility
1) Defective absorption of fluids: Absorption occurs at the villous tips and secretion
occurring from the crypts. The normal gut secretes approximately four times more fluid
that is normally ingested. However reabsorption of fluid is so complete that only about
2% of it is excreted in the faeces. Alteration in these functions however, can very rapidly
result in large amount of intestinal fluid losses and diarrhoea.
As a result of Reo virus infection, tall columnar intestinal epithelial cells were lost
and replaced by low cuboidal cells. Corona virus attacks the columnar epithelial cells of
the entire villi resulting in marked villus atrophy. However, Chlamydia destroys the
epithelial cells of the villi and crypts. As a result of these viral infections malabsorption
occurs leading to diarrhoea.
2) Increase in secretions: An E. coli organism are attached to the epithelial cells

through the antigens and then colonizes, multiplies and produce endotoxins. These
endotoxins attach to the intestinal epithelial cell membrane receptors, which in turn
activates an enzyme called Adenyl cyclase which catalise ATP to form cAMP. cAMP
operates not only by inhibiting active sodium and chloride ion absorption by villus cells
but also by stimulating anion and sodium secretion by the crypts. During this process
sodium carries water leading to diarrhoea.
3) There may be increase or decrease or normal intestinal motility during this disease.
Effect of diarrhoea:
a) As a result of diarrhoea, fluids are lost which leads to dehydration and marked
haemo-concentration which results in decreased circulating blood volume. This
will cause hypoxia initially and later on anoxia, shock, coma and death.
b) Diarrhoea causes loss of HCO3 ions from the blood into the intestine leading to
decrease in blood HCO3 levels. This will reduce the blood pH. This condition is
known as metabolic acidosis.
c) Due to diarrhoea, potassium ions move from the blood into the intestine leading to
hypokalaemia initially. Later on the body reacts by withdrawing the cellular
potassium into the blood leading to false hyperkalaemia. These changes can cause
cardiac abnormalities and death of the animals.
d) Hypoglycaemia occurs as a result of suppression of the liver function by
endotoxins and also due to malabsorption of lactose present in the milk and
anorexia.
Clinical findings:
There are 3 types of colibacillosis and they are:
1. Enteric-toxaemic colibacillosis: Affected new born animals collapse and die in a short
time of 2 to 6 hours. The out standing clinical signs are coma, sub-normal temperature,
cold extremities, collapse of superficial veins, slowness and irregularity of the heart and
mild convulsive movements. Scouring is absent.
2. Septicaemic colibacillosis: Most common during the first few days of life. The
illness is acute and the course varying from 24-96 hours. Affected animals are depressed,
weak and anorectic. There is a marked increase in heart rate and although the temperature
is high initially, it will fall rapidly to sub-normal level when diarrhoea and dysentery
occurs.
Post septicaemic localization in the joints may cause arthritis with lameness, pain
and swelling in the joints. In addition, localization in the meninges can lead to meningitis
with clinical signs like recumbency, opisthotonus, colic, paddling convulsions,
nystagmus and pus in the anterior chamber of the eye. Localization in the lungs can
cause Pneumonia but this is less common.
3. Enteric colibacillosis: This form can occur during the first three weeks of life but
commonly occurs during the first week. The faeces are watery or pasty and usually
chalky-white to yellow in colour and occasionally are streaked with blood. Defaecation is
frequent, tail and buttocks are soiled and the faeces have an offensive rancid smell. There
is usually a systemic reaction with a temperature upto 105°F and an increase in pulse rate.
The animal ceases to drink, is dull and listless and rapidly becomes dehydrated. Various
degrees of dehydration can be noticed. There may be abdominal pain on palpation, some
time tenesmus is evident and the back may be arched. Without treatment death usually
occurs in 3-5 days. All cases of colibacillosis should be carefully examined for evidence
of omphalophlebitis.
Necropsy Findings:
In acute form no lesions are detected. In the other forms, petechial haemorrhages
on the heart and serosa are seen. Peritonitis and suppurative arthritis can be seen. The
intestinal loops will be distended, oedematous, congested and may see the haemorrhagic
spots. The intestinal contents will be chalky white or yellowish and watery.
Diagnosis:
Exhibiting clinical signs of diarrhoea by neonates will be suggestive of NDC.
Confirmative diagnosis will be based on isolation and identification of the organism. For
this purpose collect the blood from the initial stages and in the later stages faecal swab
from the live animals. Also faeces, heart blood and intestinal piece from the carcasses can
be submitted to a laboratory.
Serological tests like FAT, ELISA, SNT, etc., have been used for the diagnosis of
the disease. A haematological study indicates increase in PCV, TRC and Hb due to
dehydration and the degree of dehydration can be assessed.
By using blood gas analyser, the blood pH and HCO3 levels can be estimated and
these are decreased. Total plasma or serum proteins and BUN levels are increased. Blood
K, Na and Cl levels are altered.
NDC should be differentiated from dietetic diarrhoea which is characterized by the
animal being bright and alert and the diarrhoea where in good amount of pasty to
gelatinous faeces is passed.
Treatment:
It is better to reduce the amount of milk ingested by the animal. Then the
following principles of treatment are commonly followed:
1. To overcome dehydration give fluids. The amount of fluid to be administered
depends upon the degree of dehydration.
a) 5% dehydration: Minimum amount of dehydration that can be detected by physical
examination. Skin is reduced in elasticity when grasped but assumes position to which it
is pulled.
b) 10% dehydration: Marked reduction in skin elasticity, sunken eye balls, body
surfaces are warm but extremities are cold, respiration deep and increased.
c) 15% dehydration: Signs of shock viz., cyanosis, recumbency, the body surfaces and
extremities are cold and marked sunken eye balls, shallow respiration and coma.
Fluids can be administered in two ways viz., orally (oral rehydration therapy) and
parenterally (parenteral rehydration therapy).
1) Oral rehydration therapy: If the calf is able to suckle, the fluid can be given orally
@ 3-5% of their body weight every 6-8 hours.
Example: Commercially available preparations like electral or emlyte etc. can be used.
However, one can prepare fluid as per the Asiatic formula which contain Sodium
chloride - 4 gms. Sodium bicarbonate - 4 gms, Potassium chloride - 0.75 gm and
Dextrose - 25-50 gms in a litre of water.
2) Parenteral rehydration therapy: Here the fluid is administered parenterally i.e.
intravenously.
Example: A calf weighing 30 kg and having diarrhoea and the clinical signs suggestive of
10% dehydration. 10% dehydration means the animal lost 10% of its body weight. Here
the animal weighs 30 Kg and so it lost 3 kgs of its body weight. Hence approximately 3
litres of fluid should be given slow i/v in 4-6 hours to overcome the dehydration. For
maintenance, another 40-140 ml/kg body weight should be given in another 20 hours.
Warm the fluid to 37oC before administration.
The type of fluid to be given is either Lactated Ringer's solution or isotonic
Sodium bicarbonate solution.
2. To overcome the metabolic acidosis, HCO3 ions should be supplemented: The
amount of HCO3 ions to be supplemented i.e., the base to be supplemented has to be
calculated by using the following formula:
Base to be supplemented = 0.5 x Body weight (kg) x Base deficit
Recently the factor 0.5 appears to be replaced by 0.3 in the above formula.
The base deficit can be known by:
a)Base deficit = Estimated HCO3 level in blood - Normal HCO3 level in blood.
b)For the field Veterinarians, the base deficit is approximately:
5% dehydration : 10 mEq of HCO3/litre
10% dehydration : 5-20 mEq of HCO3/litre
15% dehydration : 25 mEq of HCO3/litre
The amount of HCO3 ions can be supplemented by administering isotonic solution
containing:
Sodium bicarbonate 1.13%
Sodium chloride 0.85%
Dextrose 5.00%
Also lactated Ringer's solution can be administered i/v. This solution contains the
alkalizing agent sodium lactate which will be metabolized by the liver to yield HCO3
which will be further broken down to into –OH and CO2. Then the hydroxyl radical will
increase the blood pH. This will occur properly when the liver is normal. However, in
colibacillosis, the functions of the liver are suppressed the conversion of lactate into
hydroxyl radical may not be proper. Hence the use of sodium bicarbonate may be a better
proposition as it is broken down into HCO3 and sodium after i/v injection immediately
and changes the blood pH. HCO3.
3.To overcome hypokalaemia, Potassium to be supplemented @ minimum of 10

mEq of potassium/litre of fluid given. Commercially Potassium chloride is available as
15% injectable solution of 10 ml ampoule which supplements 20 mEq of potassium. It is
better to add this to many bottles of fluid rather than being given directly.
4.To overcome hypoglycaemia, dextrose should be administered i/v, since the

following functions of dextrose are very beneficial:
a) It overcomes hypoglycaemia
b) It supplies energy.
c) It overcomes toxaemia in two ways:
i) 10-20% dextrose acts as an osmotic diuretic, thus keeps the renal system patent leading
to more urine formation resulting in elimination of toxins.
ii) During NDC, liver is not functioning properly due to lack of energy. So when dextrose
is supplemented, it supplies energy and the liver can function better resulting in
detoxification.
d) It causes temporary hyperglycaemia leading to the release of insulin which in turn
pushes potassium back into the cells thus overcoming false hyperkalaemia.
5. To reduce intestinal secretion, chlorpromazine can be administered @ 3-5 mg/ kg

body weight i/m. Chlorpromazine decreases the synthesis of Adenyl cyclase which
results in less formation of cAMP. Thus excretion of sodium and water into the intestine
is reduced leading to retention of fluids.
6. To prevent the effect of the toxin, porymixin- B or colistin (Wallamycin suspension,

Carter-Wallace Ltd.,) @ 3-10 mg/kg body weight, orally can be administered. It has been
reported that the specific stereo chemical configurations with amino groups of these
drugs are very similar to the endotoxins which leads to competition between the drugs
and endotoxin for binding on the cell surface, resulting in the lack of binding of the
endotoxin on the surface. Thus the endotoxin cannot produce its effect.
7. To overcome the causative agent administer any one of the antibacterial agent
orally as well as parenterally since these are highly effective against Gram negative
organisms: Furazolidone (@ 5-10 mg kg, orally), Chloramphenicol (@ 25-50 mg/kg,
orally: 10-20 mg/kg, i/m or i/v, bid), Gentamicin (@ 2-7 mg/kg, i/m, bid); Ampicillin (@
10-25 mg/kg, orally, 5-10 mg/kg i/m or i/v) ; Sulfa - Trimethoprim (@ 15-20 mg/kg,
orally, i/m) ;and Sulfaguanidine(@ 130-150 mg/kg, orally), Amoxycilin (@ 5-10 mg/kg,
i/m, orally, 10 mg/kg, i/m).
Commonly after doing the antibiotic sensitivity assay, the antibacterial agent is
used for which the organisms are most sensitive. Generally, gentamicin is administered
parenterally and furazolidone orally which is found to be very effective.
Now a days, fluoroquinolones like enrofloxacin, ciprofloxacin and pefloxacin
have been advocated @ 2.5 - 5.0 mg/kg body weight parenterally eventhough they have
to be used with utmost care since they have been shown to produce erosions of the bony
cartilages of the young ones like puppies and foals.
8. To prevent the effect of histamine, anti-histamines should be administered.

9. To reduce the intestinal contractions, the use of antispasmodics is questionable and
should be used with caution as stasis of the gastro-intestinal tract may be good for the
multiplication of the bacteria which will elaborate the toxin and thus aggravating the
toxaemia.
10. To soothen the g.i. tract, astringent mixture containing kaolin, pectin and catechu,
with or without neblon can be given orally.
11.To improve the appetite and to tone up the body, B complex, yeast tablets,
Lactobacilli and Vitamin A preparations can be used.
NOTE: To overcome toxaemia, corticosteroids should be used with caution in new born
animals as the drug is an immuno-suppressant. Only in case of shock, corticosteroids like
dexamethasone @ 0.5-2.0 mg/kg body weight should be used, i/m or i/v.

a) Management practices:
1. Cows should be placed in clean maternity stall prior to parturition.
2. The udder of the cow should be washed prior to calf nursing.
3. The calf should be assisted to suckle the colostrum within an hour and should suckle
about 6% of its body weight within 6 hours of its birth.
4. Disinfect the navel with Tr.of iodine immediately after birth. If possible repeat the
treatment on 2nd and 3rd day after birth.
5. Place the calf in individual stall for at least first 2 days of life. Then place in a pen with
less than 10 calves of approximately the same age.
6. Sour colostrum: Colostrum from the first 6 milkings is pooled in large plastic
containers and allowed to ferment. The ideal temperature range for fermentation of
colostrum is -10°C to -6°C. For environmental temperature above 25°C add formalin
at a concentration of 0.1% to the colostrum. Colostrum containing blood will putrefy
and such colostrums should not be used. The calf is fed fresh colostrum from its dam
for first 2 days and then is given the pooled colostrum. The sour colostrum is diluted
2:1 with warm water before being fed twice daily. Calves fed with sour colostrum
perform as well as those fed whole milk or milk replacers and they can be given sour
colostrum for as long as 4 weeks or until weaning. This practice enables a considerable
saving in the cost of feeding calves. Another advantage of feeding sour colostrum
during the early critical period of the calf’s life is the protection provided by the
continuous presence of colostral antibodies in the intestinal tract.
b) Oral prophylactic antibiotics like tetracyclines etc., may be beneficial.
c) Use of Lactobacillus acidophilus boluses may or may not be beneficial, but it certainly
won't do any harm.
d) Vaccination:
i) E coli bacterins containing K-99 pili antigen to be administered i/m to pregnant cows
twice at 4 and 2 weeks before parturition. The calves born to such cows will suckle the
colostrum and along with it pili antibodies will get into the intestine and coat the
intestinal mucosa. Such calves when exposed to E. coli, the pili antigen of E. coli cannot
bind to the intestinal mucosa and thus cannot multiply and produce the disease.
ii) Oral vaccination : The E. coli bacterins have been given to new born calves orally for
10-20 consecutive days. But antibody response is short lived since a single exposure to
antigen does not result in an anamnestic response to 2nd exposure.
iii) Combination of parenteral and oral administration of vaccines with K-88 pili antigen
to pregnant sows is better than the ones administered alone. Parenteral administration
produced IgM antibodies and oral ones made the gut associated lymphoid tissue to react
wherein the B-lymphocytes migrated to the mammary gland and became plasma cells
and produced lot of IgA. These antibodies are passed in the colostrum and milk and
protected the piglets.
(ii) AVIAN COLIFORM INFECTIONS
E. coli affects the birds of various age groups with varied clinical manifestations
like:
1. Colibacillosis
2. Hjarre's disease (Coli granuloma)
3. Peritonitis.
4. Salphingitis
5. Synovitis
6. Omphalitis - Yolk sac infection ( mushy chick disease)
7. Air sac disease.
Etiology:
The morphological characteristics of E. coli are given under colibacillosis of
neonates. These organisms have O, K and H type of antigen and there are 141, 89 and 49
strains respectively. The most common serotypes are 01: Kl, 01:K2 and O79:K80.
Epidemiology:
a) Occurrence: Avian coliform infections are wide spread and commonly occur in
domestic fowls when they are in 4th to 5th week of age. It can occur in any age group. It
has also been recorded in turkeys, ducks and other game birds.
b) Transmission: The organisms are passed in the faeces and hence this is the common
source of infection. Usually, the portal of entry of the organisms is through the ingestion
of contaminated feed and water. Once a poultry unit is infected the entire premises
including the litter will be contaminated.
Contamination of the eggs with the faeces at the time of laying is common.
Pathogenesis:
Various stress factors play an important role in the onset of this disease. Even this
infection may be associated with mycoplasma, new castle disease, infectious bronchitis,
infectious bursal disease and coccidiosis.
Upon ingestion, the organisms get into the intestine and will get colonized and can
elaborate the toxins. The diarrhoea due to endotoxins described in other species of
demestic animals does not occur in poultry. However, mild diarrhoea noticed in poultry
may be due to mild inflammation of intestine and also due to mixing of faeces with the
urine at the time of voiding. The organisms can get into the circulation causing
septicaemia and then localize in various organs like the lungs, peritoneum, oviduct and
joints setting up inflammation and with accumulation of mucopurulent or caseous
exudate.
Clinical signs:
Sudden increase in daily mortality rate is first indication of colisepticaemia. Then
there will be respiratory distress with sucking and gurgling noises, restlessness and
lowered food consumption.
Necropsy findings :
1.Panophthalmitis : Hypopyon with blindness of one eye is seen.
2.Pericarditis : The pericardial sac is cloudy, epicardium is oedematous and it may be
filled with fibrous exudate.
3.Salphingitis : It is characterized by a large caseous mass in a dilated thin walled
oviduct.
4.Synovitis : Joints are swollen and filled with caseous exudate.
5.Coligranuloma (Hjarre’s disease): It is characterized by granuloma of liver, caeca,
duodenum and mesentery. It is histologically similar to tubercle granuloma but lesions
does not have acid fast organisms. Enteritis may or may not be seen.
Diagnosis:
The clinical signs and lesions like air-sacculitis, pericarditis and peri-hepatitis are
suggestive of avian coliform infections. These lesions are almost pathognomonic.
The disease can be confirmed by the isolation and identification of E. coli. For this
purpose collect the faecal swabs from the live affected birds and any organ with lesions
from the carcasses.
Treatment:
Administer any one of the following antibacterial agents:
1. Nitrofurantoin at a concentration of 0.02-0.04% in the feed.
2. Tetracycline @ 100-200 gms per ton of feed
3. Sulpha with trimethoprim preparations in the feed.
4. Sulphadimidine 16% solution (Diadin, PRzer) @ 30 ml in 4 litres of water for 4 days
for 100 birds.
5. Ampicllin (Roscillin oral powder, Ranbaxy) @ 30 gms in 100 litres of water to be
administered to 3000 chicks in 1st week, 1400 chicks in 2nd week, 800 chicks in 3rd
week and 670 chicks in 4th week.

1. Good hygienic measures should be followed.
2. Fumigation of eggs immediately after laying.
3. Inactivated vaccines of serotypes O78:K80 etc., has been used.
4. Avoid overcrowding.
Questions:
1. Why now a days colibacillosis of domestic animals is known as Neonatal diarrhoea
complex?
2. Why secretory diarrhoea occurs in colibacillosis and how will you over come it?
3. Why metabolic acidosis occur in NDC and how will you overcome it ?
4. Why pregnant dams are vaccinated with pili antigen of E. coli ?
5. Why oral vaccination of neonates with E. coli bacterins will not protect colibacillosis
in neonates ?
6. Why colostrum should be fed within 6 hours after birth to neonates?
7. Why sodium bicarbonate is a better drug when compared to lactated Ringer's saline in
overcoming metabolic acidosis ?
(a) Clinical signs of colibacillosis.
(b) Diagnosis of NDC.
(c) Antibacterial agents against colibacillosis.
(d) Sour colostrum.
(e) Oral rehydration therapy.
9. List out the disease or conditions caused by E. coli in poultry.
10. Describe the pathogenesis of avian coliform infections.
11 .Describe the necropsy findings of avian coliform infections.
6. NAVEL ILL AND JOINT ILL
Navel ill is a condition where there will be inflammation of umbilical vein and
umbilical cord.
Umbilical cord consists of the amniotic membrane, umbilical veins, umbilical
arteries and the urachus. The umbilical cord breaks after birth and dries up within one
week. Inflammation of the external aspects of umbilicus, umbilical veins and umbilical
arteries is known as omphalitis, omphalophlebitis and omphalo-arteritis respectively.
It commonly occurs immediately after the birth of young ones of all the species of
domestic animals and can be seen upto 3 months of age.
Joint ill is a condition wherein inflammation of one or more joints occurs. Either
the navel ill and joint ill can occur simultaneously or joint ill may follow navel ill.
Etiology:
It occurs usually due to improper disinfection of the umbilical cord after birth. It
occurs usually as a mixed infection of E. coli, proteus spp., brucella, campylobacter.
leptospira, streptococci, staphylococci, Spherophorous necrophorus and Actinomyces
(Corynebactgrium) pyogenes.
Clinical findings:
If bacteraemia and septicaemia develops, the calf may die without exhibiting signs
of illness. An umbilical abscess and suppurative arthritis appear after an interval of
several days to weeks.
This condition commonly occurs in young calves and can be seen in other species
also. This condition is usually associated with fever, diarrhoea, depression, anorexia and
weakness. In these two conditions, the affected area is swollen, painful to touch and filled
with pus. Incoordination and limping in the beginning with acute lameness and
recumbency later on. Ripening of the area which breaks open to discharge the pus will
occur and the hairs are matted with the discharge.
Necropsy findings:
At necropsy, a thickened umbilical cord is found along with the abscesses and
suppurative arthritis. The abscesses are located most often in the liver, urinary bladder
and spleen.
Diagnosis:
The clinical signs like fever, swollen umbilicus and joints in neonatal animals will
be suggestive of these conditions. It can be confirmed by isolation and identification of
the causative agents by collecting the pus from the umbilicus and joints.
Treatment:
1. Broad spectrum antibacterial agents like sulphadimidine, tetracycline.
Chloramphenicol etc. should be administered parenterally in high doses.
2. Administer antihistamines and if necessary corticosteroids parenterally.
3. If the umbilical abscesses are ripened, make a small incision to drain out the pus. Then
treat it as an open wound. Try to avoid the opening of the swollen joints, because to treat
it successfully is very difficult.
Keep the newly born animals clean and tie a knot an inch below the umbilicus and
cut the umbilical cord and apply Tr. of iodine. Keep the maternal barn and the calf shed
clean.
Questions:
1. Define navel ill and joint ill.
2. What is the significance of navel ill and joint ill.
3. Describe the clinical signs of navel ill and joint ill.
4. Describe the treatment of navel ill and joint ill.
7. ULCERATIVE LYMPHANGITIS
(Ulcerative cellulitis, Caseous lymphadenitis)
It is a contagious disease of horses and cattle mainly caused by Corynebacterium

pseudotuberculosis and is characterized by ulcers and swelling in the lower parts of the
limbs and lameness.
Etiology:
It is caused by Cory. pseudotuberculosis which is a Gram positive, pleomorphic,
non motile, non spore forming and non capsulated rod. Other pathogenic organisms like
streptococci, staphylococci, Rhodococcus equi and Pseudomonas aeruginosa have been
isolated from similar lesions.
Epidemiology:
It commonly occurs in the horses and also recorded in cattle and buffaloes.
Overcrowding and unhygienic conditions may play a role in the occurrence of this
disease.
Pathogenesis:
The organisms enter through the abrasions of the lower limbs, multiplies and
invades the lymphatics. It produces inflammation of the skin and lymphatics. Nodules
develop, break open and forms ulcers. Abscesses develop along the lymphatics.
Clinical findings:
The nodules usually appear on the fetlock and later on can be found throughout the
body. They may reach a size of 5-7 cms and rupture and discharge a creamy green pus.
The ulcers will be formed with ragged edges with a necrotic base. The lymphatics of this
area will be swollen, hard and painful and secondary ulcers may be noticed. The painful
swelling can lead to lameness. The lesions will heal in 1-2 weeks but recurrence of the
lesions can occur upto a period of one year.
The lesions in cattle is almost similar to that of horses but there will be gelatinous
clear exudate from the lesions and there can be enlargement of the regional lymph nodes.
Diagnosis:
The diagnosis of this disease is usually by clinical findings and isolation of the
organisms from the lesions.
Ulcerative lymphangitis of horses should be differentiated from glanders and
sporotrichosis. This can be done by clinical features and isolation of the organisms.
Treatment:
The lesions should be cleaned with an antiseptic solution and dressed regularly
until the lesions are healed. If the disease is severe, then administer the penicillin or
tetracyclines parenterally.
Prevention and control:

Good hygienic measures of the stables are a must. Immediately attend the injuries
to the lower limbs.
Questions:
1.Describe the pathogenesis of ulcerative lymphangitis.
2.Describe the clinical signs of ulcerative lymphangitis.
3.Describe the differential diagnosis of ulcerative lymphangitis.
8. STRANGLES
(Equine distemper)
It is an acute infectious disease of horses caused by Streptococcus equi and is

characterized by upper respiratory tract infection and abscesses of lymph nodes of the
throat region.
Etiology:
It is caused by Streptococcus equi. The organisms are Gram positive cocci and
appear in chains.
Epidemiology:
a) Occurrence: It occurs throughout the world and is one of the important diseases of the
horses. It can occur in any age group but commonly occurs in 1-5 year age group and in
cold climatic conditions. The morbidity rate can be 10% or can go upto 100%. The
mortality rate is very low (1-2%).
The following conditions can occur as sequelae of strangles:
1. Purpura haemorrhagica - may be an allergic reaction to streptococcal antigens.
2. Empyema of the guttural pouches.
b) Transmission: The portal of entry of the organisms primarily can be by inhalation and
also by ingestion. Movement of horses plays an important role in the spread of the
organisms.
Pathogenesis:
Upon inhalation, the organisms enters the mucosa of nasal cavity and pharynx and
causes rhinitis and pharyngitis. Then the organisms through the lymphatics go to the
lymph nodes of the throat and forms abscesses. These will break open discharging
creamy yellow pus. The organisms then can get into circulation and localize in kidneys,
brain, liver, spleen and joints as well and causes the suppurative inflammation.
Clinical findings:
Incubation period is 4-8 days. Initially there will be moderate fever (103-105°F),
anorexia, depression and serous nasal discharge will be seen which will be followed by
purulent nasal discharge, sneezing and coughing. Due to pharyngitis, there will be severe
pain and the animal even though ingests the feed and water with difficulty it will be
regurgitated through the nostrils.
The fever will subside in 2-3 days and reappear once again when the abscesses
occur in the lymph nodes. The lymph nodes of the throat are enlarged, hot and painful.
Due to pressure of these on the larynx and pharynx, there will be stertorous breathing and
dysphagia. Within 10 days, ripening of the abscesses occur, which will break open
discharging thick cream yellow coloured pus. The course of the disease can vary from 3
weeks to 3 months.
Atypical forms can occur which may be:
l. Involving lungs -pneumonia.
2. Involving the CNS - purulent meningitis resulting in CNS signs.
3. Involving the joints - polyarthritis, lameness.
4. Abscesses in the liver, spleen and visceral lymph nodes may break open and cause
death of the animal.
Necropsy findings:
Extensive suppuration of visceral organs, pleura, peritonium and lymph nodes of
the throat are seen.
Diagnosis:
Horses having clinical signs of fever, abscesses of the lymph nodes of the throat
and discharging of thick cream yellow coloured pus can be suspected for strangles. It can
be confirmed by isolation and identification of Strep. equi by culturing the nasal
discharge and pus from the lymph nodes.
Serological tests like passive HAT, immunoblotting, DNA restrictions and
bactericidal tests can be used for the diagnosis of strangles.
Strangles should be differentiated from:
1. Equine viral rhinopneumonitis and Equine viral arteritis where in respiratory tract
infection in foals and abortions pregnant mares are seen.
2. Equine influenza - respiratory tract infection is seen.
Abscesses in the lymph nodes of the throat and discharging of pus is only seen in
strangles but not in the above three diseases.
Treatment:
1. To eliminate the Strep. equi administer the drug of choice i.e., procaine penicillin G @
20,000 IU/kg body weight, i/m for 3-5 days.
2. Good nursing care is essential like good warm shelter, good amount of fresh drinking
water, soft palatable feed, good bedding etc.
3. After ripening, open the abscesses, drain out the pus and treat it as an open wound.

1. Good hygienic measures should be adopted in the stables.
3. Vaccinate the healthy animals with killed streptococcal vaccine, 10 ml s/c. It is a
phenol killed vaccine containing 4 different types of streptococci.
Questions:
1. Describe the pathogenesis of strangles.
2. Describe the clinical signs of strangles.
3. Describe the treatment of strangles of horses.
4. Write in brief about the sequelae of strangles.
9. GLANDERS
It is a contagious disease of horses, mules and donkeys caused by Pseudomonas

mallei and is characterized by either acute or chronic form with nodules or ulcers in the
respiratory tract and on the skin.
Etiology:
It is caused by Pseudomonas mallei which was previously known as Actinomyces
mallei and Malleomyces mallei. It is a slender Gram negative rod measuring about 1.5-
5.0 µm in length and 0.3-0.5 µm in breadth. It is a non motile, non capsulated and non
spore forming organism. It is susceptible to hypochlorite, iodine and mercuric chloride. It
can survive for about 20 days in clean water and for about 6 weeks in the stable.
Epidemiology:
a)Occurrence: It is restricted to Eastern Europe, Asia Minor, Asia and North Africa. The
animals affected are horses, mules and donkeys and the disease is highly fatal. Human
beings are also susceptible and is usually fatal. In horses commonly chronic form occurs
and in mules and donkeys acute form of the disease occurs.
b) Transmission: The organisms enter the animal mainly by ingestion and also by
inhalation.
Pathogenesis:
Upon ingestion the organisms goes to the intestine and then into the blood
resulting in bacteraemia or septicaemia. Then they localize in the nasal mucosae, lower
parts of the turbinates, lungs and on the skin commonly of the hind limbs. The nodules
develop on the nasal cavity and the skin and then ulcerates. These may coalesce together.
In the limbs lymphadenitis and lymphangitis will occur. The lymph nodes all along the
lymph vessels will be swollen and will break open discharging pus of the colour and
consistency of dark honey. This is known as 'farcy bud’. The lymph vessels will be
thickened and cord like and this is known as 'farcy cord'. The limb is swollen and appears
like the limb affected with elephantiasis. This cutaneous form is known as 'farcy’.
In the lungs, bronchopneumonia occurs and the miliary tubercles like lesions are
produced.
Clinical findings:
1. Acute form: In this form high fever, cough, nasal discharge, nodules and ulcers on the
skin and nasal mucosa are seen. Then death due to septicaemia will occur within a few
days.
2. Chronic form: In this form chronic cough, frequent epistaxis and laboured respiration
are seen. Later on the lesions described under the pathogenesis occur on the nasal mucosa
and skin of the limbs. The nasal discharge will be serous in the beginning and later
becomes purulent and blood tinged. Submaxillary lymph nodes are swollen. The course
of this form can be few months.
Necropsy findings:
In the acute form multiple petechial haemorrhages are seen throughout the body,
bronchopneumonia and enlargement of bronchial lymph nodes are noticed. In the chronic
form, miliary nodules are seen throughout the lungs, ulcers in the upper respiratory tract,
nodules and ulcers in the skin and subcutis of the limbs which are greatly enlarged.
Diagnosis:
1. Horses having high fever, cough and lesions of farcy bud, farcy cord, nodules or ulcers
in the nasal cavity should be suspected for glanders.
2. Mallein test: It is an allergic test. Mallein is the antigen of Pseudomonas mallei used
for the diagnosis of glanders. The following types of Mallein tests are used:
a) Sub-cutaneous Mallein test
b) Ophthalmic Mallein test.
c) Intradermal Mallein test.
d) Intradermo-palpebral Mallein test: This is commonly used Mallein test. Here 0.1 ml of
Mallein is injected intradermally into the lower eye lid by using a tuberculin syringe and
needle. The results are recorded after 48 hours. If there is marked oedema of lid,
blepharospasms and severe purulent conjunctivitis, then it is positive for glanders.
3. Serological test like CFT is a reliable test. Other tests used are indirect
haemagglutination test and conglutinin complement absorption test. A dot-ELISA has
been developed for field use.
4. Strauss reaction: The pus from the suspected animal is injected intra-peritoneally into
the male guinea pig. If there is severe orchitis and inflammation of the scrotal sac then it
is positive for glanders.
Glanders should be differentiated from the following diseases:
1. Epizootic lymphangitis due to Histoplasma farciminosum.
2. Ulcerative lymphangitis due to Corynebacterium pseudotuberculosis.
3. Sporotrichosis due to Sporotrichum schencki.
4. Severe strangles.
All the above diseases can be differentiated from glanders either by isolation and
identification of the causative agent or by Mallein test.
Treatment:
Usually treatment is not undertaken because glanders is communicable to human
beings and also the act on Glanders proposes the euthanasia of the affected animals. If
necessary, sulphadimidine for 20 days can be used and is found to be highly effective.

1. Quarantine measure is very essential for not only in the place of occurrence but also
when the horses are imported.
2. Positive animals should be destroyed as per the Glanders and Farcy act of India.
3. Repeated testing of the equines by Mallein test once m 3 weeks until all reactors are
identified and removed.
4. Vigorous disinfection programme should be undertaken in areas where glanders cases
were detected.
Questions:
1. Describe the mode of transmission of glanders.
2. Describe the clinical signs of glanders.
3. Define the following:
(a) Farcy bud
(b) Mallein
(c) Strauss reaction
(d) Intradermo-palpebral Mallein test.
4. How will you differentiate strangles from glanders?
10. BACTERIAL GASTRO-ENTERITIS OF DOGS
It means inflammation of the stomach and intestines caused by several species of

bacteria mainly in dogs and characterized by vomition and diarrhoea.
Etiology:
Inflammation of the stomach and intestine can occur separately or inflammation of
the stomach can end in inflammation of the intestine or both the organs can be inflamed
concurrently. It can be caused by a single or multiple causative agents like bacteria,
viruses, chemicals, parasites etc. Many a times bacteria or viruses can be primary or
secondary pathogens involved in this condition.
The following bacteria have been incriminated in this condition:
1. Escherichia coli: A Gram negative, rod-shaped, ubiquitous bacterium which is part of
the normal flora of the intestinal tract. Under certain conditions like stress it can cause
colibacillosis.
2. Campylobacter jejuni: It is a small, motile, Gram negative curved, spiral shaped rod
and causes campylobacteriosis.
3. Salmonella: More than 148 serotypes of salmonellae are isolated from dogs causing
salmonellosis. Out of these, Salmonella typhimurium and S. anatum are recovered most
frequently from dogs and S. typhimurium from cats.
4. Yersinia enterocolitica: It is a Gram negative, small rod or coccobacillus measuring
0.5-1.0 x 1.0-3.0 µm and causes yersiniosis.
3. Bacillus piliformis: It is a Gram negative, spore forming rod and causes Tyzzer's
disease.
6. Shigella dysenteriae, S. ilexneri. S. boydii and S. sonnel: They are non motile, Gram
negative bacteria morphologically indistinguishable from other entero bacteria. Shigella
is principally primate pathogens and occasionally causes shigellosis of dogs.
7. Clostridium periringens: It is a Gram positive bacillus and under certain conditions,
overgrowth of this organism causes gastroenteritis.
Epidemiology:
a) Occrrence: It is one of the important diseases of dogs and cat occurring throughout
the world. Gastroenteritis has been recorded in all age groups but commonly occurs in
young ones. E. coli commonly occurs in puppies within a week of age, whereas
salmonellae can occur in puppies as well as adults. The prevalence of salmonella
infection can range from 4-28% and the bacterium has been isolated from 1-36% of
clinically normal dogs and 0-14% of cats. Many a times it can be a burning problem
leading to very high morbidity and mortality rates. C. jejuni has been recently
incriminated as an enteropathogen in dogs and cats having zoonotic importance.
However, it causes milder clinical syndrome and low incidence rate in cats when
compared to dogs. Humans are more susceptible than animals to infection.
Poor managemental practices and poor sanitary condition of the kennels can play
important roles in the occurrence of this condition. Puppies unable to get good amount of
colostrum immediately after birth are highly susceptible.
Stress factors like overcrowding, unsanitary condition, weaning, transportation,
irradiation, glucocorticoid therapy or other forms of immune suppression due to Canine
distemper or feline panleucopaenia viruses can precipitate the occurrence of the disease.
b) Transmission: The organisms commonly enter the body through ingestion of
contaminated food and water. It can be also by contact. Raw or improperly cooked food
products for cats and dogs prepared from farm animal sources have a higher incidence of
contamination with salmonellae than pelleted and heat processed foods. In addition,
salmonellae can multiply quickly in moistened food stuffs left at room temperature.
Infected animal handlers may also be a source of salmonella in a hospital, kennel or
cattery. Neonates may acquire infections from contaminated secretions of their dams.
Abortions, stillbirths and the birth of weak puppies or kittens may result from in utero
infection. Coprophagia also plays an important role.
C. jejuni can be transmitted by houseflies mechanically.
Some organisms like B. piliformis, Y. enterocolitica and Cl. perfringens can be
found normally in the dogs without producing disease but excreting these organisms in
the faeces. Under stress such dogs can come down with this disease.
Pathogenesis:
The organism can directly enter the stomach and intestines and cause
inflammation. Some organisms like E. coli, Salmonella spp. and C. jejuni can produce
enterotoxins which can cause secretory diarrhoea by activating the Adenyl cyclase
enzyme which catabolizes ATP to produce cAMP. This cAMP increases the secretion of
sodium and chloride and prevents the absorption of Na from the gut leading to more of
water in intestines and culminates in diarrhoea.
The endotoxins produced by B. coli and salmonella are absorbed into the
circulation leading to toxaemia and endotoxic shock.
The organisms like E. coli and salmonella can enter the circulation and cause
septicaemia in young animals and can localize in various organs.
Inflammation of the gastric mucosa leads to excessive secretion of gastric juice
and vomition. This will result in dehydration and metabolic alkalosis.
Excessive intestinal secretion will lead to loss of HCO3 ions and potassium from
blood leading to metabolic acidosis and hypokalaemia respectively.
The metabolic disturbances depend upon the severity of vomition and diarrhoea.
Hence we may see either metabolic alkalosis or metabolic acidosis or no change at all.
Dehydration will lead to haemoconcentration, hypovolaemia, hypoxia, anoxia and
shock. Dehydration, metabolic disturbances, hypokalaemia and hypovolaemic and or
endotoxic shock can contribute to the death of the animal.
Clinical findings:
Peracute, acute and chronic forms of this disease can occur.
The peracute form usually will be in the form of septicaemia where in young
puppies can die without showing any clinical signs. Some can show fever, depression,
weakness, recumbency and death.
In the acute form, fever of 103-106°F, depression, weakness and vomition are
initially seen. In a day or two it can be followed by diarrhoea which can be watery or the
faeces can be pasty and rancid smelling. It can be mixed with excessive amount of
mucous or mucosal shreds. Abdominal pain is evidenced by crying and preferring to lie
down on cool surfaces. This will be followed by signs of subnormal temperature and
dehydration like sunken eye balls, loss of elasticity of skin, cold extremities, cold body
surfaces, recumbency, severe depression and tenesmus can be seen. Some time dysentery
indicated by blood clots or blood in the faeces can be seen. Cyanotic mucous membranes,
coma and death can occur in 2-3 days.
In the chronic form, there will be persistent or recurrent diarrhoea, weakness,
emaciation wherein there will be chronic weight loss. The faeces can be foetid and
watery.
Necropsy findings:
In peracute form, septicaemia is indicated by petechial haemorrhages on the
serosa, mucosa and heart. In the acute form there will be congestion, oedema and
haemorrhages in the stomach and intestine. The intestinal contents will be mixed with
excessive mucous, blood or blood clots. The mesenteric lymph nodes are enlarged and
haemorrhagic. Localized infection of visceral organs is characterized by pneumonic
changes in the lungs, necrotizing hepatitis and pyelonephrosis. In the chronic form
thickening of the mucous membranes of ileum and colon can be seen.
In Tyzzer's disease, the characteristic finding is multiple whitish grey to

haemorrhagic foci which are 1-2 mm in diameter on the capsule and cut surface of the
liver.
Diagnosis:
Puppies and adult dogs with vomition, diarrhoea and fever should be tentatively
diagnosed as gastroenteritis. Confirmation will be by isolation and identification of the
causative agent by culturing the faecal swab and sometimes blood (initial stages). The
intestinal contents, heart blood, liver and lungs should be collected upon necropsy for this
purpose.
B. piliformis cannot be isolated on artificial media and the liver suspension must
be inoculated i/v or intracranialiy into mice or embryonating eggs and can be very
helpful.
For the diagnosis of Tyzzer's disease, special stains such as Giemsa or Warthin-
starry or Gomori's silver stains can be used (to detect the organism). The organism has a
characteristic beaded appearance with the last stain.
Bacterial gastroenteritis should be differentiated from viral and parasitic
gastroenteritis.
1. Viral gastroenteritis:
a) Canine distemper is characterized by diphasic fever, pustules on the ventral aspect
of abdomen,convulsive seizures, vomition, diarrhoea, nasal and lacrimal discharges.
b) Canine parvo viral gastroenteritis can occur in two forms viz., the cardiac and
enteric form. It is characterized by high morbidity and mortality rates, pan cake
stools, dysentery etc.
c) Canine corona viral gastroenteritis is characterized by diarrhoea wherein awfully
foul smelling faeces is passed.
d) Infectious canine hepatitis is characterized by saddle shaped fever, prolonged
clotting time and diarrhoea.
e) Feline panleucopenia is characterized by fever, vomition, extreme dehydration and
praying posture in 3-5 months old cats. A persistent non-regenerative anaemia and
leukopaenia are more suggestive of this infection.
2. Parasitic gastroenteritis:
Diseases like ascariasia, ancylostomiasis, spirocercosis and coccidiosis can be
differentiated by faecal examination where in characteristic ova or oocysts can be
demonstrated.
Treatment:
Usually symptomatic treatment is given initially and after confirming the tentative
diagnosis by culturing and antibiotic sensitivity assay the specific treatment is given to
dogs suffering from gastroenteritis. The following treatment is generally given:
1. Don't allow the animal to drink water or to ingest food for first 12 hours and 24 hours
respectively. Give bland diet like rice or barley gruel, baby food, honey, milk etc.
2. To overcome the vomition administer either 0.5-1.0 ml of stemetil or 1-2 ml of
perinorm, i/m and maintain with 1/2 -1 tablet of the same preparation, orally, bid or tid.
3. If vomition is severe, then to overcome dehydration and metabolic alkalosis,
administer either Dextrose normal saline or Ringer's saline, i/v depending on the degree
of dehydration.
4. If the diarrhoea is severe, then to overcome dehydration and metabolic acidosis,
administer either isotonic sodium bicarbonate (1.13%) - dextrose(5%) solution or lactated
Ringer's solution i/v depending upon the base to be supplemented or degree of
dehydration respectively. Base to be supplemented is calculated by using the formula:
Base to be supplemented = 0.6 x body weight (kgs) x Base deficit.
Base deficit is calculated by:
a) Base deficit = Normal blood HCO3 level - Estimated blood HCO3 level
b) Base deficit in field conditions is approximately;
5% dehydration : 5 mEq of HCO3 / litre
or
5 % (mild) dehydration : 3 mEq of HCO3/kg body weight
10 % (moderate) dehydration : 6 mEq of HCO3/kg body weight
15 % (severe) dehydration : 9 mEq of HCO3/kg body weight
After knowing the base to be supptemented (HCO3), the required amount of
isotonic sodium bicarbonate is administered intravenously.
Orally fluids prepared by using Asiatic formula or commercially available
preparation like Electral can be used. The dose is 50-100 ml/kg/day. For details
refer NDC.
Transfusion of plasma @ 130-250 ml/dog may be more beneficial than
fluid therapy when mucosal disruption and increased g.i., permeability lowers
albumin concentration to less than 2.0 g/dl. If necessary go in for blood
transfusion.
5. To neutralize the acid and to soothen the g.i. tract sodium bicarbonate/Gelusil
MPS/gastrointestinal sedative is given orally and also pectokab / kaltin / salvacol /
pesulin can be used.
6. To overcome E. coli and salmonella administer any one of the antibacterial agents both
orally and or parenterally: Sulpha-trimethoprim (@ 15-30 mg/kg, bid); Chloramphenicol
(@ 25-50 mg/kg, bid, tid); Gentamycin (@ 5-10 mg/kg, bid); Furazolidone (@ 5-10
mg/'kg, bid); Amoxicillin (@ 10-15 mg/kg, bid, tid) and Ampicillin (@ 10-20 mg/kg, bid,
tid).
The antibacterial agent should be used parenterally in dogs infected with
salmonellae and having systemic signs. In Tyzzer's disease the treatment has not been
successful as affected animal die before it can have an effect.
For infection with C. jejuni it is better to use Erythromycin @ 30-40 mg/kg/day
divided tid or tylosin @ 45 mg/kg/day divided bid for 5 days orally.
7. To prevent the effect of the toxin administer either colistin sulphate @ 5-10 mg/kg or
polymixin-B @ 1-2 mg/kg orally.
8. To overcome the toxaemia adminster 20% dextrose and dexamethazone, i/v.
9. To reduce the intestinal secretion, administer largactil @ 3-4 mg/kg or indomethacin @
5-10 mg/kg body weight or aspirin @ 10-25 mg/kg, divided daily orally.
10. To reduce the bleeding from the g.i. tract administer either botrupase or stadren /
clauden / siochrome, 1-2 ml, i/m.
11. To improve the appetite, administer either B-complex (vibelan) or B-complex liver
extract (Belamyl/Neohepatex), 1-3 ml, i/m.

The following preventive and control measures can be adopted:
1. The umbilical cord of puppies should be tied, cut off the excessive part below the knot
and apply good amount of Tr. of iodine immediately after birth.
2. Good amount of colostrums is given immediately after birth since it not only
supplements essential nutrients but also antibodies which gives protection in the g.i. tract
and systemically also.
3. Good nursing care of the newly born puppies is very essential.
4. Good hygienic measures like proper disposal of excretions and cleaning and
disinfecting the kennels should be followed.
5. Isolate the sick animals and treat them.
6. Vaccinate the pregnant bitches against E. coli and other commonly occurring viruses
causing gastroenteritis. Proper schedule should be adopted.
Questions:
1.Define gastroenteritis and list out the etiological agents involved in this disease.
2.Describe the metabolic disturbances of this disease and how will you overcome these
disturbances?
3.How will you control bacterial gastroenteritis?
4.Write short notes on:
a) Clinical signs of bacterial gastroenteritis.
b) Diagnosis of bacterial gastroenteritis.
c) Zoonotic importance of bacterial gastroenteritis.
11. KENNEL COUGH

(Infectious tracheobronchitis)
Infectious tracheobronchitis is an acute or chronic infectious disease of dogs
caused by multiple etiological agents and is characterized by inflammation of the trachea
and bronchi and can end in fatal bronchopneumonia in puppies and debilitated adult or
aged dogs. Since it is a highly contagious disease, it can spread rapidly among animals
that are closely confined as in hospitals or kennels or dog shows. Hence it is called as
'kennel cough'.
Etiology:
Several viruses, bacteria and mycoplasma appear to be involved in the etiology of
kennel cough. Some are of the opinion that viruses are the principal agents involved
which is later complicated with bacteria. Others are of the opinion that bacteria especially
Bordertella bronchiseptica is perhaps the single most important cause of kennel cough.
However, simultaneous infection with several of the agents cannot be ruled out.
The infectious agents involved in kennel cough are:
1. Viruses: Viruses like CD virus, canine adenovirus 1(ICH virus), canine adenovirus 2,
Canine PI virus, canine reoviruses types 1, 2 and 3 and canine herpes virus are involved
in kennel cough.
2. Bacteria: Bacteria like Bordertella bronchiseptica (principal agent), pseudomonas
spp., E. coli and Klebsieiia pneumoniae are involved.
3. The role of Mycoplasma spp., in kennel cough has not been firmly established. Stress
and environmental factors such as cold, drafts and high humidity may increase
susceptibility.
Epidemiology:
a) Occurrence: One of the important diseases of dogs and has been recorded in many
parts of the world and in all age groups. The morbidity and mortality rates vary a lot
and this depends upon the pathogen(s) involved.
b) Transmission: The main mode of entry of the organism is through aerosol route. It
can spread rapidly among the animals in the kennels, hospitals and dog shows by
aerosol transmission, by direct contact and in heavily contaminated environments by
fomites.
Pathogenesis:
The organisms upon entering the nasal cavity cause rhinitis and then cause
tracheitis and bronchitis leading to the accumulation of viscous purulent exudate. This
will cause plugging of bronchi and bronchioles leading to hypoxia. Complicated cases
end in bronchopneumonia and death.
Clinical findings:
Clinical signs usually develop in 3-5 days after initial exposure and are generally
serous nasal discharge which becomes muco-puruient later on. This is followed by a dry,
hacking and often paroxysmal cough. The cough is easily induced by gentle palpation of
the larynx or trachea and also by exercise. Later on there will be retching and gagging.
Affected dogs are active, alert and afebrile and will recover in 7-10 days.
Signs of bronchopneumonia with fever, purulent nasal discharges, profound
depression and anorexia may occur in young puppies or debilitated older dogs.
Diagnosis:
The clinical signs and the history of recent exposure are only suggestive of kennel
cough. The disease can be confirmed by isolation and identification of the causative agent
by culturing the nasal swabs and tracheal washings.
Treatment:
Most cases of kennel cough recover without treatment within 7-10 days. However,
some dogs will suffer for weeks altogether and such cases should be treated with the
following:
1. Commonly antibiotics like gentamicin, kanamicin, chloramphenicol, tetracyclines and
sulpha-mmethoprim combinations are used. Parenteral administration of any one of
these is not effective in clearing the trachea and bronchi of B. bronchiseptica as there
will be inadequate concentrations of the antibiotics in the tracheo-bronchial secretions.
Hence the drugs should be administered parenterally or orally and also by aerosol
(nebulization) or intra-tracheal route.
Example: Gentamicin or kanamicin @ 5-10 mg/kg body weight, i/m, bid for 10-14
days. Gentamicin 30 mg or Kanamicin 200 mg per treatment of aerosol or intra-
tracheal route, once in 12 hours on the first day and once a day for 5-7 subsequent
days.
2. To reduce the inflammation of the respiratory tract, corticosteroids like dexa or
betamethasone @ 0.2-0.4 mg/kg body weight can be administered along with the
antibiotics as aerosols or intra-tracheal injection. In addition, the same can be
administered parenterally or orally @ 0.5 -1 mg/kg body weight for 2 weeks.
3. Broncho-dilators like Deriphyllin, 1-2 ml, i/m or i/v can be administered.
4. Expectorants like Piriton or Corex cough syrups can be used orally to facilitate the
clearance of secretions from the lower respiratory tract.
5. Cough suppressants like Dextromethorphan hydrobromide or Butorphanol are
indicated only if the cough is non-productive and is persistent or interfering with sleep.
General hygienic measures are indicated here also. Keep the kennel clean,
disinfected and properly ventilated.
Vaccinate the healthy dogs by using either the canine viral vaccines and also with
killed bacterins of B. bronchiseptica i/m or s/c or live avirulent strains of B.
bronchiseptica intranasally. Both the types of Bordetella vaccines will reduce the
morbidity and severity but will not prevent the infection when dogs are exposed to B.
bronchiseptica. The intra-nasal vaccination can be done to nursing pups before weaning
as maternal antibodies will not interfere with intranasal vaccines. The immunity lasts for
10-12 months and as such annual revaccination is required.
Questions:
1. Why infectious tracheobronchitis is also known as kennel cough?
2. Describe the etiological agents involved in kennel cough.
3. Describe the clinical signs of kennel cough.
4. Describe the treatment of kennel cough.
5. Why intra-tracheal treatment is advocated in kennel cough?
6. What do you mean by nebulization?
12. SWINE ERYSIPELAS

(Diamond skin disease)
It is an infectious disease of pigs caused by Erysipelothrix rhusiopathiae

(insidiosa) and is characterized by diamond shaped skin lesions in the acute form and
non-suppurative arthritis and vegetative endocarditis in chronic form.
Etiology:
It is caused by Erysjpelothrix rhusiopathiae (insidiosa). It is a Gram positive rod
which may be curved or straight and measures about 1-2µm in length. It is killed by 2%
formalin and 5% phenol.
Epidemiology:
There are atleast 22 serotypes of E. rhusiopathiae known to exist and not all
serotypes isolated from pigs are virulent. In addition, the serotype antigens are
immunologically distinct and one will not give protection against others.
a) Occurrence: Swine erysipelas occurs through out the world. Pigs of all ages are
susceptible. However adult pigs and sucklings are more susceptible when the strain of
bacteria involved is of low virulence and highly virulent respectively. Human beings are
susceptible and hence it is of zoonotic importance.
b) Transmission: The organism enters the pigs by ingestion of contaminated feed and
water and also through the skin abrasions. The source of infection is faeces.
Veterinarians can get the infection while handling the virulent vaccines used for
vaccination.
Pathogenesis:
Upon ingestion the organisms go to the intestine and then get into the blood. It
causes bacteraemia or septicaemia and then localizes in the skin, joints and valves of the
heart.
In the skin it causes square / rectangular / rhomboid urticarial patches which are
about 2.5-5.0 cms in diameter and pink to dark purple in colour. In the joints there will be
hyperaemia of the synovial membranes. Increase in synovial fluid and later on thickening
of the joint capsule. In the valves of the heart, it causes vegetative endocarditis, wherein
nodular or cauliflower like lesions occurs on the valves. Emboli can be detached and
through circulation can localize in any organ especially kidneys causing pyaemic
nephritis.
Clinical findings:
Three forms of this disease are seen:
1. Acute form: IP is 1-7 days. Some pigs may die without showing any clinical signs.
Other pigs can have high fever (108°F), depression, anorexia and ocular discharge.
Later on incoordination and shifting lameness is seen. Within 2-3 days, diamond skin
lesions can occur on snout, ears, shoulder, back, sides, abdomen and throat. These are
square / rectangular / rhomboid urticarial patches which are about 2.5-5.0 cms in
diameter and pink to dark purple in colour.
2. Sub-acute form: Similar to acute but milder.
3. Chronic form: Cardiac insufficiency characterized by dyspnoea, cyanosis and sudden
death can occur in pigs with endocarditis. Joints are enlarged, hot and painful in the
beginning and within 2-3 weeks the joints will be quite firm and ankylosis of joints
occur. Alopecia, sloughing of the tail and tips of the ears and hyperkeratosis can occur.
Necropsy findings:
In the acute form, diamond skin lesions are pathognomonic. The large ecchymotic
haemorrhages are seen through out the body but commonly clearly visible in the pleura,
peritoneum and under the capsule of the kidney. Infarcts may be sometimes seen in the
spleen and kidney.
In the chronic form the most characteristic lesion is the non suppurative
proliferative arthritis of limbs and intervertebral joints, vegetations of the valves of heart
and infarcts of the kidney can occur.
Diagnosis:
1. By clinical signs.
2. By lesions.
3. Isolation and identification of the organisms: In acute form, blood can be examined
after staining and also can be cultured. In the chronic form synovial fluid from live
animals and endocardial vegetations and kidney infarcts from carcasses also yields
organisms. Also it can be injected to mouse and pigeons.
4. Haematology reveals monocytosis.
5. Serological test: CFT can be used. Also agglutination test can be used and a titre of
1:25 and above is considered as positive. ELISA also has been used.
Swine erysipelas should be differentiated from hog cholera and salmonellosis
wherein there will be enteritis, tremors and convulsions are seen. This disease also should
be differentiated from streptococcal septicaemia and endocarditis.
Treatment:
1. To eliminate the causative agent administer penicillin which is the drug of choice @
30,000 lU/kg body weight, i/m, for 3 days. Chronic cases do not respond well to
treatment.
2. Administer cortisone 75 mg, s/c for pigs having arthritis.

1. Follow good hygienic measures.
2. Vaccinate the pigs with any one of the following:
a) Serum simultaneous method: This is the old method of immunizing the pigs. Here
the blood from the infected animal and anti-serum are administered
simultaneously to produce milder infection.
b) Bacterins also can be administered.
c) Live attenuated vaccines and tissue culture vaccines have been used orally or by
injection for the prevention of swine erysipelas.
The vaccine prepared from the prevailing local strains should be used.
Questions:
1. Why swine erysipelas is also known as 'diamond skin disease?
2. Describe the clinical signs of swine erysipelas.
3. What do you mean by vegetative endocarditis?
4. How will you treat swine erysipelas?
5. How will you control swine erysipelas?
13. ACTINOBACILLOSIS
(Wooden Tongue)
It is an infectious disease of cattle caused by Actinobacillus lignieresi and is

characterized by chronic sappurative granulomatous inflammation of the tongue and less
commonly, the oesophageal groove and phryngeal lymph nodes.
Etiology: It is caused by Actinobacillus lignieresi. It is a Gram negative bacilli

interpersed with cocci which is known as ‘Morse code’ appearance. Non motile, non
capsulated and non spore forming organism.
Epidemiology:
a) Occurrence: It occurs throughout the world. It is a sporadic disease. Commonly
cattle are affected. It occurs in buffaloes and sometimes sheep are also affected. In
sheep the tongue is not affected and only the soft tissues of head and neck are
affected.
b) Transmission: The organisms are commonly found in the mouth and rumen.
Whenever there is trauma they will get into the tongue. The trauma may be due to
ingestion of bearded grasses, thorns, wires and awns.
Pathogenesis: Initially the organisms will get into the tongue and causes acute
inflammation leading to marked swelling of the tongue and salivation. Later on chronic
supporative granulomatous inflammation of the tongue occurs which results in hardening
and shrunkening of the tongue giving the wood like appearance of the tongue. Then it
spreads to the lymph nodes of the throat region and similar changes occur. This results in
swelling of the lymph nodes which may come in the way of deglutition and respiration.
Ripening of the lymph nodes may occur which may break open discharging thin non
odorous pus.
Clinical findings: In the beginning, the tongue is swollen and may be protruding from
the mouth, excessive salivation and unable to ingest feed and water properly are noticed.
If the tongue is handled it may be painful and may resent the handling of the tongue. This
may be accompanied with moderate to high fever.
Due to involvement cf the retro-pharyngeal lymph nodes there will be interference
in swallowing and loud snoring respiration. The submaxillary and parotid lymph nodes
will be swollen and visible. The lymph nodes will ripen, break open and discharge thin
non-odorous pus. As the condition becomes chronic nodular type of lesion can be seen
on the lateral surface of the tongue and few ulcers also can be seen. Then the tongue
becomes hard, shrunkened and immobile leading to inanition, starvation and death
Cutaneous form has been recorded and is very rare. Here swellings upto 15 cms
can occur in the neck, thorax and abdomen.
Diagnosis:
1. By clinical signs of tongue and lymph nodes.
2. Examination of sulphur granules: Collect the pus in a test tube and add normal saline.
Mix the contents well and pour it on to the petri dish. Search for sulphur granules which
are yellow coloured small tiny granules. Pick one or 2 granules and put it on a slide and
add 1 or 2 drops of distilled water. Then place another slide over it and by applying
pressure crush the granules. Then with draw both the slides slowly in the opposite
direction so that both the slides will have the smear. Then air dry it, heat fix it and do the
Gram's staining.
Differential Diagnosis: Because there is salivation this disease has to be differentiated
from:
1. Rabies - Persistent bellowing, tenesmus etc.
2. FMD — Vesicles, ulcers in the oral cavity and foot.
3. RP - Blood shot eyes, erosions on the oral cavity, diarrhoea.
Because lymph nodes are enlarged it has to be differentiated from the following diseases:
1. Tuberculosis - Tuberculin testing.
2. Bovine leukaemia - leukocytosis, all the lymph nodes of the body are swollen and
enlarged.
3. Abscesses of the throat region.
Treatment:
1. To -overcome the etiological agent use any one of the following:
a. Streptomycin (Ambistrin) - drug of choice and is administered @ 5-10 mg/kg
body weight, b.i.d., i/m for 3 to 10 days
b. Chloramphenicol - 3-10 mg/kg, i/v or i/m
c. Oxytetracycline - 5-10 mg/kg, i/v or i/m
2. To reduce the fibrous tissue reaction administer any one of the following:
a) Sodium iodide - 1 g/15 kg as a 3-10% solution, slow- i/v, once
b) Potassium iodide - 5-10 g/cow, orally, once a day for 6-10 days.
c) Lugol's iodine - 3-30 ml/cow, dilute in equal quantity of distilled water and
administer it as slow i/v injection once in 3 days, 3 or 4 times.
3. Drain out the pus from the lymph nodes by incising and pack with gauze soaked in Tr.
Iodine or lugols iodine.
4. Along with antibiotic, isoniazid @ 10 mg/kg, orally, daily for 3-4 weeks has given
very good results.
14. ACTINOMYCOSIS (Lumpy Jaw)
It is an infectious disease mainly of cattle caused by Actinomyces bovis and is

characterized by rarefying osteomyelitis of mandible and maxilla.
Etiology: It is caused by Actinomyces bovis. In Greek Actino means ray like and myces
means fungus i.e., ray like fungus. It is a branching filamentous Gram positive organism.
The filaments are divided by segmentation giving a beaded appearance to the organism.
Epidemiology:
a) Occurrence: Recorded throughout the world and sporadic. It has been recorded in
cattle, buffaloes and human beings. In horses the organism is associated with fistulous
withers and in swine with mastitis.
b) Transmission: The organisms are normally present in the upper respiratory and
digestive tracts of cattle. The organisms enter the bone when there is trauma due to
ingestion of bearded grasses, sharp awns, wires etc.
Pathogenesis: Actinomycosis is characterized by rarefying osteomyelitis of the mandible

and maxilla. Here the reaction seen is chronic suppurative granulomatous inflammation.
Here the lumps are seen originating from the bones and these lumps are hard and
immovable. These go on increasing in size and break open discharging sticky honey like
fluid which leads to formation of fistulous tracts.
Some times soft tissues like testes, brain, lungs and rumen can be affected and
abscesses will be formed.
Clinical findings: Initially, small lumps (nodules) will be seen at one place in the
mandible or maxilla. This will increase in size day by day and within few weeks or
months it can become a very big lump. This lump is very hard and immovable and
painful to touch. This may break open discharging sticky honey like fluid containing
sulphur granules. Within few days or weeks after the appearance of this lump, other
lumps can appear in other parts of mandible or maxilla. If the maxilla is affected, there
may be dyspnoea. If the swelling is near the teeth, the teeth will be malaligned and
painful and come in the way of mastication.
In swines, the mammary glands are affected in this disease.
Diagnosis:
1. Clinical signs - lumps originating from the mandible/maxilla, almost suggestive of
Actinomycosis.
2. Examination of sulphur granules: The technique is similar to actinobacillosis.After
staining and examining under the microscope, it has to be differentiated from the sulphur
granules of actinobacillosis and botryomycosisby looking at the morphological
characteristics of the organisms and the club shaped structures.
Botryomycosis Actinobacillosis Actinomycosis

Staphylococcus aureus Actinobacillus lignieresi Actinomyces bovis
Gram positive Gram negative Gram positive

Cocci in the Form organisms in morse branching filaments
of bunch of grapes code appearance
Differential diagnosis: Actinomycosis should be differentiated from actinobacillosis by:

1. Lymph nodes and other soft tissues are affected only in actinobacillosis but not in
actinomycosis.
2. Sulphur granule examination- Actinomycosis, actinobacillosis and botryomycosis
can be easily differentiated as mentioned above.
3. Tongue is affected in actinobacillosis and jaw bones are affected in actinomycosis.
Treatment: Similar to actinobacillosis and in addition the following also can be done:
1. Surgical extirpation of the growth in the initial stages is the treatment of choice.
2. X-ray irradiation of lesion at very low doses repeatedly has been shown to be
effective.
3. Injecting the antibiotic like streptomycin, 2-3 g to the lesion has also been tried
along with parenteral administration.
15. TUBERCULOSIS
a) Tuberculosis of Domestic animals
(Kshaya roga, Pearl's disease, consumption, Scrofula, Pthisis)
An infectious disease of all domestic animals and human beings caused by

Mycobacterium bovis / M. tuberculosis / M. avium and is characterized by progressive
development of tubercles in any of the organs.
Etiology: TB can be caused by Mycobacterium bovis, M. tuberculosis & M. avium
Mycobacterium bovis - Primary host is cattle and secondary host can be any
species of domestic animals and human beings.
Mycobacterium avium - Primary host is birds and secondary host can be pigs,
cattle, horse, sheep etc.
Mycobacterium tuberculosis - Primary host is human beings and secondary host
can be pigs, monkeys, dogs, cattle, etc.
Morphology: These are slender rods measuring about 1.5 - 4.0 u x 0.2 - 0.6 u. They are
acid fast organisms and the acid fastness is due to a lipid called Mycolic acid. The
organisms are non spore forming, non-motile and aerobic. They are resistant to
commonly used disinfectants and antiseptics but susceptible to ethyl alcohol.
Epidemiology:
a) Occurrence: Recorded through out the world. It has been recorded in almost all
species of domestic animals and several wild animals, domestic and wild birds. It is a
disease of economic importance of dairy industry. Mortality and morbidity rates are not
easy to define. It may cause 10-23% of production loss.
Tuberculosis is a disease of zoonotic importance. Even though TB is in existence
from time immemorial and lot of work has been done, big break through in diagnosis,
treatment or control has not occurred.
Detailed systematic work was done in India by Lall and published in Veterinary
Bulletin as a Review article way back in 1969. The salient features of this report are:
1. There is no difference in virulence of Indian strains of tubercle bacilli as compared
to European strains.
2. There was no difference in the susceptibility of indigenous breeds as compared to
exotic or cross-bred cattle.
3. The incidence of TB was much higher in buffaloes (13.83%) when compared to
cows (7.4%).
4. Isolated M. tuberculosis from humans and M. bovis from cattle.
5. Unable to isolate tubercle organisms from milk by culturing or Guinea pig
inoculation. Hence tubercle mastitis in India is very rare.
Tuberculosis is a zoonotic disease and the source of infection from animals to

human beings may be:
1. Raw milk.
2. Exhaled air of tuberculous animals.
3. People handling the tissues and organs of affected animals.
According to Ratledge (1979) there were about 1.5 to 2.0 crores of people
suffering from TB in the world. They will be spreading the disease to 5-10 crores of
people every year. About 30 lakhs of people die of TB every year. These figures appears
to increase every year.
According to an article in recently published in Prajavani, Dr. Robert Koch has
identified the causative agent of TB and the birth day of him is 24-3-1882 and in honour
of him every year 24th March will be celebrated as World tuberculosis day where public
awarenwss camps are organized throughout the world.. Every year 8.0 million people are
added to the TB list in this world and 30 million people are dying of TB every year in the
world. In India, 5 lakh people are dying of TB every year i.e., one person is dying of TB
every minute. There are more than one crore people suffering from TB in India.
Culturing: Can be cultured in either Dorsett's egg medium or Petragnani's medium or
Lowenstein-Jensen medium. The medium contains:
1. Basic dyes like Malachite green, crystal violet which will inhibit the growth of
Gram positive bacteria.
2. Glycerine which prevents drying and promotes growth.
3. Serum, egg or potato extract which supplies nutrients and neutralizes the toxic
effect of long chain fatty acids.
Incubate the suspected material in the medium for 6 weeks.

By animal inoculation the species present in the suspected material may be identified -
Guinea pig Rabbit Chicken
M. tuberculosis + + -
M. bovis + + -
M. avium - + +
b) Transmission: The source of infection is exhaled air, sputum, faeces, milk, urine,
vaginal and uterine discharges and discharges from the opened peripheral lymph nodes.
The entry of the organisms may be by inhalation or ingestion of contaminated feed

and water. The organisms can survive for 18 days in stagnant drinking water and for 6-8
weeks in faeces. It can be transmitted through coitus or A.I.
In calves, the infection can be due to:
1. Ingestion of milk from the affected cows.
2. Intra-uterine transmission from the affected cow to the developing foetus. This
route is strongly suspected since very young calves without showing much of the
clinical signs die suddenly and at autopsy had very well developed tubercles in
various organs especially liver.
Pathogenesis: There are two stages in the body:

i. Primary complex - In the primary complex the portal of entry and the regional lymph
nodes are affected and the lesions are seen. If the entry is through inhalation, these
types of lesions are seen in the lungs. If the portal of entry is through ingestion, this
type of lesion is seen in g. i. tract (but not in cattle).
ii. Post primry dissemination - Here the organisms from the primary complex can get
into the blood directly or through the lymphatics. Then through the circulation the
organisms go to various tissues and organs. Here commonly miliary tubercles are
produced. .Also nodular tubercles can be formed.
Tissue reaction:
In the beginning congestion, oedema and infiltration of neutrophils occur around
the organisms. The neutrophils can phagocytize the organisms but cannot kill the
organisms. After some time these neutrophils will die. Then there will be infiltration of
mono-nuclear cells especially macrophages will occur. For 8-10 days, these macrophages
phagocytize the organisms but cannot kill the organisms, which may be due to non-fusion
of phagosome with lysosome. After 8-10 days the tempo of events increases and the
macrophages may get the power of killing the organisms. The syncytia formation occur
leading to the formation of epithelioid cells. Epithelioid cells may fuse together to form
giant cells. The commonly seen giant cell is the Langhan’s giant cell i.e., the cell having
many nuclei at the periphery. Surrounding these cells will be monocytes and then
lymphocytes. Finally, fibroblasts develop around these forming the capsule. This is
nothing but typical chronic granulomatous inflammation resulting in tubercle formation.
The lesion in TB is a classical tubercle. The tubercles can be of two types viz,
(l) Nodular tubercle which will be greyish white in colour and bigger in size.
(2) Miliary tubercle which is small in size and appear like a millet seed. This is
commonly seen in generalized TB.
Even though the tubercle bacilli do not produce the toxin, toxaemia is seen. This
may be due to the destruction of the tissues and the products of cellular destruction
getting absorbed into the blood. Thus chronic toxaemia may be responsible for the going
down in condition.
The nodules conglomerate on the pleura or peritoneum and appear like bunch of
grapes or a chain of pearls. Hence the term 'Pearl's disease' is used in TB in cattle. This is
the pathognomonic lesion of tuberculosis in cattle.
Two types of pleuricy are produced in TB -

a) Dry pleuricy - here the accumulation of exudate in the thoracic cavity is scanty.
This is seen in cattle.
b) Wet pleuricy - here the exudate accumulated in the thoracic cavity is more. This is
seen in dogs.
Clinical findings:
Cattle: Capricious appetite and fluctuating temperature. Coughing is not loud and is not
paroxysmal. Coughing will be once or twice at a time and it is slow, suppressed and
moist. It can be easily stimulated by squeezing the pharynx. In advanced stages, when too
much of lungs are affected, increase in rate and depth of respiration and dyspnoea is seen.
Then due to enlargement of lymph node and its pressure on the different organs, the
following can be seen. :
1. Bronchial lymph node - dyspnoea
2. Mediastinal lymph node - persistent and recurrent tympany
3. Retropharyngeal lymph node - dysphagia and noisy breathing.
The submaxillary, prescapular, precrural and supramammary lymph nodes can be
enlarged.
Tuberculous metritis can result in interferance with conception or abortion in late
gestation or if the calf is alive after birth, it will die and generalized TB lesions will be
seen.
Tuberculous mastitis can occur and for the details refer the topic on mastitis.
Orchitis in males will be characterized by large indurated, painless testicles.
There will be progressive loss of weight leading to severe emaciation at the
terminal stages.
Sheep and Goats: Symptoms of broncho-pneumonia are seen.
Pigs: Commonly pharyngeal and cervical lymph nodes are affected. Some times
generalized form can also occur and involvement of meninges and joints can occur.
Horses: Cervical vertebrae are affected with painful osteomyelitis. Here stiffness of neck
occurs which will be painful, so that the animal may not stretch its neck downwards
resulting in inability of the animal to ingest feed and water. Less common signs includes
coughing, enlargement of lymph nodes, nasal discharge and fluctuating temperature.
Dogs and cats: Loss of weight, intermittent fever, coughing, dyspnoea, pneumothorax,
ascites and palpable masses in the abdomen. Chronic ulceration of the skin can occur in
dogs, but most commonly seen in cats.
Necropsy findings:
Cattle: Nodular or miliary tubercles in lungs, pleura, liver, peritoneum, kidney, lymph
nodes and osteomyelitis of ribs, vertebrae and flat bones of pelvis. Bunch of grapes like
lesions on the pleura and peritoneum. Histopathologically all the changes of the classical
tubercle is seen.
Buffaloes: Similar to cattle but calcification is uncommon.
Horses: The lesions appear like sarcoma and rarely caseation or calcification is seen.
Primary complex is in the alimentary canal.
Sheep and goat: Very similar to cattle.
Pigs: Can be localized or generalized. Primary complex is alimentary or respiratory tract.
Cats: Primary complex is alimentary tract. Susceptible to bovine type but resistant to
human type.
Dogs: Wet pleuricy with lot of milky exudate in thoracic cavity. Giant cells, caseation
and calcification are not commonly seen. Firm beige or white nodules are scattered over
the visceral and parietal pleura. Instead of caseation necrosis, liquefactive necrosis occurs
that is why exudate is milky.
Diagnosis:
1. By clinical signs of fluctuating fever, chronic cough not responding to commonly
used antibiotics, going down in condition, emaciation etc. is suggestive of TB.
2. By lesions and histopathology - Tubercles in various organs and histo-
pathologically presence of chronic granulomatous inflammation with acid fast
bacilli.
3. Isolation and identification of the causative agent: Collect the samples like
sputum, nasal discharge, urine, faeces, oesophago-pharyngeal fluid, liver and
biopsy material like lymph node, liver and exudate from thorax and abdomen of
suspected animal and make smears and do AF staining and also do isolation of the
organisms after culturing of these materials.
4. X-ray of thorax and abdomen of dogs and cats.
5. Serological tests: CFT, FAT, Precipitation, HAT, HIT and ELISA have been used
for the diagnosis of TB. Latex agglutination test has been used for the diagnosis of
TB with much success.
6. CMI tests: (a) Allergic test: Here tuberculin test is done. Tuberculin is an antigen
extracted from the tubercle bacilli. There are 4 types of tuberculin test:
A. Single intradermal tuberculin test:
Procedure: In India this test is commonly done in the neck region and in many other
countries it is done in the caudal fold i.e., below the anus. The procedure followed in
India is as follows:
1. Shave a small area in the neck of cattle.
2. Measure the thickness of the skin fold by using a Vernier’s calipers which will be
the initial reading.
3. By using the tuberculin syringe and needle inject 0.1 ml of tuberculin
i/d which is indicated by a small pea like swelling.
4. After 48-72 hours examine the site of injection and again measure the thickness
of the skin fold which will be final reading.
Interpretation:
Positive: The site is erythematous, oedematous, warm to touch and painful upon
palpation and the skin fold thickness is increased by 3 mm and above.
Negative: The above changes are negligible or absent.
Example:
Positive Negative
Final reading 12 mm 8 mm
Initial reading 4 mm 5 mm
Difference 8 mm 3 mm
Mechanism: Tuberculin positive: The lipid and protein present in the antigen will
initially attract few neutrophils and these will die and also the skin reactive factor causes
erythema and oedema. Later on large number of MN cells will be attracted to the site.
The monocyte or macrophage will phagocytize antigen and modulates it and present it to
the sensitized T- lymphocytes which will produce various lymphokines like -
(1) Macrophage chaemotactic factor (MCF) which attracts more number of macrophages
to the site; (2) Macrophage aggregating factor (MAF) which will aggregate the
macrophages at the site; and (3) Macrophage migration inhibition factor (MIF) which
will inhibit the macrophages going away from the site. Because of these changes
thickening of the skin occurs and the swelling will be hard.
Tuberculin Negative: In an animal not sufferring from TB the sensitized T-lymphocytes
are absent. Hence the above reaction will not occur.
False positive reaction to tuberculin test:
It means that even though the animal is not suffering from TB it will give positive
reaction to tuberculin test. It may be due to:
(1) Presence of saprophytic or non-pathogenic Mycobacterium in the body.
(2) Infection due to Mycobacterium avium, M. paratuberculosis and Nocaradia
farcinicus.
False negative reaction to tuberculin test:
This means that even though the animal is suffering from tuberculosis, it will be
negative to tuberculin test. .
This may be seen in:
1) Initial stages of TB i.e., first 6 weeks after the exposure to the bacilli.
2) Advanced cases of tuberculosis.
3) Cows from the act of parturition to 6 weeks after parturition. Here the stress of
parturition releases corticosteroids which are immunosuppressive.
4) Aged cattle.
5) Hydatid cyst, sarcoidosis, Hodgkin's disease, Uraemia and lymphoma.
6) Administration of corticosteroids.
7) Repeated tuberculin testing at 30-60 days interval.
Such animals are called 'Anergic' animals and the population of such animals is
about 4-5%. The mechanism of anergy is not clearly understood. It may be due to:
1) Compartmentalization of the reactive cells - here the sentitized T-lymphocytes might
have gone out of the blood into the spleen and lymph nodes.
2) Presence of suppressor cells which will suppress the immune response.
3) Presence of humoral suppressor factors.
(ii) Double intradermal tuberculin test:
Here the procedure, interpretation and mechanism is similar to single
intradermal tuberculin test. But the tuberculin is injected twice at an interval of one
week at the same site and the results are recorded 24 hours after the second injection.
(iii) Subcutaneous tuberculin test (Short thermal test):
Here record the temperature of the animal first and then inject 4 ml of
tuberculin s/c. Then record the temperature after 4, 6 and 8 hours. If the temperature is
increased by 2°F and above, then it is considered as positive.
(iv) Intravenous tuberculin test:
Record the temperature of the animal and inject 1 ml of tuberculin
intravenously. Then record the temperature at 4 hours interval for 3-4 times. If the
temperature is increased by 1.7°C or above, then it is considered as positive,
(v) Comparative tuberculin test:
This test is used in doubtful cases.
Procedure: Technique, mechanism and interpretation is almost similar to single
intradermal tuberculin test. However, avian and mammalian tuberculins are injected at
two different sites in the neck one below the other at a distance of 12 cms simultaneously.
The results were recorded after 48-72 hours.
Interpretation: If the reaction to mammalian tuberculin is greater than avian tuberculin,
then the suspected animal is suffering from Mycobacterium bovis or M. tuberculosis. If
the reaction to avian tuberculin is greater than mammalian tuberculin, then the suspected
animal is not suffering from tuberculosis and this reaction may be due to Mvcobacterium
avium or M. para tuberculosis. This test is used to overcome the false positive reaction to
tuberculin test in cattle.
Site of testing for intradermal tuberculin test:

Cattle and buffaloes - Neck or caudal fold
Pigs - Base of the ear
Poultry - Wattle
Dogs - Tuberculin will not give very good results. Hence, 0.1 - 0.2 ml of BCG is
administered intradermally and the results are recorded after 48-72 hours. BCG is not
useful in cats.
Human beings - The single i/d tuberculin test is also known as Mantoux test. Now it is
known as Heaf test. Here the diameter of the erythema is measured by using a scale. If
this test is positive, it may be due to tuberculosis or BCG vaccination.
b) Lymphocyte stimulation test: appears to give very good results but is expensive. Here
stimulation index of 3 and above is considered as positive to TB.
c) Macrophage migration inhibition test is used but not commonly for the diagnosis of
TB.
a) Cough: Pneumonia of many types like bacterial, viral, parasitic and aspiratory etc.
occur in domestic animals Bacterial pneumonia - Similar to TB signs. Best way is to treat
pneumonia by using sulphadimidine and sulpha-trimethoprim combinations. If the animal
responds to treatment, then it will not be having tuberculosis.
Parasitic/verminous pneumonia - it can be differentiated by: (1) Faecal examination
reveals the presence of ova or larvae of lung worms and (2) Responds to treatment with
Levamisole and the above two facts are absent in TB.
Aspiratory pneumonia - In this condition there will be a history of wrong drenching and
the animal may die in 7-10 days.
CBPP - Responds to treatment with tylosin. Can be confirmed with CFT.
b) Involvement of lymph nodes:

i) Retropharyngeal lymph node - when it is swollen it exerts pressure on the larynx and
causes stertorous breathing sounds. Hence this condition should be differentiated from
nasal schistosomiasis and rhinosporidiosis by examining the nasal cavity and nasal
discharge/scrapings for the presence of either boomrang shaped ova or double walled
spores respectively.
ii) Lymph nodes of throat - It should be differentiated from:
a) Actinobacillosis - pus is collected from lymph nodes and the sulphur granule is
examined for the presence of Gram negative, morse - code appearing organisms.
b) Theileriosis - blood smear examination reveals the presence of theilerial organisms
inside the RBCs.
c) Bovine leukaemia - persistant leukocytosis and DLC reveals lymphocytosis.
The best way to differentiate TB from the above conditions is by tuberculin test.
Treatment: Treatment in domestic animals is usually not undertaken because:

1. The suffering animal will be a source of infection to human beings and other
domestic animals.
2. The cost of treatment is very high since it involves large dose of drugs and that too
it will be for a prolonged period of time. In addition, the treatment will be
effective in some animals and may not be effective in some animals.
The following drugs have been used for the treatment of tuberculosis in human beings:
1. Para-amino-salicylic-acid (PASA): This drug competes with PABA (Para-amino-
benzoic-acid) required for the synthesis of folic acid. Thus cell wall synthesis is
inhibited.
Dose: 5-6 g Bid.
2. Isoniazid: It inhibits mycolic acid synthesis there by cell wall synthesis is
inhibited. It is available as Isonex tabs (Pfizer). Dose: 25 mg/kg body weight,
orally for 60 days. Then once in two days for 60 times.
3. Streptomycin: It inhibits the synthesis of polypeptide by m RNA. Dose: 0.75-1.00
g, i/m once a day for 60-120 days.
4. Combination of PASA, isoniazid and Streptomycin has been commonly used.
5. Rifamycin - available as Arzide - 450 mg capsule. Rifampin - available as Coccid
- 150, 450 mg capsules. Both inhibit the DNA dependant RNA polymerase
resulting in decreased nucleic acid synthesis. Dose: 10-25 mg/kg or 600 mg/day
or 1 capsule/day, orally. Rifamycin and isoniazid combination is also used.
6. Ethambutol - available as Bacibutol, Biddlebutol, Ethambi, Combutol as tablets of
400 or 800 mg.
7. Pyrizinamide - available as Coxamide tablets of 500 mg. Dose: 20-40 mg/kg, in 2
to 3 divided doses.
Only in exceptional cases like animals of high pedigree, treatment of such animals
is being undertaken. Otherwise the animals affected with TB will be euthanised.

1. Screen the herd by tuberculin testing and dispose off the positive cases.
2. BCG vaccine - Calmette and Guerin developed this vaccine by growing bovine
tubercle bacilli in potato glycerine like cultures and sub-cultured several hundred
times to attenuate the bacilli. Hence, Bacille calmette and Guerin vaccine is an
attenuated vaccine.
Dose: 50-100 ml, s/c, and repeated annually.
In India BCG has been used regularly on the day birth in babies for a long time.
However, recent field trials in Malawi and India (Tamil Nadu) by the WHO indicated
that BCG vaccine is not protective against tuberculosis in human beings. This created lot
of arguments on this aspect and was withdrawn for a short period. Again the practice of
vaccinating the babies has been introduced in our country.
b) AVIAN TUBERCULOSIS
It is a contagious disease of poultry caused by Mycobacterium avium and

characterized by chronicity, persistence in a flock once established, unthriftiness,
decreased egg production and death.
Etiology:
Mycobacteritim avium- There are 3 serotypes namely Mycobacterium avium
serotypes 1, 2, 3 affecting the birds. The organisms are bacillary with rounded ends, they
measure about 1-3 um in length. They are Acidfast organisms. Eventhough they are
aerobic their growth is enhanced under 5-10% of CO2. They require glycerine for their
growth. They have to be incubated for 3-4 weeks in incubators i.e., the suspected material
in the media has to be cultured for 3-4 weeks for best growth.
The organisms are resistant to environmental condition and survive for a long
time.
Epidemiology:
a) Occurrence: World wide. The birds affected are domestic fowls, ducks, geese,
peacocks, pigeons, sparrows, wood pigeon, black bird, owl etc.
It is not a common disease in turkeys.
In 1968 in USA 16 crores of birds were examined and out of which 2 lakhs birds
had T.B.
b) Transmission: The source of infection is the faeces of bird suffering from T.B.
Hence the mode of transmission is by ingestion of contaminated feed and water.
Route of entry of organism through inhalation is very rare or absent. It is also
transmitted on attenders feet, clothes and hands or on crates, equipments and
implements. Transovarian transmission may or may not occur.
Pathogenesis: Upon ingestion organisms get into the intestine and then in to the
mesenteric lymph node setting up of chronic granulomatous inflammation. This is the
primary foci. Then the organism through the lymph enters the blood and through
circulation disseminated in various organs.
Commonly the liver and bones are involved. Less commonly the organs like
spleen, kidney, serous membranes, genital system and CNS are involved. In all these
places, 2 types of tubercles are formed i.e., miliary and nodular.
Here the characteristic difference is the absence of calcification. One of the
important causes of death is rupturing of the nodules in the liver or spleen resulting in
internal bleeding and death.
The nodular lesions usually affect all the layers of intestine and they ulcerate
leading to discharging of the organisms in to the intestinal contents. Hence the faeces
contain good number of organisms and will be a constant source of infection.
Clinical findings: Emaciation, going down in condition, loss of weight, and the keel
bone becomes prominent because of the atropy of the muscles, covering the breast bone.
The combs become pale and shrunkened, diarrhoea, and decreased egg production. One
of the important sign is lameness of one leg resulting in "hopping" because of the
movement of bones and joints.
Necrpopsy findings: Refer to pathogenesis, nodules and millet seed like lesions are seen
in various organs. The nodules will be elavated from the surface of the organ.
Diagnosis:
1) By clinical signs
2) By lesions
3) By acid fast staining technique
Live bird-faeces
Carcasse- material from the lesions
4) Culturing
5) Tuberculin testing: Single 1/d tuberculin test is performed in one of the wattles.
According to O. Thoen 0.03-0.05 ml (0.03-0.0l ml) avian tuberculin is injected by using
25-26 gauge needle i/d in to one of the wattles. After 48 hours the wattle is examined. If
there is hot, soft and doughy swelling of the wattle is present then it is considered as
positive. In some birds the swelling may be pronounced where the size of the wattle will
be 1-5 times that of the normal wattle. Swelling is due to oedema. The swelling gradually
subsides and disappears within 5 days.
6. Serological tests
i. Rapid whole blood AT is better than tuberculin test but false positive reactions can
occur. This test is done by mixing a drop of blood with a drop of antigen and
looking for clumps/granules i.e., Agglutination
ii. ELISA
Treatment: The affected birds are not treated and they will be culled.
1. Good hygienic measure is very important.
2. Testing and elimination of the reactors and if necessary culling the entire flock and
keep the pen idle for 6 months.
3. Vaccination: Live young M. avium serotype-6, administered orally to chickens,
gave 70% protection.
16. PARATUBERCULOSIS
(Johne's Disease)
It is an infectious disease mainly of cattle and also of sheep and goats, caused by
Mycobacterium paratuberculosis and is characterized by progressive emaciation of all
species affected and chronic diarrhoea and thickening and corrugation of the intestine in
cattle.
Etiology: It is caused by Mycobacterium paratuberculosis. It is a short thick rod

measuring about 1-2µ in length x 0.5 µ in diameter. They may appear singly or in
clumps. They are acid fast; aerobic and grows at a temperature of 37°C. They can be
cultured in Dorsett's egg medium containing the extract of other acid fast bacilli called
Mycobacterium phlei. This extract is an aluminum complex and is known as Mycobactin.
The cultures should be incubated for 4 weeks.
There are three strains. One is from bovine origin and the other 2 is from ovine
origin. All these three strains can cause disease in cattle.
The organisms are susceptible to 10-20% chlorinated lime, 5% formalin, 5% Lysol
and 5% caustic soda or potash.
The organisms persists in the contaminated soil for one year. Soil pH plays an
important role. Animals reared on alkaline soils will have high incidence but with little
clinical manifestations. Animals reared on acid soil will have very severe form of the
disease.
Epidemiology:
a) Occurrence: Johne's disease occurs through out the world. It is usually a sporadic
disease, but sometimes outbreaks can occur. Since it is a chronic disease resulting in
progressive emaciation and not responding to treatment, it causes economic losses in the
form of decrease in production.
The animals affected are - mainly cattle, and followed by buffaloes, sheep, goat,
camel, Llamas, yaks, deers, reindeers and antelopes. Usually young ones are highly
susceptible and they pick up the infection. But when they become 2 years and above of
age, they exhibit the clinical manifestations of the disease.
Morbidity rate is very difficult to assess. Annual mortality rate can be 10%. Certain
stress factors like the act of parturition, transportation and nutritional deficiencies can
trigger the onset of the disease.
b) Transmission:
1. Ingestion of contaminated feed and water. The main source of infection is the faeces
of suffering animal and also from animals 15-18 months before showing clinical
manifestations of the disease.
2. Intra-uterine transmission - from dam to the foetus.
3. Milk from affected cows also may be a source of infection to the calves.
Eventhough the organisms have been isolated from the semen, the significance is not
clearly understood.
Pathogenesis: After ingestion, the organisms go to the intestine and at first the posterior
part of the intestine and their mesenteric lymph nodes are affected. These organisms can
be disseminated to other parts of intestine. In very advanced cases the entire intestine can
be affected.
The organisms enter the mucosa and sub-mucosa of the intestine. This will attract
lot of mononuclear cells. The macrophages fuse to form epithelioid cell. This results in
syncytia formation and stops at symplasma stage. There is no caseation, calcification and
encapsulation in cattle. But in sheep, caseation is commonly seen and calcification is
seen in 25% of the cases. Because of the massive infiltration of macrophages in mucosa
and submucosa, thickening occurs and mucosa is thrown in the form of folds resulting in
corrugations resembling that of brain. This is the pathognomonic lesion.
Because of these changes, the food is not digested and absorbed properly. And the
motility of the intestine is increased. This results in diarrhoea. Because of malabsorption,
the body reserves are utilized. Since it is a chronic disease, the animal becomes
emaciated and the rib cage will be very prominent. Serous atrophy of fat occurs.
Clinical findings: Chronic diarrhoea which is not responding to the commonly used
antibiotics is the most important clinical sign. Diarrhoea may be continuous or
intermittent. The faeces are of the consistency of thick pea soup and without foul smell.
The excessive mucous, shreds of epithelium, blood/blood clots are absent. Animal may
show slight improvement in the consistency of the faeces which may be of normal in
advanced gestation. Immediately after parturition diarrhoea will start. Bottle jaw,
progressive emaciation, weakness, dehydration and finally prominent rib cage with
marked sunken eye balls will be seen and then death.
In sheep and goat, progressive emaciation and shedding of wool are seen.
Diarrhoea is not severe.
Necropsy findings: The carcass is emaciated. The s/c fat, mesenteric and coronary fat
are absent. The cavities may contain slight excessive quantities of serous fluid. Serous
atrophy of fat occurs in the coronary grooves. Upon opening of the intestines, the mucosa
of the intestine is thickened 3-4 times and there will be corrugations on the mucosa. Most
commonly these are seen on the ileo-caecal valve and can be seen on ileum, caecum and
colon and in advanced stages from duodenum to rectum. The mesenteric and ileo-caecal
lymph nodes are enlarged and oedematous. No lesions in the foetus.
In sheep, the intestines are thickened but corrugations may not be seen. Caseation
is commonly seen and calcification is seen in 25% of the cases.
Histopathology: Similar to pathogenesis. In addition, arteriosclerosis of the intestinal

vessels in advanced cases can be seen.
Diagnosis:
1. By clinical signs like chronic diarrhoea not responding to treatment and prominent
rib cage.
2. Isolation and identification of the causative agent: Each and every method
employed for the isolation of the causative agent is having one or the other draw back.
a) The faeces is collected and processed according to the centrifugation method. A
small quantity of the sediment is placed on a glass slide and a thick smear is made.
Air dried and fixed by heat. Then acid fast staining is done and examined under the
oil-immersion lens. If pink or red coloured organisms are found in singles or clumps
then it is positive for Johne’s disease.
After centrifugation method, add 5 or 10% sodium or potassium hydroxide
solution to the sediment and mix the contents and allow to stand for 24 hours. Then
centrifuge it, make a smear and do acid fast staining.
Draw back: Since the organisms passed in the faeces is few in number, chances of
missing are there.
b) Rectal pinch method: Hold the blunt end of the scalpel in your hand and insert the
hand in the rectum as deep as possible and then scrape the rectal mucosa. Then
withdraw the hand in such a way that the scalpel will not touch the rectum. Make a
smear and do acid fast staining.
Draw back: About 25% of the suffering animals will not have lesions in the rectum
and chances of demonstration of the organisms is less.
c) The faeces and rectal scrapings can be submitted for culturing of the organisms.
3. By lesions: Presence of corrugations on the mucosa of the intestines is a
pathognomonic lesion of Johne’s disease. Sometimes, in the initial stages of the disease,
such lesion may not be seen. In such conditions, the intestine should be submitted for
histopathology and detection of symplasma and also doing acid fast staining on sections
to demonstrate the presence of acid fast organisms.
4. Serological tests: CFT is commonly used and will detect 90% of the cases. Non-
clinical carriers and early stages of the disease will not be detected.
FAT can be done, but it is very difficult to differentiate M. paratuberculosis from
M. avium as these organisms are antigenically related.
AGPT also can be used.
ELISA has been used recently and found to be good.
5. CMI tests:
Johnin test: Johnin is the antigen of M. paratuberculosis and has been used from a long
time for the diagnosis of Johne’s disease. The following types of Johnin tests have been
used:
a) Single intradermal johnin test: The procedure and interpretation of this test is very
similar to tuberculin test. Increase in skin fold thickness by 3 mm or above will be
considered as positive.
b) Double intra-dermal johnin test: It is almost similar to double intra-dermal
tuberculin test, but the second injection of johnin is made 48 hours after the first
injection.
c) Intravenous johnin test: Record the temperature of the animal and inject 4 ml of
johnin intra-venously. Again record the temperature after 3, 4.5, 6 and 7.5 hours after
injection. If the temperature is increased by 1.5° F and above, it will be considered as
positive.
In India the single intra-dermal johnin test and in U.S.A. the intravenous johnin
test is commonly used for the diagnosis of Johne’s disease.
Differential Diagnosis: Since diarrhoea is the most common clinical sign of Johne's
disease, it should be differentiated from the following diseases:
1. Salmonellosis: Here diarrhoea is present with watery and foul smelling faeces
containing excessive amount of mucous, mucosal shreds. Dysentery and fever are
also present. These things are absent in Johne's disease,
2. Amphistomiasis: Diarrhoea with foul smelling faeces containing shreds of
mucosa, sometimes blood clots and even the immature flukes which are absent in
Johne's disease. Presence of characterisitc ova during the faecal examination will
differentiate amphistomiasis from Johne's disease.
3. Parasitic diarrhoea: Presence of characteristic ova of various nematodes will
differentiate parasitic diarrhoea from Johne's disease.
4. Fascioliasis: is characterized by alternating diarrhoea with constipation. It can be
differentiated from Johne's disease by faecal examination and detecting the
characteristic ova of Fasciola sp.
5. Coccidiosis: is characterized by diarrhoea, dysentery and anaemia. It can be
differentiated from Johne's disease by faecal examination and demonstrating the
presence of characteristic oocysts.
Treatment: Usually the treatment of animals suffering from Johne's disease is not
undertaken and such animals will be culled.
Recently, animals suffering from Johne's disease were treated with streptomycin
and isoniazid. The severity of this condition in these animals was reduced but the
organisms were demonstrated upon culturing even after treatment.

Good measures are not available for the control of Johne's disease. However, the
following methods can be adopted:
1. Testing the herd with johnin test and culturing and disposing of the positive cases.
Repeated testing, 2-3 times at an interval of 6 months will be useful. This method
is being adopted in advanced countries, wherein compensation is being paid to the
owners for disposing of the positive cases. Such measures in developing countries
will be very difficult because of economy.
2. Test the herd and isolate the reactors so that two groups will be formed i.e.,
infected and non-infected groups. Immediately after the birth of a calf from
infected cow, it is removed and reared in the healthy group. How far it is useful is
questionable as congenital transmission has been recorded.
3. Vaccination:
a) Vallee's vaccine: It is a live non-attenuated vaccine prepared by mixing live M.
paratuberculosis organisms with oil of paraffin and powdered pumice stone. This
is injected s/c and resulted in the formation of a granuloma. Hence organisms
were supposed to be present for a long time and giving protection for a long tune.
b) Latest vaccine: In 1982, a vaccine containing live attenuated organisms along
with oil of paraffin and pumice stone were used on a large scale and appears to be
successful.
c) Sigurdsson's vaccine: It is a old vaccine and contains killed organisms.
These vaccines will raise the reactivity of the animal to tuberculin test by 8
times than that of the normal cattle. Thus it will be coming in the way of control
of tuberculosis. So vaccination against Johne's disease is not commonly used
where TB eradication programme is being launched.
17. SALMONELLOSIS
a) Salmonellosis of domestic animals
(Paratyphoid)
It is an infectious disease of all domestic animals caused by various species of

salmonellae and is characterized by 3 major syndromes viz., peracute septicaemia, acute
enteritis and chronic enteritis.
Etiology: About 2200 serotypes of Salmonellae have been recorded throughout the
world. Common species are:
Cattle: (1) Salmonella typhimurium - Commonly affects calves under 6 months of age
and recovered calves will not act as carriers.
(2) S. dublin - affects both calves and adults equally. The recovered animals will
become carriers and will be a source of infection to other animals.
(3) S. newport etc.
Sheep: S. typhimurium, S. dublin and S. anatum
Pigs: S. choleraesuis and S. typhimurium.
Horse: S. typhimurium causes acute enteric form and will be very severe. Other serotypes
are S. anatum, S. newport, S. enteritidis, S. heidelberg, S. arizona and S. angona.
These are Gram negative rods and measure about 3-4 µ x 0.6 µ. These are usually
motile, non-spore forming and non-lactose fermenters. For the isolation of Salmonellae
concentration procedures are used by culturing in selenite brilliant green broth and
McConkey's medium.
Epidemiology:
a) Occurrence: World wide affecting almost all the species of domestic animals.
Young animals are more susceptible when compared to adults. Morbidity rate in pigs,
sheep and calves is usually high often reaching 50% or more. But in adults (cattle),
sporadic cases have been recorded. Mortality rate can reach 100%. Certain
predisposing factors precipitate the onset of this disease. They are starvation,
exhaustion during transport, recent parturition and inter-current infection.
It causes severe economic losses and is one of the most important diseases of
domestic animals.
It is a disease of zoonotic importance and the source of infection to human beings
is contamination of drinking water, ingestion of contaminated milk and meat. Pork
sausages, eggs and egg products and dried milk are the important source of infection.
b) Transmission: Salmonellae are spread by direct (infected animals), or indirect
(Environment, primarily feed and water supplies) means. Commonly by ingestion of
contaminated feed and water. The source of infection is the faeces which contaminate
the water, feed and pasture. These faeces may be from suffering animals, carriers and
other domestic animals. Another important source of infection is the contaminated
bone meal. This may be due to contamination of rendering plant leading to
contamination of bones and then preparing the bone meal from such bones and adding
it to the feed. Air-borne transmission of S. typhimurium can occur.
Pathogenesis: Upon ingestion, the organisms either through the pharynx or intestines
will go to the lymph nodes and multiply. Through the lymphatics, they get into the blood
causing bacteraemia and septicaemia. After a short period, they localize in various organs
like intestines, liver, spleen, mesenteric lymph nodes, gall bladder and joints. In pigs,
they can localize in lungs and meninges.
In the intestine, they cause acute haemorrhagic enteritis characterized by
congeston, oedema, sloughing of mucosa and haemorrhages. The intestinal contents will
be mixed with mucosal shreds, excessive mucous, blood or blood clots.
Diarrhoea results in:
1. Severe dehydration leading to marked haemoconcentration which results in hypo-
volaemic shock.
2. Loss of HCO3 ions from the Mood into the intestine will result in decrease in
blood HCO3 level and blood pH which is nothing but metabolic acidosis.
3. Loss of K ions from the blood into the intestine will result in hypokalaemia which
may end in heart failure and death.
All the above change will results in death of the animal.
Clinical signs:
1. Septicaemic form: Seen in calves, foals, piglets, lambs and kids from the day of
birth to 4 months of age. High fever (105 - I07°F), depression, weakness, anorexia
and death within 24-48 hours. In young pigs and calves CNS signs like
incoordination, nystagmus, tremors and paralysis can be seen where in 100%
mortality can occur.
2. Acute enteric form: Commonly seen in adult animals of all species. Mortality
rate can be 75% or more. High fever (104-106°F) depression, weakness, anorexia,
atony of rumen marked decrease in milk production. Later on watery diarrhoea which
is foul smelling and then dysentery where the faeces may contain blood clots or
blood, excessive mucous and mucosal shreds. As the condition worsens, marked
dehydration indicated by sunken eye balls, red mucous membrane, loss of elasticity of
the skin, increase in heart and respiratory rates will be seen. Clinical signs of colic
like frequent getting up and lying down, kicking at the abdomen, restlessness,
groaning and rolling and looking at the flank are seen. The course of the disease is 2-5
days.
A sequal to this form is the development of dry gangrene of the extremities
including ear tips, tail tip, and the limbs from the fet lock down.
3. Sub acute enteritis: Mild fever, anorexia and slight diarrhoea are seen.
4. Chronic enteric form: Commonly seen in pigs and the symptoms exhibited are
persistent diarrhoea, severe emaciation and intermittent fever.
Pregnant animals can abort.
Necropsy findings:
Septicaemic form : Petechial haemorrhages on the serosa, mucosa and endocardium.
Acute enteric form: Acute haemorrhagic enteritis.
Chronic form: Button like ulcers in the caecum and ileo caecal valve is a very
characteristic finding.
.
Diagnosis:
1. By clinical signs like, fever, diarrhoea and dysentery.
2. Isolation of the causative agents: Since the organisms are not excreted in the faeces for
two weeks after the commencement of the clinical signs, culturing of the faeces may be
negative. Hence, the faeces from the neighboring animals irrespective of species of
animal and from recovered animals should be submitted for culturing. The materials to be
submitted from carcasse are - heartblood, spleen, liver, bile, mesenteric lymph nodes and
intestinal contents.
Usually, gall bladder will have Salmonella and hence the contents of the gall bladder
and thick impression smears from the wall of the gall bladder must and should be
submitted. It should be remembered that the source of Salmonella in the faeces of carrier
and suffering animals is from the gall bladder. Drinking water and feed for culturing
should be undertaken.
3. Serlological tests: Indirect HAT, tube agglutination test, Coomb's test and FAT have
been used for the diagnosis of salmonellosis.
Differential Diagnosis: Since diarrhoea and dysentery are commonly seen in
salmonollosis, the following diseases should be differentiated:
a) Coccidiosis: In this disease the fever is absent and it can be confirmed by
demonstrating the oocysts in the faeces.
b) Calf scours: In this disease the faeces is chalky white and dysentery is not
commonly seen.
c) Rinderpest: In this disease the oral lesions are present, and this is absent in
salmonellosis.
d) Bovine virus diarrhoea: Oral lesions are present.
e) Arsenic poisoning: In this poisoning diarrhoea and dysentery are present but the
fever is absent.
f) Johne's disease: This disease is characterized by chronic diarrhoea which is not
responding to treatment. The faeces are thick pea soup like and without mucosal
shreds, blood or blood clots. Fever is absent.
g) Amphistomiasis: Fever is absent. It can be confirmed by demonstrating the ova
during faecal examination.
Treatment:
1. To overcome the etiological agent administer the chaemotherapeutic agents to
which the organism is sensitive. Commonly chloramphenicol is administered
parenterally at the rate of 20 mg/kg body weight, at 6-12 hourly intervals and Neftin
(furazolidone) @ 20mg/kg body weight, b.i.d. for 3 days.
Other drugs which can be used are:
Sulphadimidme 130-150 mg/kg body weight, orally, i/v.
Sulpha-trimethoprim 15-30 mg/kg b.wt. bid i/m orally
Gentamicin 5 mg/kg, b. wt, bid, i/m
Enrofloxacin/Ciprofloxacin 2.5-5.0 mg/kg body weight, i/m or i/v
Treated animals can become carriers and to eliminate such condition is
difficult.
2. To overcome the dehydration and metabolic acidosis administer the following
mixture intravenously:
Sodium bicarbonate 1.13 g
Sodium chloride 0.85 g
Dextrose 5.00 g
Distilled water 100.00 ml
Dose: According to the percentage of dehydration.
3. To overcome hypokalaemia, admmister potassium chloride intravenously or orally
@ 1 g KCl (13 mEq) per liter of fluids given.
4. To soothen the gastro-intestinal tract administer the astringent mixture (Kaolin,
catechu, pectin and cretapreparata) @ 50-100 g per cow, b.i.d. or t.i.d.

2. Use good hygienic measures like:
a) Keep the barn clean.
b) Keep the animal clean.
c) Proper disposal of the excretions.
d) Disinfect the area.
3. Provide fresh and clean water ad libidum to the animals
4. Good vaccines are not available eventhough killed bacterins and live attenuated
vaccines have been used.
b) SALMONELLA INFECTIONS OF POULTRY

The following diseases are caused by various species of Salmonella :
1. Pullorum disease
2. Fowl typhoid
3. Fowl paratyphoid.
i) PULLORUM DISEASE
It is an infectious disease of poultry caused by Salmonella pullorum and it is

characterized by drooping of wings, inclination to huddle together, loss of appetite,
chalky white diarrhoea and high mortality in 2nd or 3rd week old chicks.
Etiology: Salmonella pullorum is a long slender rod and measures about 1-2.5 x 0.3-0.5
µm. It is a Gram negative, non-motile, non-spore former and facultative anerobe. It grows
well in beef extract agar or broth. It produces rapid decarboxylation of ornithine which is
most important characteristic. It produces only somatic antigens.
Epidemiology:
a) Occurrence: World wide in its occurrence and very important disease of poultry. The
birds susceptible are domestic fowls, turkeys, ducks, pigeons, guinea fowl, pheasants,
sparrows and other wild birds. Young chicks are more susceptible than adults. Maximum
mortality can occur in 2nd or 3rd week old chicks. Adults are also susceptible with or
without signs and they are carriers of this organism and mortality rate is very low.
b) Transmission:
1. Main mode of transmission is by transovarian transmission (vertical transmission i.e.,
hen to chick). The female birds have the organism in the ovary and when the eggs are
formed these organisms are transmitted to the eggs. Thus transmitted to the
offsprings.
2. In the hatchery, when such type of eggs hatch the infected young ones can spread
disease to other chicks (Lateral spread - chick to chick in hatchers).
3. Also by attendants - hands, feet, clothings.
4. By egg eating - cannibalism
3. Through the contaminated feed and water.
Pathogenesis: The organism enters the circulation and causes bacteraemia and then
localize in the various organs and tissues like liver, pericardium, heart and even pleura
and peritoneum etc. In these places there will be hyperaemia, congestion, focal
degeneration and necrosis. These are especially seen in the liver. In the adults, the ovaries
are affected. Individual ovules are misshapened, angular and attached to the body of the
ovary by stalks. The contents of the ovules are firm, cheesy, yellow or dark red and blood
stained. The ovules are shrunkened and sometimes detached in to the peritoneal cavity
leading to peritonitis.
Clinical Findings: Some chicks just after birth may not show any signs and suddenly
die. Other chicks may be depressed, loss of appetite and ends in death. Some chicks
may have inclination to huddle together, drooping of the wings and destorted body
appearance. They may also exhibit a shrill cry while passing the faeces and the faeces
will be chalky white in colour. That is why it is also known as ‘bacillary white diarrhoea’.
Chalky white faeces is not always seen and so the chicks may pass greenish brown
faeces, hence the name bacillary white diarrhoea was changed into pullorum disease as
the causative agent is Salmonella pullorum.
The adult birds may not show the clinical manifestation of the disease and
occasionally depression, anorexia, diarrhoea and dehydration are seen.
Necropsy Findings: In chicks and fowls the liver is enlarged and congested and streaked
with haemorrhages. Necrotic foci or nodules may be present in cardiac muscle, liver,
caeca, large intestine and gizzard and pericardium in some. In adults, ovaries are
shrunkened and ovules are coalesced.
Diagnosis:
1. By clinical signs- No characteristic signs but bacillary white diarrhoea and high
mortality in 2-3 weeks of age may give a clue.
2. Necropsy findings - Pathognomonic lesions are absent but lesions of the ovary in
adults may give a clue.
3. Isolation and identification of the organism - Material to be submitted - faeces in
live bird and a piece of liver, pericardium, myocardium, gizzard, pancreas, lung and
yolk sac from the carcasse. For culturing, beef infusion agar is used.
4. Serological tests - Commonly serum or whole blood Rapid Plate Agglutination
Test (RPAT) is used in fowls but not in turkeys. Whole blood RPAT - 1 drop of
whole blood + 1 drop of antigen within 1 minute clumping of the antigen into large,
well marked, purple flakes with clear interspaces is considered positive. Other tests
like tube agglutination test, micro agglutination test, haemagglutination test and
micro antiglobulin test also can be used.
Treatment: Eventhough many drugs have been used for the treatment of pullorum
disease, they are incapable of eliminating the infection from the treated flock i.e.
treatment is only effective in suppressing the multiplication of the bacteria which results
in over coming the severity of the infection and saving the life of many chicks. However,
it will not prevent the carrier state of the bird. It is well known that a bird which gets
Salmonella pullorum will never get rid of the organism, through out its life and thus it
becomes a carrier and will be a source of infection to other birds. Any one of the
following drugs can be used -
I. Sulphonamides:
1. Sulphadiazine and sulphamethazine are most effective.
2. Sulphathiazole and sulphaguanidine are intermediate.
3. Sulphasuccidine and phthalyl sulphathiazole and sulphanilamide are least efjfective.
Any one of these is administered at a concentration of 0.5% level in mash for 5-10
days from the date of birth or when clinical manifestations are seen.
II. Nitrofurans: Nitrofurazone and furazolidone at 0.04% level in mash for 10-14 days is
also very effective.
III Antibiotics:
1. Chloramphenicol - 0.5% concentration in feed for 10 days.
2. Chlortetracychne - 200 mg/kg of the ration.
3. Colistin.
Prevention and Control: Since good treatment which will not eliminate the carrier and
good vaccines are not available it is very difficult to control and eradicate the disease.
Hence, the best way is to follow the control measures -
1. Test the entire flock of the birds, especially the ones used for the breeding purpose
and eliminate the positive ones.
2. Do not use the eggs from poultry unit having pullorum disease for hatching of the
eggs or day old chicks from such farms should not be used for breeding purpose.
3. Fumigation of the incubator and the eggs with the formalin and potassium
permanganate mixture may or may not be beneficial.
ii) FOWL TYPHOID

It is a septicaemic disease of domesticated birds caused by Salmonella gallinarum
and characterized by acute or chronic syndrome with moderate to very high mortality
rate.
Etiology: It is a short plump rod, measuring 1-2 µm in length and 1.5 µm in breadth.
Occurs singly or in pairs, they are Gram negative, forms spores but not capsule and non
motile. Very difficult to differentiate from Salmonella pullorum and the most important
difference is S. pullorum decarboxylates ornithine where as S. gallinarum does not
decarboxylates ornithine.
Epidemiology:
a) Occurrence: World wide occurrence in domestic fowls, turkeys and also sometimes in
ducks, pigeons, peacock and guinea fowl.
It was first recorded in 1888 in England and was thought to be fowl cholera and
supposed to be caused by, Bacillus gallinarum. Moore in 1895 gave the term 'infectious
leucaemia and named the organism Bacillus sanguinarum. Curtice (1902) called it as
‘fowl typhoid'
Fowl typhoid is one of the common diseases of the poultry industry causing severe
economic loss. The mortality rate can vary from 4-50% or more. The mortality in
1,2,3,4,5 and 6 month old birds can be 25.6, 35.5, 24.9, 19.2, 13.8 and 2.7 per cent
respectively. The above figures indicates that high mortality occurs in one to three
months of age.
b) Transmission:
1) Transovarian transmission can occur but not very common.
2) Penetration of the egg shell by the bacterium after the eggs are laid is the most
common mode of transmission wherein when such eggs hatches in the hatchery it will
be a source of infection to other chicks. This is the most important mode of
transmission.
3) Also transmitted by attenders and by the sexing persons by carrying organism on their
hands, feet, and clothes.
4) The carcasse is the good source of organism therefore organisms can survive for
several months.
5) Dogs, cats and rats can carry part of the carcasse to the neighboring farm and spread
the disease.
6) Trucks and feed sacks are source of infection.
The organism is killed by the 1:1000 phenol, 1:20,000 Bichloride of mercury, 1%
of Potassium permanganate in 3 minutes and 2% formaline in 2 minutes.
Pathogenesis: The organism enters the circulation causing septicaemia and localizes in
various organs like liver, spleen, heart, peritoneum etc. The organism produces an
endotoxin which may be responsible for haemolytic anaemia. The exact mechanism is
not understood. It may be erythrophagocytosis.
Clinical findings: IP is 4-6 days.

Chick and fowl: Very similar to pullorum disease. Some chicks die without showing any
clinical signs and in addition laboured breathing or gasping may be seen.
Growers and adults: Acute out-breaks can occur where in sudden drop in feed
consumption, droopy, ruffled and pale combs will be noticed. Fever may be seen after 2-
3 days and will be remaining high until a few hours before death.
Necropsy Findings: The liver, kidney, spleen are swollen and red in colour. The surface
of liver after exposure to air usually shows the distinct greenish - bronze sheen and this
lesion is almost pathognomonic lesion of fowl typhoid. Greyish white foci of miliary
type nodules in the liver and myocardium is seen. Pericarditis, peritonitis, haemorrhagic,
mishapen and discoloured ova and catarrhal inflammation of intestine are seen.
Diagnosis: Similar to pullorum disease.

Sample collected from dead bird: Liver, spleen and a piece of heart and peritonial ftuid.
From live birds, serum and whole blood are used for RPAT.
Treatment: Similar to pullorum disease.

1. Sulphaquinoxalene - 0.1% in the feed.
2. Furazolidone - 0.04% in the feed for 10 days.
3. Streptomycin, chloromycetin, chlortetracycline.
Prevention and Control: Similar to pullorum disease.

1. Vaccination:
(a) Fowl typhoid vaccine (Alum precipitated) (IAH & VB): Formalinized culture of S.
gallinarum and alum precipitated vaccine is used for prophylaxis and during outbreaks
and the dose is 0.5 ml, i/m. For protection it is administered to 6 months old birds. The
container size is 250 ml.
(b) S. gallinarum vaccine (Intercare) – Nobilis strain 9R is incorporated as a live
attenuated vaccine and the dose is 0.2 ml, s/c. The first dose and the second dose is
administered at 6 weeks and 16-18 weeks of age respectively. The container size is 500
doses (Rs.2500/-).
2. Thorough cleaning of eggs in antiseptic solution immediately after they are laid is a
very good preventive measure.
iii) AVIAN PARATYPHOID
It is an infectious disease of poultry caused by various species of salmonella
excluding Salmonella pullorum and Salmonella gallinarum and characterized by
anorexia, increased thirst, diarrhoea, weakness, emaciation and tendency of the birds to
huddle together.
Etiology: More than one thousand serotypes of salmonella have been recorded and out of
which 200 serotypes have been isolated from fowl. Among these important ones are:
1. Salmonella typhimurium
2. Salmonella thompson
3. Salmonella virchow
They are Gram negative, nonspore former, and measures about l-4 µm x 0.4 - 0.6
µm. They are motile by means of peritrichous flagella. They are grown in beef extract
agar or broth and beef infusion agar or broth. They also bring about decarboxylation of
ornithine.
Epidemiology:
a) Occurrence: The distribution of Avian paratyphoid is world wide and causes severe
economic loss. Mortality rate is very high in chicks in first two weeks of their life and in
adults it is very low.
b) Transmission: Very similar to fowl typhoid.
The organisms are regularly or intermittently excreted in the faeces, because the
organisms are localized in the gastro-intestinal tract.
The litters and feeds are also contaminated.
Pathogenesis: The organisms upon ingestion go to the various parts of gastro-intestinal

tract and commonly localized in the crop and caeca. Here it causes catarrhal
inflammation and also haemorrhages. The organisms can also get in to circulation and
can localize in liver, spleen, heart and peritonium and causes inflammation. These
organisms elaborate endotoxins which is responsible for the death of the bird.
Clinical findings: Very similar to pullorum disease and fowl typhoid and very difficult
to differentiate from these diseases. The clinical signs noticed are- sudden death without
exhibiting signs in new born chicks. In others the tendency of birds to huddle together
near the source of heat is seen. The tendency of the bird to stand in one position with the
head lowered, eyes are closed, drooping of the wings and ruffling of the feathers also
seen. Marked anorexia and thirst with profuse watery diarrhoea can be seen.
In some chicks unilateral blindness and conjunctivitis can be seen. As the chicks
become 3-4 weeks and above of age clinical signs may not be seen and they become
carriers and will be source of infection to others.
Necropsy findings: Emaciation, dehydration, coagulated yolk, congested liver, spleen

with haemorrhagic streaks and pinpoint necrotic foci, congested kidney and pericarditis
with adhesions catarrhal enteritis are seen during post mortem.
Diagnosis: Serological tests like RPAT, whole blood AT, MAT, Antiglobulin test, Tube
agglutination test and CFT have been used.
Rapid whole blood AT is a good test for the diagnosis of pullorum disease and
fowl typhoid but it is not a good test for fowl paratyphoid.
Treatment: Treatment is very similar to pullorum disease i.e., sulpha drugs are
commonly used.

1. Good hygienic measures are very important.
2. Fumigation of the incubator with potassium permanganate 0.6 gm and formaline 1.2
ml/cu.ft.
3. Dipping of the eggs in antiseptic solutions like quartemary ammonium compounds,
formalin, sodium hydroxide, sodium orthophenyl phenate or dipping of eggs in
antibiotic solutions like kanamycin, neomycin, gentamicin, spectinomycin.
4. Testing and eliminating the carriers.
5. Vaccination: Bacterins and live attenuated vaccine have been used experimentally.
Heat inactivated Salmonella typhimurium vaccine have been administered orally to
day old chicks and was found to be effective.
Food poisoning or salmonella infection in Human Beings:

An estimated 2.5 million cases of human illness occur every year. About 5 lakh
cases require hospitalization and 9000 people die. This has been attributed to food
poisoning due to salmonella and out of which 39% cases occurs through the meat of
poultry.
Avian paratyphoid and Avian typhoid are the diseases of Zoonotic importance.
18. INFECTIOUS KERATITIS OF CATTLE

(Pink eye, Blight)
It is an infectious disease of cattle caused by Moraxella bovis and is characterized

by keratitis and conjunctivitis with corneal opacity and corneal ulcers.
Etiology: It is caused by Moraxella bovis. It is a Gram negative rod and measures about
1.5 - 2.0 µ x 0.5-1.0 µ. It occurs in pairs and also in short chains. It is non capsulated and
non-sporulating. When cultured in horse blood agar a zone of haemolysis occurs. The
production of the condition due to this organism only is questionable. Hence, certain
other factors are also involved, like the organism and the eye being exposed to the
sunlight.
Epidemiology:
a) Occurrence: Commonly seen in many countries during summer. Cattle and buffaloes
are affected and young ones are highly susceptible.
b) Transmission: Commonly through the face fly - Musca autumnalis.
Pathogenesis: The organisms are directly introduced into the eyes and they multiply
elaborating a 'dermonecrotic endotoxin' which damages the different parts of the eye.
Clinical findings: Incubation period can be 2-3 days to 3 weeks. Copious watery
lacrimation, blepharospasms, photophobia, injection of the corneal vessels and
congestion, oedema of the conjunctiva, slight to moderate fever, moderate anorexia and
decreased milk yield are seen.
Corneal opacity starts at the centre of the cornea and then spreads peripherally.
The colour is white to deep yellow. Later on ulcers on the cornea can be seen.
One or both the eyes can be affected and may end in recovery within 3-5 weeks
and some may become blind.
Diagnosis:
1. By clinical signs of the eyes.
2. Submitting the conjunctival swab for culturing.
Deferential Diagnosis: It should be differentiated from

1. Trauma of the eye: Visual keen observations.
2. IBR: Here the corneal opacity starts from periphery to centre.
3. Bovine malignant catarrhal fever: Not only the signs of the eyes but also signs of the
CNS and other organs also are seen.
4. Thelazia rhodesii: Worms can be demonstrated in the eye.
Treatment:
1. To overcome the etiological agent administer the antibiotics parenterally as well as
locally into the eyes. Apply eye ointments or applecaps containing OTC /
chloramphenicol / Gentamicin daily 2-3 times for a week.
2. To prevent the effect of histamine administer antihistamines like avil, chloril,
cadistin, cural parenterally.
3. Cornea! opacity/ulcer: The above treatment can be given and if it is not successful,
then administer:
(a) Combination of gentamicin or chloramphenicol 1-2 ml with dexamethasone 1-2
m!,subconjunctivally, once a day for 5-7 days.
(b) Prepalin forte - 2-6 ml, i/m, once in 3 days for 3-4 times.
© Placentrex 6-10 ml, i/m once in 3 days for 4-5 times.
(d) Milk proteins-can be given subconjunctivally or parenterally.
(e) Ulcer can be cauterized with Silver nitrate sticks.
EYE WORMS
Thelazia species which commonly affects the eyes of cattle and
buffaloes. They are transmitted by flies and is characterized by excessive
lacrimation, photophobia, conjunctivitis, keratitis, comeal ulceration and abscess on
theeyelids.
Diagnosis:
1. Movement of worms in the anterior chambers of the eye can be observed.
2. Take a plastic syringe loaded with normal saline and introduce the nozzle into
themedial canthus of the eye and push the saline with force. Collect the fluid that
iscoming out through the eye in a bowl. The eye worms can be seen in this fluid.
Treatment: Levamiso!e as 1% solution is applied as eye drops, b.i.d. for 2-3 days or
Levamisole @ 7.5 mg/kg body weight can be administered orally or parenterally as
single treatment.
19. CONTAGIOUS PLEURO PNEUMONIA

(a) CONTAGIOUS BOVINE PLEURO PNEUMONIA
(CBPP, Lunger's)
It is a specific infectious and contagious disease of cattle caused by Mycoplasma

mycoides and is characterized by bronchopneumonia and pleurisy.
Etiology: It is caused by Mycoplasma mycoides which is an organism which is in

between bacteria and virus. Previously it was known as pleuro pneumonia like organisms
(PPLO). They lack cell wall and reproduce by binary fission. It is sensitive to tylosin,
kanamycin, tetracyclines and resistant to sulphonamides and penicillins.
Epidemiology
a) Occurrence: Recorded in Eastern Europe, Asia, Africa and Iberian peninsula. It is
eradicated from USA in 1892 and from South Africa in 1916. It is recorded somewhat
commonly from North Eastern India. Recorded commonly in cattle only. Adults are more
susceptible than the young ones. Mortality can be upto 50%, morbidity can be upto 90%
and 25% remain as recovered carriers.
b) Transmission: Mainly by means of inhalation.
Pathogenesis: Upon inhalation the organisms are carried to bronchi, bronchioles and
then alveoli. Here the inflammation results in the formation of croupous membrane. Then
the organisms enter the interlobular septa and causes inflammation resulting in oedema
and accumulation of lot of fibrin. The inter-lobular septa are prominent and give a
marbled appearance and various stages of pneumonia may be seen.
Because of the distension of the inter-lobular septa the pressure on the vessels and
lymphatics leads to less supply of blood and results in necrotic changes and results in
necrotic anaemic patches. Around the patches encapsulation can occur resulting in the
formation of a sequestrum, which contains good amount of organisms, which can live
upto 3 years. Due to certain stress factors the sequestrum can break open releasing the
organisms which may result in:
1. Bronchopneumonia in the same animal.
2. Spreading the organisms to other healthy animals. Such type of animals is called as
'Lungers'.
Inflammation of the pleura resulting in deposition of lot of fibrin can occur.
Clinical findings: IP is 3-6 weeks and can be upto 6 months. High Fever (105-106°F),
anorexia, marked depression, atony of the rumen reduction in milk yield occurs. Initially,
coughing will occur upon exercise and later on can occur repeatedly with chest pain and
the animal stands with the elbows out, the back arched and the head extended.
Expiratory grunting, pleuritic friction rub and moist rales can be heard on auscultation of
lungs. About 50% of the affected animals die and 35% becomes carriers.
Necropsy findings; Refer pathogenesis.

Diagnosis:
2. By necropsy findings.
3. Culturing - nasal discharge and lung piece.
4. Serological Test: CFT is the test of choice and even detects the carriers. RPAT also
being used.
1.Pneumonic pasteurellosis Demonstrating the bipolar
2.Haemorrhagic septicaemia organisms in these diseases
3. Verminous pneumonia of calves - demonstrating the larva upon faecal examination
and good response to treatment with anthelmintics.
4. Tuberculosis - by tuberculin test.
Treatment: The drug of choice is tylosin administered @ 5-10 mg/kg b. wt., i/m or
orally, b.i.d., for 3 days. Tetracyclines also can be used.
Control:
2. Detect the carriers and eliminate them.
3. Vaccinate the healthy animals.
a) CBPP (live attenuated) vaccine: prepared by repeated sub-culturing in serum both.
b) Nasal vaccines and Avianized vaccines have been also used
(b) CONTAGIOUS CAPRINE PLEUROPNEUMONIA (CCPP)

It is a contagious disease of goats mostly caused by Mycoplasma strain F-38 and is
characterized by fever, cough, dyspnoea, open mouth breathing and salivation.
Etiology: Mycoplasma strain F-38 is now recognized as the cause of this disease.
Epidemiology:
a) Occurrence: It occurs only in goats and the organism cannot be transmitted to
cattleand sheep. Morbidity is 100% and mortality can be 60-100%.
This disease has been reported from North Africa, Spain, Mediterranean littoral,
Asia Minor and India.
b) Transmission: It is mainly transmitted by inhalation.
Pathogenesis:
It is very similar to CBPP but the sequestra are not formed in the lungs and the
reaction of the interlobular tissue is much less. The lesions may be confined to only one
lung.
Clinical findings: Similar to CBPP.
Necropsy findings: Refer pathogenesis.
Diagnosis:
Serological tests like CFT, ELISA and a latex agglutination test are used.
It should be differentiated from pneumonia due to Mycoplasma mycoides sub sp.
Capri; M. mycoides sub sp. mycoides and M. capricolum.
Treatment: Similar to CBPP
1. Isolate the infected goats and treat them with tylosin.
2. Vaccinate the healthy goats by
a) Sonicated antigens of F-38 strains in incomplete freund's adjuvant.
b) Lyophilized, saponin killed vaccine.
c) CCPP (live attenuated) vaccine: Prepared by repeated subculturing in Bennett's broth.
Dose is 0.1 ml, i/d at the base of the tail of the goat.
The above vaccines are effective in protecting the goats against CCPP and do not
produce local adverse reaction as seen in CBPP.
20. LEPTOSPIROSIS
(Ili jwara, Asymptomatic abortion, Red water of calves, Leptospiral mastitis)
It is an infectious disease of domestic animals caused by various serovars of

Leptospira and is characterized by septicaemia, haemolytic anaemia, haemoglobinuria,
jaundice, abortion, mastitis and interstitial nephritis.
Etiology:
All leptospires are now classified into one species called Leptospira interrogans
containing over 212 serovars arranged into 23 serogroups. They are spiral shaped
organisms with the ends bent into the shape of hook. They measure about 8-12µ x 0.1 -
0.2µ. They are non-flagellated organisms but still motile. They are not stained with
aniline dyes. The following staining technique can be used.
1. Silver stain of Fontana, modified silver impregnation staining.
2. Silver stain of Leviditi and Warthin Starry.
3. Hoyer's Congo red.
4. Geimsa stain
For culturing of the Leptospirae, Stuart’s, and Fletcher’s media containing
5-10 % serum is used.
Epidemiology:
a) Occurrence: World wide occurrence wherein all the species of domestic animals are
affected and even human beings are affected. It can occur in any age group. Many
wild lives are also susceptible and will be source of infection to domestic animals.
This disease causes severe economic losses in the form of mortality, abortions,
mastitis, decreased milk production etc.
It is a zoonotic disease where in it represents occupational hazard to butchers,
farmers and veterinarians.
Each serovar is adapted to particular maintenance or reservoir host and they may
cause disease in any mammalian species. A serovar behaves differently within its
maintenance host species but not in incidental or accidental hosts.
Ex. Li. pomona has pig, skunk, racoon, oposssum as maintenance host.
Cattle and Horses: Li. pomona, Li. icterohaemorrhagiae, Li. canicola, Li.
grippotyphosa, Li. hardjo.
Morbidly rate can be 100%, mortality rate is 5% and abortion rate is 30%. In
calves the mortality rate is high. Calves under one month of age are highly susceptible.
Sheep: Li. pomona - mortality upto 20%.
Goats: Li. grippotyphosa - mortality upto 45%.
Pigs: Li. pomona, Li. canicola, Li. icterohaemorrhagiae.
Dogs: Li. canicola, Li. Icterohaemorrhagiaewere considered previously but now a days
others also – Li. pomona, Li. grippotyphosa, Li. hardjo etc..
b) Transmission: The source of infection is urine, aborted foetuses, and infected uterine
discharges. Young pigs can pass leptospira in the urine for 1 year. The organisms
enter the body through the cutaneous or mucosal abrasions.
Pathogenesis: After penetration of the skin or mucosa, the organisms get into the blood.
For few days, septicaemia occurs. These organisms elaborate a toxin known as
haemolysin, which causes lysis of RBCs. This results in haemolytic anaemia. The
haemoglobin is released and some is excreted through the urine resulting in
haemoglobinuria. Some haemoglobin in the RES is broken down into haem, porphyrin
and globin. Porphyrin is converted into biliverdin and then into bilirubin which
accumulates in the blood and coats serosa and mucosa giving yellow colour which is
known as jaundice.
Then the organisms localize in the liver and cause hepatitis and afterwards
localizes in the kidneys and causes interstitial nephritis. The organisms are excreted in the
urine.
Clinical findings: IP is about 3-7 days.

Cattle: Acute, subacute or chronic form can occur.
(a) Acute form: High fever (103-107°F), anorexia, depression, petechial haemorrhages
on the mucosa. Jaundice, haemoglobinuria and haemolytic anaemia, characterized by
increase in heart and respiratory rates, pale mucous membranes and also dyspnoea.
Acute mastitis characterized by almost complete stoppage of milk production. The
secretion is red coloured or contains blood clots and the udder is limp and soft.
(b) Sub-acute form: Very similar to acute but milder in degree.
© Chronic form: Abortion storms during the last trimester of gestation.
Horses: Sub-acute form occurs and the condition called periodic ophthalmia is associated
with this disease. Here photophobia, lacrimation, conjunctivitis, keratitis, hypopyon and
iridocyclitis occur. Repeated occurrence of this condition results in blindness.
Dogs: It is also known as Canine typhus, Stuttgart's disease of infectious jaundice. Per-
acute, acute and chronic forms have been recorded. Refer acute and chronic nephritis for
details.
Diagnosis:
1. By clinical signs of haemoglobinuria, jaundice, anaemia, abortion.
2. By lesions
3. Isolation and identification of the organisms:
The samples to be collected during the acute phase are blood and during the
chronic phase is urine. Milk should be collected from leptospiral mastitis cases. Kidneys,
lungs and pleural fluid should be collected from aborted foetuses. Liver and kidneys
should be submitted from carcasses.
To isolate leptospira from a live animal is very difficult. The urine is submitted
after adding 1 drop of formalin for 20 ml of urine to prevent the over growth of other
bacteria. To demonstrate leptospira, dark field microscope is used. Also suspected
material is stained with silver stain wherein the leptospirae will take black colour.
From a live animal, blood, urine or milk is injected intra-peritoneally into the
Guinea pig or cultured in special media to isolate the leptospirae.
4. Serological test: Usually, the diagnosis is made by demonstrating the antibodies in
the serum by:
a) Micro-agglutination test: This is the most commonly used test. Titres of
1:500 in cattle. 1:200 in pigs is considered as positive.
b) Standard tube agglutination test
c) Rapid plate agglutination test
d) Others- CFT, ELJSA, IPT, FAT.
5. Haematology: PCV, TRC, and Hb are decreased.
6. Liver function test: Serum arginase, SGPT, SGOT levels are increased.
7. Indirect Van den Bergh test is highly positive.
Differential diagnosis: Since anaemia is present in this disease, it should be

differentiated from other haemolytic diseases like:
1. Babesiosis: It can be differentiated by examining the blood smear for the presence
of intra-erythrocytic Babesia organisms.
2. Bacillary haemoglobinuria: To demonstrate the Clostridium haemolyticum from a
live animal is difficult.
3. Post parturient haemoglobinuria: This disease can be diagnosed by estimating the
blood phosphorus level wherein it is decreased.
4. Kale and Rape poisoning.
Treatment:
1. To eliminate the causative agent administer streptomycin which is the drug of choice
since it is excreted by the kidneys. It is administered @ 10 mg/kg body wt. bid, i/m for 3-
5 days.
Tetracyclines and doxycycline also can be used
2. To overcome anemia -
a) Blood transfusion in very severe cases and
b) Administering haematinics in mild to moderate cases.
3. Sodium bicarbonate is administered to make the urine alkaline wherein the
haemoglobin is soluble so that it can be eliminated without causing any damage to the
renal tubules.
4. Administer liver extracts, B-complex preparations.

1. Eliminating the carrier animals - this can be done either by (a) Administering very
high dose of Streptomycin @ 25 mg/kg body weight once or (b) by disposing of
the carrier animals.
3. Eliminate the rats which are the source of leptospirae.
4. Prevent the wild life coming in contact with the domestic animals.
5. Vaccinate the healthy animals - calves above 3 months of age and pregnant dams
in their advanced gestation.
a) Killed bacterins which is alum precipitated is widely used in many countries of
this world. In India it is only available for dogs.
b) Egg attenuated vaccines have also been used.
c) Formalin killed aluminium hydroxide adsorbed vaccines are also used.
21. LISTERIOSIS
(Circling Disease)
It is an infectious disease mainly of sheep, goat and cattle and is caused by Listeria
monocytogenes and is characterized by meningo-encephalitis, abortion or septicaemia.
Etiology: It is caused by Listeria monocytogenes which is a Gram positive small rod

measuring about 1-2 µ in length x 0.5 µ in breadth. It is motile, catalase positive, non-
spore forming and non-capsule producing organism. There are 13 serovars and the
common ones are 4B, l/2a, l/2b and 3.
Epidemiology:
a) Occurrence: Most important disease in New Zealand, North America, Europe,
U.K. and Australia. It is also recorded in India. Animals susceptible are sheep, cattle,
buffaloes, goats, horses, pigs, cats, rabbits and also human beings are affected. In human
beings it is often fatal. The spoiled silage acts as a predisposing factor because the pH of
the silage is about 5.5 in which bacteria survive and multiplies. Whereas in good silage
where in the pH is 4-4.5, the bacteria may survive but will not multiply.
b) Transmission: By ingestion of silage and also contaminated feed and water. The
source of infection is faeces, urine, aborted foetuses, uterine discharges and milk. Also
ticks and fleas have been shown to transmit the organisms.
Pathogenesis: Upon ingestion the organisms go to intestines and then into the blood
causing bacteraemia and septicaemia. The organisms produce haemolysin i.e.,
listeriolysin B which can cause lysis of the RBCs and can act on pace maker of
contractile cardiac muscle fibres leading to electrical arrest of heart. Then the organisms
localize in various organs especially meninges and brain causing meningo-encephalitis.
Also ascending infection from the abrasions of oral mucosa or trauma to deciduous or
permanent tooth, the organisms may enter the trigeminal or other cranial nerves and get
in to the CNS. The inflammation of the brain stem is unilateral. It causes micro abscesses
in the brain stem which is a pathognomonic lesion of this disease. Perivascular cuffing
with lymphocytes, histiocytes, eosinophils and neutrophils can occur. In visceral organs
like liver, spleen, endo and myocardium multiple foci of necrosis occur.
Clinical findings: In monogastric animals and young ruminants, visceral listeriosis with
or without meningitis is seen. But in adult ruminants meningoencephalitic form is seen.
(a) Meningoencephalitic form: Fever of 104-107°F is seen initially. Animal may stand
for long periods with drooling of saliva and food hanging from the mouth. The
characteristic clinical sign is unilateral facial paralysis where in only half of the face is
paralysed i.e., left or right side. The ear, eyelids and lips of that region are affected and
drooping of one side is seen. Deviation of the head can occur and even after setting right
this condition, it will go back to its original position. Head pushing and circling are also
seen. Panophthalmitis can occur. The course of the disease is about 1-2 weeks in cattle
and for 3-4 days in sheep. The morbidity rate is 10% and the mortality rate is 100%.
(b) Abortion form: In cows abortion at 7th month or above of gestation is common and
there will be retention of placenta. It can have a fever of 105°F. In ewes and does
abortion at 12th week of pregnancy can occur and it can be 15%. Aborted lambs having
small yellow foci of necrosis in the liver, small abomasal erosions and yellow orange
meconium are almost pathognomonic findings.
© Septicaemia form: In this form fever, depression, weakness, emaciation, diarrhoea and
corneal opacity occur. The course of the disease can be 12-24 hours.

Diagnosis:
1. By clinical signs of unilateral facial paralysis and circling, one can suspect it as
listeriosis.
2. Histopathological examination: Micro-abscesses in the brain stem are a
pathognomonic lesion.
3. Isolation and identification of the organisms: The samples to be submitted from a
live animal are faeces, urine and milk, uterine discharges and from an aborted
foetus collect all the organs including stomach contents. Isolation of the organisms
is difficult and it is better to send the brain stem in ice box, keep it for 3 weeks and
then culture it.
The side most affected is collected in formal saline and submitted for
histopathological studies and the other half of the brain, is frozen and submitted for
culturing.
1. Nervous form of ketosis } The unilateral facial
2. Pregnancy toxaemia in sheep } paralysis is absent in
3. Rabies } all these diseases
4. Brucellosis - do STAT
5. Septicaemia due to E coli. Salmonella etc.
Treatment: is effective in the initial stages but not so effective in later stages. The
following drugs may be useful:
Tetracyclines - 10 mg/kg body wt., i/v or i/m for 5 days can be useful.
Streptomycin can be useful.
Chloramphenicol was considered as the drug of choice previously as it used to cross the
blood brain barrier (BBB). However, recent studies have indicated that eventhoufg it
crosses the BBB and found in good concentration in the CSF, but the concentration
fluctuates. In addition, it is a bacteriostatic drug. Hence, now a days it is not considered
as the drug of choice for CNS disorders.
Now a days it is better to treat the CNS disorders by using very high concentration
of the antibacterial agents (3-5 times the normal dose) and 2-4 times in a day is very
essential. Then the agent should be bactericidal. The following drugs have been
advocated for the CNS disorders:
(1) Sulpha –Trimethoprim @ 15-30 mg k/g, i/v, tid, qid. Recent studies have indicated
that this combination of drugs will pass through the BBB and the effective concentration
of the drugs is maintained in the CSF for a long time. Now it may be the drug of choice
for CNS disorders.
(2) Penicillin G 40000 IU/kg, Qid.
(3) Ampicillin 25-50 mg/kg, iv, Qid,
1. The most important control measure is avoiding of feeding of spoiled silage to the
animals.
2. Administering tetracyclines in the feed.
3. No good vaccines are available in India.
22. BRUCELLOSIS
(a) Brucellosis in cattle
(Bang's Disease)
It is an infectious disease mainly of cattle caused by Brucella abortus and is

characterized oy abortion late in pregnancy and a subsequent high rate of infertility.
Etiology: It is caused by Brucella abortus. It is a short rod or cocco bacilli and measures
about 0.3-2.0µ x 0.5 µ. It is a Gram negative, non-motile and non-spore forming
organism. It needs 5-10% CO2 for its growth.
Epidemiology:
(a) Occurrence: It occurs throughout the world and cause severe economic loss in the
form of abortion, infertility problem and decreased milk production. Animals affected
are cattle,buffaloes, bison, yaks, deer, racoons, coyotes, opossums and camels. Human
beings are also susceptible especially Veterinarians, farmers and butchers where in it is
an occupational hazard.
(b) Transmission: It enters the body through ingestion of contaminated feed and water,
by inhalation and through the conjunctiva and intact skin. Also by coitus and artificial
insemination where in the bull is infected and the organisms are found in the semen.
Congenital infection may occur in calves born from infected dams. Embryo transfer is
safe.
The source of infection is uterine discharges, foetus, foetal membranes and milk.
Pathogenesis:
Br. abortus is a facultative intracellular parasite which is capable of multiplication
and survival within host phagocytes. The organisms are phagocytosed by PMNs in which
some survive and multiply. These are then transported to lymphoid tissues and foetal
placenta. The organism is also able to survive within macrophages because it has the
ability to survive as the formation of phagolysosome may not occur. The organisms enter
the body and then get into the blood and localizes in the pregnant uterus, udder, testicles
and accessory male sex glands, lymph nodes, joint capsules and bursae. The udder plays
an important role because the organisms are found usually in the udder without damaging
the udder. Here the organisms can lie dormant for a very long time. From this organ the
organisms can get into the uterus and through the milk into the calf and human beings.
The calf can get the infection through the milk or uterus, and the organisms lie dormant
in the calf and will get into the uterus upon sexual maturity. It is a disease of the sexually
matured animals.
Upon invading the gravid uterus, it spreads to the uterus and causes severe
ulcerative endometritis of intercotyledonary space. Then it invades the allantochorion,
foetal fluids and placental cotyledons and results in destruction of the villi. Because of
this abortion occurs in 5th month or more than 5th month of gestation.
A substance called ‘erythritol’ is produced by placenta of cows, swine, bitches and
ewes. It probably attracts the organisms to the placenta and stimulates the growth of
Brucella. So abortion is common in these species of animals.
In the bull, orchitis and epidydimitis occurs which result in acute painful swelling
of the scrotal sac to twice its normal size. The testes are not enlarged and finally atrophy
occurs and testis disappears (liquefactive necrosis). The seminal vesicles may be
enlarged.
In the joints, non-suppurative synovitis occur leading to hygroma.
Clinical Signs: Abortion at the 5th or more than 5th month of gestation occurs. Usually it
occurs as abortion storms where in the abortion rate can be 90%. Sometimes, individual
animals can abort. After aborting for once or twice, abortion subsides and the rate may be
10-25%. Usually, such cows will have retention of placenta which usually ends in
metritis. Such cows will give very small quantity of milk. Some cows will have hygroma
of the knee joint which appears like a sac (swelling) filled with water like fluid.
In bulls, the scrotal sacs are swollen and painful and finally the testes will
disappear and such animals are sterile.
In horses, Brucella abortus may be associated with fistulus withers.
Diagnosis:
1. By history of abortion storm.
2. By clinical signs of abortion over 5th month of gestation, hygroma, ROP, infertility
problems etc.
3. By isolation and identification of the organisms: Materials to be submitted are uterine
discharge, contents of various organs, lymph nodes of foetus, placenta, milk and
vaginal mucous. The suspected materials may be cultured in blood agar or Trypticase
soy agar and also by injecting into Guinea pigs. It requires 5 days to 2 weeks for
growth.
4. Serological tests:
A. Agglutination tests:
i) Rapid plate agglutination test (RPAT): It is a screening test used for the diagnosis of
Brucellosis in a herd. This test is first conducted by using the serum and if this test is
positive, then standard tube agglutination test (STAT) is performed to confirm
Brucellosis previously. Now a days ELISA is being used as a confirmatory test.
ii) Standard tube agglutmation test (STAT): After the RPAT is positive, then this test is
used. Then the following criteria is used to differentiate vaccinated animals from
infected i.e., non vaccinated animals:
Vaccinated Non-vaccinated animals
Positive 1 : 200 1 : 100
Suspicious 1 : 100 1 : 30
Negative 1 : 50 Less than 1:50
It is better to submit two serum samples - the first sample during the acute phase
and the second sample during the convalescent phase i.e., 2-3 weeks after the first sample
collected immediately after abortion to arrive at a meaningful diagnosis. If there is
increase in titre by 3-4 fold, then it is considered as positive. For example:
Positive animal Negative animal
Acute phase 1 : 40 1 : 40
Convalescent phase 1 : 640 1 : 80
iii) Card agglutination test: This test was introduced as a screening test for the diagnosis
of Brucellosis in beef cattle. This test is similar to RPAT and is performed on a card by
using plasma instead of serum. Commercially test kits are available in foreign countries.
iv) Rose Bengal agglutination test: This test is also similar to RPAT. Hers the antigen
stained with Rose Bengal dye is used. It appears that it is better than RPAT. This test is
commonly used as a screening test.
v) Rivanal and 2-mercaptoethanol test: Here the suspected serum is mixed wnh
either rivanol or 2-mercaptoethanol and kept for some time. Then the STAT is
done. Here these agents will destroy the IgM. That means the level of IgG is
measured in these tests. This test is used to differentiate the vaccinated from
infected animals. If the elevated titre is due to IgM then it is considered as
vaccinated animal and if the elevated titre is due to IgG then it is considered as
infected animal. For example:
Vaccinated Infected
animal animal
Titre of STAT 1 : 640 1 : 640
Titre of 2 ME test 1 : 80 1 : 640
vi) Cervical mucous plate and tube agglutination tests: These tests are similar to RPAT
and STAT and instead of serum, the cervical mucous is used. In the tube test lower
dilutions of the cervical mucous is used as compared to the higher dilutions of serum
used in STAT.
vii) Whey agglutination test: Here the milk is treated with rennet and the whey is
separated and is used for RPAT and STAT.
viii) Seminal plasma agglutination test: Semen from a suspected bull is collected and
treated with a chemical to get seminal plasma which is used for RPAT and STAT.
ix) Whole milk agglutination test: Instead of serum whole milk is used to perform RPAT
or STAT.
x) Milk ring test or Abortus Bang ring test: This test is used to diagnose brucellosis in a
herd. Here the pooled milk from a dairy farm is used.
Procedure:
Take 2 ml of milk in a test tube and then add 2-3 drops of Brucella antigen stained
with Haemtoxylene. Mix the contents by rolling the tube in between the palms. Keep the
tube in a water bath or incubator at 37°C for one hour. Then take out the tube and keep at
room temperature for 1-2 hours.
Interpretation:
If there is intensely cherry red coloured ring at the top most level of the milk, then
it is positive for Brucellosis. If the milk is uniformly light pink through out then it is
negative for Brucellosis.
Mechanism:
The antibody present in the milk combines with the Brucella antigen and forms a
antigen-antibody complex. This complex along with the fat globules rises to the top
giving an intensely stained cherry coloured ring at the top which will be considered as
positive for Brucellosis. In a negative sample, since antibodies to Brucella are absent, the
antigen-antibody complex will not be formed. Hence the antigen gives uniform light pink
color to the entire milk sample.
B. Other serological tests like CFT, FAT, ELISA, western blot technique etc have been
used for the diagnosis of Brucellosis. Now a days attempt has been made to use Milk
ELISA as a screening test.
5. CMI test:
a) Lymphocyte stimulation test (LST): This test is used for the diagnosis of this
disease. In this test, if the stimulation index is 3 and above then it is positive for
Brucellosis.
b) Whole blood lymphocyte stimulation test: In this test whole blood is used instead
of purified lymphocytes to save time and money. The interpretation is similar to LST
and the results are comparable with that of LST.
c) Macrophage migration inhibition test: This test is not as popular as LST.
d) An intradermal test is also being used for the diagnosis wherein the Brucellin is
injected i/d either in the neck or in the caudal fold.
Differential Diagnosis: Since there is abortion, Brucellosis should be differentiated

from:
1. Trichomoniasis: Here abortion occurs commonly at 2-4 months of gestation. There
will be also pyometra and purulent uterine discharge. Abortion rate is about 5-
30%.
2. Campylobacteriosis: In this disease foetal death and resorption; and abortion at 2-
4 months of gestation can occur. Abortion rate is about 5-20%. Repeat breeding is
a common finding.
3. Leptospirosis: This disease is characterized by abortion at 6 months and above of
gestation and the abortion rate is 25-30%. This disease can be diagnosed by micro-
agglutination test, urine examination and culturing.
4. Infectious bovine rhinotracheitis: Abortion occurs at 6 months and above of
gestation and the abortion rate is about 25-50%. The aborted foetus is autolysed
and the presence of focal areas of necrosis in the liver of the foetus are
pathognomonic findings of IBR. Also respiratory and eye forms occurs with
accumulation of white necrotic material on the respective mucosae.
5. Listeriosis: Abortion occurs at about 7th month of gestation and may be also
Associated with CNS signs.
6. Epizootic viral abortion: In this disease abortion occurs at 6-8 months of gestation
and the abortion rate is 30-40%.
Treatment: No good treatment is available in domestic animals suffering from

Brucellosis. Usually the treatment is not undertaken. Various drugs like Sulphadiazine,
Streptomycin and chloramphenicol have been tried parentarally without much success.
Also used as intramammary infusions to eliminate the Brucella from the udder, but not
successful.
Long acting OTC @ 20 mg/kg b. wt., i/m at an interval of 3-4 day along with
streptomycin @ 25 mg/kg b. wt. i/m or i/v daily for 7 days was partially successful in
cows.
The treatment is not effective because Brucella is intra-cellular organism and
effective concentration of the drug inside the cells may not be there to eliminate the
bacteria. Recently, drug target delivery system has been used wherein the liposomes
having the anti-bacterial agent have been administered intravenously, making the
macrophages to phagocytise them. This resulted in the higher effective concentration of
the antibacterial agent inside the cell.
Usually the treatment of animals is not undertaken because brucellosis is a
zoonotic disease.
Control: There are two methods employed:
1. Testing of the animals by using serological tests and culturing and disposing off the
positive animals. This is the method employed with compensation in various
foreign countries like USA, Canada etc., where the main aim is to eradicate the
disease.
2. By vaccination: Most commonly used vaccine is Brucella abortus strain 19 vaccine
(IVRI) and is a live attenuated vaccine. Dose is 5 ml, s/c.
Calf hood vaccination: Here the calves between 3-6 months of age are vaccinated with
this vaccine. The antibody titre develops, exists for few months and then subsides. In few
countries, vaccination of calves is compulsory and is administered only once.
Adult vaccination: The same vaccine can be used in cows during the outbreak of
brucellosis in a herd. Even after vaccination, abortion continues and will subside after 45-
60 days. But this is not done commonly.
This vaccine will give protection for about 5 gestations. Bulls should not be
vaccinated.
Levamisole when administered 7 days after vaccination has enhanced the antibody
response to the vaccine.
Precautions while handling this vaccine: Accidental injection, inhalation or falling of
vaccine in the eye will cause undulant fever in human beings. Hence it should be
handled very carefully and following precautions should be undertaken.
a) Wear gloves while vaccinating the animals.
b) Avoid self pricking.
c) While adjusting the column of vaccine in the syringe do not spray.
This vaccine has been used intradermally and sub-conjunctivally with reduced
dose (1/20th of the s/c dose), but the s/c route is slightly better.
Killed Brucella Vaccine (Duphavac): K45/20A strain has been used with adjuvant. The
advantages of this vaccine are:
a) It will not spread to other animals and produce the disease.
b) It produces non-agglutinogenic antibodies and hence will not come in the
way of diagnosis of the disease.
c) Very safe to handle by the Veterinarian.
d) Can be very easily administered during an outbreak of Brucellosis.
3. Adopt good hygienic measures.

4. Eliminate the bulls suffering from Brucellosis.
(b) Brucellosis caused by Brucella ovis
It is an infectious disease of sheep caused by Brucella ovis and is characterized by

infertility in rams due to epididymitis, abortion in ewes and neonatal mortality. Natural
infection occur only in sheep and experimentally goats can be infected. Ram is much
more susceptible than ewes.
Acute oedema and inflammation of the scrotum occurs. Systemic reaction like
fever, depression and increase in respiratory rate can be seen. The epididymis is enlarged
and hard, more commonly at the tail. Scrotal tunics are thickened and hardened and the
testicles usually atrophic. The infected rams finally become sterile and this may be due to
autoimmune mechanism.
This condition is diagnosed by CFT, physical palpation of the contents of scrotum
and cultural examination of semen.
Killed B. ovis and B. abortus strain 19 combined vaccine has been used for
control.
© Brucellosis caused by Brucella suis
It is characterized by sterility and abortion in sows, heavy piglet mortality and

orchitis in boars.
B. suis has no prediliction for localization in the uterus and udder. It is found in
all body tissues. It is a disease which is similar to undulant fever in man.
Sows abort only once. Lameness, incoordination and posterior paralysis occur
commonly which is due to arthritis and osteomyelitis of lumbar and sacral vertebral
bodies.
No suitable vaccine is available.
(d) Brucellosis caused by Brucella melitensis
B. melitensis causes brucellosis in goats and Malta or Mediterranean fever in man.

It is very similar to bovine brucellosis and also systemic reaction with fever, depression
and loss of weight occurs.
Laboratory diagnosis is not easy and usually attempt to diagnose this disease is
made whenever human brucellosis is diagnosed.
Elberg’s Rev 1 vaccine which is a live avirulent vaccine is used.
(e) Brucellosis in dogs
It causes early embryonic death in bitches and epididymitis and testicular

degeneration in male dogs. Brucella canis are found in the blood for a very long time
like 1-2 years. Hence blood should be collected for culturing and is the best way of
diagnosis. Serological tests are not reliable because other organisms give cross reaction
leading to false positive reaction.
(f) Brucellosis in Human beings
It can be due to B. abortus and B. melitensis. Sometimes it can be due to other

species of brucella. Usually, infection occurs by ingestion of raw milk from the cows or
goats suffering from brucellosis. Commonly Veterinarians, animal attenders and butchers
are frequently exposed to the organisms due to handling of ROP, aborted cases and
slaughtered animals.
Clinical findings: Intermittent fever, repeated headaches, back pain, loss of weight,
arthritis and finally orchitis and sterility.
Diagnosis: It is done by STAT and ELISA.
Treatment: The following treatment is very effective.
Streptomycin - 0.75 - 1.00 gm/person, i/m, daily for 2 weeks.
Simultaneously, tetracyclines - 0.25-0.5 gm, t.i.d., orally for 3-4 weeks.
The response to treatment is good
Doxycycline and minocycline also have been used recently.
No good vaccine is available
CAMPYLOBACTERIOSIS
(Vibriosis)
It is a venereal disease of cattle caused by Campylobacter foetus sub sp. foetus and
is characterized by early embryonic death, mild endometritis and prolonged oestrus cycle
in cows and asymptomatic in the bulls.
Etiology: Previously the causative agent was known as Vibrio foetus and in 1973, the
name of the organism was changed to Campylobacter foetus sub sp., foetus. It is a small,
Gram negative, micro-aerophilic, curved to spiral rods that have a single polar flagellum.
They are motile with a characteristic cork screw kind of movement.
It is closely related to Campylobacter foetus sub sp. intestinalis and
Campylobacter foetus sub sp. jejuni. Neither of these two sub species are involved with
the venereal disease of cattle although Campylobacter foetus sub sp. intestinalis
occasionally causes abortion in cattle.
Epidemiology:
a) Occurrence: It has been recorded throughout the world wherein cattle are commonly
affected and sheep and goats may be susceptible.
b) Transmission: is by coitus or by artificial insemination in cattle and in sheep and
goats it is by ingestion.
Pathogenesis: Upon coitus or A.I. the organisms get into the cervix and then into the
uterus and causes mild cervicitis, endometritis and salphingitis. These changes may be
responsible for early embryonic death and abortion at 2-4 months of gestation.
Clinical findings: Transient infertility in breeding females results from early embryonic
death, endometritis and prolonged oestrus cycle. Abortion commonly occurs at 2-4
months of gestation which may commonly go un-noticed. This may be noticed by the
owner when the animal comes to heat even inspite of regular service or A.I. Many cows
may fail to conceive even after repeated A.I. which may end up as a repeat breeder.
The infection is confined to the genital tract and there is no systemic reaction.
In the bulls it is asymptomatic because the organisms are localized in the prepuce
which will not interfere with the semen quality or breeding ability.
In ewes, abortion occur near about the 6 weeks and above of gestation without any
previous signs.
Sub-acute and chronic forms of Campylobacteriosis have also been recorded in older
cows.
Diagnosis:
1. Herd history of repeat breeding and history of abortion and prolonged oestrous cycle
should make one to suspect Campylobacteriosis.
2. Demonstration of organisms from cervico-vaginal mucous and from gastric content of
aborted foetus either by staining or by culturing.
3. Serum agglutination test is not reliable because it is not a systemic infection.
4. Cervical mucous agglutination test is extensively used. This test is positive only after
60 days after infection. This test should not be done at the time of oestrus as
antibodies are diluted in cervico-vaginal mucus. The blood from either metestral
bleeding or from rough manipulation of the vagina during collection can result in a
false positive test.
Treatment: Infusion of 1 gm of Streptomycin in 20-30 ml of distilled water into the
uterus is effective. In case of males, douching the preputial cavity with Streptomycin
solution and administration of Streptomycin parenterally are commonly practiced.

1. Vaccination: Vaccinate the breeding females twice (1st dose: 4.5 months prior to
breeding; 2nd dose: 10 days prior to breeding) with adjuvant bacterins every year.
2. Antibiotics in semen extenders will be very useful.
3. Storing of the semen at 5°C will prevent the multiplication of the organisms.
4. Freezing the semen will not kill the bacteria.
5. Periodically test all the breeding bulls.
23. CORYNEBACTERIUM PNEUMONIA IN FOALS
It is a disease of equines and mostly of young foals caused by Rhodococcus equi

and is characterized mainly by pneumonia and abscesses of the lungs.
Etiology: It is caused by Rhodococcus equi and the old name of this organism is
Corynebacterium pneumoniae. It is a Gram negative, small, pleomorphic rod and occurs
in chains or singles or pairs. It is a non motile, non spore forming and aerobic or micro
aerophillic organism. It reduces sugars and catalase positive The organism is not
resistant to environmental temperature but lives in most soil for 12 months.
This organism affects principally foals but also found in lymph node abscesses of
pigs and in cattle also associated with ulcerative lymphangitis. Coryne.
pseudotuberculosis and C. pyogenes can also cause this disease.
Epidemiology:
a) Occurrence: Wherever equines are present, 5% of the infectious diseases of foals is
due to this organism. The mortality can be 80%. The mortality decreases as the
age of the foals increases i.e., after 3 months of age. Foals of 2 weeks to 6 moths are
susceptible with peak prevalence between 1-3 months. In older foals the morbidity rate is
high but the mortality rate is less. The foals do not grow properly and the age of maturity
is delayed.
b) Transmission: The exact mode of transmission is not known. Previously a genital

mode has been proposed but now a days it is of no importance. Now, it is mainly by
ingestion, inhalation and navel route. Predisposing causes in the horse are unknown, but
the disease can be produced experimentally by oral or intra nasal route.
Pathogenesis:
The organisms get into the blood and cause bacteraemia and then localize in
various organs, particularly in the lungs and to a lesser extent in the joints and
subcutaneou tissues and causes abscesses. This leads to toxaemia.
Clinical findings: Clinical signs vary with the age of the foal. The earliest affected foals
may run acute course of the disease. The foal becomes suddenly ill showing the signs of
pneumonia, arthritis, anorexia and raise in the body temperature.
In older foals the disease runs a sub-acute course showing cough and fever,
shallow breathing, dyspnoea and moist rales on auscultation. The foal continues to take
milk, but emaciation progresses. Sometimes there is severe diarrhoea and animal may
die within one or two weeks. No enlargement of the regional lymph nodes.
Diagnosis: For culturing of the organisms, tracheal fluid aspiration, nasal swab and even
the cervico-vaginal swab from suspected breeding mares should be used.
An intradermal test and ELISA has also been used.
Necropsy finding: Suppurative bronchitis and abscesses in the lungs and the ventral
border of the lungs are vastly involved. Mediastinal lymph nodes are enlarged.
Differential diagnosis: This disease should be differentiated from EVR, EVA,
Strangles and Salmonellosis.
Treatment: Chloramphenicol, tetracyclines and penicillins can be used. Now a days a

combination of Erythromycin @ 25 mg/kg body weight, t.i.d. and Rifampicin @ 5 mg/kg
body weight, b.i.d., orally for at least 30 days has been recommended.
NSAIDs anti-inflammatorics, bronchodilators and mucolytics can be used.

1. Eliminating the breeding mares which are known to carry the infection.
2. Good hygienic measures especially at the time of foaling.
3. Disinfecting the umbilical cord after foaling.
4. Injecting the long acting penicillins as a precautionary measure.
5. Feeding of the colostrum to the neonate as early as possible.
6. Administering the hyper-immune serum to the foals when they are one month of
age.
7. Vaccinating the pregnant mares is not very useful.
24. CHLAMYDIOSIS
Chlamydia psittaci causes many diseases in domestic animals and all the birds
causing severe economic loss.
Etiology: It is now classified under rickettsia. It is in between bacteria and viruses.

Because they are intracellular organisms they are considered as viruses. They contain
both DNA and RNA, have good cell wall and susceptible to antibiotics and
sulphonamides and hence considered as bacteria.
Chlamydia psittaci causes Avian chlamydiosis in all the birds.
Chlamydia psittaci causes Psittacosis, Ornithosis and urethritis in human beings.
Chlamydia trachomatis causes conjunctivitis, vaginitis and urethritis in human
beings.
These organisms are also associated with cat scratch fever in human beings.
In domestic animals Chlamydia psittaci causes various syndromes. Various strains
are there which are all related antigenically. The elementary body measures about 200-
300 nm and the initial body measures about 1000 nm.
Mode of Replication: The elementary body is pinocytized by the epithelial cells and it
develops into initial body. The initial body undergoes repeated binary fission to produce
many elementary bodies. These will be found in a sack like or vacuole like structure and
by rupture of the epithelial cells, the elementary bodies will be released.
Diagnosis:
2. By isolation and identification of the organisms: It is very difficult to demonstrate
the organisms in a suspected material. Hence, the suspected material should be
mixed with phosphate buffer solution and then injected into the yolk sac of the 3-7
day old chicken embryo and incubated. With in 5-12 days, the developing chicken
embryo die, then open the egg and make a smear of the yolk sac and do the staining
with any one of the following staining techniques to demonstrate the organisms:
a. Geimsa stain: The organisms appear purple coloured.
b. Macchiavello's and Gieminez stain: The organisms are red colored.
c. Casteneda’s stain: The organisms take blue colour.
Chlamydia psittaci causes the following diseases:

1. Sporadic bovine encephalomyelitis (SBE): It is also known as ‘Buss disease’ and
‘transmissible serositis’. This disease occurs in adult cattle and young calves under 6
months of age. The morbidity rate is more in calves when compared to adults and the
mortality rate is higher in adults when compared to calves.
Clinical findings:
IP is 4 days to 4 weeks. High fever (105-107°F), depression, nasal discharge,
salivation, coughing and dyspnoea in the beginning are noticed. Later on knuckling of
fetlocks, incoordination, circling, collapse and death will occur. The course of the disease
can vary from 1-3 days to 3 weeks.
Necropsy findings: Presence of lot of fibrin in the pleura, thoracic cavity, abdominal
cavity and joints which is known as fibrinous serositis is a very characteristic finding of
this disease.
Diagnosis:
1. By clinical signs and lesions.
2. By isolation and identification of the organisms in the developing chicken
embryos.
3. By serological tests like FAT and CFT.
Treatment: Commonly OTC is administered @ 10 mg/kg body wt, i/m or i/v

for 3-5 days.
Prevention and control: Formalin killed vaccine has been used and will give protection
for 3 years.
2. Enzootic bovine abortion: It is also known as 'foot hill' abortion where in abortion
occurs in late gestation. The abortion is 60% and even pregnant heifers are also affected.
There is no ROP and no adverse effect on the breeding capacity of the cow. In young
bulls it causes epidydimitis and also the accessory sex glands are affected.
3. Pneumonitis and Conjunctivitis: Domestic animals like sheep, cattle, goat and dogs
are affected where in there will be purulent discharge from the eyes and nose; and
dyspnoea. Sulphadimidine and tetracyclines are effective.
4. Polyarthritis: It occurs in sheep, cattle and horses. Here many joints are affected and
there will be swelling of the joints and lameness.
5. Bovine enteritis: Here the abomasum and ileum of the calves are affected resulting in
diarrhoea.
6. Avian chlamydiosis (Psittacosis or omithosis): Almost all the birds are affected and
can cause mortality rate of less than 5%. It is transmitted by contact and inhalation. Upon
inhalation they are phagocytosized by the phagocytes and through circulation localize in
respiratory tract, liver, spleen, kidneys, intestines etc. The IP is 5-8 days or it can be 2-6
weeks. Serous or purulent discharge from the nostrils or eyes, loss of appetite,
depression, diarrhoea with greenish grey faeces, gelatinous in consistency and may be
blood stained. There will be severe decrease in egg production. It can be a severe
disease in turkeys when compared to fowl and mortality can be upto 30%.
It can be diagnosed by culturing the faeces and also by demonstrating the small
discrete, pink coloured inclusion bodies in the impression smears of liver and spleen.
Also FAT and CFT are commonly used.
It is treated with chlortetracycline @ 500-800 gms/ton of feed for 3 weeks.
Handle the affected birds with care since the human beings can come down with the
disease.
25. AVIAN MYCOPLASMOSIS

Class: Mollicutes
Order: Mycoplasmatales
Family: Mycoplasmataceae
Species: Mycoplasma gallisepticum Turkeys
Mycoplasma synoviae Chicken
Mycoplasma meleagridis - Turkeys
Mycoplasmas are in between bacteria and virus. About 20 serotypes have been
isolated from avian sources. Out of which the above three mentioned are important. They
are the smallest free living organisms. They measure about 200-800 nm. They are
filterable. They have no cell wall. But have a triple layered plasma membrane.
(a) Chronic Respiratory Disease
The 'chronic respiratory disease (CRD)’ is caused by Mycoplasma gallisepticum.

It occurs through out the world and causes severe economic loss. Birds of any age can be
affected but young ones are more susceptible.
It is transmitted by inhalation and also through the infected eggs to ovaries to the
eggs. I.P. is 6-21 days. The signs noticed are sneezing, coughing, moist rales and
breathing through the beaks. In turkeys both the infra-orbital sinuses will be swollen so
much that complete closure of eyelids can occur. In both the birds mild conjunctivitis
will be seen.
Necropsy reveals the catarrhal exudation in the respiratory tract. Pneumonia with
pericarditis, peritonitis and perihepatitis which are similar to E.coli, infection are also
seen.
Diagnosis:
1) By histological studies and necropsy findings.
2) Isolation and identification of organisms - Tracheal, airsac, lung, turbinate and sinus
exudate should be used for culturing by using broth or agar medium. The culture should
be incubated for 5-7 days and 2-3 sub cultures should be done. The colonies will have
nipple like structures at the centre which is characteristic of mycoplasma.
The smears can be made from the colonies and stained with Giemsa to
demonstrate the small coccoid organisms often in clumps.
2) By serological tests: RPAT, HIT.
(b) Mycoplasmal arthritis

Mycoplasma synoviae causes arthritis in birds. Morphologically it can not be
differentiated from M. gallispticum. Clinical signs noticed are depression, paleness of
combs and face, rapid loss of condition and swelling of the joints especially the feet and
hock resulting in lameness.
The synovial membrane will be thickened and oedematous, the joints will be filled
with clear fluid initially and creamy white exudate later on.
The treatment and prevention and control for CRD and arthritis are same.
Treatment:
Tylosin tartarate is the drug of choice for both the diseases. The other drugs used
are, Tiamulin, Spectinomycin Lincomycin, Speromycin, Gentamicin, Erythromycin and
Oxytetracycline. These can be administered in drinking water.
1. Dipping of the eggs in any one of the antibacterial agents mentioned above. Ex. 7 ml
of Gentamicin is mixed with 493 ml of distilled water and 1000 eggs are dipped in this
solution for 10 seconds.
2. Testing and eliminating the reactors, if necessary the whole flock.
II. VIRAL DISEASES
1. FOOT AND MOUTH DISEASE
(Kaalu baayi jwara/bene/roga, Kurkatt in kannada)
(FMD, Aphthous fever, Aftosa, Epizootic aphthae)
It is an extremely contagious acute disease of all cloven footed animals caused by

a picorna virus (FMD virus) and characterized by fever and vesicular eruptions in the
mouth and on the feet and teats.
Etiology:
Family: Picorna viridae
Genus: Aptho Virus
It is a very small RNA virus and it measures 20-30 nm. It is having a cubical
symmetry. It is non-enveloped.
This virus is having 7 major serotypes. They are O, A, C and Asia (1,22). They
occur commonly in our country. The commonest in our country is ‘0’ and least common
is ‘C’. In the recent 3 years, the type C has not been encountered in our country. The
other 3 more major serotypes are called SAT (South African Territories) 1, 2 and 3 which
occur commonly in Africa, and they are not recorded in our country.
In addition to the above major strains, there are many substrains (about 80)
because this virus undergoes mutation readily. There is no cross protection between
strains and substrains.
The virus is very resistant to commonly used disinfectants and many
environmental factors. The virus can survive for over a year in infected premises and for
10-12 weeks on feed and clothings. All meat tissues including bone will remain infective
for very long periods if these are quickly frozen. The virus is destroyed by 1-2% sodium
hydroxide or formalin or 4% sodium carbonate (washing soda).
In 2004, the FMD virus was detected in milk 33 hours to 14 days before exhibiting
clinical signs.
Epidemiology:
1) Occurrence: It is common in Africa, Asia, Europe, South America, Japan and
Phillippines. USA is not having FMD from 1929. Australia and New Zealand never had
FMD. It is a very common disease in our country causing severe economical loss to the
dairy industry (4500 crores of Rupees). According to ADMAS, 28 states out of 32 states
of our country encountered an attack rate ranging from 51 to 65,000 cases per million
susceptible population.
Species: Cloven footed animals - common in cattle, and then followed by pigs, goats,
sheep and buffaloes. Also occurs in camels and deers. Many wild animals are susceptible
and may act as reservoirs.
In an outbreak, morbidity can reach 100%. The mortality is below 2% in adults
and but it is 20% in calves, because in calves the heart is affected leading to myocardial
failure. Some times the case fatality rate can reach 50% in exotic adult cattle. This may
be due to HS, BQ, Anthrax affected cattle coming down with FMD or recovered cattle
from these diseases and then having FMD.
Human beings are slightly susceptible where in vesicles may develop in the mouth
or head. They can carry the virus in the nasal mucosa for 28 hours.
This disease causes severe economic loss, in dairy industry which is due to
mortality rate, decreased milk production, decrease in working capacity of the animals
loss of skin and hide, infertility and sterility problems, sequalae to FMD like panting,
over grown hairs (hyper trichosis). The economic loss due to FMD according to latest
estimate in our country may be Rs. 4,500 crores loss per year.
2) Transmission: The source of infection is the saliva, milk, faeces, semen and urine.
Mainly this virus is transmitted by -
1) Ingestion of contaminated feed and water.
2) By inhalation- aerosol transmission (through air the FMD virus may be transmitted
upto 250 kms). Other ways of transmission may be through semen and artificial
insemination. Birds and many wild lives act as carriers and hence they can also transmit
to domestic animals. Many arthropodes like fleas, ticks, and flies can transmit the virus.
Recovered sheep and cattle will be shedding the virus upto a period of 6 months.
The virus can be transmitted from one country to another by:

1) Importing of animals or animal byproducts like meat from countries where FMD is
common.
2) Importation of frozen semen.
3) Human beings.
Pathogenesis: Irrespective of route of entry of virus, the virus gets into the blood and
there will be viraemia for a short period. Then the virus localizes in the epithelium of the
oral cavity and interdigital space and in some animals also on the teat and udder. The
virus causes hypertrophy and hyperplasia of epithelium, leading to formation of vesicles.
The small vesicles fuse (coalese) together to form bulla. The vesicles/bulla are thin
walled and will be filled with clear straw coloured fluid. Because of prehension
mastication and walking, the vesicles will rupture leading to formation of ulcers. In
calves the heart is affected. There will be coagulative necrosis which gives a greyish
white appearance arranged in parallel rows and this condition is known as tigroid
appearance of heart.
Clinical findings: IP is 1-21 days but commonly it is 3-8 days. The first sign noticed is
high fever - 104-107°F. Depression, anorexia, decrease in milk production and formation
of vesicles or bullae in the oral cavity and also the dorsum of the tongue. Later on due to
rupturing of these there will be ulcer formation. There will be profuse salivation which
will be rope like or strand like and smacking of the lips occurs. Initially limping of the
animal is noticed and later on the animal may be recumbent because of lameness. The
rupturing of vesicles in the inter-digital space can lead to ulcer formation which can be
complicated with bacterial infection. Finally formation of maggots and foul smelling
discharge from the lesions occurs. If the wound is existing for prolonged period of time
overgrowing of the hoof can occur. Pregnant animals can abort.
The vesicles can be formed on the teats and lower aspect (portion) of the udder.
Because of pain, proper letting down of milk may not occur. The cow may not allow the
owner for milking. These vesicles rupture during milking and can be complicated with
secondary bacterial invaders, which may lead to mastitis.
In young calves similar clinical signs can be seen and after 5-6 days after starting
of the signs there will be dyspnoea, weak and irregular heart action, convulsions and
death occurs. In some cases diarrhoea/dysentry can be also seen.
In sheep, goats and pigs mild form of disease occurs. Most of the animals will
recover within 1-2 weeks. Some may require 1-2 months.
Necropsy findings: Vesicles, bullae and ulcers in the oral cavity and tongue are
commonly seen. These lesions also can be seen in pharynx, oesophagus, forestomach and
intestines. Some times from the trachea to bronchi. In young calves tigroid appearance of
the heart is seen.
Diagnosis:
1) By clinical signs
2) By lesions
3) Isolation of the virus - The vesicular fluid, tongue epithelium, saliva, faces, milk,
oesophago-pharyngeal fluid should be collected and can be cultured in BHK-cell, tongue
epithelium and in developing chicken embryos, Guinea pigs and unweaned mice.
Commonly the tongue epithelium is collected and placed in a container having glycerine
with PBS or normal saline which is supplied by the FMD centre of IAH & VB,
Bangalore. The sample is submitted along with the filled in questionnaire to the FMD
centre in IAH & VB, Hebbal, Bangalore for isolation and identification of the FMD
virus. The samples which will be recorded as doubtful/negative will be submitted by the
authorities to the FMD centre, IVRI, Izatnagar for further studies.
4) Serological test: Neutralization test, CFT, FAT, IPT, ELISA and the virus infection
associate (VIA) antigen test have been used for the diagnosis of FMD.
Differential diagnosis: The diseases to be considered are Vesicular stomatitis, Vesicular

exanthema, BT, BVD and RP.
The details of animal inoculation test are as follows:
Sp. of animal FMD Vesicular Vesicular Blue tongue
stomatitis exanthema
Cattle + + - +
Pig + + + -
Sheep, Goat + + - +
Horse - + - -
Treatment: There is no effective treatment for this virus. However supportive therapy is
given. They are-
1) To overcome the secondary bacterial invaders a course of broad spectrum antibiotics
like Dicrysticin/vetopen i/m. 1 LD for adults or Tetracyclines like OTC, chlor
tetracycline @ 5 mg/kg body weight, i/m, for 5 days is administered.
2) To reduce the fever and pain administer antipyretics and analgesics like novalgin,
analgin, 8ml/100 kg body wt. (500 mg/mi) or Esgipyrin - N (3 ml & 5 ml ampoules) 10-
20 ml/animal orally or Diclofenac sodium @ 1 mg/kg body weight for 3-5 days is
administered.
3) The mouth is washed with either the PP lotion, 0.5-1% sodium hydroxide or 1-2%
sodium carbonate solution. Then boroglycerine or borax glycerine is applied. Boro
glycerine contains 1-2 gms of boric acid (antiseptic) in 100 gms of Glycerol
(smoothening agent). Borax glycerine is available as such (10 gm, 20 gm). Sometimes
one can think of using G-32 tablet either by crushing 1-2 tablets into powder and mixing
with coconut oil or Honey and applying to the lesions and or administering orally 5 tab,
b.i.d.
The foot/udder lesions were cleaned with PP lotion and then any one of the following
is applied:
a) Lorexane cream (Benzidine hexa chloride) - prevents maggot formation.
b) Betnovate N ointment - reduces pain, itching.
c) M & B antiseptic cream
d) Himax.
If maggots are allready formed, then to remove them, oil of terpentine/
Phenothiazine/carbon tetrachloride/neem oil is applied.
5) In 1979 in experimentally produced FMD in cattle and pigs, a chemical called
Methisoprinol has been tried at a dose of 28 mg/kg in cattle and 110 mg/kg in pigs, i/m
once a day for 2 days with complete recovery within 3-5 days.
Prevention and control: It is very difficult to prevent and control FMD because-
1) Highly potent vaccine inducing immunity for long period are not available.
2) The FMD virus readily undergoes mutation.
For the control and eradication of this disease in some countries testing and
slaughtering of reactors and in contact animals has been followed and the owners were
paid compensation and this has given very good results. This method has been followed
in recent outbreaks of FMD in United Kingdom.
In developing country like India commonly the following measures were followed:
i) Isolation of the affected animals
ii) Treatment of affected animals
iii) General hygienic measures
iv) Vaccination of healthy animals
Ring vaccination wherein the animals at the periphery of a village or a group of
villages were vaccinated first and then moved on to the centre to contain outbreak is
followed in some countries like India.
Vaccines: The vaccines used in our country are all killed vaccines and aluminum
hydroxide adsorbed vaccines. They are all polyvalent. Efforts have been made to produce
this vaccine by using the local strains. These vaccines produce immunity for 6-8 months.
Hence they should be repeated in a year i.e., twice a year. Since in most of the places
FMD out breaks occur in January the animals are commonly vaccinated in November/
December.
The following vaccines are available.
1. Raksha FMD vaccine (Indian Immunologicals) O, C, Al ,A22
Dose: Cows, buffaloes & calves - 3 ml s/c.
Sheep & goat - 1 ml s/c
2. FMD vaccine (IVRI) - both polyvalent & monovalant vaccines are available.
Dose: Polyvalent (O,A, C Asia-1) - 10 ml
Monovalent - 2. 5 ml
3. FMD vaccine (BAIF) similar to no. 2.
4. FMD vaccine (Hoechst) similar to no. 2
In the market if the approximate rate/dose is Rs.10 then if the vaccination is done
in Veterinary hospitals it is subsidized i.e., Rs. 2/dose.
Recently, the Indian Immunologicals has introduced the following inactivated
vaccines:
1. Raksha-Ovac – It is an oil adjuvant vaccine. It is unique oil in water in oil emulsion
offering both efficient release of FMD antigens and depot formation. It contains
inactivated tissue culture FMD virus antigens – O, A, C and Asia 1 adjuvanted with
mineral oil.
Dose: Cattle, buffaloes and pigs - 2 ml.
Sheep and goats - 1 ml.
Route: Deep i/m
Schedule: 1st dose – 4 months of age
Subsequent dose – every 9 months.
2. Raksha biovac - FMD + HS
3. Raksha Triovac – FMD + HS + BQ, 3 ml by deep intramuscular route at mid neck
region. It is a homogenous double oil suspension (water in oil in water wmulsion).
Primary vaccination is done at 4 months of age, first revaccination is done 9 months after
the primary vaccination and subsequent revaccination will be done annually.
Adverse reactions due to repeated vaccinations:
In some animals allergic reaction has been observed in the form of wheal, or
nodules on the back and slight dyspnoea. This is due to various proteins present in the
tissue culture system.
The latest vaccine produced is by using genetic engineering technology or gene
splicing or DNA recombinant technology in USA. Out of these, viral protein-1 (VP-1) is
the most important one which is involved in the immune response against this disease.
Then the gene responsible for VP-1 is identified and separated and incorporated into E-
coli. This gene orders E-coli to produce VP-1. This protein is isolated and purified and
used as vaccine @ 250 µg/animal.
Immuno-modulators: It has been shown that when levamisole was administered 3 days
after FMD vaccination, the protection given was much more than the protection given by
the vaccine alone.
In Lab animals poly I:C when administered along with the FMD vaccine
potentiated the response by 10 times.
Sequalae to FMD: Many sequalae viz., Panting, overgrown hairs (hyper-trichosis),

infertility, sterility and overgrown hooves have been recorded in cattle recovered from
FMD after few weeks to few months.
Panting and overgrown hairs: The exact mechanism involved in panters is not clearly
understood. However, involvement of the thyroid gland is strongly suspected.
In normal animals, Thyroxine is the hormone produced by the thyroid gland and
one of the important function of thyroxine is thermoregulation.
In FMD, the thyroid gland is affected hence the amount of thyroxine produced is
reduced. Thus thermo regulation is affected and to remove the excess of heat from the
body the animals breath fast i.e., the respiratory rate is increased and hurried. This
condition is known as ‘panting’ i.e., hurried respiration. When such animals are exposed
to sunlight the panting is severe. Panting can be continuous or intermittent. In some
cases panting is more in night. Most of the persons will confuse this condition for
Asthma. The other signs noticed are drooling salivation, moderate increase in
temperature (l03-105°F) and decrease in milk production. Most of these animals will
have overgrown hairs also and the hairs will be thick and rough.
Diagnosis is done by clinical signs exhibited and the previous history of animal
having FMD and also by estimating the level of protein bound iodine (PBI) where this
level is decreased.
Recent study in this college ruled out the possibility of the involvement of
Prostaglandin-E in Panters.
Treatment:
1) Supplementation of thyroxine by administering Eltroxin or proloid or thyroxine tablets
0.1 and 1 mg tablets (100 tabs in one bottle).
Dose: 5 tabs bid/animal orally for 15-30 days.
Thyroglobulins were also tried in panters.
2) To increase the production of thyroxine iodine containing preparations like KI @ 5-6
gm/cow/day once in 3 days, 5 times may be used.
Most of the animals used to improve after the above treatment. In some animals in
the beginning the severity of the condition is increased and after few days the severity
goes on decreasing and within 1-2 months time, animal will be almost normal. In some
cases there may not be improvement at all.
3) Aspirin a Cox-2/3 inhibitor leading to decrease in PG-E has been tried in this college
@ 10 mg/kg body weight for 10-15 days orally but the animals were not cured.
To improve the condition of hairs, Acetylarson (M&B, 10 ml ampoule containing

23.6% of arsenic) @10 ml /cow, s/c or i/m everyday for 5 days or once in 3 days for5
times can be administered.
2. VESICULAR STOMATITIS
Vesicular stomatitis is an infectious disease caused by a virus mainly affecting
horses and also in cattle and pigs and is characterized by the development of vesicles in
the mouth and feet.
Etiology:
It is caused by a vesiculo virus belonging to the family: Rhabdoviridae. It is a
RNA virus. There are two antigenically distinct types namely New Jersey and Indiana.
There are 3 subtypes under Indiana namely Fort Lupton, Alagar (Brazil) and cocal
(Trinidad). The new Jersey strain is the most virulent and most common. The virus is less
resistant to environmental conditons than FMD virus.
Epidemiology:
a) Occurrence:
Cattle, horses, donkeys and pigs are susceptible. Goats and sheep are resistant.
Outbreaks are most common in cattle. Calves are much more resistant to infection than
adult cattle.
Occasionally human beings are affected and mild infection resembling influenza
occurs.
Geographically the disease is limited to the western hemisphere and is enzootic in
parts of North, Central and South America.
The morbidity rate varies considerably. It can be usually 5-10% and it can reach
even 80%. There is usually no mortality.
Deers can be an amplifier host.
Seasonal incidence - rapidly decreases with the onset of cold weather.
b) Transmission:
Mainly by ingestion of contaminated feed and water and also can be by ingestion
of contaminated pasture the virus enters the body.
Vectors also can play a role in the transmission since the virus isolated from biting
flies like Simulium vittatum, Phelobotumum spp., Sandflies and Aedes Spp. (Mosquitoes).
Pathogenesis: It is very similar to FMD.
Clinical findings:
It is very similar to FMD. However in some outbreaks involving thousands of
cattle, vesicles are not seen.
Oral lesions are common and lesions on the udder and feet are rare.
Recovery is rapid and affected animals are normal in 3-4 days.
Secondary complications are rare.
In horses, the clinical signs are similar to that of cattle. In pigs, the lesions are
commonly seen in the snout and feet and lameness is commonly seen, when compared to
other animals.
Diagnosis:
1. It is very essential to isolate the causative agent since the clinical signs of Vesicular
stomatitis are very similar to that of FMD. The saliva and vesicular fluid should be
collected and used for Animal inoculation test and culturing in developing chicken
embryos.
2. Serological tests - following tests can be used:
a) CFT can be used to differentiate VS from FMD virus and also in identifying the
strains.
b) Resin Agglutination inhibition test
c) Serum neutralization test
d) Counter immunolectrophoresis.
Vesicular stomatitis should be differentiated from
1) FMD
2) Vesicular exanthema - occurs only in pigs
3) RP
4) BVD
5) Bovine malignant catarrh.
Treatment: is similar to FMD.
Prevenion and control:
1. Good hygienic measures
2. Quarantine mesures
3. Vaccination - A formaline killed cell culture vaccine administered twice has been
experimentally used.
3. VESICULAR EXANTHEMA OF SWINE
Vesicular exanthema of swine is an acute, febrile, infectious disease caused by a

calicivirus and is characterized by clinical signs very similar to that of FMD, VS and
swine vesicular disease.
Etiology:
It is caused by a calicivirus and there are 13 strains wherein the virulence of the strains
varies. The virus can be outpored in tissue culture.
Epidemiology:
1) Occurrence: It has been reported from Hawai, Iceland and USA. This disease is
eradicated from USA in 1959. Only pigs are susceptible and all ages and breeds are
affected. It is a mild disease with a low mortality rate i.e., less than 5%. Severe loss of
body weight can occur. Pregnant sows may abort and lactating sows may go dry with
resultant heavy losses in baby pigs.
Experimental transmission to horses can occur.
2) Transmission: The sources of infection are infected live pigs and infected pork.
Infected pigs excrete the virus in saliva and faeces for 12 hours before vesicles develop
and for 1-5 days afterwards.
Raw garbage containing infected pork scraps is the most common medium of
spread from farm to farm.
On infected premises the disease is spread by direct contact. Ingestion of infected
material is sufficient to produce infection.
There is a hypothesis that the primary reservoir for vesicular exanthema is in
marine animals (Sealions, fur seals, grey whales, feral swine). Epizootics in pigs may
have been initiated by the feeding of marine meat or garbage containing marine animal
products.
Pathogenesis:
It is similar to that of FMD.
Clinical findings:
The incubation period is usually 1-3 days. The clinical findings are very similar to
FMD. In addition, the lesions are seen on the coronary skin, the sole, the heel bulbs and
between the claws. The lesions on the feet may predominate in some outbreaks wherein
they may be of little significance.
Recovery in uncomplicated cases is usually complete in 1-2 weeks.
Diagnosis:
1. By clinical signs this disease can be suspected and can be confirmed by Animal
inoculation test and by tissue culturing of the fluid from the vesicles.
2. Serological tests like CFT, VNT and AGPT have been used.
It is very difficult to differentiate from FMD, VS or swine vesicular disease by
clinical signs alone. It can be differentiated only by Animal inoculation test and
serological tests.
Treatment:
Hyper immune serum appears to be very effective. The other treatment used for
FMD can be tried.
1. Quarantine measures
2. Slaughtering of infected animals
3. Boil the garbage and then give it to the pigs.
4. The infected premises should be thoroughly cleaned and disinfect the area with
2% sodium hydroxide solution.
5. Do not feed the marine products.
6. Vaccinate the pigs with formaline killed vaccine.
4. SWINE VESICULAR DISEASE

Swine vesicular disease is an infectious disease of pigs caused by an enterovirus
and is characterized by clinical signs similar to FMD.
Etiology:
SVD is caused by an enterovirus belonging to the family picarnaviridae. This virus
is related to the Human coxseckie B5 virus. Several variants of the virus are now in
existance.
The SVD virus can be cultured in tissue culture and the characteristics can be
useful in distinguishing this virus from FMD, VS and VE. This virus is extremely
resistant to chemical and physical influences. It is inactivated by 2% sodium hydroxide,
8% formaline and 0.04% sodium hypochlorite.
Epidemiology:
1) Occurrence: SVD was first recorded in Italy in 1966, then in Hongkong in 1970,
England in 1972, many countries of Europe in 1972-74, Japan in 1973 and Malte in 1975.
2) Transmission: The sources of infection are oral and nasal secretions, vesicular fluid
and shed vesicular epithelium.
Infection generally occurs through minor abrasions on the feet. Transmission
occurs by direct contact.
The disease may also be spread by the feeding of uncooked garbage.
Pathogenesis: is similar to FMD.
Clinical findings:
Incubation period is 2-14 days. The morbidity rate varies from 25-65% and can
even go upto 100%.
The clinical signs are almost similar to that of FMD.
The course of the disease is 2-3 weeks and the mortality is uncommon.
Rarely CNS signs are observed.
Diagnosis:
1) By clinical signs SVD can be suspected. It can be confirmed by culturing in the tissue
culture.
2) Serological tests like FAT, CFT, VNT, AGPT, Counter immunoelectrophoresis and
ELISA have been used.
SVD should be differentiated from FMD, VS, VE and Foot rot in pigs.
Treatment:
No treatment is indicated. However treatment used for FMD can be used.
1) Slaughtering the affected and in contact animals
2) Disinfection of the area
3) Boiled garbage should be fed.
4) Use of inactivated vaccine may be useful.
5. RINDERPEST
(Dodda roga, RP, Mata, cattle plague)
The names given to Rinderpest in different places are:
Latin: Typhus bovum French: Peste bovine
Punjab :Burree Bengal: Pasunga
It is an acute highly contagious disease of ruminants and swines caused by a

paramyxo virus and it is characterized by high fever and focal erosive lesions mostly
confined to the mucosa of the alimentary tract.
Etiology:
Family: Paramyxo viridae
Genus : Morbilli virus
Species: RP virus, PPR virus, CD virus, Measles virus
It is a RNA virus, it is mostly spherical in shape but also can be ovoid and
elongated and measures about 100-300 nm. It is enveloped and envelope is having
spikes or projections and it is a single stranded RNA virus. The symmetry is helicle.
The virus is susceptible to ether, chloroform and β propiolactone. It is a very fragile
virus (can be easily killed) and when exposed to sunlight it is inactivated within two
hours.
It can be cultured in embryonic kidney, calf kidney, embryonic skin, testes,
thyroid and leukocyte tissue cultures (commonly used is calf kidney cell culture). In
these tissue cultures it produces cytopathogenic effect like giant cell formation and
syncytia formation.
Many strains of RP virus are available with varying pathogenicity. All the
strains are almost antigenically identical. Hence one strain gives protection against
the other strain.
Epidemiology:
a) Occurrence: It is enzootic in Asia, North and equatorial Africa. Countries like
Japan, Philippines, New Zealand and Australia are now free from this disease. It is not
recorded in the western hemisphere (Canada, USA). This disease is a very old disease
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because it is existing from time immemorial. It causes very severe economic loss,
because according to previous estimations the number of cattle died of RP is much
more than or almost-equal to the number of cattle died of all the other diseases of
cattle. The mortality rate is as follows:
Exotic and cross bred cattle -- 90-100%
Indigenous breed of cattle -- 20-50%
Buffaloes -- 75-100%
Sheep and goat -- 10-90%
Because of the RP eradication scheme (RPES) which was launched in India in
1954 for the control and eradication of RP, the outbreak and mortality have been
significantly reduced.
Animal Animals
Outbreaks
affected dead
Before RPES 8000 4 lakhs 2 lakhs.
Vth plan 130 2800 1200
Last 3 years
Since from last 6-7 years RP cases have not been recorded in India, the Office
International des Epizooties (OIE) has certified that our country is free from RP.
Sp. of animals affected:
1) Cattle: Cattle of exotic and cross breeds are severely affected. Indigenous breeds
are also affected but they are some what resistant.
2) Buffaloes
3) Sheep and goats: Previously they thought that RP was not affecting the sheep and
goats in a large scale. Now a day it is a very important disease in our country.
From 1942 in Ex-French territories of West Africa a disease called 'peste des petits
ruminants was recorded in sheep and goats. It was caused by a virus and the viral
characteristics were very similar to RP virus. Finally it was concluded that it is a RP,
caused by a strain of RP virus which has lost its virulance to cattle.
4) Swines
5) Camels: Disease produced but virologically not confirmed.
6) Many wild animals (Hippopotamus, Sambar deer, water bug, European Bison) are
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susceptible to RP virus and they suffer from this disease and many wild lives are
dieing of this disease. It appears that they may be the source of infection to domestic
animals.
b) Transmission: Most important mode of transmission is by close contact between
infected and non infected animals. It can be also transmitted by ingestion of
contaminated feed and water and by inhalation. The source of infection are all the
secretions and excretions of the affected animal i.e. saliva, nasal discharge, tears, urine
and faeces etc.
Even though many vectors have been shown to carry virus they will not
transmit the disease.
Pathogenesis: The virus enters the body through naso pharyngeal mucosa, goes to the
tonsils then to regional lymphnodes. It replicates and through the lymph enters the
blood in mononuclear cells. Then there will be viraemia which may vary from 3-10
days. The virus is having affinity for lymphoid tissue and epithelial tissue. Hence
through circulation the virus localizes in the epithelial tissue like the oral mucosa and
the gastro-intestinal tract. Here it causes congestion and haemorrhages and this is
commonly seen in the abomasum and through out the intestines. The haemorrhages
and erythema running transversely across the colonic mucosa and on the rectal folds
of mucosa will be clearly visible and gives an appearance of "zebra markings" which
is a pathognomonic lesion of R.P. It also causes pin point greyish-white necrotic
patches (1-5 mm) in the oral cavity and abomasum and the intestines. These lesions
are seen on the tongue especially on the ventral aspect of the tongue and they appear
like as though sprinkling of the bran on the mucosa. These will be sloughed off
leading to formation of erosion and later on small ulcers which can coalesce together
to form large ulcers.
The virus also localizes in the lymphoid tissue i.e., spleen and the payers
patches of the ileum. In the beginning congestion, oedema, hyperplasia leading to
hypertrophy/swollen appearance, hyperplasia and oedema can occur. As a result of
which there will be swelling and later on they will be sloughed off leading to crater
like lesions. Lysis of lymphocytes can occur resulting in leucopaenia. The respiratory
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tract is also affected where in congestion, oedema, haemorrhages and erosion can be
seen. In the lungs, pneumonic changes are seen and also emphysema can be seen.
Clinical findings: IP is 6-9 days. In the beginning there will be moderate fever like
104°F, depression, anorexia, restlessness, dry muzzle and constipation. Within 1-2
days nasal and lacrimal discharges appear, which will be in the beginning serous like
and later on becomes mucoid or mucopurulent. There will be excessive thirst,
photophobia, leucopaenia and rough hair coat. By 2nd or 3rd day oral lesions appear
and salivation is seen. The type of salivation is drooling salivation. The temperature
goes on increasing and by 3rd or 5th day it can be 106-108 °F.
Then diarrhoea starts and as a result of which the temperature drops down and
can be normal and at the ending stage it will be subnormal. Later on there will be
dysentery. The animals will be extremely dehydrated, weakness, sunken eyeball,
marked depression, subnormal temperature, recumbency, coma and death.
In the beginning there will be severe congestion of visible mucus membranes
especially the conjunctiva leading to blood shot eyes.
The course of the disease is 6-12 days.
Sheep and Goats: The clinical signs seen are fever, discharges from the eyes and
nostrils, salivation, diarrhoea, dysentery and pneumonic signs. The oral lesions are not
commonly seen.
In cattle respiratory signs like coughing, laboured breathing and the expirations
are halting type can be seen.
Pregnant animals can abort 3-6 weeks after onset of illness.
Skin form: is also being recorded wherein the systemic signs are absent and small
pustules are seen on the neck, wethers, inside the thighs and serotum.
Necropsy findings: Refer pathogenesis and some of the important findings are:
1. Erosions in mouth and erosions and haemorrhages in the abomasum and
intestines.
2. Zebra marking in rectal mucosal folds.
3. Crater like lesions in payer's patches.
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Diagnosis: RP in a single case is difficult to diagnose. Examination of a group of

animals for the signs and lesions should be considered while diagnosing RP.
1. By signs: oral lesions, fever, diarrhoea, blood shot eyes, respiratory signs.
2. By lesions: zebra marking, erosions in oral cavity, crater like lesions.
3. Isolation and identification of the causative agent. From a live animal during the
first four days of fever the (a) 30 ml of blood can be collected in a container having 10
ml of EDTA (EDTA 1.3 gm, Sodium chloride 0.7 gm. and Distilled water 100 ml) and
tongue scrapings, impression smear also can be collected.
(b) The biopsy material collected from the prescapular lymph node also can be
submitted. The suspected material is added to tissue culture and observed for CPE.
4. Serological test: Virus neutralization test, CFT, FAT, AGPT, IPT, SNT, ELISA,
CIEP and passive HA have been used. A rapid dot-enzyme immune assay test
suitable for field use has been developed.
In our country commonly AGPT is used.
For IPT & FAT you can send impression smears. Acetone is used as fixing agent
which increases cell permeability, Using specific cDNA probes isolates of RP and
PPR viruses can now be differentiated.
5. Cell-mediated immune response test (CMI test)
1) Lymphocyte stimulation test: The RPV causes immunosupression. Hence
mitogenic and antigenic response of lymphocyte is reduced.
2) Allergic test: Not successful.
Differential Diagnosis: RP should be differentiated from BVD, FMD, Vesicular

stomatitis, Malignant catarrhal fever, Coccidiosis, Salmonellosis, IBR and Arsenic
poisoning.
Treatment: Before treatment of RP cases it is the bounden duty of Veterinarian to

inform RPES, Bangalore. The following treatment may be useful.
1. To overcome secondary bacterial invaders give a course of broad spectrum
antibiotic like OTC.
2. To overcome dehydration and metabolic acidosis, give lactated ringer's and
Sodium bicarbonate solution.
216
3. To supplement energy, administer 5-10% dextrose by i/v.

4. If there is too much of blood loss due to dysentery think of blood transfusion.
5. To soothen the gastro-intestinal mucosa administer astringent mixture, ie., kaolin,
pectin, catechu and creta preparata.
Control: The RPES was started in 1954 and its objectives were-
1) Strict quarantine measures: When there is an outbreak that area was cardoned off
to prevent the entry and leaving of animals from that village i.e., quarantine measures
were strictly followed.
2) To develop good resistance in susceptible animals by massive vaccination
programme. Here all the animals i.e., cattle, buffaloes, sheep, goat and pigs of 6
months and above of age of that area and the surrounding areas were compulsorily
vaccinated. After vaccination branding mark was applied on the hind quarters, to
identify vaccinated animals. For this purpose an RPES squad was given which
comprised of a veterinarian, few VLJs and few animal attenders. This squad was
also provided with a jeep.
3) Separating the affected animals from healthy animals and treating the affected
ones.
From April 1992, the National project for Rinderpest Eradication (NPRE) has
been implemented to achieve RP zero i.e., complete eradication of RP from our
country.
The following vaccines have been used.
1) Goat tissue vaccine (GTV): it is a live attenuated vaccine. Here the virulant RP
virus was repeatedly passaged in goats and at the 250th passage the virus was
attenuated i.e., at this stage the virus was unable to produce disease in cattle.
Such attenuated virus was stored and used for preparation of vaccine. Here this
virus was injected to goats and at the height of the fever i.e., 3rd day, the goats were
slaughtered and the spleens were collected. These spleens were ground and the
required quantity was placed in ampoules, sealed and freeze dried.
The ampoule may contain 0.125 or 0.25 gm of the freeeze dried vaccine. The
ampoule was broken and the contents were transferred into a mortar, then small
217
quantity of chilled normal saline was added and the contents were triturated by using
pestle and mortar. Then the remaining normal saline was added and the contents were
mixed. If it is 0.125 gm ampoule then 50 ml of normal saline was added and if it is
0.25 gm ampoule then 100 ml of normal saline was added. The contents are
transferred to a sterilized beaker and the beaker was kept on ice.
Dose: 1ml s/c.
Type of animals vaccinated: This vaccine is used for native (indigenous) breeds of
cattle. It is not used in exotic or cross bred cattle and sheep and goats. It causes RP in
sheep and goats.
Duration of immunity: minimum of 5 years and maximum of life long. In advanced
stage of pregnancy and calves below 6 months of age should not be vaccinated with
this type of vaccine. This vaccination has been used in indigenous breeds of cattle for
a very long time. It has played a very important role in reducing the incidence of RP
in our country. This vaccine has been withdrawn and not in use in India.
2) Cell culture vaccine/RP tissue culture vaccine (TCV).
Kabete '0' strain of RP virus has been repeatedly cultured in calf kidney cell culture
and at the 90-96 passage the virus got attenuated. After 96 passage the virus is
stored by freezing. ,
Whenever the vaccine is produced, the seed virus is inoculated into the calf kidney
cell culture and observed for CPE. Once CPE develops the tissue culture is harvested
and processed, transferred to ampoules or vials and freeze dried.
The ampoule is broken and the contents are transferred into a morter and a small
quantity of physiological saline is added. The contents are triturited and then rest of
the physiological saline was added. The total amount of physiological saline used is
100 ml/ampoule. The contents are transferred to a beaker and the mouth of the beaker
is closed with aluminium foil. Immediately the animals will be vaccinated.
Dose: 1 ml, s/c.
Types of animals vaccinated: Exotic cross bred and indigenous cattle, sheep, goats,
pigs, buffaloes and the dose is 1 ml, s/c. Animals in advanced stage of pregnancy is
also vaccinated. Calves of any age can be vaccinated but commonly of 6 months and
above of age are vaccinated. If any calf under 6 months of age are vaccinated, it is
218
better to revaccinate the calves when they are of 6 months and above of age.
This was the only vaccine available now in our country for the prevention and
control of RP. From last 6-7 years our animals are not vaccinated for RP.
3) Lapinized vaccine: Here the virus is repeatedly passaged in rabbits and at 700-800
passages the virus gets attenuated. While preparing the vaccine this attenuated virus is
inoculated into the rabbits and on the 3rd day the rabbits are killed. The blood, spleen
and mesenteric lymph nodes are used in vaccine production. The contents of one
ampoule is reconstituted in 80-160 ml of normal saline.
Dose: is 1 ml, s/c in exotic and cross bred cattle. This vaccine is of historical
importance only i.e., now it is not commonly used because lot of rabbits are required
to produce huge amount of vaccine.
4) Chicken embryo adopted vaccine: The virus is repeatedly passaged in developing
chicken embryoes, so that it gets attenuated. This attenuated virus is used for
preparing the vaccine from the developing chicken embryoes. This is also not
commonly used.
5) Lapinized avianized vaccine: Here the RP virus is repeatedly passaged in the
rabbits for the virus to get attenuated. This attenuated virus again passaged in
developing chicken embryoes for the further attenuation i.e., why it is known as
lapinized avianized vaccine.
6) Killed or inactivated vaccines: In the olden days this method was used, but later on
discontinued. Now it appears that killed vaccines are needed for vaccination of
animals in countries where RP does not occur but the risk of its introduction is high.
7) Measles vaccine: This vaccine can be used in calves and adult cattle. It is used in
calves born to immunized dams where in the above vaccines do not elicit good
immune response due to interference from colostral antibodies.
8) Recombinant vaccines: Such vaccines are being under trial now. This can be used
in calves having maternal antibodies. This vaccine appears to be not expensive.
9) 2001 – Intranasal vaccine for RP: Powder form, applied intranasally and gave
protection.
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6. PESTE DES PETIS RUMINANTS

(PPR, Goat Plague or Kata)
Peste des petits ruminants is an acute, highly contagious viral disease of goats
and sheep caused by a morbillivirus (Paramyxovirus) and is characterized by fever,
anorexia, necrotic stomatitis, diarrhoea, oculo-nasal purulent discharge and respiratory
distress.
Etiology:
PPR is caused by a morbilli virus (belonging to the paramyxoviridae family)
and is closely related to rinderpest virus, canine distemper virus and measles virus.
The African and Asian strains have some biochemical differences.
Epidemiology:
a) Occurrence: It is a RP like disease in Africa and Asia and is highly fatal in goats
and less so in sheep. It was first described in West Africa in 1942. It is possible that
some of the earlier reports of RP in sheep and goats in Asia might have been PPR as it
is very difficult to differentiate them by clinical manifestations.
In India, it was first reported in Tamilnadu in 1989 and then in different states
by several workers. It was reported in Andhra Pradesh in 1991 and then later on in
1997 and 1998. Also Sudarshana et al. (1995) provided data on the seroprevalence of
PPR and RP specific antibodies in small ruminants in Karnataka. Since then several
reports were published in Karnataka.
During the past 7 years many of the states of our country have reported PPR as
a major morbilli virus infection of small ruminants. Currently the differentiation of
RP and PPR are being done and reported separately as per OIE guidelines. India is
free from clinical RP for the past 6 years.
The state wise RP/PPR status during the last 7 years indicate that out of 32 states
only 7 states comprising of HP, West Bengal, Orissa, MP, AP, TN and Karnataka
encountered attack ranging from 2 to 4,080 cases per million susceptible population.
Except a few cases of RP in southern states, the rest of the cases are of PPR. The
remaining 25 states and union territories have not reported or had negligible cases of
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PPR.
Cattle and pigs can have the antibodies but do not come down with the disease
upon inoculation of PPR virus. Natural disease may occur in the Gazelle, Laristan
sheep, gemsbok and ibex. Deers are susceptible. The domestic and wild animals may
not act as reservoirs.
Outbreaks invariably occur when new stock is introduced into a farm.
Morbidity rates can range from 50-90%. The case fatality rates are higher in goats
(55-85%) than in sheep (less than 10%). Goats are more susceptible to PPR than sheep
and kids over 4 months and less than 1 year of age are most susceptible.
b) Transmission:
Infection is mainly by inhalation and also can occur through the conjunctiva and
oral mucosa. Insects are not regarded as vectors of the virus. Large amounts of the
virus are present in all body excretions and secretions of the affected animals.
Pathogenesis:
PPR virus penetrates the retropharyngeal mucosa and enters the blood and
causes the viraemia. Then it localizes in the alimentary, respiratory and lymphoid
systems and damages them. This results in severe diarrhoea, dehydration and death. In
some, diarrhoea is followed by pneumonic signs.
Clinical findings:
Two forms of the disease viz.. acute and subacute forms have been recorded,
1). Acute form: It is mainly seen in goats and is almost similar to RP. Incubation
period is about 3-6 days. Initially high fever, dullness, sneezing and serous discharge
from the eyes and nostrils are seen. After a day or two, there will be discrete necrotic
lesions in the mouth which can spread to the entire oral mucosa forming diphtheritic
plaques. Then there will be halitosis and anorexia. The nasal and ocular discharges
become mucopurulent, which will dry up leading to matting of the lids and partial
occlusion of the nostrils. Within 3-4 days of fever, there will be diarrhoea which is
profuse and the faeces may contain mucous and even blood. Then coughing
and dyspnoea will occur which will be worsened by seconday bacterial invaders.
Superficial erosions also have been recorded in the mucosa of the vulva and prepuce.
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The animals can die within a week.

2). Sub acute form: This form is common in sheep and can be seen in goats also. The
clinical feature is mild and few animals may die within 2 weeks. However, majority
of the animals will recover.
Necropsy findings:
Discrete or extensive areas of erosion, necrosis and ulceration are present in the oral,
pharyngeal and upper oesophageal mucosa and can extend upto abomasum and small
intestine. Zebra markings are seen in the ileo-caecal region, colon and rectum. The
retro-pharyngeal and mesenteric lymph nodes are enlarged and the spleen may be
enlarged. Muco-pumlent exudate in the nostrils and upto the larynx, congestion and
oedema of the trachea and bronchi are seen. Pneumonic changes like red consolidation
and atelectasis particularly of the right lobe is very common. Purulent or fibrinous
broncho-pneumonia and pieuritis due to complications with secondary bacterial
invaders can be seen.
Diagnosis:
1. The clinical signs and necropsy lesions are suggestive of PPR.
2. Isolation and identification of PPR virus confirms the diagnosis. For this purpose
ocular, nasal and pharyngeal secretions and faeces of affected animals should be
collected and submitted to a laboratory. From the carcasse, lymph .nodes and tonsils
should be collected. For histo-pathological studies, a piece of lung, small and large
intestine, oral mucosa and mesenteric lymph node should be collected and submitted
to a laboratory.
3. Serological tests like Agar gel precipitation test (AGPT), counter immuno-
electrophoresis technique, serum neutralization, complement fixation test (CFT), dot-
ELISA and cDNA probes have been used.
PPR should be differentiated from Rinderpest, Blue tongue, Pneumonic
pasteurellosis, Contagious caprine pleuro pneumonia, Contagious ovine pleuro
pneumonia, entero-toxaemia and coccidiosis. It is very difficult to differentiate PPR
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from RP and Blue tongue and the best way is to either by isolating and identifying the
causative agent or by serological tests.
Treatment:
The following therapeutic measures may reduce the severity and may even save the
animals:
1. A broad spectrum antibacterial agent is administered parenterally to overcome the
secondary bacterial invaders.
2. Good amount of fluids like Lactated Ringers solution is administered parenterally.
3. Frequent cleaning of the eyes, nostrils and mouth is required.
4. Give liquid diet tike jowar or rice or ragi gruel with jaggery, salt and Sodium
bicarbonate in small quantities repeatedly.
5. Give astringent mixture or neblon or diaroak orally.

1. Prevent the entry of new stock from unknown sources. It is better to isolate the new
stock and test them for PPR and then allow them with the old stock.
2. PPR vaccine is now available in our country. IVRI, Izatnagar has prepared this
vaccine which is similar to RP tissue culture vaccine and the dose is 1 ml, s/c which
may cost Rs.1.10. The vaccination should be done at the age of 3-4 months and
repeating after one year.
7. BOVINE VIRUS DIARRHOEA

(B.V.D, Mucosal disease complex)
It is a mild to very severe disease of cattle caused by a Toga virus and is
characterized by fever, erosions and ulcers in the alimentary tract mucosa, corneal
opacity, and the lesions in the foot.
The virus comes under the Family: Toga iridae
Genus : Pesti virus.
The virus is having cubicle symmetry and enveloped and measures 30-70 nm. It
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is seen mostly in cattle and young animals in the age group of 8 months - 2 years. The
disease can be very mild to very severe depending on the virulence which can be non-
pathogenic to highly pathogenic. Hence the mortality rate can be very low to very
high. Congenital transmission of this virus with tolerance has also been recorded.
The virus is present in mononuclear (MN) cells of blood. Hence blood should
be submitted for culturing in addition to faecal swab, nasal swab and tongue scrapings.
This virus grows well in turbinate cells and cardiac cells and the CPE produced
is vacuoles.
The lesions seen are erosions, ulcers in the oral cavity and g.i., tract. Payer's
patches are also affected like in RP. But zebra markings in rectal mucosa are not seen.
10% of the cases will have corneal opacity and 10% of cases may have foot
lesions like FMD.
Good vaccines which are highly potent are not available. This is the most
common disease in USA and Canada causing severe economic losses.
The main differences between RP and BVD are:
Particulars Rinderpest BVD
1.Sp. of animals affected Cattle, buffaloes, sheep, Only cattle
goats & swine
2.Mortality 90-100% Low to High
3.Lesions Erosions and ulcers Erosions and Ulcers
4.Eye form Absent Present
5.Foot lesions Absent Present
6.Good vaccines Available Highly potent vaccines
are not available
8. BOVINE MALIGNANT CATARRH

(Malignant Head Catarrh, Malignant catarrhal fever)
Bovine malignant catarrh (BMC) is an acute, highly fatal infectious disease of
cattle and farmed deer caused by a virus and it is characterized by the development of
an erosive stomatitis and gastroenteritis and erosions in the upper respiratory tract,
kerato-conjunctivitis, encephalitis, cutaneous exanthema and lymph node enlargement.
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Etiology:
BMC is really two diseases, clinically and pathologically indistinguishable, but
caused by two different infectious agents namely:
1. Alcephine BMC Virus (Wildebeest associated Virus, bovid herpesvirus 3, AHV-1)
and is transmitted from blue wildebeest.
2. An unidentified infectious agent (sheep associated BMC virus) probably a
herpes virus, similar to AHV-1 and transmitted from sheep.
Both the viruses are not transmitted from the one cattle to other cattle. Also they
will not cause disease in their principal host i.e., wildebeest and sheep.
The sheep associated agent is difficult to isolate from the blood. The agent has
been transmitted with difficulty by intracerebral inoculation in rabbits to hamsters and
to other cattle by transfusion of large volumes of blood.
The African virus is the wildebeest associated virus and it can be readily
transmitted by several routes. It has been adapted to grow on egg yolk sac and tissue
culture and transmission to rabbits-to yolk-sac-to cattle has been achieved.
Epidemiology:
1) Occurrence:
BMC occurs in most countries but most frequently in Africa and at a low
incidence in the USA, Canada, Australia, New Zealand, Europe, Scandinavia and the
East Indies. African BMC occurs in most African countries in cattle which co-mingle
with clinically normal wildebeest and hartebeest.
European-American-Australian BMC occurs in outbreak form in cattle which
co-mingle with sheep and sporadically in cattle running as sole cattle herds.
The disease is almost invariably fatal. The morbidity rate varies. Commonly it
occurs as isolated cases and rarely as outbreaks affecting 50% cattle. Commonly
occurs in late winter, spring and summer.
The clinical disease occurs only in cattle and buffaloes and inapparent infection
in sheep and goats among the domestic animals, Blue wildebeest in Africa, white
tailed deer, housed red deer, buffalo, American and European bison are also affected.
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2) Transmission:
The mode of transmission of sheep associated BMC is unknown and probably it
may be by ingestion.
Vaginal discharge of ewes after lambing, congenital from ewes to lambs?
Vector borne ?
The method by which wildebeest associated BMC spreads naturally is
uncertain. It may be probably by inhalation of aerosal or ingestion of pasture
contaminated by virus excreted by young wildebeest (upto 3 months) in nasal and
ocular discharges. Spread by direct contact between cattle does not seem to occur.
Pathogenesis:
BMC is a fatal, multisystemic disease characterized by lymphoid hyperplasia,
and widespread vascular epithelial and mesothehal lesions which are morphologically
associated with lymphoid cells. Involvement of the vascular adventitia accounts for the
development of gross lesions, including the epithelial erosions and
keratoconjunctivitis. The lymph node enlargement is due to atypical proliferation of
sinusoidal cells and the cerebromeningeal change, usually referred to as encephalitis,
and is in fact a form of vasculitis. There is commonly a synovitis, especially involving
tibiotarsal joints. This is associated with a lymphoid vasculitis. The disease is
essentially an immunological dysfunction in which a subset of T lymphocytes is the
target. Subsequent changes result in widespread Iymphoid cell hypoplasia and tissue
necrosis, the characteristic lesions of BMC.
Clinical findings:
The incubation period varies from 3-8 weeks. However after artificial infection
it is 22 days (14-37 days).
BMC is described as occurring in a no. of forms but these are all gradations and
depending on the predominent clinical signs, the various forms have been described.
1. Head and Eye form: In this form, there will be high fever (106-107°F), anorexia,
agalactia, increase in heart rate (100-120 per minute), a profuse mucopurulent nasal
discharge have been recorded. Due to obstruction of the nasal cavities with exudate
there will be dyspnoea and stertorous sounds can be heard.
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There will be ocular discharge, oedema of the eyelids, biepharospasms and

congestion of scleral vessels. Corneal opacity is always present and occurs as a narrow
gray ring at the corneo-scleral junction and spreading centripetally.
There will be a diffuse reddening of the buccal mucosa on the 19th or 20th day
after infection. Discrete local areas of necrosis appear on the hard palate, gums and
gingivae. Due to pain, the animal moves its jaws carefully with a smacking sound. It
will be difficult to open the mouth. The erosive mucosal lesions may be localized or
diffuse and occur on the hard palate, the dorsum of the tongue, the gums below the
incisors, the commissures of the mouth or inside the lips. There is excessive salivation
and the saliva is ropy, bubbly and hanging from the lips.
The skin of the muzzle is extensively involved commencing with discrete patches
of necrosis of the nostrils, which soon coalesce causing the entire muzzle to be covered
by tenacious scabs. Similar lesions may occur at the skin-horn junction of the feet
especially at the back of the pastern. The skin of the teats, vulva and scrotum in acute
cases may slough off entirely on touching or become covered with dry tenacious scabs.
The horns and rarely the hooves may be shed.
Nervous signs like weakness in one leg, inco-ordination, muscle tremors,
nystagmus, head pushing, paralysis and convulsions are seen. Trismus also occurs.
Superficial lymph nodes are enlarged.
The consistency of the faeces varies from constipation to profuse diarrhoea with
dysentery. In some cases there is gross haematuria with the red colouration most
marked at the end of urination.
The course of the disease is 3-7 days and rarely can go upto 14 days. Some
animals will have apparent recovery but usually will die within 7-10 days due to acute
encephalitis.
2. Peracute or Alimentary tract form:
The course of the disease is short and it is about 1-3 days. The clinical signs of
this form is different from that of the head and eye form.
High fever, dyspnoea, marked diarrhoea and minor eye changes like
conjunctivitis are seen.
This form can occur as an outbreak when cattle are in indirect contact with
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sheep. This is characterized by brief period of slight illness followed by the final
fulminating disease.
3. Mild form:
This form has been recorded most commonly in experimental animals. In this
form there will be a transient fever and mild erosions on the oral and nasal mucosae
and usually animals will recover.
Diagnosis: It is based on
1) Clinical signs and lesions.
2) Isolation of causative virus by doing transmission to cattle or rabbits by using whole
blood (500 ml), nasal swabs or washings and lymph node extracts.
3) Haematological studies - leukopaenia at first illness and progressing to a level of
3000-6000/µl and this is due to agranulocytosis. Usually moderate leukocytosis is
seen.
4) Serological tests -
a) VNT
b) FAT For the detection of African (Wildebeest-associated) virus.
c) CFT
d) ELISA
The sheep-associated infectious agents undetectable serologically.
Necropsy findings:
Minor degrees of haemorrhage and erythema through extensive, severe
inflammation to discrete erosions occurs in the mouth, nasal cavities and pharynx.
They may be shallow or deeper and covered by cheesy diphtheritic deposits.
Longitudinal, shallow erosions are present in the oesophagus. Erythema, or
haemorrhages or erosions can occur in a mild form in the fore stomachs and more
marked in abomasum catarrhal enteritis of moderate degree and swelling and
ulceration of the payer’s patches are constantly seen. The faeces may be loose and
blood stained.
Similar lesions can occur in trachea and sometimes in the bronchi but lungs are
not involved.
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Liver is swollen and degenerated. All lymph nodes are oedematous, swollen and
often haemorrhagic. Peterchial haemorrhages in the brain and meninges occurs.
Histologically BMC is characterized by perivascular, mononuclear cell cuffing in
most organs and by degeneration and erosion of affected epithelium. The
pathognomonic lesions are a necrotizing vasculitis, thrombosis, infiltration of tissue
with dividing lymphocytes and macrophages and an intense inflammatory reaction
with hyperaemia and exudation of fluid pointing to a hypersensitivity like reaction.
Acidophilic, intracytoplasmic inclusion bodies in neurons have been described and
controversy exists.
BMC should be differentiated from
1. BVD
2.RP
3. IBR
4. Pneumonic pasteurellosis
5. Sporadic bovine encephalomyelitis
6. Calf diphtheria.
Treatment:
Treatment of affected animals is unlikely to influence the course of the disease.
Non steroidal anti inflammatories may ease the discomfort.

1. Isolate the affected cattle.
2. Separate the cattle and sheep
3. Avoid the introduction of sheep from areas where the disease has occurred,
4. Vaccination is not successful eventhough good antibody titres occurs after
vaccination indicating that CMI plays an important role in giving protection.
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9. INFECTIOUS BOVINE RHINOTRACHEITIS

(IBR, Red nose)
It is an infectious disease of cattle caused by a herpes virus and it is

characterized by pneumonic form, eye form, abortion form, encephalitic form,
systemic form and vulvo-vaginal form.
Etiology: IBR virus known as Bovine herpes virus-1 comes under the
Family : Herpeto viridae
Genus : Herpes virus.
It is a DNA virus, spherical in shape, enveloped and having cubicle symmetry.
The CPE produced is rounding off of the cells. The virus replicates in the nucleus and
hence intranuclear inclusion bodies are produced.
Epidemiology:
a) Occurrence: IBR has been recorded in many countries of the world. It is common
in USA, Canada, New Zealand, Australia, UK, Africa, Europe and Asia. Recently
according to the 1985 report by Singh et al, in several dairy forms of our country about
47.63% were serologically positive for IBR. According to ADMAS studies from 1995-
98 from 11 states of India, the seroprevalence of IBR in cattle is 45% and in buffaloes
is 11%. The disease is more severe in beef cattle when compared to dairy cattle. All
ages and breeds of cattle are susceptible.
Type of cattle Morbidity rate Mortality rate
Beef cattle 20-30% 6-12%
Dairy cattle 8% 3%
According to one estimate economic loss due to reduction in milk yield, body
condition and abortion is 25-50 US dollars/cow. Commonly cattle are affected,
however, goats, swine and buffalo can be affected but their significance is unknown.
Wild ruminants like various types of deers are also susceptible.
b) Transmission: Commonly the IBR virus is transmitted through inhalation and also
can be by contact and natural service or artificial insemination.
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Pathogenesis: Upon inhalation the virus gets into the respiratory tract causing rhinitis,
laryngitis and tracheitis and then can get into the circulation causing viraemia and then
localizing in the respiratory tract, eye or mucosa of the vagina or vulva. The virus also
can get into the meninges and brain causing non-purulant leptomeningitis and
encephalitis.
In the mucosa, it causes congestion and later on formation of small pustules.
These pustules coalesce together to form white necrotic patches. These patches
contain firbrin, leucocytes and necrotic epithelial cells. These lesions are commonly
seen in nostrils, larynx, trachea, conjunctiva, vulva and vagina. This is the
characteristic lesion of IBR. When this necrotic material is removed ulcers can be
seen.
Clinical signs:
1) Respiratory form/pneumonic form:
IP: 3-7 days. This is the classical form of IBR. Clinical signs noticed are high
fever (106-108°F), decreased milk production, anorexia and depression. The mucosa
of the nostrils are severely congested and appears pink i.e., why it is also known as
red nose. Nasal discharge is seen in the beginning and then becomes mucopurulant.
Sneezing, coughing, hurried respiration and laboured breathing (dyspnoea) occurs.
Upon ausculation vesicular murmurs are increased. Finally open mouth breaming can
also be seen. Lesions of IBR on the nasal mucosa are seen.
2) Eye form:
Initially conjunctivitis characterized by serous discharge in the beginning and
mucopurulant discharge later on, congestion of conjunctiva and later on IBR lesions
and corneal opacity can occur.
3) Abortion form:
Abortion can occur at any stage of gestation but commonly occurs in the last
trimester of gestation. About 25% of the pregnant cows can abort. Aborted foetuses
will be dead several (2-5) days before their expulsion. Hence the lesions in the foetus
cannot be seen properly. However upon histopathology of the liver, adrenal glands and
kidneys, focal areas of necrosis with intra nuclear inclusion bodies are seen and this is
pathognomonic lesion of IBR.
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ROP also can occur. Such cases can end in metritis and temporary failure of
conception.
4) Encephalitic form:
Calves less than 6 months of age are affected. Salivation, inco-ordination,
circling, licking at the flanks, convulsions, blindness, recumbency, coma and death
occurs.
5) Systemic form:
Seen in neonatal calves where in it is severe and highly fatal. High fever,
respiratory distress, excessive salivation, rhinitis and conjunctivitis, hyperaemia of the
oral cavity, erosions on the soft plate, acute pharyngitis and laryngitis. Most of the
calves die.
6) Infectious pustular vulvo-vaginitis (IPV):
The first sign noticed is failure of the tail to return to its original position, after
defaecation/micturition. This indicates perineal pain and proper examination reveals
oedema, mucopurulant discharge, pustules and white necrotic material on the mucosa.
In bull, it causes severe balanoposthitis with IBR lesions. The bulls get the infection
during coitus and they can transmit the virus through semen.
Necropsy Endings:
Refer to pathogenesis.
Diagnosis:
1. By clinical signs of various forms of IBR.
2. By lesions of live animals and histological changes of aborted foetus.
3. By isolation and identification of IBR virus. Materials collected form the live
animals are nasal swabs. In the initial stages where, the nasal discharge is serous in
nature is a very good material. The other samples to be collected are conjunctival
swabs, vaginal swabs and also blood buffy coat and from a carcasse -trachea, lungs.
4. Serological tests like SNT, FAT, DPT. ELISA and FAT are commonly used.
The definitive diagnosis of IBR is difficult as development of serum neutralizing
antibodies is slow (upto 18 days) and the duration of demonstrable titre is extremely
variable between animals. Hence serological diagnosis is not enough and it should be
coupled with clinical findings and isolation of the virus.
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5. CMI test like lymphocyte stimulation test, macrophage migration inhibition test and
allergic test are also used.
BVD, RP, Malignant catarrhal fever - all have oral lesions and same is not
found in IBR. Shipping fever and allergic rhinitis also should be considered.
Treatment:
1. Good nursing care.
2. Administer a course of broad spectrum antibiotics.
3. To reduce the respiratory distress and coughing administer expectorant and avil.
4. To eye form, 2-deoxy-D-glucose at a concentration of 20 mg/ml has been used as
eye drops twice a day and the animals recovered from this form. However it is
useless if it is administered i/v.
1. General hygienic measures.
2. By vaccination. Vaccines used are-
a) Modified live virus vaccine for i/m use, should not be used in pregnant cows.
b) Modified live virus vaccine for intranasal use: Can be used in pregnant cows. Here
vaccine is administered intranasally so that the local immune response occurs in the
respiratory tract. Here IgA and interferon is produced, which will give protection.
c) Subunit vaccine: Envelope is used for production of vaccine. No question of
transmission to other animals. The administration of interleukin enhances the effect
of sub unit vaccines.
b) Inactivated vaccine - controversy exists.
Recently a vaccine is available in our country of tissue culture inactivated oil
adjuvant IBR vaccine (Intervet Lab., Hyderabad) known as Ibrivax (20 ml container)
and the dose is 2 ml s/c and the duration of immunity is one year and hence has to be
repeated annually.
Rapid diagnositic kit will be released by Hoechst Roussel Vet in collaboration
with BAIF in India shortly.
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10. BLUE TONGUE

Blue tongue is an infectious disease mainly of sheep and occasionally of cattle
caused by an orbivirus (Reo virus) and is characterized by catarrhal stomatitis, rhinitis
and enteritis and lameness due to laminits and coronitis.
Etiology:
Blue tongue virus (BTV) is an arthropod-borne orbivirus in the family
Reoviridae. It measures about 50-80 nm. It is a RNA virus and produces large
cytoplasmic inclusion bodies. There are 24 serotypes recorded in the world and one
will not give protection against the other. The serotypes recorded in India are 18 (1, 2,
3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 14, 15, 16, 17, 19, 20 and 21).
The BTV are stable and resistant to decomposition and sodium carbonate. They
are susceptible to 3% sodium hydroxide solution and complex organic iodides.
Epidemiology:
a) Occurrence:
BT is common in many countries of the world. It has been recorded in African,
American, Australian and Asian continents wherein some parts are endemic.
BT was first reported by Hutcheon (1881) as epizootic catarrh from Africa.
From African continent, the disease moved towards Europe and further to North
America. In the Indian sub-continent the disease was first reported from Pakistan in
1959. Subsequently the first outbreak of BT in India was recorded by Sapre in 1964
among sheep and goats of Maharashtra state. Later on, it has been recorded from many
states of our country. An USDA sponsored project entitled 'Studies on epidemiology
and immunobiology of Blue tongue virus' in collaboration with the CCS Haryana
Agricultural University, Hisar, Haryana was implemented and research work on this
aspect was done. It covered 5 North Indian states (Haryana, HP, Jammu and Kashmir,
Punjab and Rajasthan).
Under natural conditions infection occurs in sheep and cattle. Clinical BT outbreaks
in sheep occur throughout the year in different geoclimatic regions of India and cause
colossal economic losses. The outbreaks have been reported in exotic, crossbred and
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indeginous sheep, but exotic and crossbreds are severely affected. In Karnataka the
disease has been reported from many northern and eastern districts where the sheep
population is high. The incidence of BT is usually noticed at the end of southeast
monsoon and the beginning of northeast monsoon when the breeding and population
of culicoides is at its peak.
The past 10 year data indicate that only 7 states (AP, Karnataka, Kerala, TN,
Maharashtra, HP and Gujarat) out of 32 states of our country encountered the attack
rate ranging from 3 to 8,747 cases per million susceptible population. Highest attack
rate is seen in AP and lowest in Gujarat. Twenty five states and union territories did
not report nor had negligible cases of blue tongue.
The disease has been also recorded in Elk, white tailed deer, pronghorm
antelope, camels and other wild ruminants. Natural infection rarely occurs in goats but
the infection can be transmitted experimentally.
In India, clinical disease in cattle and buffaloes has not been reported and
majority of the workers is of the opinion that cattle are reservoirs of BT virus for
sheep.
When the disease occurs in a flock for the first time the incidence of clinical
disease may reach 50-75% and the mortality 20-50%.
It is one of the common diseases of sheep in our country causing severe
economic loss, which may be due to:
1. Mortality
2. Loss of wool
3. Overgrown hooves
4. Wrinkling and crackling of skin.
b) Transmission:
BTV is mainly transmitted by the vectors. Both biological and mechanical
vectors are involved.
1) Biological vectors: BT virus is biologically transmitted by certain species of
Culicoides (called as kurudu nona in kannada). There are about 1000 species of
culicoides in the world and only 7 have been shown to transmit the disease. 42 out of
46 species of culicoides have been identified in India and the exact species involved in
235
the transmission of BT virus is yet to be identified. The cycle of transmission in the

vector takes 10-15 days and the flies infective for life (about 70 days). Culicoides are
about 1-5 mm in length and can pass through the mosquito net or screen and can bite
humans and cause allergic reaction. They breed very well in swampy areas, stagnant
water and hot and humid conditions are good for their multiplication.
2) Mechanical vectors: Here the BT virus without multiplication in the vector is
transmitted from one animal to another animal. The sheep ked (Melophagus ovinus)
acts as a mechnical vector. Mosquitoes may play a role in transmission and Aedes sp.
and Anopheles sp. is suspect.
Pathogenesis:
The virus gets into the circulation through the bite of the vector, then there will
be viraemia and localization in the endothelium of the oral cavity, nasal cavity and
lamina and coronary band. Initially there will be congestion and oedema. Due to
stagnation of blood in the vessels, the tongue appears cyanotic i.e., blue in colour i.e.,
why the disease is called as "blue tongue". Later on necrosis leading to sloughing of
the mucosa, resulting in ulcers on lateral borders of the tongue can occur. In the
muscles there will be hyaline degeneration and haemorrhages.
The lesion that is perhaps most consistent and closest to pathognomonic for Bt
is focal haemorrhage, petechial or upto 1 cm wide by 2-3 cms long in the tunica media
at the base of the pulmonary artery. These haemorrhages are visible from both the
internal and adventitial surfaces and may be present in clinically mild cases with few
other lesions. Another important finding is the formation of pseudo-membrane in the
dental pad.
Clinical findings:
IP is less than a week.
1. Sheep: Initially there will be fever (105-106°F), anorexia, increase in heart and
respiratory rates. By 48 hours there will be discharge from the nostrils and eye which
will be serous in the beginning and becomes mucopurulant later on. There will be
excessive salivation which will be drooling in the beginning and later it can be ropy.
Severe congestion of the oral mucosa especially of the tongue resulting in cyanosis
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(blue colour), hence known as 'blue tongue' disease. Later on ulcers occur on the
lateral borders of the tongue and thus the saliva can be blood mixed. Swelling and
oedema of the lips, gums, dental pad and tongue can occur. Respiration is obstructed
and stertorous. Diarrhoea and dysentery can be also seen. Laminitis and coronitis can
occur which can be seen in some nimals and usually when the mouth lesions are
healing. Such animals will be lame or limping or recumbent. An important sign
noticed is appearance of dark red purple band on the skin just above the coronet. Wry
neck with twistmg of the head and neck to one side occurs in few cases. The lower
parts of the face, ears and jaws are oedematous. A break in the staple of the fleece can
occur. In some animals vomition and aspiration pneumonia can occur. Deaths usually
occur after 6 days of onset of clinical signs.
2. Cattle: In cattle it is known as pseudo FMD. Clinical signs are very similar to sheep
but will be milder. An important clinical sign is the burnt and cracked appearance of
the muzzle. Also ulcers of the teats can be seen.
Abortion can occur in both the species and deformed foetuses can be thrown out.
Necropsy findings: The lesions mentioned in pathogenesis are seen.
Diagnosis:
1. Clinical signs
2. Lesions
3. Animal inoculation: Blood from infected sheep is collected and inoculated to
healthy sheep.
4. Serological tests: CFT is good for sheep but not for cattle. Other tests like AGPT,
VNT, FAT, Competitive and blocking ELISA are also used.
BT should be differentiated from RP and FMD. In RP of sheep and goats, the
oral lesions may or may not be seen and foot lesions are absent and clinical signs of
fever and pneumonia are seen.
It is very difficult to differentiate BT from FMD since oral cavity and feet are
affected in both the diseases.
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Treatment:
The following therapeutic measures can be adopted:
1. Wash the mouth and foot lesions with potassium permanganate solution.
2. A broad spectrum antibacterial agent like OTC is administered parenterally for 5
days.
3. Antipyretic, analgesic and anti-inflammatory agents are administered to reduce the
fever and pain.
Diclofenac sodium – 1 mg/kg body weight, i/m for 5 days or
Meloxicam (Qik, Sarabhai zydus) – 1 ml (5 mg) / 10 kg body weight, i/m or 0.5
– 1 bolus orally; for 3-5 days.
4. Give jowar or rice or ragi gruel with jaggey, salt and cooking soda to the animal in
small quantities and frequently.
5 Administer balanced electrolyte solution with 5% Dextrose (Ex. Arolyte-M)
parenterally.
1. Keep the sheep and goats inside the sheds during evening and night hours.
3. Prevent the coming in contact of sheep with culicoides.
This can be attempted by:
a) Burning of dry neem leaves around the sheep shed to produce the repellent action.
b) Applying the following preparation all over the body of sheep except eyes and this
will produce the repellent action:
Kerosene oil 80 ml
Naphthalene ball 10 gms
Nilgiri oil Few drops
Neem oil Few drops
c) Controlling the culicoides by
1) Spraying of kerosene oil to stagnant water.
2) Spraying of gamma BHC @ 500 gms/acre of land will kill the larvae of culicoides.
3) Spraying of other commonly used ectoparasiticidal agents like malathion, sumithion
etc.
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3) Painting the screen with 8% malathion in alcohol.

5) Biological control of culicoides has been attempted without much success. In
future this may be the most effective method of control of culicoides.
d) Vaccination: In our country no vaccine is available for the prevention and control of
BT. Now efforts are on to produce a suitable vaccine by incorporating the local
strains of BTV in Karnataka, Tamil Nadu and other states of our country.
In foreign countries like South Africa, USA and UK polyvalent live attenuated
vaccines prepared from chicken embryoes and Tissue cultures have been used.
However, the use of vaccines in the 5th or 6th week of gestation my result in deformed
lambs.
It appears that the killed vaccines have not given encouraging results.
11. BOVINE EPHEMERAL FEVER

(Three day sickness)
It is an infectious disease of cattle caused by a bullet shaped virus and is

characteized by inflammation of mesodermal tissues resulting in fever, muscular
shivering, lamensss and enlargement of peripheral lyph nodes.
Etiology : It is a bullet shaped RNA Virus. It is enveloped and having helicle

symmetry. There are 4 serotypes viz., DDP 63, CSIRO 368, DDP61 and FUK 11. It is
grown in unweaned mice, Hamster and also in tissue cultures like BHK 21, calf kidney
cells, foetal bovine kidney cells and testes.
Epdemiology:
a) Occurrence: Ephemeral fever is common in Africa, Asia and East Indies and
Australia. Cattle are affected and any age group can be affected but commonly adults
are affected. The morbidity rate can vary from 25-90% but commonly 35%. Mortality
rate is 0.8-1.6% but most of the animals willl recover. Bulls and fat cows are severely
affected.
239
b) Transmission: is by sand fly- ceratopoganidae species. However it is not

transmitted by culicoides species and also not by contact.
Pathogenesis: The virus is introduced into the blood through the bite of the flies and
there will be viral septicaemia. Lateron the virus localizes in the mesodermal tissue
like joints, muscles and lymph nodes. Here it causes hyperplasia of the endothelium of
the venules and cappillaries. Later on there will be oedema and perivascular
neutrohillic infiltration. This can lead to partial/complete occlusion of vessels which
may result in necrosis of the vessel walls. The skeletal muscles will have focal
necrosis.
There may be hydropericardium, hydroperitonium, rhinitis, tracheitis and
pulmonary emphysema.
Clinical findings:
IP 2-10 days . The signs are fever (105-1060F) peripheral lymph nodes are
enlarged, anorexia, sharp fall in production of milk; in some animals constipation and
in others diarrhoea, increase in heart and respiratory rates. Muscular shiverning,
stiffness of the muscles, swelling in the shoulders, neck and back; limping
lameness/recumbency can be seen or weakness of the hindlimbs. There may be ocular
and nasal discharges. Joints may be swollen.
The temperature mostly will be normal within 3 days and the animal start
ingesting feed and ruminating. It will take another 3-4 days for animals to overcome
lameness.
Many animals may have paresis/paralysis of the pharyngeal muscles and if such
animals are drenched it may get into the respiratory tract causing aspiratory
pneumonia. Here probably it may be due to improper opening and closing of epiglotits.
Necropsy finding:
Similar to pathogenesis.
Diagnosis:
1.Clinical signs.
240
2. Serological tests like SNT, FAT, CFT, AGID and blocking ELISA.
3. Biochemical changes like increase in plasma fibrinogen level and a siginificant
hypocalcaemia has been recorded.
1. Traumatic reticulitis- No enlargement of lymphonodes. No lameness.
2. Acute laminitis: Very rate.
3. Parturient paresis/Milk fever- Responds to calcium therapy and Milk lever-no fever.
4. Acute mastitis: By examining the milk.
Treatment:
1. To reduce the fever, pain and swelling give agents which will cause antipyretic,
analgesic and anti inflammatory effect.
a) Esgipyrin – N ( Analgin 150mg + phenyl butazone 150mg( available as 3 ml
and 5 ml ampules.
Dose: 10-20ml/m once a day for 3-5 days.
b) diclofenac sod @ 10-20 ml/cow, i/m
c) If Esgipyrin-N not available give analgin Analgin 8 ml/100 kg body weight ie.
40 mg/kg
d) Sodium salicylate if Analgin not available. It is better to give injectable in
morning and oral in evening.
2. Give a course of broad spectrum anitbiotics to overcome secondary bacterial
infection.
3. Rhustox-500 It is homeopathic drug, 8-12 drops placed on the tongue once or
twice a day three or four times.
4. Adminisiter calcim borogluconate @ ½ to 1 bottle/cow, i/v, s/c
5. Good nursing care is required.
Control:
1. Control of vectors is difficult
2. No vaccine is available in our country. However formaline inactivated mouse
brain vaccine, live attenuated vaccine and b-propiolactone inactivated vaccine in
Freund’s adjuvant have been used in foreign countries.
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RABIES
( Lyssa, Hydrophobia, Rage, Tollwut)
Rabies is hihgly fatal infection of CNS of al warm blooded animals caused by

Rhabdo
virus and is characterized by either the attack complex or ascending paralysis or both.
Latin word Rebere Rabies = To rare + T0 attack.
Etilogy: It is a RNA virus and its enveloed and symmetry is helicle.
It is one of the large viruses and it is relatively fragile, because it is destroyed
within few hours when exposed to sunlight. It is sucepitble to most of the disinfectants
like 70% alcohol, carbolic acid and idodine. It can be cultured in developing chick
emryoes and hamster kidney tissue culture etc.
There are minor and major antigenic variants of Rabies virus. Commonly two
strains are seen-
1. Street virus: This is the virus which is existing in nature.
2. Fixed virus: This strain is obtained by passaging the street virus in the brain of
rabbits, 50 or more times, It is called fixed virus because its characteristics like
incubation period, formation of negribodies are fixed.
Sl.N Particulars Street virus Fixed virus

o.
01 IP Variable and Fixed and short
long
02 Rabbits Death occurs in Death occurs in
14-20 days 7days
03 Salivary glands Affected Not affected
04 Negri bodies Usually present No usually present
05 Type of disease Furious from Paralytic form
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Epidemiology:
a) Incidence: Rabies occur in most of the countries of the world, but Australia and
Newzealand never had Rabies. One of the important disease of our country. Usually it
never occurs as a big outbeak and i.e. why it is not a disease of economic importance,
However it is very important disease of zoonotic importance. Because it appears that
20,000 people die of rabies every year and about 5 lakh post exposure vaccination
have done every year in our country. This is increasing every year.
Almost all warm blooded animals with possible exception of opossums are affected.
There is no variation in susceptibility to age. Usuallly it is a fatal disease However
non fatal rabies has been recorded in human beings and ogs, But the number is very
less. Three cases of rabies in human beings with recovery has been recorded. All these
three cases had paralytic form.
According to WHO, dogs were responsible for 91% of all human rabies cases
followed by cats(2%), other domestic animals (3$), bats(2#), foxes(1%) and all other
wild animals (less than 1%)(.
There are two reports in big indicating rabies as not fatal. Veeraraghaan et al
(970) had reportoed that a dog without shwing clinical signs of rabies had biten a
body who dies of rabies on 44th day . Also the virus was isolated from that dog 13
times in first 4 months and once a year for 4 eyars. IN the second report four dogs
were injected i/m with rabies virus. Two dogs died of rabies and two recovered from
rabies.
It has been also reported that mice can be infected by inhalation and also to an
extent by ingestion and without much rfatality. Thus it appears that mice/rate may act
as carriers reservoir of rabies virus.
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Transmission: It is always through the bite of an animal. Also it can be transmitted to

human beings when they handle the oral cavity of the rabid animal with bare hands
having abberations, wounds/cuts. In rats or mice experiments it has been proved that it
can be transmitted by inhalation and to an extent ingestion.
The source of infection to human beings is commonly infected dogs and to an

extent other rasbid animals. The source of infection to domestic animals is commonly
rabid dogs and also by wildlife, like foxes, skunksd, wolves, bats, raccoons and
squirrels.
There are 3 types of bis( viz Insectivorous, fruits eating and vempire rats). The rabies
virus will not invade. Nervous system but replicate in fatty tissue. I.e. why they are
known as – “Symptomless carriers”, Interbat spread and sprread from bats to other
species is principally by bites and by Inhalation also can occur.
The incidence of rabies apapears to be common in summer because the wildlife
move fromn place to place in search of food and also for mating.
The saliva of all bites may/may not have the virus. The rabies virus can occur
in the saliva. 5 days before the onset of the clinical sings.
Pathogenesis: The virus gets into the body through the bitten wound as the saliva
contains the virus. The virus gets into the peripheral nerve and migrates through the
nerves and enters the spinal cord and then the brain. In the brain it causes
oncyphalitis. The neurons and perkinfe cels are affected and the virus roduces intra
cytoplasmic inclusion bodies known as negri bodies. The numebr one casue of
encephalitis in catle is Rabies. Then through the crnial nerve gets into the salivary
glands and replicates in this glands, i.e how the saliva gets the virus. Recently it has
been shown in cattle that the virus from the brain gets into the olefactory nerve and
then into the taste buds and other sensory end organs in the cropharynx and thus the
saliva gets the virus.
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In the brain no gross lesious are produced. But only the histological lesions are
prduced. The excact cause of pareris/paralysis or manical behaviour of the animal is
not clearly understood. The paralyss may be due to degenerative changes and lateron
the distruction of the neurosns. The manical bheaviour may be due to irritation of the
CNS. The signs of excessive salivation, pica, excessive libido ( mounting of inaminate
objects or homosexuality) paralysis of the bladder ( etensiion of urine) and anus(
tenesmus), are indicative/suggestive of the involvement of the autonomaic nervous
system during Rabies.
Clinical findings: Two forms of rabies occurs- Furious form/Maniacal

- Paralytic form/mild.
The IP varies and it depends on the site of bite of an animal i.e. the
length/distance the virus has
to travel from wound to the brain. Usually IP can be 3 weeks but it can vary from
2 weeks to several
months.
1. Mild or paralytic form: Knuckling of the fetlock, sagging of swaying of hind
quarters while walking are initially seen. Flaccidity of the tail and deviation of the tail
to one side is also seen. Decreased sensation, tenesmus, which is due to paralysis of
the anus and it is a very important sign of rabies. Drooling of saliva can be seen from
start to the end of the disease, the voiceless attemps to bellow ( yawning) and paralysis
of the penis also occurs. Within 2 or 3 days the animal will be down and in another 48
hours it may be dead. The course of the disease of this form may b3 6 to 7 days.
2. Furious form: or Maniac form: The animal will be alert and hypersensitive to
sound and movements. The animal will have a staring look and the eyeballs follows
the movement of the object infront of it. Slight provovation may make the animal to
attack. Constant, repeated bellowing is a very a important sign in cattle. Such
animals may tear the rope and may run wildly, and trying to bite and attack the other
animals or objects infornt of it. Sexual excitement with repeated mounting of the
same sex/objects. Pica also can be seen. Within 24-48 hours such animals will be
down depressed and may collapse and die within 1-3 days.
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In both the forms anorexia, and ingestion of water may or maynot be present.
Hydrophobia may/may not be present. In both the forms salivation is commonly seen.
The temperature of both the forms may be normal or 1-3-105 F.
Buffaloes: Characteristic signs are not common.

Sheep: Similar signs are seen and in addition to it vigorous wool pulling may be seen.
Horses: Furious form is common where in there will be blind charging sudden falling
and rolling and chewing of the skin can be seen.
Dogs: 25% of cases are of furious form where in characterisitc signs are seen and
howling is seen. 75% of cases are of dumb form/paralytic form.
Dumb form is so atypical that, it is very difficult to diagnose rabies. Some of

the tips which can be kept in mind in such cases are
1. Any animal showing salivation and off feeding should be suspected for Rabies.
2. Any animal showing CNS abnormality should be suspected for Rabies. Well
trained dogs will follow the instructions of the owner, but in this form of rabies, such
dogs will not respond or may respond very slowly.
3. Such dogs will be very much depressed, weak and appear as though morosed.
Swines: Twitching of the nose, rapid chewing movements, excessive salivation,

backword walking and squeal continously.
Necropsy findings: Gross lesins are absent and histopathologiclal changes changes
mentioned in pathogenesis are seen.
Diagnosis:
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1. By clinical signs: When characteristic signs are present it is easy to diagnose

rabies. In many cases the signs are not so chararcteristic in the beginning and it will
be very difficult to diagnose it. In such cases one should suspect for rabies and should
isolate such cases. Then symptomatic treatment should be given by wsearing good
gloves ( PM gloves) and by not touching the oral cavity. Such animals should not be
euthanised, because without allowing the complete course of the disease it is very
difficult to demonstrate negri bodies for confirmation of our diagnosis. If isolated,
such animals if dies within 10 days then it may be rabies. If such animals are still alive
after 10 days then it is not rabies.
2. Demonstration of negri bodoes. Immediately after opening the brain make
impression smears of the Ammon’s Horn/Hippocampus major of the braina.
Iommediately do the straining before it is dried. The routinely used staining techniuqe
is seller’s staining.
Composition of the seller’s stain:
Solution A – methylene blue 10 gm
Acetone 100ml Acetone- 500ml
Solution B
Basic fuchsin – 5 gm
Acetone- 500ml
Prepare the above solutions, filter it and store it in amber coloured bottles.
While doing the staining prepare the staining solution freshly by mixing 2 parts of
soluton A and 1 art solution. B.
Procedure: Immerse the impression smear slides in seller’s stain for 1-5 secs and take
out the slides and wash in tap water. Air dry it and take out the slides and weash in tap
water. Air dry it and see under the oil immersion lens, for the presence of negri
bodies. The negribodies are round, about 1-27 in diamter and there may be 1-20 negri
bodies in the cytoplasm of neuron. These negribodies will be bright red or megenta in
coloure and the ctytoplasma of the the neuron will be ple blue in color.
The presence of negri bodies indicates that the animal had rabies. However only
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70% of the cases will be positve for negri bodies. If it is negatie for negri bodies one
should not come to the conclusion immediately that is is negative for rabies. IN such
cases the brain should be submitted for further testing. Half of the brain after cuttng
into small pieces is preserved in 10% for maline and in the same manner the other haf
preserved in 50% Glycerol saline ( Ex- 100 ml Gluycerol + 100 ml of 0.9% sodium
chloride/normal saline). These sampales are submitted to the nearest Veterinary
College where the facilities are available for further testing or to the Pasteur Institute
of South Indian in Coonoor – 643103, Nilgiris, Tamilnadu.
The brain preserved in 50% Glycerol saline is used for mouse inoculation test.
Here the brain tissue is ground well and the extract is injected intracisternally to a
batch of mice. These are observed for 7-21 days. If the mice comes down with rabies
and dies then the brain is opened and testing for the negribodies is done. Also FAT is
done. If both the tests are positive then the diagnosis of rabies is confirmed. This will
be intimated to concerned Veterinarian through the post card.
The other half of the b raina is used for the routine histopathological studies.
Here the changes of ancephalitis and negri bodies will be obsered.
In dogs, neuroons of hippocampus major and in cattle perkinje cells of
erebelum will be commonly examined for the presence of negri bodies.
3. Other serological tests- CFT, HIT, ELISA, IPT ( recently used by Indian
workers).
Corneal imprint: Here from the live animal impression smear of the cornea is taken
and then FAT is performed to demonstrte the virus..
1. Lead poisoning: Blindness is noticed.

2. Lactatin tetan: Attacking is usually not noticed.
3. Listeriosis: Unilateral facial paralysis.
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4. Thrombo-embolic meningo encephalitis ( TEM): is caused by Haemophilus

somnus and is characterized by CNS sign high fever and haemorrahgic infarcts in the
brain.
5. Sporadic bovine encephalmycelitis: ( SBE): Is caused by Chalmydia psittaci
and characterized by CNS signs high fever and fibrinous serositis.
6. Nervous form of bovine ketosis:- Ketone breath test the urine for ketone bodies.
7. Choke: In dogs especially, where ingested bones will obstruct in pharyux or
oesophagus and this can be diagnosed by X-ray.
Treatment : There is no treatment . In human beings interferons have been injected

into theCSF and also antiserum has been used. The effectivenses may be – or
depending on seerity. The wound due to dog bite should be thoroughly cleaned with
soap and and water and carbolic acid may be applied.
Prevention and Control
1. Educating the public regarding rabies.

2. Elimination of the stray dogs.
3. Compulsory vaccination of the dogs.
Type of vaccines available for animals are :
1. Anti Rabies vaccine- pre exposure ( IAH & VB): It is prepared from the brain
of sheep, It is a killed vaccine. The sheep are injected with the Rabies virus
intrascisternally. These sheep come down with the disease and on 6th –8th day these
sheep as killed and the brain is collected. The brain is cut into small pieces and
triturited and then treated with 1% phenol.
This vaccine contain 20% sheep brain suspension. This is used in dogs- 5ml and cats-
3ml by s/c route.
The first dose is administered when the dog is 6 months of age. The duration of
immunity is 6 months. I.e. this vaccine has to be repeated once is 6 months.
It is called as pre exposure vaccine because it is used only in those animals
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which are not exposed to Rabies virus that is dog bite.

2. ARV- post exposure ( IAH & VB): It is similar to AR preexposure vaccine and
difference is it is 5% sheep brain suspension
It is called post exposure vaccine beacuase it is used in animals which are bitten by
rabid dogs and this is used in all species of domestic animals.
Dose: dogs & cats- 2-5 ml heifers – 10 ml.
Calf, sheep, goat – 5ml Camels
Adult ( cows, buffaloes, horses) – 15-30 ml
Elephants- 30-60 ml
It is administered s/c daily for 7-14 days.
Adverse reaction: After pre or post- exposure vaccination , some dogs

will be having
presis/paralysis of the hind limbs. This may be due to
demyelinization. Such dogs
should be treated with corticosteroids and anitihistamines. Such
animals may or may not
Completely recover.
3. High egg passaged vaccine: Here the rabies virus is passaged repeatedly in
deeloping chicken embryoes at 180th –190th passage level; dose: cattle 5 ml, i.m cat
1ml, i./m.
4. Low egg passaged vaccine The Flury strain of rabies virus gets attenuated after
40- 50th passage in developing chicken embryoes. This is used only in dogs2-3 ml/
i/m, duration of immunity 3 years.
5. Nobi-Vac-R ( inter care): It is a inactivated vaccine and the chemical used is B
propiolactone. Available as single dose. Dogs and cats can be vaccinated when they
are 3 month of age and cattle and horses after 6 months of age, repeat after one year
administer i/m or s/c.
2. Pentadog; ( Serum institute of India ) Rabies V-killed, CDV – live attenuated,
ICHV- Live attenuated, Leptosopira icterohaemorrhagiae- Killed, L- canicola- Killed.
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Dogs- dose 1 ml s/c or i/m,

Schedule: 1 st injn. At the age of 7 weeks and above,
IInd injn. At the age of 3-4 weeks after the first.
IIIrd Booster injn. 1 year after the second and then every year cost: Rs. 85/dose.
4. Rabisin: ( Serum institute of India) Beta0 propiolactone inactivated cell culture

vaccine and adsorbed on aluminium hydroxide. This vaccine can be used in all
species. Ages and breeds.
Dose: 1 ml s/c or i/m in all species.
Pre- exposure –
Schedule: 1 st injn. Small animals 4 weeks and above

Large animals 8 weeks and above.
2nd injn. 3-4 weeks after the first in dogs and cats only.
Booster : One year after the above. Duration of immunity three years.
Post-exposure: dose 1 ml, s/c or i/m,
Schedule: day 0” –1 st injn. 2nd injn. Day 3, 3rd injn. Da 7, 4th injn. Day 14.
Ist booster – day 30, Iind booster day 90 I ml vial 10ml vial.
Vaccines for Human beings:
1. Sheep brain vaccine. Now not commonly used.
2. Suckling mouse brain inactivated vaccine. The brain of suckling mice doses
not have much of myelin, and when injected, the adverse reaction in the form of
demyelination will not occur.
3. Duck embryo vaccine- inactivated with Propiolactone.
4. Human diploid cell culture vaccine i.e. Marioux ( sli) verocel Iml i/m. No
adverse reaction. 1 ml cost Rs. 360/-
5. Rabipur = chikcen embryo vaccine ( inactivated ) 1 dose Rs. 200/-
Vaccinatin wilf life: Vaccinating the foxes is a must. The live attenuated vaccine in
liquid form in chicken heads as bait isd being used with success in some foreign
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countires.
PSEUDORABIES
( Mad tch, Aujeskey’s disease )
It is an infectious disease mainly of pigs and occasionally of cattle, sheep,
dogs, and cats, caused by a hepes virus. In young pigs it is characterized by acute fatal
encephalitis and in other species it is characterized by both encephalitis and marked
local pruitus.
Etiology:
Faimily : Herpetoviridae
Genus: Herpes virus.
It is a DNA virus with cubical symmertry and enveloped. It replicates. Inside
the nucleus and produces intranuclear inclusion bodies.
It can be grewn in developing chikcen embryo and can be passaged in rabbits
and unweaned hamster.
Epidemioloy.
a) Incidence: Pseudorabies occurs in many countries of the world. Pigs are
commonly affected and rarely cattle, sheep, dogs and cats are affected. Human beings
can be affected but it is not fatal. In young suckling pigs the morbidity and mortality
rte can be 100% . In adult pigs the mortality rate is very low. In cattle it is usually
fatal.
b) Transmissison: Not clearly understood. It has been shown to spread from pigs
to pigs by contact. But it will not be spread by contact in other domestic animals.
Shopes hypothesis: According to this hypothesis, the cattle suffered from psuedorabies
and they die. The rats will ingest small amount of carcasse and then they migrate to
the piggery unit and then die. The pigs ingest the rats and they will come down with
this disease.
The portal of entry is through the abraded skin or the intact nasal mucosa.
Pathogenesis: The virus gets into the circulation and there will be
viraemia for
ashort period. Then the virus localizes in the respiratory tract and
252
replicates. Through
the olefactory, glassoharyngeal or trigeminal nerve gets into the brain
and causes
encephalitis. When the virus gets through the abraded skin it gets into the
peripheral nerves
and causes irrigation which is responsible for the pruitis.
Clinical findings: In young pigs i.e. less than one month of age the
disease is ery serve . In the beginning, high feer of 107 F and the inco-ordination of
hindlimbs and recumbency are seen. Tremors, paddling movements, lateral deviation
of head, frothy salivation, nystagmus and convulsions occur. Within 12 hours death
can occcur. IN some pigs blindness due to an extensive retinal degenertion can occur.
In adlut swines the disease is very mild. The signs noticed are anorexia,
dullness, agalactia and constipation. Mummifie foetuses, stillbirths, late abortions can
also occur. Pruritus is absent in young piglets.
Cattle: Intense local pruritus with iolent licking, chewing and rubbing of the part. This
can be seen in any part of the body but msot commonly it is seen on the head. Flansk
or the feet. CNS excitement in the form of constant bellowing maniacal behaviour,
circling and convulsions can be seen. After wards paralysis wll occur which is
accompanied with respiratory distress and ataxia. Within 6-48 hours the animals may
be found dead.
The signs are similar in dogs and cats but it is very rate.
Necropsy findings: Considerable damage to local areas of skin and extensive s/c
oedema, pneumonica changes in lung, haemorrhages in the endocardium and the fluid
accumulation in the pericardial sac.
Histopathologically encephalitic changes are seen ( perivascular cuffing
degenerative changes of neuron). Intranuclear inclusion bodies are seen in the neurons
of the cerebral cortex of pigs.
Diagnosis:
1. By clinical signs
2. By histopathology – intranuclear inclusion bodies.
253
3. Samples to be submitted are

a) local tissue of pruritus.
b) Part of local nerve trunk.
c) Piece of cerebellum.
The suspected material is injected into the rts or mice and they comedown with the
disease.,
Serological tests: FAT, SNT, VNT, ELISA
Tretment – No treatment.
Control:
1. Distruction of rats
2. Reariong of cattle and pigs separately.
3. Vaccionation: Killed and attenuated vaccines have been used. The vaccine is
administered intramuscularly and peripherelly. No vaccine is available in our country.
Genetically vaccines are now available for the control of seudorabies.
SWINE INFLUENZA
(Swine/Hog/Pig flu )
It is an acute infectious respiratory disease of swines caused by a myxo virus

type A, influenza virus and it is characterized by sudden onset of high fever,
coughining, anorexia, dyspnoea. Prostration and rapid recovery.
Etiology:
Family: Orthromyxo viridae
Genus: Influenza virus
Type A - Swines, equines, avians.
B & C - Human beings
It is a RNA virus and measures about 8-100 mm. Helicle symmetry, single
stranded RNA in 8 segments and enveloped. This virus can be cultured in
developing chicken embryo and other tissue culture system. They agglutinate RBC s
254
of fowls and some mammals. The virus is susceptible to phenol and formaline. The
virus contain two agglutinis. I.e. Haemagglutinin and Neuraminidase which varies in
subtypes.
A Type /swine/Karnataka 1/89.
Tpidemiology:
a) Incidence; Swine influenza occurs in many countries of the world. Only swines are
affected. It is common in Agugust and September affecting almost all piglets in that
region and by November-December the disease wanesoff.
In pigs the first out break occurred in 1918. From that time it occurs every year all of
a sudden and goes off. The mortality rate is less than 1-2% . The reason for this type
of incidence may be-
a. Due to the appearance of new crops of pigs every year.

b. Lung worm- earth worms combination.
However along with swine influenza in 1918 a pandemic of human influenza occurred
and killed 20 million people throughout the world. After this pandemic it went off.
The reason for this may be due to Darwin's theory- survival of the fittest.
1. Transmission : Is not clearly understood.
It may be due to the lungworm- earthworm hypothesis. After the recurrence of
the disease is few animals it can be spread to other animals very fast through
inhalation.
Pathogenesis: The virus is present in respiratory tract causing inflammation

Clinical signs: It occurs suddenly in almost all pigs where in, pigs will be sick at
sametime. Fever of 108 F marked anorexia and depression occurs initially. The a
imals will be lying on the sternum with the forelimbs stretched forward and the head
lying on the ground, laboured jerky respiration, coughing, nasal dischargfe, lacrimal
discharge and considerable loss of wt. Occurs By 6th or 7th day all the pigs will
recover from this condition and will be very active.
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Necropsy findings; Inflammation of respiratory tract and pneumonic changes. The

respiratory tract will be filled with tenacious fluid.
Diangosis:
1. Clinical signs.
2. Culturing- Nasal swab from live animal, swab from any part of respiratory tract
and a piece of lung from the carcasse, can be collected for culturing.
3. Serological tests: HAT, HATT, FAT.
Treatment:
1. Administration of expectorants.
2. A course of broad spectrum antibiotics/sulphonamides.
Control: Vaccinating the pregnant sows.
HOG CHOLERA
( Swine fever)
It is an infectious disease of pigs caused by a Toga virus and it is characterized

by septicaemia haemorrhages through out the body and high morbidity and mortality
rate.
Etiology: F : Toga viridae G. Pesti virus.

It is a RNA virus measures about 40-60mm, cubicle symmetry and is
eneveloped.
It is antigenically related to BVDV. It is cultured in cell culturesof kidney cells
of cattle. Sheep and goat. There are several strains, some cause CPE and some does
not cause CPE.
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Epidemiology:
a) Incidence: Hog cholera occurs in many countires of world. It is a very
important disease of swine industry. Since it causes severe economic loss. This
disease has been eradicated in USA in 1978.
b) TransmissionL By inhalation and ingestion the virus gets into the body. It
appears that feeding of garbage is the most important source of infection.
Pathogenesis: The virus gets into the tonsils and multiplies. Then through lymphaties
gets into the circulation and replicates leading to septicaemia. The virus is having an
affinity for the endothelium of vessels. Here it replicates and causes hydropic
degeneration and proliferation of the endothelium. This leads to partial/complete
occlusion of vessels leading to infarcts. It is also having affinity for lymphoid tissue
leading to depletion of lymphocytes in the lymphoid organs and also leucopaenia.
Clinical findings: IP 5-10 dauys.
1. Peracute: Withtout signs many young ones will be found dead.

2. Acture: High fever 105-107 F anorexia, depression, disinclined to move upon
force and hanging of the tail. Most of them likes to lie down and burrow in to the
bedding and even piled one on of the other. Constipation followed by diarrhoea and
vomiting can occur. Diffused purplish colouring of the skin on the ventral aspect of
abdomen, thorax, inside of the thigh and perenium. Lateron necrosis on the edges of
ear, trail and lips of vulva is seen. Nervous signs are also seen in the early stages,
circling inco-ordination, muscular tremors and convulsions. The course of the disease
is about 5-7 days.
3. Chronic: Milder form occurs as a result of low virulent strains of virus and
many of the clinical signs of acute form are seen. Skin lesions are common. This
chronic form appears to be common now a days.
It can also cause foetal resorptions. Ummified fetuses. Stillbirths, and congenital
anomalies like cerebellar hypoplasis.
Necropsy finding: Petechial haemorrhages on serosa and mucosa. These
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haemorrahges are clearly noticeable under the capsule of the kidneys. Ileo-caecal
vlve, urinary bladder, larynx and lymphonodes. The spleen is enlarged and having
marginal infarcts. Infarcts in the mucosa of gall bladder, larynx and lymphonodes.
The spleen is enlarged and having marginal infarcts. Infarcts in the mucosa of gall
bladder is almost a pathognomonic lesion of hog cholera. The mucosa of colon will be
having circular raised button ulcers and no a days it is not common.
Histopathologically non suppurative encephalitis is a very important lesion and
the lesiors of the blood vessles are noticed.
Diagnosis: 1. By signs 2. By lesions

4. Haematology: Leucopaenia occurs where in TLC of 4000-9000/cumm is seen
Normal TLC in 6-12 week old pigs 14,000-40,000/mm3 ( Average 21,000 /mm3)
5. Culturing the material: Blood, brain stem & lymph node.
6. Serological tests: FAT, SNT, CFT, AGPT, HIT, ELISA, AGPT is commonly
used where in pancreas from the carcasse is rested.
7. Intradermal test.
8. Animal inoculation test.
Swine erysipelas. Salmonellosis, anthrax, acute pasteurellossis, salt poisoning

African swine fever. Eoinopthilic perivascular cuffing in salt poisoning is very
characteristic.
Treatement: Administer hypermmune serum - 50-100 ml,s/c and do symptomatic

treatment.
Conttrol : Hog cholera free area.

1. Test and slaughter.
2. Strict quarantive measures.
3. Good hygienic measures.
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Enzootic area: Vaccination.
1. Serum simultaneous method: Here 2 ml of whole blood from infecged animal is

injected s/c and at the same time 20-75 ml of hyperimmunized serum s/c injected.
2. Inactivasted vaccine (a) Blood from infected animal is collected and crystal
violet is added 5-10 ml of this vaccine is administered s/c. b) Formaline inactivated
vaccine.
3. Attenuated vaccine:
4. a) Lapinized vaccine( IVRI vaccine) 10# spleen suspension. Dose - Im s/c,
duration of immunity is 1 year.
b)tissue culture vaccine: Porcine kidney cells are used
TRANSMISSIBLE GASTROENTERITIS (TGE)
It is a highly contagious enteric disease of pigs caused by a corona virus and it

is characterized by diarrhoea, vomition and high mortality rate.
Etiology: Family: Corona viridae. Genus: Corona virus.
It is a RNA virus. It measures about 80-100mm, helicle symmetry and enveloped.

The envelope is having petal shaped projections. It is cultured in porcine kidney cell
culture. Porocine thyroid and ( porcine) tests. CPE is characterized by rounding off of
cells and datachement of cells, It is susceptible to Bita propiolactone and saponin.
Epidemilogy:
a) Incidence: TGE occurs through out the world. Very important disease of swine
industry causing severe economic loss in the form of high mortality rates ( 100%) of
piglets under 2 weeks of age. The virus is photosensitive and hence the disease is not
common in summer but common in winter.
259
b) Transmission: By ingestion and inhalation. It is very contagious disease.

Pathogenesis: The virus upon ingestion and inhalation goes to small intestine and it
is having very good affinity for tall columnar epithelial cells of the villi of the small
intestine. The virus replicates in the cells and cells are destroyed. Rate of distruction
is more than the rate of replacement. Hence contraction of the villi occurs and is
covered with low cuboidal epithelial cells. This results in the shortening of the villi.
The above changes results in reduction in prodction of certain enzymes

reaquired for diagestion. Hence lactose is not hydrolysed and not absorbed. Presence
of lactose in creases the osmotic presuure which results in withdrawal of lot of fluids
leading to diarrhoea - dehydration - haemoconcentration..
Here also metaboalic acidosis and hypokalaemia occurs which may be

responsible for death of the piglet.
Clinical findings: IP 18 hours- 3 days. Vomition and then diarrhoea occurs. Faeces
will be watery yellow in colour and foul smelling and also it contain small curds of
undigested milk. Signs of dehydration are also seen.
Courseof the disease is 2-7
Necropsy findings: The stomach and small intestine are congested and contain
curdled milk. The intestinal wall is thin and almost transparent.
In normal pigs the chyle which is white or milky fluid and contain lymph and
emulsified fat is present in the mesentric lympatics. But in TGE it is absent. Examine
the villi with a handlens; villi: Crypt ratio is 1:1 (normally it is 7:1)
Diagnosis:
1. By signs
2. By lesions
3. Culturing: Faecal swab, piece of small intestine.
4. Serological test: VNT, FAT, IPT, HIT, competitive ELISA.
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1. Colibacillosis: No vomition.
2. Clostridium perfringens type C: Haemorrhages in intestine, blood in the faeces.
3. Swine dysentry: Adult swines are commonly affected.
Treatment:
1. To overcome dehydration - fluid administration Lactated ringer’s solution i/p.
2. To overcome hypokalaemia - potassium to be supplimented.
3. To overcome metabolic acidosis - Soda bicarb.
4. To overcome vomition-perinorm, stemetil.
5. To overcome diarrhoea - Astringent mixture.
6. To overcome secondary baterial invaders - chloromycetin, Neftin, Gentamicin.
Control:
3. Vaccination: Lot of research work has been done on this aspect by using
killed/attenuated/ inactivated vaccines in piglets or pregnant sows. The
vaccine have been administered i/m, s/c, orally, intrammamarily, either to
the sow or piglet without much susccess. Later on it was found that when a
moderately virulant TGEV is administered orally to pregnant sows is
highly beneficial. Here the IgA producing B-lymphocytes present in the
intestine was (were) exposed to the virus and these lymphocytes gets into circulation
and gets localized in the mammary gland. After farrowing these lymphocytes become
plasma cells and start secreting IgA. The piglets when they suckle colostrum and the
milk they ingest good quantity of IgA which goes to the intestines and coats the
mucosa. The IgA is resistant to the acidic pH of stomach and hence good amount of
IgA present in the intestine. When such pigletsingest virulant TGEV it can bind to the
epithelial cells and cannot replicate and thus cannot produce the disease. Hence this is
most commonly used method for the prevention of TGE.
POX DISEASE
Family : Pox-viridae. 6 genera.

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They are DNA viruses, oval shaped when hydrated and brick shaped when
dehydrated. They are enveloped. The symmetry is complex, measure about
300x240x100 mm. These viruses can be cultured in developing chick embryo and also
cell culture.
Cow Pox
It is beningn contagious skin disease of catttle caused by ortho-pox virus and it is

characterized by typical pox lesions on the teat and udder.
Etiology: Cow pox virus which is related to horse-pox and small pox viruses.
Epidemiology:
a) Incidence: World wide, it is a sporadic disease, now a days not common.
b) Transmission: By milkers hand and milking machine.
Pathogenesis: The virus enters the prickle celle layer of skin and causes inflammation
resulting in congestion and this is known as ‘roseola’ stage. Epithelial cells undergoes
hypertrophy which leads to the formation of papules and this is known as ‘papular’
stage.
Then the fluid accumulates leading to the formation of vesicles and this is known as
vesicular stage. These vesicles are umbilicated. Then there will be infiltration of
neutrophils into the vesicles and pus formation occurs which is known as ‘pustular’
stage. These break open and dries up and forms scabs. Normally these scabs will
detach and fall off which is known as stage of desquamation.
Because of milking habits only scabs may be seen in cows.
Clinical findings: Scabs of 1-2 cms in diameter which are thick, tenacious and yellow
brown to red in colour are seen on the teats and udder of the cows. Sometimes deep
ulcers also can be seen.
The course of the disease is 2-3 weeks. Almost all the cows will recover.
Because of these lesions, it may end in mastitis.
Diagnosis: is by signs and lesions.

Differential diagnosis: Cow pox should be differentiated from:
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1. Pseudo cow pox: Here the lesions are large and more in number and less
painful.
2. Bovine ulcerative mamilitis: Here plagues and ulcers are seen in the teats.
3. FMD: Here the vesicles are seen on the teats, udder, mouth and feet and they
rupture forming ulcers.
Treatment:
1. Clean the lesions and apply antibiotic and corticosteroid containing ointments
like Betnovate- N, Beclate-N, Neosporin-H. This will reduce the pain and allow for
proper letting down of milk and also prevents mastitis.
2. Give a course of broad spectrum antibiotics parentarally.
Control: No vaccine is available. Follow good hygienic measures.
SHEEP POX AND GOAT POX
Benign and malignant form occurs in sheep and goats.

The benign formoccurs in the adults where the lesions are seen at the
base of the tail. The malignant form is seen in the lambs where the lesions are seen in
the oral and nasal cavity.
Etiology: The virus belongs to the genus Capri pox. The virus agglutinates RBCs of
ducks, fowl, sheep and Guinea pigs. It can be cultured in kidneys, thyroid and
testicular cells of sheep.
a) Incidence: It is common in Africa, Asia and Europe. It is the most severe form
of pox disease of the domestic animals and the mortality rate can be 50% in lambs.
b) Transmission: is by contact and by inhalation.
Clinical findings: IP is 2-14 days. Two forms of the disease occurs and they are:
1. Malignant form: This form occurs in lambs. Some may die without showing
any signs. Some will have high fever, marked depression, discharge from the eyes and
nose and the typical pox lesions occur in the lips, oral cavity, nostrils and nasal
cavities, uro-genital tract mucosae and also can be on the unwooled skin. The
mortality rate is 50%.
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2. Beningn form: This form occurs in adults. The pox lesions are seen under the
tail and there is no systemic reactions. The mortality rate is 5%.
In ewes, the lesions can occur on teats and udder leading to severe mastitis
which may be fatal.
Necropsy findings: Pox lesions in the mouth, pharynx, larynx, trachea and may be
even in the abomasum.
Diagnosis:
1. By signs and lesions.
2. By culturing the scab material.
3. By serological tests like CFT, FAT, AGPT, HAT, HIT.
Differential diagnosis: Sheep pox should be differentiated from Blue tongue and
contagious echthyma.
Treatment: is similar to cow pox.
Control: is usually done by vaccination.
1. Sheep pox vaccine (IAH & VB): it is a live un-attenuated sheep pox virus
suspended in 50% glycerol saline.
Clean the inner surface of the ear and then scarify by using a rotary
scarificator and then rub a small quantity of the vaccine.
After one week examine 10% of the vaccinated animals randomly for the
appearance of takes i.e. pink raised areas and also scab formations in the vaccinated
area. If takes are present in more than 50% of the animals then it is OK. If more than
30-35% of the animals does not have takes, then repeat the vaccination in the other ear.
Even after second vaccination ‘takes’ are absent then consider them as immune.
Precautions: This vaccine should be used when there is an outbreak i.e., it should not
be used in clean flocks.
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RANIKKHT DISEASE
It is an infectious highly contagious and destructive disease of domestic fowls

and wild birds caused by a paramyxo virus and characterized by high morbidity and
greenish coloured diarrhea.
Histroy: It was first described in 1926 in England, Java and Korea. In 1927, this
disease was first recorded at a place called Ranikhet near Almora in U.P., and hence it
is known as Ranikhet disease in our country. The name New castele disease is given
because it was first repoted in place called New Caste in Tyne in England. Tyne in
England . Throughtout the world it is nown as new castle disease.
Epidemiology:
a) Incidence: Occurs throughout the world over 200 species of birds are
susceptible. It is very common in chikcen, and also has been recorded in turkeys.
Peahens, Guinea hens, pheasants, quails and pigeons. Ducks and geese can also be
affected. It is very important disease of poultry industry causing severe economic loss
and severe headache.
Three panzooties have been recorded . First panzootic occurred in fowls in mid
1920 starting from Far-East and spreading throughout the world. Second one
occurred in fowls in the Middle East in the ater 1960 and covered all continents
by1973. Third one occurred in poieons in middle East in 1970 and by 1980 covered
the world.
The economics loss is due to-
1) High mortality rate
2) Loss of meat
3) Decreased egg production
Etiology: It is caused by paramyxo virus. It is a RNA virus and symmetry is helicle.
It measures about 100-200 nm in diamter
It is also known as paramxo virus 1 (PMV). The Neuraminidase.
Haemagglutinin
The virus causes haemagglutination- erythrocytes of amphibia, reptiles, birds man,
mouse G. pigs( This is not a Ag – aby reaction )
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It can be cultured in developing chicken embryos and also in monolayers of

chickens fibroblast.
b) Transmission: It is transmitted by inhalation or ie., by aerosol method. It can
be also tansmitted by ingestion of contaminated feed and water.
Pathogenesis: The virus upon inhalation or ingestion will get into circulation and is
having a great affinity for the vascular endothelium and the lymphoid tissue . IN
endothelial cells of blood vesxsels it causes damange and necrosis. Hydropie swelling
of tunica media also occurs. All these changes can resultin formation of hyaline
thrombi in the blood vessels. In the lymphoid tissue, necrotic changes occur and
hyperplasia of reticulum. Various organs like proventriuculus, duodenum, caecum,
lungs, trachea, CNS are affected where in congestion, edema, haemorrhages are seen.
The changes noticed depends on the virulance of the virus because strains of
New castle disease virus of low, moderate and highly virulant in nature have been
recorded.
They are also classified into the following type.
1) Lentogenic virus – These are almost avirulent. They are (1) Hitchner’s Bl (2)
Lasota strain (3) F-strain: These are used for vaccine production.
2) Mesogenic type- (1) Roakin, 2) Komarov, 3) Mukhteswar. These strains are
also used fr vaccine production/
3) Velogenic type :- (1) Herts, (2) Great Britain 3) Ca- 1082.
Clinical findings: Four types of New caste disease:
1) Doyle’s form: In this form CNS signs with systemic signs are seen. Mortality
rate is 90%
2) Beach’s form: Here respiratory isgns along with CNS signs occur, commonly
10% of mortality and even can go to 90%
3) Beauder’s form: Acute repirtory signs of adult chicken.
4) Hitchner’s form :- Moderate from in adult birds and can cause mortality of
30%. The signs are not vry clear cut.
Common clinical signs: I.P.- 2-18 days and commonly 4-5 days. Dllness, fever hdding
together ruffled feathers, dropping of the one or both the wings folowd by in co-
ordination and then paresis or paralysis of one or btoh the limbs. Twitching of the
266
head and neck. Torticollis. At this time greenish watery diarrhoea can be seen. In
addition, respiratory signs like marked dysponea with stretching of the neck and trying
to breath through nose or beaks can be seen and birds may fall down and die due to
asphyxia.
Severe form of the disease is commonly seen in young chickens when
compared to the adults. Hwever severe outbreaks.have been recorded in adults also
recently. The birds recovered from Newcastle disease will be having decreased egg
production for aprolongedf period and also there will be marked decrease in meat also.
Necropsy findings: Catarrhal inflammation of the trachea which may even become
haenorrhagic tracheitis, lungs may be normal or may see the lesions of pneumonia,
which thickening of mucous membrane of air sacs, containing catarrhal or caseous
contents. In gasdtro intestinal tract hemorrhages in the proventriculus which was in
olden days considred as the pathognomonic lesion of NCD, is not being considered
same at the present time. Hemorrhages and necrosis of the oaecal tonsils, ulceration
oof the intestine and even formation of diptheroid necrotic inflammation of intestine
appearing like Hocholera can be seen. Ovaries will be haemorrhagic and sometimes
necrotic.
Diagnosis:
1) By clinicsl signs
2) By lesion
3) Isolation of virus- From carcasse- the materials to be collected are lung, spleen,
traciea bone marrow. In live bird – the materials to be sent are tracheal or cloacal
swibs.
The suspected material is injected into allantoic cavity of 9-11 day chicken embryos.
Every day the eggs are candled Those which dies with in 24 hours are discorded and
the other which dies after 24 hours will be taken in to account. Hence the embryos are
markedly haemorrhagic and stunted. The allontoic fluid is used for Haemagglutination
inhibition test to confirm the virus.
Serological test:
1. Haemagglutination test (HAT)
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2. Haemagglutination inhibition test (HAIT) commonly used test for the diagnosis
of N.D.
4) FAT 4) CFT 5) AGPT 6) ELISA 7) Phage neutalization test.
Differential Diagnosis: ILT, Fowl plague, Avian influenza, Avian Eoryza, Marek’s
disease Fowl cholera T.B. Avian Mycoplasmosis and Avian encephalomyelitis.
Treatment: No treatment
1) Good hygienic measures: Thimmaiah et al ( 1955) IVJ 72 (6) : 562-564 Virex(
Polchem Hygiene lab. Pune ) 1 Gm+99 ml of strile Dist. Water 1% soln. I litre/cubic
mater sprayed by ysing A – 1 gum sprayer. Has viricidal activity against NDV and
IBDV, sulfomic it contains potassium persulphate ammoniunun perisulphate. Malic
acid Acid and dodecyle be\zne sulfamic acid oxidizing agent ozone.
2) Good management practices.
3) Vaccination:
1. Ranikhet disease vaccine(R2B strain) (IAH & VB): It is a live attenuated
vaccine, prepared from chikcen embryos . It is avilable as freeze dried vaccine in 200
doses.
Mix the contents of the ampoules in 100 ml of sterile normal saline or distilled water
and use it within 2 hours.
Dose: 0.5ml i/m or s/c per bird in the wing. Used in birds of 6-8 weeks of age.
Adverse reactions: Some birds may have drowziness and later on may develop
paralysis. Such birds should be separated and if there is no improvement with in 10
days, they should be culled.
This vaccine should be used in healthy flock. If coccidiosis and worm
infestation is there. Then first treat for these condition and then vaccine the birds.
2. Ranikhet disease Vaccine (F strain) (IAH & VB): it is a modifed living virus of
British origin used for immunization of young chicks of 6-10 days old. The contents
of the ampoules is mixed with 10 ml of sterile normal saline or distilled water which
will be enough has for 100 chicks.
Mode of administration : Instil one drop of the vaccine to the eye and one drop to the
nostril.
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4) New Castel disease vaccine (BAIF): it contains F. strain ( Lasota ) it is a live

modified lasota vaccine.
Container size: 200 ,500, & 1000 doses with diluents
Procedure; Reconstitute the vaccine with the diluent.
Apply a drop of the vaccine to each nostrils.
Day old to 7 day old chicks are vaccinated.
4) N.D. Vaccine( BAIF): Muktheswar strain. It is a live modifed measogenic
vaccine.
Available as 200,500, 1000 doses with diluents.
VI. Sulpha Drugs:
These drugs are still, very effective against coccidiosis of poultry.
1. Coxicure granules (Cedilla): is available as 200 gins tin which contains:
Sulphaquinoxalene - 85 gm
Diaveridine - 15 gm
Dose: for prevention: 200 gm / ton of feed.
2. Sulphaquinoxalene:
For treatment: 0.1% for 2-3 days followed by a break of 3 days and 2nd dose @
0.05% for 2 days, then a break of 3 days and then give for 2-3 days.
This is the old schedule which was devised on the basis of the life cycle of the
parasite where in the invading stage of the parasite .is attacked with drugs.
3. Sulmet solution (ICI): 12.5% solution, 450 ml bottle. It contains 12.5% of
sodium sulpha dimethyl pyrimidine.
Dose: 30 ml/4 litre of water for 2 days and then 15 ml/4 litre of water for 4
days.
4. Paquine powder (Ranbaxy): is available as 30 gms sachet which contains 7.5
gm of sulphaquinoxalene
VII. Other drugs tried in foreign countries:
1. Moneusin available as Coban
2. Lasalocid
3. Nicarbazine
4. Halofuginone
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5. Aprinocid
6. Butynorate
Any one of these drugs is used for the treatment of coccidiosis
of poultry.
1. Prevention is usually done by administering any one of the drug mentioned
under treatment either in the feed or drinking water to day old chicks and continued for
a prolonged period of time. Here the prophylactic dose of the drug is used. Commonly
this is the practice used in each and every poultry farm in our country.
2. Good hygienic measures are a must.
3. Over crowding should be avoided as much as possible.
4. Still vaccines are not commercially available in our country. However
attempts being made to prepare the vaccines. Live virulent oocysts have been
administered as vaccine in low doses. Attempts are also being made to prepare live
attenuated vaccines.
HISTOMONIASIS (BLACK HEAD)

It is a protozoan disease caused by Histomonas meleagridis and is
characterized by necrotic foci in the liver and ulceration of the caeca.
Incidence: It is world wide in its occurrence. It affects turkeys, chickens, pheasants,
partridges, pea fowls, quails and Guinea fowl. It causes a severe disease in turkeys
when compared to chickens. Commonly chickens of 4-6 weeks of age and turkeys of
3-12 weeks of age are affected. It can cause aa economic loss of 2 million dollars in
turkey industry.
Etiology: It is caused by Histompnas meleagridis. It can be spherical or wheel shaped
protozoa, having a single flagellum and several pseudopodia. These protozoa can be
stained with H & E stain, PAS and Hollande's Cupric- picro-formol stain.
Transmission: Commonly the chickens are considered as the source of infection to
the turkeys. This disease is transmitted by the caecal worm i.e. Heterakis gallinarum,
because these protozoa are present in the eggs of this worm. And also the earthworms
are associated with the mechanical carrying of the eggs of H. gallinarum. Hence, the
270
birds pickup the infection either by ingestion of feed and water contaminated with the
eggs of this worm or by ingestion of earthworm containing the larvae of this worm.
Pathogenesis: Upon ingestion of the eggs, they go to the intestine and the eggs hatch
to release the larva. These larva releases the Histomonas meleagridis in the intestine,
which penetrates the epithelial cells of the intestine causing congestion and catarrhal
inflammation. There will be excess secretion of mucoid like material which will
undergo caseous necrosis. Later on there will be ulcer formation in and goes to the
liver and causes necrotic foci in the liver. These foci are circular, depressed area
of necrosis measuring upto 1 cm in diameter and the periphery of the foci will be
elevated.
Clinical Findings: The most important sign in the early stage is passing of sulphur
colored (deep yellow) faeces. Drowsiness, drooping of wings, walking with stilted
gait, closed eyes, head down close to the body or tucked under a wing.
Anorexia, fever and the head may or may not be cyanotic.
The course of the disease is 10-22 days and even it can cause a
mortality rate of 20% in turkey fowls.
Necropsy findings: Similar to pathogenesis.
Diagnosis:
1. Faecal examination from the live bird or intestinal contents or intestinal
scrapings or liver impression smears from a carcass and examine under the microscope
to demonstrate the protozoa, and also by various staining techniques.
2. By post mortem findings.
Treatment: Any one of the following drugs can be used:
1. Furazolidone @ 0.011 - 0.022% in the feed.
2. Carbarsone
3. Dimetridazole
4. Impromidazole
5. Nitarsone
1. By eliminating the vectors like caecal worms and earthworms. For ceacal
worms administer the anthelmintic regularly.
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2. Avoid rearing of chickens and turkeys together.

TRICHOMONIASIS
It is disease caused by Trichomonas gallinae in pheasants, turkeys, chickens
and other wild birds. It causes necrotic ulceration on the mucosa of the buccal cavity,
sinuses, oesphagus, crop and proventriculus.
Treatment: Dimetridazole
HEXAMITIASIS
It is a disease caused by Hexamita meleagridis in turkeys, pheasants, quails, pea
fowl, partridges and chickens. It causes infectious catarrhal enteritis where in watery
diarrhoea occurs initially which becomes yellowish later on.
Treatment: Butynorate, Furazolidone, Chlor and Oxy tetracyclines.
BLOOD PROTOZOA
Leukocytozoonosis: In chickens it is caused by Leukocytozoon caulleryi where in the
organisms are present in the RBC, monocytes, and Lymphocytes. It is characterized by
anaemia, leukocytosis, splenomegaly and liver degeneration. It is transmitted by
Culicoides.
Treatment: Clopidol
ECTOPARASITES
1. LICE
Species of
Biting lice Sucking lice
Animal
Cattle Bovicola bovis Haematopinus eurysternus
(Damalina bovis) Linognathus vituli
Buffalo - Solenopsis capillatus
Haematopinus tuberculatus
Sheep Bovicola bovis Haematopinus
quadripetrusis
Goat Bovicola caprae Linognathus pedalis
Linognathus stenopsis
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Horse Bovicola equi Linognathus asini

Dogs Trichodectes canis
Heterodoxus spiniger
Cats Felicola subrostratus -
Pigs Haematopinus suis
Life Cycle: Occurs entirely on the host.

Symptoms:
They cause irritation, itching, scratching which leads to at annoyance to the
animal. This results in decrease in milk production and anaemia.
Fleas: Ctenocephalidis canis – dogs - IH for Dipylidium caninum. Catenocephalidis
felis - cats.
Ticks:
Life Cycle: The adult female ticks lay eggs in cracks and crevices of the barn. These
egg hatches and larva comes out. The larva attaches to the animal body and sucks
blood or lymph and engorges arid moulds to become the nymph. There may be one or
two or three nymphal stages. They moult to become imago, which develops in to the
adults.
Ticks are classified into one host or 2 hosts or 3 hosts, ticks
One host tick: All the stages of the life cycle occur on a single host. eg:- Boophilus
annulatus.
Two host ticks: The larva suck blood engorges and moulds to become nymph and
drops off. Then it moults to become imago which attaches to the second host and
develops into adults.
eg :- Ryhiphicephalus evertsi
Rjphiphicephalus bursa
Hyslomma species
Three host ticks: All the 3 stages in the life cycle of tick occur in 3 different hosts.
eg: Ixodes species
Hyalomma species
Haemophysalis species
Amblyomma species
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Ornithodorus species
Dermacentor species
Rhiphicephalus species
Argas persicus
Harmful effects of ticks:

1. The ticks transmit various diseases, Ex. Blood protozoan diseases like
theileriosis, Babesiosis, Rickettsial disease - Anaplasmosis. Bacteria - Brucellosis,
Ticks pyaemia (Staphylococcus aureus).
Viruses: EEMV (Equine encephalomyelitis virus), FMD.
2. They suck blood and causes anaemia.
3. They can cause tick paralysis which may be due to the toxins produced
in the ovaries (ticks) which is introduced into the animal through the saliva, (tick
bite). It is an ascending paralysis starting from hind quarter and progresses towards the
neck region.
4. Sweating sickness.
5. Tick pyaemia.
6. Tick worry.
7. Damage to the skin and hide.
Treatment and control of Lice, fleas and Ticks:
1. Hand picking and destroying.
2. Arsenic and Nicotine dips - This is out dated.
3. At present various chemicals have been used.
a) Chlorinated hydrocarbons.
i) D.D.T. (Dichloro Diphenyl Trichloroethane)
It is used at a concentration of 0.25 - 0.5% it is available as
powder.
ii) B.H.C. - Benzene hexachloride.
Gamma isomer of BHC is very effective, commonly
0.025 - 0.1% concentration is used.
iii) Toxophene 0.75 to 2%
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iv) Aldrin - 0.1%

v) Dieldrin - 0.1 to 1%
Toxic effects of chlorinated hydrocarbons:
They bring about stimulation of CMS. The animals will be alert, muscular
tremors, falling down and convulsion; with frothy saliva sticking to the mouth. These
symptoms are very similar to symptoms of fits of human beings. All of a. sudden, the
normal animal exhibits the signs by falling down and having convulsion. The duration
of the convulsion may vary from 1-10 minutes. After this, the animals become normal,
will be standing on their feet, ruminating and defaecations and micturitions will be
normal. At this (stage) time the animals appear all most normal and if we record the
temperature, the temperature can be 104-106o F, which will mislead the clinician. The
rise in temperature is due to tremors and convulsions. This episode can be once or
twice or thrice a day or once in 2-3 days. Some animals may die after a single
episode. Also animals can exhibit unusual postures.
1. Administer calboral 100 ml to 450 ml i/v, because in this type of toxicity,
hypocalcaemia occurs and hyperkalaeraia.
(Blood potassium level increased.)
2. Administer good amount of Magnesium sulphate orally to cause purgation, so
that evacuation of gastro intestinal contents occurs and along with it the removal of
ectoparasiticide occurs which is ingested.
3. Give a very good water bath so that further absorption of ectoparasiticide from
the skin is prevented.
II. Organophosphorus Compounds:
a) Malathion available as "Cythion" (Cyanamid) and it contains 50% malthion it is
available in container size of 250 ml, 500 ml, 1 litre, 25 litres. The concentration used
is 0.25 - 0.5%
"Cyban" - Scented Malathion, it is a preparation, meant for the use in human
beings.
b) Sumithion: It is 50% w/v Fenitrothion available as 100 ml bottle. Concentration
of 0.25 - 0.5% is used.
c) Ronnel: it contains Fenchlor phos. 0.5% concentration is used.
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d) Neguvon: 0.25 - 0.5% concentration is used.

e) Asuntol: It is made by Jagath chemicals and it contains 50% coumafos wettable
powder, as 15 gm sachet and 1 kg (800 Rs)
Concentration → Young ones - 0.25%
→ Adults - 0.5%
Toxic effects of all these: Salivation, dyspnoea, diarrhoea, abdominal, pain, muscular
tremors and ataxia.
They inhibit cholinesterase, resulting in over stimulation of parasympathetic
nervous system i.e. increased cholinergic effect.
Treatment for toxic effect:
1. 2-PAM (Pyridiae Aidoxime Methiodide): It is available as such, 20 ml
ampoule, containing 500 mg.
Dose: 20-50 mg/kg slow i/v, if necessary repeat after 30 minutes. Administer within
24-48 hrs after ingestion of poison. It helps in the regeneration of cholinestarase.
2. Atropine sulphate:
Cattle 30 mg / 45 kg b. wt (0.2-0.5 mg/kg body wt
Sheep 50 mg / 45 kg b. wt
Horses 6.5 mg / 45 kg b. wt
Dogs 2-4 mg / dog
1/3rd dose slow i/v and 2/3rd dose i/m or s/c every 3-6 hrs. In dogs, we should be
careful when using the Atropine sulphate because it causes death of the dog if the
diagnosis is not correct.
Available as 1 ml Ampoule/ of Atropline sulphate containing 0.65 mg. For this,
we should give half dose i/v and then half dose s/c. Also available as 10 ml vial (1
mg/ml).
3. Carbamates:
"Sevin" 50% wettable powder, 0.5% used.
4. Formamidine compounds:
Amitraz - 0.11 – 0.25 % concentration can be used.
5. Other:
a) Notix scrub (petcare) - carbaryl 10% in shampoo base, 30 g.
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b) Notix Talc (petcare) - carbaryl 5% Dusting, 150 g.

c) Pestoban liquid (Indian Herbs) 100 ml 1 litre, dilute in 8-10 times of
water and apply to the animal as a sponge bath or spray. Allow for 48
hours. Repeat after 3 or 4 days.
d) Blaze Liquid (Indian Herbs) 100 ml, Apply and rub.
e) Sumicidin 20% EC (Rallis) - Fenvalerate 20% w/'v 0.5 ml in 1 litre of
water. 100 ml, 250 ml, 500 ml; 1 litre and 5 litres.
f) Butox (Deltamethrin), 2 ml/litre.
g) Ivermectin 200 µg/kg body weight s/c, repeat after 4 weeks.
Mode of application:
1) Select a sunny day for spraying an ectoparasiticide because it will not allow the
drug to be absorbed into the body.
2) Put a basket to mouth of the animal or tie the mouth in case of dog to
prevent licking.
3) Prepare the required concentration of drug. The veterinarian should be very
careful in preparing the solution.
4) Apply the drug to the body of the animal either by using the sponge in the form
of a bath or by spraying by using the pumps. Allow the animal for 2-3 hours and
even by exposing to the sunlight.
5) After this time is over give a good water bath and expose the animal to sunlight
for drying.
Schedule: The ectoparasiticides are applied once in a week or 2 weeks for 2-3 times,
then once in 3 months regularly.
Some times even after following the schedule the number of ticks is not reduced
drastically which may be due to the developing of resistance to the ectoparasiticides. If
such a situation occurs, better switch over to another ectoparasiticide.
When ever spraying is done to the animals it is better to spray the cattle shed
especially of cracks and crevices by using higher concentration of drug like 5-10 times
the concentration used for the animals.
To control and eradicate the ectoparasites is very difficult and even by using the
above schedule it is not possible to eliminate all the parasites. By using the above
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schedule the intensity of the ectoparasites will be reduced. Another method of control
is vaccinating the animals with tract of various stages of the parasite.
eg:- Ticks, This method results in good immune response which will make the
tick to fall off from the body of the animal, which may be due to Agn-Aby reaction.
Other methods of control:
1) Burning of pasture.
2) Rotational grazing.
3) Vacating the barn for 3 months.
Ivermectin: 200 µg/kg s/c Repeat at 4 week interval.
Flumethrin: 1 mg/kg – spray 100% effective 28 days after treatment. Amitraz:
is also effective.
MANGE
1. Sarcoptic mange (scabies):
It is one of the mange commonly seen in almost all domestic animals caused by
Sarcoptes scabiei and characterized by itching, scratching, thickening and wrinkling of
skin and development of crusts on the skin surface.
Incidence: World wide, all species of domestic animals.
Etiology: Sarcoptes scabiei.
Transmission: Direct contact.
Life cycle: The adult female mite burrows deep in the skin forming tunnels and lays
eggs @ 3-5 eggs per day and total of 40-50 eggs per mite. These eggs hatch in 3-5
days and larvae comes out. The larva can stay in tunnel or will come out on to the
surface of skin and again burrows into the skin, forming mould packets. The larva
moulds to become nymph which again moulds to nymphs. These develop into adults.
Larva, nymph and adults can be transmitted from one animal to another animal upon
contact.
Pathogenesis: They suck lymph and feed on epithelial cells and this causes irritation
leading to itching and scratching. Also Keratinization and proliferation of connective
tissue occurs leading to thickening and wrinkling of skin. Later on vesicles develops
which is filled with lymph and ruptures leading to formation of crusts. Because of all
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these things we see alopecia.

Symptoms: The lesions are seen in different parts of different species which is as
follows.
Cattle: Head, neck, brisket, inside of thighs and scrotum.
Horses: Head and neck.
Sheep and Goat: Ears and face.
Pigs: Nose, ear, root of tail, around eyes, back and feet.
Dogs: Muzzle, elbow, hock and root of tail.
In advanced cases the lesions are generalized, irritation, itching, scratching,
thickening and wrinkling of skin, development of crusts and alopecia.
The mites usually (preferably) present on the hair free parts of skin. In
generalized infestation loss of wt, progressive emaciation and some can die.
Diagnosis:
1) By symptoms and lesions.
2) By skin scraping examination.
Treatment: To overcome the etiological agents, use any one of the following:
1) Lime sulphur dip: Once a week for 3-6 weeks.
2) Tetmosol Tetraethyl thiuram monosulphate (ICI) available as
a. Soap or cake contains 5% of this compound
b. Solution 25%, 50 ml and 1 litre 5% solution is applied to the body.
3) Benzyl benzoate: Available as Ascabiol (M&B), 25% white emulsion, 125
ml, 1000 ml container.
Clip the hairs and give a good bath so that the crust will be removed.
Then apply this emulsion. If the lesions are generalized, mix the emulsion with
equal quantity of water and apply. If the lesions are localized - apply as such.
Apply at an interval of 3-6 days for 2-3 times. This is the drug which is
commonly used in dogs. The field veterinarians also used this in other large
animals also- but the text books have not mentioned for the use of large
animals. It is contraindicated in cats.
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4) Gamma BHC: These are indicated in large animals in the text.

5) Malathion: Concentration 0.25 -0.3% as spray or bath once a
6) Asuntol: week for 2-3 weeks.
7) Oil of Karanj: It is oil obtained from Pongama pinnata. Daily for 2-
8 days applied to lesions.
8) Taramira oil: It is extract of Rapeseed Mustard. It is applied, twice at an interval

of 5 days.
9) Hippush: It is an extract from Juniperus communis. 50% oil extract apply
daily for 6 days. Then give a break of one week, and repeat this course.
10) Cedrus deodara oil: 15% of this oil in castor oil is used; apply daily for 10 days.
Available as Flematic skin oil (TTK) 90 ml bottle. Effective against fleas, mites and
ticks. Apply liberally and allow for 60 minutes.
11) Lazin vet: Once a week for 3 weeks.
12) Ivermectin (USA) Ivomec, (Merc sharp and Doom MSD USA). By Thimmappa
Rai and Yathiraj (1988) Bangalore.
Dose: 0.2 mg/kg, b.wt. s/c.
Majority of cases were cured when administered once others require 2-3
injections at an interval of one week.
13) No tick powder. Applied daily.
PSOROPTIC MANGE
It is an ectoparasitic infestation of all domestic animals except clogs caused by
Psoroptes species and characterized by itching, scratching and formation of crust on
the skin.
Cause: Psoroptes ovis and P. bovis.
Very common in sheep, causing mortality
Transmission and pathogenesis: Symptoms and diagnosis are very similar to
sarcoptic mange. Here the infestation is superficial and tunnel formation is absent.
Treatment: Similar to sarcoptes and other drugs used are
1) Crotoxyphos - 0.3%
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2) Ivermectin.
The following supportive therapy can be used in both sarcoptes and psoroptes
mange,
1) To reduce itching - administer,
i) Antihistamine like Avil.
ii) Corticosteroid like Dexavet or Hostacortin.
2) To improve skin texture administer Acetylarson (M&B)
9.4% for dog 1-3 ml, s/c or i/m.
23.6% for cattle 3-10 ml, s/c or i/m.
3-4 injections have to be given at interval of 3-4 days
3) To bring about good healing and proper growth of epithelium of skin
administer, vitamin - A.
Prepalin forte (Glaxo) Dog - 1-2 ml
Cattle - 2-6 ml i/m
3-4 injections have to be given at an interval of 3-4 days.
4) Also administer 3-4 injections of B-Complex at an interval of 3-4 days.
5) Also administer 5-10% Dextrose, i/v.
DEMODECTIC MANGE
(Demodicosis, Follicular Mange, Red mange)
It is a infestation of skin of all domestic animals caused by Demodex species

and characterized by either squamous or pustular type.
Incidence: World wide. All domestic animals including man are affected. Stress
factor and vit. A deficiency may predispose to this type of mange.
Etiology:
Demodex canis It is a small, elongated mite and its body is divided
Demodex bovis into three parts- head, thorax and abdomen.Thorax
Demodex ovis contains four pairs of stumpy legs and abdomen
Demodex equi contains cross striations.
Transmission: By contact.
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Life cycle: Rot clearly understood larva and 3 nymphal stages have been recorded
before becoming adults.
Pathogenesis:
1. The mites get into hair follicles and damage them resulting in alopecia.
2. The mites invade sebacious glands and causes inflammation resulting in.
excessive secretion of 'sebum' which appears like flakes or scales on skin sue face.
3. Hypertrophy of epithelial cells resulting in thickening and wrinkling of skin.
4. The damage to the skin by these mites will predispose to the secondary bacterial
invaders like staphylococci (58%), proteus (23%) and pseudomonas (19%) which
results in formation of nodules and pustules. Generalized lesions can result in
toxaemia and death of the animal.
Symptoms:
Squamous form: Alopecia, thickening and wrinkling o£ skin, initially skin will be
coppery red in colour and later on it will be black in colour.
Pustular type: Nodules or pustules which may break open discharging pus. This
type can occur in all species of domestic animals but nodular type is common in
ruminants.
Parts affected:
Cattle: Neck, brisket, wether, dewlop shoulder and forelegs.
Dogs: Around eyes, forehead and nose.
Sheep: Back and flank.
Goats: Neck, chest and shoulder.
Course of disease: Few weeks to months to years.
As the condition progress, loss of weight, weakness, emaciation also will be
noticed.
This parasite suppresses the CMI response hence such animals are more susceptible to
bacterial and viral infection like pneumonia.
Prognosis is poor in old dogs and demodicosis complicated with pseudomonas.
Diagnosis:
1. By symptoms.
2. By lesions.
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3. By skin scraping examination - the mites should be present in

good numbers and the presence of one or two may be normal. Refer the
chart.
Treatment: To treat demodectic mange is very difficult. The following drugs have
been used:
1. Rotenone in Olive oil is applied to the lesions once in 5 days for
several weeks.
2. Benzyl benzoate + 0.25% BHC.
3. Lime sulphur dip.
4. 0.5% Malathion
5. 0.5% Neguvon Once a week for 2-3 weeks
6. 0.25% Asuntol
7. Closantel: First injection 5 mg/kg b.wt., s/c Second injection - 2.5 mg/kg
b.wt. s/c. Totally injections, at an interval of 1 week. Very effective.
8. Cypermethrin: 1.25% solution in propylene glycol applied locally, daily for
10-15 days and then twice a week until cured.
9. Ivermectin: 0.1 - 0.2 mg/kg b.wt., s/c once a week for 7-8 weeks. This is tried
by Dr. Sudhirkumar Borikar, and Dr. Yathiraj.
It is better to administer 5-10% Dextrose, intravenously to animals having
disorders of the skin.
The supportive therapy mentioned for Sarcoptic mange can be used in
Demodectic mange except- the use of corticosteroids should be avoided since the
immuno-suppression is already existing.
Always treat with antibacterial agents to overcome the secondary bacterial
invaders.
Control: Genetics plays an important role. Hence, do not use bitches having
Demodectic mange for breeding purpose.
KNEMIDOKOPTIC MANGE
Knemidokoptes mutans causes scaly leg in chickens, turkeys, pheasants and
other gllinaceous birds. The mites burrows in the epidermis of the legs, causing
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scales to loft and become loosened and the legs thickened and deformed.
Knemidokoptes pilae and K. jamaicanen is cause mange of the legs, base of
the beak, vent area and back of parakeets and canaries respectively.
K. gallinae, depluming mite of chicken, pigeons, pheasant and geese is found
at the base of feathers and the back, or top of the wing and on the vent, breast and
thighs. It causes intense pruritis leading inturn to feather pulling.
CHORIOPTIC MANGE
Chorioptes bovis is a cosmopolitan, superficially dwelling parasite, displaying a
distinct preference for the tail escutchen and legs of the cattle, where it feeds on
epithelial debris. Although cattle are the principal hosts, C. bovis may also be found on
the tail and legs of horse, sheep and goats and in the ear canal of rabbits.
Asymptomatic infestation is far more common obvious dermatitis.
The life cycle of Chorioptis bovis is very similar to that of Psoroptes spp and is
complete in 3 weeks. The first sign in horse is usually violent stamping of the feet
and rubbing of the back of the hind pasterns, on wire, rails or stumps. This is moat
evident during periods of rest; and at night in cases of long duration, the skin is
swollen, scabby, cracked and usually greasy and small amounts of serous exudate may
be attached to most hair in the affected area.
Chorioptic mange in cattle usually appear during the late winter as a superficial,
mildly pruritic, flaky dermatitis involving the tail, escutchean and hind legs.
Chorioptis bovis causes exudative dermatitis on the lower legs arid scrotum of
rams. In extreme cases the crusts may be associated with chorioptic mange lesions
covering more than 1/3rd of the scrotum and was apparently related to elevation of
testicular temperature.
OTODECTIC MANGE
Otodectes cynotis infests the external ear canal and adjacent skin of dogs, cats,
foxes and ferrets causing intense irritation. Copious dark cerumen is characteristic of
Otodectic otitia. Aural pruritis sometimes causes the animal to rub and scratch its ears
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and shake its head violently enough to produce haematoma of the aural pinna.
NOTOEDRES MANGE
It is caused by Notoedres cati in cats, rats and rabbits. It occurs chiefly on the
ears and back of the neck but may extend to the face, foot, hind paws and in young
cats to the whole body. The mites burrow into the skin and causes elopecia and marked
hyperkerotosis with abundant epidermal flakes.
Characteristics of Mites:
The mites will be identified by looking at the morphological features of the
mite.
1. Sarcoptes scabiei: The mites are small, globose or circular in shape, the
pretarsi have long, unsegmented pedicels and the anus is at the posterior edge of the
body. All the legs of the both sexes are short and the third and fourth pairs do not
project beyond the margin of the body.
2. Psoroptes Spp.: The mites are bigger than the mites of Sarcoptes
scabiei, are oval in shape, the legs are long and the pretarsi have long, three
segmented pedicles.
3. Demodex Spp: The mites are elongate, usually about 0.25 mm long
and they have a head, a thorax which bears four pairs of stumpy legs and an
elongate abdomen which is transversely striated on the dorsal and ventral surfaces.
4. Chrorioptes bovis: The mites resemble psoroptes. The pretarsi of C. bovis have
short, unsegmented pedicels on first, second and fourth pairs of legs of the female
and all legs of the male. The male has two turrets like lobes on the posterior margins
of the body.
5. Notoedres cati: The mites resemble Sarcoptes but are small and its anus is on
the dorsal surface instead of on the posterior margin of the body.
6. Otodectes cynotis: The mites resemble Chorioptis. The pretarsi of O. cynotis
have short, unsegmented pedicles on the first and second pairs of legs of the female
and on all legs of the male. The body of the male is only weekly bilobed posteriorly.
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ECTOPARASITES OF POULTRY
I. Lice:
They belong to the order Mallophacra. These are the biting lice and they do
not suck blood, but if blood is available, they will ingest it. The entire life cycle occurs
on the skin.
a. Monocanthus stramineus: Chicken, body louse or chicken yellow body louse.
It is about 3 mm in length and found on the skin of the breast, thighs and near
the cloaca. Eggs are laid in clusters on the base of the feathers.
b. Cuclotogaster heterographa: Head louse, 3 mm long, dark grey in colour.
Since they are found in the head, they are called as 'head louse'.
c. Lipeurus caponis: Wing feather louse.
d. Gonicotes gallinae: Fluff louse found in down feathers.
II. Mites:
i. Dermanyssus gallinae: They feed only at night, they suck blood. They may
transmit, Spirochaeta.
ii. Ornithonysaus sylviarum: Northern fowl mite.
iii. Knemidocoptes mutans: ‘Scaly leg mite'. It lives in the tissues beneath the
scales of the legs and causes severe local reactions resulting in thickening and
deformation of the legs.
iv. Cytodites nudus: 'Air sac mite'. They are found in lungs, air sacs and bronchi
and may cause nodules.
v. Laminosigptes cystiocola: It causes nodules in the skin.
III. Ticks:
Argas persicua
Harmful effects of ectoparasites:
1. Since these are found on the surface of the skin and move all over
the body, they cause uneasiness, annoyance and irritation.
2. Since, some of the lice, mites and ticks suck blood, they cause anaemia.
Heavy infestations causes weakness, loss of gain in body weight, emaciation, decrease
in egg production and finally the death of the birds.
286
3. Some ectoparasites like Dermanyssus gallinae can transmit spirochaetes.

Diagnosis: The ectoparasites are usually present at the base of the feathers and in
between the feather. Hence thoroughly search these areas for the presence of either the
eggs, nymphs or adults.
After picking these parasites, they can be easily identified as lice or ticks. The
exact species of ectoparasite can be identified by processing the ectoparasite end,
studying their morphological characteristics under the microscope.
Treatment and Control: The use of chlorinated hydrocarbon compounds is contra-
indicated in poultry because of the residues present for a long period in meat and eggs
which are used for human consumption.
In our country, the commonly used ectoparasiticides in poultry are :
1. Malathian: is available an Cythion 50% EC (Cyanamid) in container sizes of 250
ml. 500 ml, 1 litre, 5 litres. The concentration used for spraying of birds is 0.25-0.5%.
Mix 80-160 ml in 10 litres of water which is sufficient for 300 birds. Spray the birds
thoroughly.
For the building mix 200-220 ml of Malathion in 4 litres of water. Avoid
contamination of feed, feeding troughs and water fountains.
The antidote for this type of poisoning is Atropine sulphate.
2. Asuntol: 50 wettable powder (Jagat chemical): It contains Coumafos 50%. It is
available as 15 gms sachet (Rs. 25/-) and 1 kg (Rs. 800/-). 2 gms of Asuntol is mixed
in 1 litre of water and sprayed on the birds. For the house the concentration is
doubled.
The Powder is used for dusting of poultry house. For this the area of the
poultry unit is calculated and the required amount of powder is uniformly placed on
the litter to cover the entire litter and the litter is slightly mixed.
3. Sumicidin 20% EC (Rallis India): It contains 20% Fenvalerate. For dipping,
sponging or spraying 0.5 ml of Sumicidin is mixed in 1 litre of water and for building
1-2 ml per litre of water.
While preparing the required concentration of the ectoparasiticide, the
available concentration of the drug should be presumed as100%.
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FUNGAL DISEASES
Fungi are filamentous or unicellular organisms with chitin, chitosan, gluconand
mannon in their cell wall.
Nutrients is absorptive, both carbohydrates & nitrogen sources must be
supplied. Fungi are autotropic in respect of vitamin requirement with exception of
some species of Trichophyton
The fungi are either saprophytes, symbionts or parasites. Some have become
highly adopted parasites of animals and man and cause a variety of diseases of the skin
and internal organs.
Historically, fungi have been regard as relatively insignificant causes of
infection and until recently clinical laboratories offered little more than interest in
providing mycological services. During past few years, however, the literature has
shown a sharp increase in the number of case reports of fungal infection. The fungi
are now well recognized causes of infection and physician awarness of the importance
is much more common. Come clinical microbiology laboratories have kept pace
with the changing times, but unfortunately many still offer only minimal mycological
services. The emergence of continuing education programmes presenting a practical
aspects of clinical mycology and a no. of recent text books in the same area, along
with the increased number of journal -publications, now makes mycology available to
all clinical microbiology laboratories where it should be included as an important
component.
The fungi can affect the skin, mucous membranes and internal organs.
1. LOCAL INFECTION
RING WORM
(Dermatophytosis, Microsporosis, Dermatophilosis, Girth itch, Dermatomycosis,
Trichophytosia)
It is a fungal infestation of skin of all domestic animals and man caused by
various species of fungus belonging to Trichophyton and Microsporum genus and is
288
characterized by ring like white crusty lesions.

It is an integumentary disease.
Incidence: By contact. However, indirect contact with any inanimate objects,
particularly bedding, harness, grooming kits and horse blankets, is probably more
important. Spores can exist on the skin without causing lesions, and "carrier
animals" of this type may act as important sources of infection. Premises and harness
may remain infective for long period because fungal spores can remain viable for years
provided they are kept dry and cool. Moderate heat and desiccation destroy them.
Transmission between species occurs readily and in rural areas 80% of human
ring worm may be derived from animals. Ringworm of animal origin affects adult
humans as well as children and diagnosis and treatment are often very difficult.
The lesions progress if suitable conditions of environment exist for mycelial
growth including a warm humid atmosphere and a slightly alkaline pH of the skin.
Fungi are strict aerobes.
Pathogenesis: Fungus usually affects the hairs and keratinized portion of skin
including nails. Fungus can grow inside or out side the hair shaft to destroy it and
eventually it falls off (alopecia).
Organism produces a toxin / irritant / allergen that are responsible for
inflammation (congestion, erythema). Fungus can not survive in inflamed area and
keeps on moving away abaxially in a ring like manner.
Secondary bacterial complications can result in formation of vesicles and
nodules in the area.
Etiology:
Cattle:
Trichophyton verrucosum (Common one)
T. mentagrophytes
T. megnini
Lesions: Lesions are seen, in head, neck, and perineum or could be a generalized one.
Classical ring like lesions which are circular, 1-3 cms diameter and are like white thick
crusts. Later the lesions can fall off leaving erythematous patch. Itching does not
occur and secondary acne is unusual. Equines:
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Etiology: Trichophyton equinum, T. quickeanum, T. mentagrophytes, T. verrucosum,

Microsporum equinum, M. gypseum
Lesions can be deep or superficial, superficially round patches of raised hair.
Lesions will be sore to touch. This can fall off within a week and. scab may appear and
heals up appearing like moth eaten appearance. It could be more than 10 mm in size.
Girth, axillary region, covers trunk, later on rump, neck and head and limbs
Canines & Cats:
Etiology: Microsporum canis (70% in dogs & 98% in cats)
M. gypseum,
T. mentagrophytes.
Classical lesions, but irregular and diffused forms are not uncommon.
KERION
Is a red, swollen area which is infected with bacteria and is ulcerated. Sheep:
Trichopyton verrucosum var ochraceum (common one).
T. quinckeanum
T. mentagrophytes
T. gypseum
T. canis.
Pigs: T. mentagrophytes (common)
T. Yerrucosum var descoidae
Microsporum nanum
Goats: T. errucosum
Diagnosis :
1. Wood's lamp: produces ultra violet rays and when held against lesions, the
lesions emit bright green yellow fluorescence. It is characteristic to M. canis (also
M. adouni and M. distortum).
2. Skin biopsy: PAS (Periodic - Acid - Shiff) gives reddish colour to fungi.
3. Culturing: using SABOURAUD'S Dextrose agar, this contains
chloramphenicol and cycloheximide (to prevent saphrophytic fungi), incubated in
dark for 21-30 days.
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Characteristic colonies visible.

Treatment:
Orally: Griseofulvin is an antifungal, antibiotic and is fungistatic and available as
Grisovin tabs (Glaxo), Fulvin -M tabs (Medopharma) and Edifulvin (IDPL). Each
tablet contains 125 mgs of griseofulvin/250 mg also.
Dose: 30 mg/lb b.wt per day bid/tid. Causes vomition if given to empty
stomach. Once response is seen reduce the dose to half and continue for 3-4
weeks, 25 nig/kg body wt. for calves upto 7-10 days, 5-7 mg/kg b.wt., for 1-2
weeks. Absorption takes place rapidly with fatty diet, and the drug is
contraindicated in pregnant bitches. Has good affect on Microsporum and
Trichophyton.
Topical: antifungal agents should be used.
1. Whit field's ointment : 450 gms. This causes inflammation and
hence fungi can not survive.
2. Salicylic acid ointment, 450 gms. it has keratolytic effect and hence fungi
can not grow.
3. Mycoderm (FDC) 100 gms powder, contains -
Salicylic acid, benzoic acid, camphor, menthol, starch, talc and kaolin
light.
4. Multifungin powder and ointmaet
5. Quadriderm cream contains beta methasone, gemtamicin, Tolnaftate and
lodochlorohydroxyl guincline.
6. Miconazole nitrate available as - "DAKTARIN GEL"(Ethnor; It is a
broad spectrum antintycotic with bactericidal action (against gram positive bacilli
and cocci.) Apply the gel to the lesion twice daily and rub the
medication gently for 2 weeks to prevent relapse. Available in 20 grams
tube.
7. Tinea fax 20 grams and 40 gms oint /powder.
8. Mycozol liquid 50 ml tube.
9. Mersagel gelly 40 gms tube.
10. Betnovate 'C' contains chinoform and beta methasone.
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11. Thiabendazole 2-4%, paste in shark liver oil and apply to lesions once in
3 days for 3 times gives good results in calves.
12. Badional gel (Bayer) used for treatment of burns. Has been tried in calves
against Tr. verrucosum. Once in a day for one week.
13. Captan - Apply 1:300 or 1:400 once or twice, 2 weeks, apart.
14. Sodium iodide i/v 1 gm/14 kg b.wt. as 10% solution one injection.
Control :-
1. Isolation and treatment of infected animals.
2. Clean and disinfect the barns and kennels with phenol - 2.5 - 5%, Formaline -
5%, Sod. hypochlorite -5% 0.25% and 1% chlorinated lime and peracetic
acid - 1% caustic soda.
3. Leave the stall unoccupied for some time.
4. Vaccination : No vaccine available in India.
A) Trichophyton verrucosum vaccine - calves vaccinated 10-20 ml 3 doses -
3 days apart.
Resistance for a year. Tried in Russia.
B) Trichophyton equinum - Live vaccine, i/m twice. Horses protected for 5
years.
C) Yinokuror et al (1975) tried and vaccinated animal, by using live
Trichophyton fariform.
2. SYSTEMIC FUNGAL INFECTIONS

(Systemic Mycoses)
Systemic mycoses in animals are usually sporadic infections which occur by
chance and cause non specific syndromes because of variation in the organs in which
they localize most commonly the mediastinal and mesenteric lymph nodes. Their
epidemiology is based on the failure of the diseases to be transmitted from one host to
another, all the infections deriving from sources in the environment. The causative
fungi exist as saprophytes in organic matter and the portal of entry is most commonly
by inhalation of dust containing fungal elements, with a primary focus developing in a
lung. Another common, form of infection is alimentary mycosis, in which the
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forestomachs, abomosum and intestines of young ruminants and poultry are involved.
Various systemic fungal infections of domestic animals and birds are as
follows.
1. BLASTOMYCOSES
A. It is systemic fungal infection caused by Blastomyces dermatitidis commonly
in dogs, also recorded in a horse, Siamese cats, Sea lion, and Man. It is confined to the
USA, Canada and Africa.
The organism cause a chronic granulomatous inflammation, of the skin and
internal organs mainly lungs. Three clinical forms blastomycosis have been
identified:
1. Primary pulmonary infection: Cough, dyspnoea, ocular and nasal discharges.
2. Disseminated disease: Ocular disease is a frequent finding in dogs with
disseminated blastomycosis, which is the most common form of oculomycosis in
dogs. Uveitis, glaucoma subretinal granuloma formation or retinal detachment is
frequently found on ophthalmological examination. Corneal oedema, exophthalmia
and conjunctivitis may be present.
Osseous involvement also occurs.
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BABESIOSIS
(Piroplasmosisor or Red water fever or Cattle tick fever)
It is an haemoprotozoan disease of domestic animals caused by various spp of
Babesia and it is characterized by high fever, haemolytic anaemia, jaundice and
haemogiobinuria.
Incidence: Babesiosis occurs throughout the world. All the spp of domestic animals
including man are susceptible. Cattle of 6-12 months of age group are highly
susceptible. Severe form of the disease has been recorded in puppies, when compared
to adults.
In cattle, exotic and cross bred animals are highly susceptible, Indigenous
breeds are also highly susceptible. It is one of the important diseases of the dairy
industry causing severe economic loss. It is common in our country.
Etiology: Babesia is pear shaped organisms inside the RBCs. Commonly occurs in
pairs with the narrow ends opposing each other at an acute angle. There are 2 types of
piroplasms.
1) Large piroplasm which measures about 4-5µ x 2µ in size.
2) A small piroplasm which will be half the size of the large piroplasm.
Spp:
Cattle: Babesia bigemina (Large Piroplasm)
Babesia bovis (Small Piroplasm)
Babesia dwergens (Small Piroplasm)
Baliesia argentine (Small Piroplasm)
Babesia major (Small Piroplasm)
Sheep & Goat: B. motasi, B, ovis, B. foliate.
Swine: B. trutmanni, B. peroncitoi.
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Horse, Donkey, Mule: B. caballi, B. equi, usually four in number, arranged like cross
Dogs: B. canis. Sometimes more than 16 organisms are seen in one RBC.
B. gibsoni
B. vogeli
Cats: B. felis.
Transmission:
(1)By ticks, here stage LO stage transmission (i.e. transtadiai) and trans-ovarian
transmission are seen.
(2)By Blood transfusion.
(3) By intrauterine, transmission,
Life cycle: Female tics suck bloodand along with it the irregular shaped organism
preset in the RBCs also gets into the ticks. Lot of Such things get into the gut of the
ticks, but only few will survive. These develop into two types of spherical bodies. First
form of spherical body will give rise to the elongated forms while the second form
gives rise to oval form. These two fuses together to form a zygote. This point is still in
controversy. Some people call the zygote as “Cigar shaped” body. Then zygote
develops in to a spherical body which invades the epithelial cells of gut and transforms
into a fission body which give rise to vermicules. These vermicules will migrate
through the gut wail in to the haemolymph, ovaries and other tissues. !n other ovaries
it goes in to ovum and usually in the yolk of ovum, it is found. They can undergo one
more cyclical change i.e. vermicules fission body vermicules. When the larva moulds
to become nymph, the vermicules migrates to the salivary glands. Here they are
transformed to spherical bodies, then spherical bodies to pyriform bodies. When the
tick bites these pyriform bodies are released into blood stream which finally enters the
RBCs. in the RBCs they divide repeatedly by binary fission which leads to lysis of
RBCs and the pyriform bodies which comes out of the lysed RBCs will invade the
other RBCs and the same cycle is repeated.
Pathogenesis: in this condition lysis of RBCs occur, the mechanism of lysis may be
1) Since pyriform bodies of babesia multiply by binary fission inside the RBCs it may
end in lysis of RBCs.
2) Recently Eli salde et al., proposed a hypothesis regarding lysis of RBCs. According
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to them cortisol and cholesterol level may play a role. Here liver synthesize the
cholesterol and by the action of the progesterone on cholesterol, cortisol is produced.
These workers have shown that the liver is damaged in babesiosis and hence the
production of cholesterol is reduced leading to hypochoiesterolaemia which inturn
leads to less formation of cortisol resulting in hypocartisolaemia.
Since the function of the corticosteroid is maintenance of homeostasis, and also
for the stabilization of the cell membranes. These functions are altered in babesiosis,
because of hypocortisolaemia. This results in the ceil membranes of the RBCs
becoming more fragile ending in lysis of RBCs.
The same workers have also reported that there is increased prostaglandin level
in babesiosis. Because of this the increased affects of prostaglandins is seen.
1) increase in the vascular permeability
2) Inhibition of the most of the immune function
3) Initiation of the systemic piafcieiei aggregation.
All these results in vascular stasis and subsequently hypoxia of parenchymatous
organs. These results in clinical manifestation of the diseases.
Severe haemolysis results in haemolytic anaemia, lysis of RBCs results in
release of haemoglobin in to blood leading to haemoglobinaemia. The haemoglobin is
filtered in the kidneys and exerted in the urine resulting in haemoglobinuria.
Haemoglobin is broken down into haemoglobin and porphyrin. Porphyrin is
converted into biliverdin, which inturn is converted in to bilirubin which will stain the
mucosa and serosa yellow which is known as jaundice.
Clinical findings: I.P. is 2 weeks. High fever, anorexia, atony of the rumen,
depression, symptoms of anaemia like pale mm, increase in heart and respiratory rate
and weakness will be seen, when the anaemia is severe we hear a sound called
thumping sound of the heart which is due to cardiac palpitation. These sounds are like
the sounds coming from beating of the heart without auscultation.
Jaundice i.e. yellow staining of mm and haemoglobinuria i.e. pacing of coffee
dictation coloured urine or dark brown coloured urine will be seen.
Necropsy findings:
Pale muscles, accumulation of fluid in the cavities, haemorrhages on serosa and
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mucosa, enlargement of liver, fatty degeneration and centrilobular necrosis,

enlargement of spleen, le splenomegaly with dark and soft pulp. Gall bladder will be
distended, with dark granular bile, kidneys will be dark in colour, and Urinary bladder
will be distended with coffee coloured urine.
CNS form of babesiosis is also recorded, but very rare. In this form CNS signs
will be seen and characteristic histopathological lesion is clogging of cerebral
capillaries with RBCs.
Diagnosis:
1) By symptoms of high fever, anaemia and haemoglobinuria.
2) By blood examination
a) Make a blood smear do the Giemsa or Leishman or wrights staining and
examine under oil immersion lens, Here we see pyri form or pear shaped
organisms inside the RBC commonly two organisms are seen in a RBC.
b) Wet mount method
c) Haemotology: PCV, TRC, Hb are reduced. After doing the PCV examines the
plasma part in capillary tube, it will be reddish in colour indicating the
haemolysis.
3) Serological tests: CTAT, card agglutination test, HIT, CFT, Indirect FAT, ELISA,
latex agglutination test, etc.
4) Macrophage migration inhibition test.
1) Anaplasmosis: Anaemia, No Hb uria, blood smear examination spherical bodies
either at the center or periphery of the RBC.
2) Theileriosis: Anaemia, high fever, enlargement of peripheral lymph nodes. No
Hburia and blood smear examination reveals rod, comma, and oval bodies.
3) Leptospirosis: Fever, haemoiytic anaemia, hburia, Blood smear examination where
in pear shaped or pyriform organisms are seen in babesiosis and no organisms will be
seen in leptospirosis.
4) Post parturient Hburia: Seen after parturition, anaemia, Hburia is seen. It is due to
P deficiency Analysis of feed for Ca and P ratio and estimation of blood P tevei which
is decreased. Best way is to going for biood smear examination for the presence of
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babesia organisms.
5) Bacillary Hburia: It is due to Cl. Haemolyticum. Fever, haemoiytic anaemia,
Hburia is noticed. Best way is going for blood smear examination for the presence of
Babesia. In our country, babesiosis is much more common than bacillary
haemoglobinuria.
6) Ephemeral fever or 3 day sickness: Fever, enlargement of peripheral lymphnodes,
and lameness. Blood smear examination is the best way for the detection of theiieria.
7) Coccidiosis: Seen in young animals having diarrhoea, dysentery anaemia. Best way
is to do faecal examination for the presence of oocyst.
Treatment:
1) Trypan blue: Available as stain and it is a powder make 1% solution with distilled
water and filter it.
Dose: Cattle 50-100 ml slow i/v one injection is enough if necessary repeat
once more. Avoid peri-vascular infiltration, dog → 5-10 ml.
2) Acriflavin: Available as powder, prepare 5% solution in distilled water and filter It.
Dose 20 ml/cattle i/v.
3) Quinorium derivatives.
4) Aromatic dismidines and carbanilides:
a) Berenil: 4 diamidino, diazoamino benzene diaceturate tetrahydrate. Availability
22.5g bottle and 5.0 gm bottle. They are yellowish granules. One gram of
powder contains 0.444g of active ingredients. Along with this battle one
measuring spoon is available one spoon equals 0.8 gm of granules.
Dose: 1-2 spoonful/100 kg body weight or 3-4 mg of active ingredient/kg
body weight. One spoonful of the powder is dissolved in 5 ml of distilled water.
Route: Deep i/m. Only once is enough. If necessary once more can be
administered. Still this drug is very effective against babesiosis in our country
and this is the drug of choice for babesiosis in our country.
The same dosage can be used in other spp. of animals also and it is very
safe.
b) Midocarb: Foreign Tradename (Imizol)
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Dose: Cattle 1-2 mg/kg body weight

Horse: 2-4 mg/kg body weight
I/m or s/c single dose is enough and if necessary repeat after 2-3 days
once more, it is very effective but still not available in our country.
c) Amidocarb.
d) Dimidin:
To overcome anaemia
1) Severe cases blood transfusion.
2) Moderate cases use haematinics.
To supply energy and fluids
5-10% Dextrose, 1-2 litres i/v
To improve the appetite
Administer Beekom-L or Vibelan and anorexia mix.
Any haemoglobinuria cases
It is better to administer sodium bicarbonate because sodium bicarbonate makes
the urine alkaline where in haemoglobin is soiubie which will prevent the damage to
the tubules of the kidney.
100 ml of commercially available Sodium bicarbonate i/v and also
administering 1-2 ounce of Sodium bicarbonate orally bid, for 2-3 days.
Most of the animals will recover but it takes nearly 2-4 weeks for the animal to
return to the normal condition.
Control:
1) To eliminate the ticks give, sponge bath or spray the animal with Malathion,
Sumlthion, Asuntol, Butox etc.
2) Vaccinate the healthy animals.
a) Passaging of the virulent Babesia organisms in splenectomized calves and
blood from such calves is used as vaccine.
b) Recently in Australia, the blood from infected animal is irradiated and used as
vaccine.
c) Chemoprophylaxis or chemo-immunization. In this method the virulent Babesia
organism is injected and at the same time Imidocarb is administered.
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TRYPANOSOM1ASIS (Surra)
It is a blood protozoan parasitic disease of most domestic animals caused by
Trypanosoma evansi and it is characterized by recurrent fever, anaemia, conjunctivitis
and debility. Surra means rotten.
Incidence: Africa and Asia, India, Animals affected are horses, donkeys, cattle,
buffaloes, mules, dogs, camels and elephants.
Etiology: T. evansi which measures 25-38µ x 1.5-3.5µ. It is an extra erythrocytic
organism.
Transmission: By vectors like Tabanus, stomaxys, Lyperosia.
Pathogenesis: Causes anaemia, and it is due to auto immune mechanism and also due
to suppression of the bone marrow. In this condition, severe, hypoglycaemia is seen,
since the organisms utilize the blood glucose.
Clinical findings: I.P. 2-3 weeks.
Cattle: Usually are carriers and disease can occur under stress. Fever, anorexia
decreased milk yield, conjunctivitis and CNS signs like circling, depression, coma and
death. Chronic cases debility, weakness and oedema.
Buffaloes: Similar signs can be seen in buffaloes also.
Horses: Similar to cattle and in addition urticarial eruption on skin, oedema on lower
part of the limb, thorax, ventral abdomen, up to prepuce. Course is up to 6-8 weeks.
Camels: Acute and chronic form chronic form can be for 3 years where in anaemia,
emaciation and death.
Necropsy findings: Marked emaciation, splenomegaly, lymphadenopathy, serous
exudates in body cavities, petechiae on serosa. Ulceration of tongue and gastric
mucosa.
Diagnosis:
1) Symptoms
2) Blood examination (a) Blood smear (b) Direct method
3) Serological test; Passive haemagglutination test, CFT, FAT, AGPT, ELISA.
4) Other tests: Mercuric chloride Test
a. Take 1 ml of 1:25,000 solution of mercuric chloride in a test tube. Add 1
300
drop of serum from a suspected animal. If a white precipitate occurs with

in a few minutes then it is positive.
b. Stilbamide test: Take 1 ml of 0.3% stilbamide and add 1 ml of serum. If
opalescence appears within 1-2 minutes then it is positive.
c. Formal gel test: Take 1 ml of suspected serum in a test tube and add 2
drops of formaline. Allow for 2 hours. If complete gel formation occurs
then it is positive.
Treatment:
1. To eliminate Trypanosoma give
a) Antrycide methyl sulphate (Quinpyramine sulphate) (ICI) as 1 gm envelope.
Make 10% solution with distilled water.
Dose: 3 mg/kg s/c.
b) Antrycide Prosait (quinpyramine sulphate 1.5gm and chloride 1.0 gm) 2.5 gm
and 25 g container add 12 ml - 15 mi distilled water
Dose: 3-5 mg/kg s/c.
c) Antrypol (Suramin) 25g bottle. Make 10% aqueous solution
Dose: 1-2 g/ 100 kg l/v.
Similar to Antrypol is Naganol.
d) Samorin (M&B) (Isometamedlum chloride) 1% solution
Dose: 1 .25 mi/45 kg., deep i/m one injection.
e) Berenil @ 3.5-7.0 mg/kg body wt. i/m as such.
f) Cymerlasan @ 0.3-0.6 mg/kg body weight, s/c effective in camels also.
2. To overcome hypoglycaemia give 10$ Dextrose, 1-2 litres i/v.
3. To overcome anaemia similar to theileriosis.
Control:
1. Eliminate the vectors by spraying the ectoparasiticides.
2. Test the affected animals, separate them and treat.
No vaccine is available.
Trypanasoma thelleri is a non pathogenic protozoon of blood.
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COCCIDIOSIS
It is a protozoan disease of all the domestic animals, caused by various spp of
Eimeria and Isospora and it is characterized by diarrhoea, dysentery, anaemia and
hindered weight gain.
Incidence:
It is world wide in its occurrence and ail the spp. of domestic animals are
susceptible. Young ones are highly susceptible and come down with the severe form of
the disease when compared to adults. It commonly occurs in young ones 3 weeks and
above.
Stress factors like overcrowding, malnutrition, poor sanitation, etc play an
important role in the onset of clinical manifestation of the disease.
Etiology:
Cattle: Eimeria zurnii, E. bovis, E. elipsoidalis. They are in the caecum, terminal
ileum and colon.
Sheep and Goat: E. arlongi, E. parva, E. faurei, found in small intestine.
Swine: E. debleicki, I. siuis
Horses: E. leuckarti
Dogs & Cats: I. bigemina, I. rivolta; I. felis, E. canis.
Transmission: By ingestion of sporuiated oocysts.
Life cycle: Sporulated oocyst contains in Eimeria, A sporocysts and each sporocyst
contains 2 sporozoites and in Isospora 2 sporocysts and each sporocyst contains 4
sporozoites. When such sporulated oocysts are ingested, it will rupture and releases
sporozoites. These sporozoites penetrate the epithelium of the intestine and develop in
to trophozoite. These trophozoites develop in to schizonts. The chromatin material left
the schizonts undergo repeated binary fission leading to formation of merozoites. Due
to this rupturing of the epithelial cells occur, releasing the merozoites. These
merozoites get in to the other epithelial cells and develop into schizonts. Schizonts
again give rise to merozoites. These merozoites are released after rupturing of the
epithelial ceils. The repetition of the part of the life cycle can occur once or twice and
this varies with the spp. of the Eimeria involved.
Sexual form of life cycle: Merozoites develop in to macro and microgametocytes.
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Macrogametocytes give rise to macro gametes and microgametocytes to microgamete.

Macrogamete combines with microgamete and forms the zygote which secretes a cyst
around it to form an oocyst. The oocysts are thrown out of the body through the faeces.
Further development of the oocyst occurs under suitable environmental condition to
form sporulated oocyst.
Pathogenesis:
The damage to the epithelial ceils occur when the trophozoite develop to
schizonts and schizonts in to merozoites. This causes the destruction of the epithelial
ceils. When this part of the life cycle is repeated and the number of repetition is more,
severity is also more. Because lot of destruction of the epithelium occurs, this leads to
diarrhoea. Due to destruction of epithelium damage to the capillaries occurs which
leads to dysentery, dehydration haemoconcentration, hypovolaemia, shock and death.
Dysentery → loss of blood → anaemia
Effects of diarrhoea (1) Metabolic acidosis. (2) Hypokalaemia.
Clinical findings: IP. is 16-30 days. Sudden onset of diarhoea i.e. soiling of hind
quarters and tail. Faeces will be foul smelling, lot of mucous and epithelial of weight,
inability to stand, pale mm, emaciation, increase in heart and respiratory rate,
depression, dyspnoea and death. Some animals may show CNS signs like muscular
tremors, hyperaesthesia, tonic or clonic spasms, ventral flexion of head and neck,
nystagmus. In such case mortality rate is 80-90%. Course of the disease is one week.
Necropsy finding:
Hemorrhagic enteritis, i.e. Sloughing off of the epithelium ulcers and the
contents of the intestines will be having more of epithelial shreds, mucous and blood.
Diagnosis:
1) By symptoms of diarrhoea, dysentery and anaemia in young ones.
2) By faecal examination to demonstrate the oocyst which may be spherical, oval.
1) Calf scours: seen less than 2 weeks of age. Fever and chalky white diarrhoea will be
seen.
2) Salmonellosis: seen in any age group of animals especially in adults it causes
diarrhoea, dysentery, fever.
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3) Enterotoxaernia: Sudden death of well grown animals are affected some animals
may have diarrhoea, dysentery.
The best way to differentiate these diseases is by faecal examination, where in
parasites especially the coccidial oocyst can be demonstrated.
Treatment:
1. To eliminate the Etiological agent administer any one of the following
a) sulphaguanidine-available as such. Dose: 130-150 mg/kg body weight orally for 5
days. Since it is a gut acting sulpha, it may not produce the same effect as that of
suiphadimidine.
b) Sulphadimidine - available as such.
Tabs: Sulpha bolus (Sarabhai) Diadin tabs (Pfizer) 5 g. Dose: 130-150 mg/kg orally
every day for 5 days.
TOXOPLASMOSIS
Toxoplamosis is a contagious protozoan disease of all species including human
beings caused by Toxoplasma gondii and is characterized by encephalitis, pneumonia,
and neonatal mortality in all species and abortion and still births in ewes.
Etiology:
Toxoplasma gondii is a systemic coccidian and member of the suborder:
Eimeriina.
There appear to be a number of strains which differ appreciably in their
virulence.
Epidemiology:
1) Occurrence:
It occurs in most parts of the world.
Toxoplasmosis is a true zoonosis occurring naturally in man, and in
domesticated and wild animals and birds.
Recent national surveys in swine in the USA and in Canada show a
seroprevalence of 24% and 9% of samples positive. On a world wide basis the
seropositive prevalence in swine is 22% with a range of 0- 97 %, for sheep 21%, goats
25%, horses 15%. True seroprevalence in cattle is believed to be low and reflective of
the relative unimportance of Toxoplasmosis in cattle.
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In farm animals the infection is sub clinical and it has Virtually no importance
as a cause of clinical disease in farm animals with the exception of that associated with
abortion and neonatal disease in sheep. The major importance of toxoplasmosis in
farm animals is its zoonotic potential.
2) Transmission:
The sole source of infection for sheep, cattle and horses is the oocyst passed in the
faeces of the cat family.
Cats become infected and shed oocysts in their faeces, as a result of ingesting
tissues of intermediate hosts Infected with the parasite. Commonly these are the
rodents and small birds, but all animals can be I.H. for T. gondii.
Rodents pass the organisms from generation to generation through congenital
infection and thus can provide a reservoir of infection in an area for a long time with
the potential for infection of cats and the triggering of massive oocyst contamination of
the environment. Following infection of the cat the period of excretion of oocysts is
short, approximately 2 week., but it is intense {I and several million oocysts are
excreted in the faeces. The cats can defecate in hay, straw, grain stores and thus
providing the potential for direct infection of livestock feeds.
Oocysts are extremely resistant to external influences and can survive in the
environment for at least 1 year.
Infection of farm animals can occur by ingestion of contaminated stored feeds,
contaminated pastures and contaminated water supplies.
Humans are I.H. for T. gondii. and approximately % the population of USA is infected.
They get the infection by ingestion of contaminated food, meat or tissues that are
eaten or handled, it poses an occupatinal risk for Veterinarian farmers and slaughter
house workers who handle infected materials.
Life History:
Toxoplasma gondii is an enteric coccidian of the domestic cat (Felis catus) and
other members of the family Felidae: Cats are the only known definitive I hosts
and therefore only infected cats shed oocysts of this parasite in their
faeces. The Oocysts is very small (11-13 urn) contains a single sporont and is non
infective when passed in the faeces. Sporulation is completed in 1-5 days and results in
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formation of two sporocysts each of which contains 4 sporozoites.

Fully sporulated oocysts are infective upon ingestion to essentially all warm
blooded animals including cats. Therefore, almost any warm blooded animal may
serve as IH of T. gondii.
Upon ingestion, sporulated oocysts rupture in the intestine and release the
sporozoites. These enter and multiply in cells of the intestine and associated lymph
nodes to form tachyzoites which spread to all other tissues of the body and they invade
cells and continue to multiply. Eventually, tissue cysts containing bradyzoites are
formed in the brain, striated muscles, and liver and viable for the life of the host. Both
tachyzoites and bradyzoites are infective upon ingestion to essentially all warm
blooded animals and behave very much in the same manner just described for
sporozoites. Thus I.Hs, become infected with Toxoplasma gondii by ingesting
sporulated oocysts from cat faeces or tachyzoites and/or bradyzoites in the tissues of
other IHs. Transplacental migration of tachyzostes from dam to foetus in utero also
occurs but varies in importance from sp. to sp. of host.
When a member of the cat family ingests tissue, cysts of T. gondii the
bradyzoites penetrate the epithelial cells of the small intestine undergo a series of
asexual cycles and finally undergo the sexual cycle, which culminates in the shedding
of oocysts. Cats shed Toxoplasma oocysts in their faeces 3-10 days after eating mice
infected with encysted bradyzoites but not until 19 to 48 days after ingesting
sporuiated oocysts or mice infected with tpchyzoites. Apparently the asexual
reproduction preceding formation of bradyzoites in the IH satisfies a major portion of
the developmental requirements preceding sexual reproduction. Cats may also
serve as IHs in as much as multiplication of tachyzoites and cysts formation occurs in
their extraintestinal tissues.
Clinical findings:
The clinical syndrome and the course of Toxoplasmosis vary a great deal
Cattle:
Usually acute farm is seen where in there will be a fever, dyspnoea, and
nervous signs including ataxia and hyperexcitability, in the early stages followed by
extreme lethargy. Still born or weak calves which die soon after birth may also be
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observed. Does not play significant role in abortion.

Congenitally affected calves show fever, dyspnoea, coughing, sneezing,
nasal discharge, clonic convulsions, grinding of the teeth and tremor of the head and
neck. Death occurs after a course of 2-6 days.
Pigs:
They are highly susceptible and in outbreaks pigs of all ages can be affected.
In adult pigs there is debility, weakness, incoordination, cough, tremor and
diarrhoea, but no fever.
Young pigs are often acutely ill with a high fever of 40-42°c and develop
diarrhoea and die after a course of several weeks.
Pigs of 2-4 wks. Of age have additional signs including wasting, dyspnoea,
coughing, nervous signs, especially ataxia.
Pregnant sows commonly abort, piglets are premature or still born or survive
and develop the above syndrome at 1-3 wks of age.
Sheep:
The systemic disease in the eve is rare.
The commonly occurring things are foetal resorption, abortion, the birth of
mummified or stillborn lambs, neonatal death, and the birth of full term lambs that
show locomotor and sucking disorders. Abortion commonly occurs during the last 4
wks of pregnancy and the rate may be as high as 50%. Full term lambs from infected
ewes may be born dead or alive but weak, with death occurring with in 3-4 days of
birth. Lambs effected after birth show fever and dysponoea but a fatal outcome is
uncommon. Fetal resorption can occur in ewes infected in early pregnancy.
Goats:
Perinatal deaths, including abortions and still birth. However , the systemic
disease, with a high case fatality rate \ft more common, especially in young goats.
Horses:
It is rare
Diagnosis:
Serological tests are commonly used to determine the presence of
toxoplasmosis but the results vary.
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1. CFT - late in the disease.

2. Sabin - Feidman dye test - Early stage.
3. Indirect IFT
4. Indirect HA - Cross reaction
5. ELISA
6. Modified direct Aggl. Test - serological surveys.
Necropsy findings:
Multiple, proliferates and necrotic granulomatous are characteristic lesions.
Such lesions with calcification in cattle occurs in nervous system, myocardium
and lungs.
In visceral involvement, there will be pneumonitis, hydrothorax, ascites,
lymphodenitis, intestinal ulceration and necrotic foci in the liver, spleen and kidneys.
In sheep, in the foetal lambs there will be focal necrotic lesions in the brain,
liver and lungs and there will be white spots in the placenta.
Histologically, Toxoplasma can be found in the cells of most organs
particularly the lungs and brain.
Causes of abortion and neonatal death in lambs should be considered.
The presence of /tecroscopic white foci of necrosis in the placenta and
histological findings of multiple foci of necrosis in the placenta and microscopic foci
of necrosis in the brain, liver, lung, kidney and heart of the lamb are highly suggestive
for Toxoplasmosis.
Treatment:
Pyrimethamine or Sulphadiazine have limited value when used alone,
combination is highly effective pyrimethamine.
Sulphapyrimidines (SD/SM/Suiphadiazine)
Effective against proliferating in the acute stage usually will not eradicate infection.
Ltd. activity on the tissue cysts. Toxic in cats.
Clindamycin is used in cats and is reported as being effective. It will not
eliminate oocysts shedding in cats, it will reduce oocysts shedding.
Control:
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1. Exposure to cat faeces should be avoided.

2. Feeding of Monejsin @ 15 mg/head per day for the first 100 days of pregnancy has
been shown to reduce lamb loss.
3. DecoQuinate - More palatable and less toxicity.
4. Killed Vaccines
PARASITIC DISEASES
HELMINTHES
NEMATODES TREMATODES CESTODES
I. TREMATODES
Hepatic distomiasis or hepatic fascioliasis or liver rot or fluke disease
It is a parasitic infestation of most of the domestic animals caused by the

various genera of flukes and characterized by either acute or chronic hepatic
insufficiency.
Etiology:-
Fasciola hepatica: - Present in bile duct of sheep, goat cattle, buffaloes, pigs,
elephants, dog, horse, cat & man. It is leaf like and having broad shoulders. It
measures 13 mm x 13mm,
Fasciola gigantica : - Similar to F. hepatica, but it is bigger in size and having
narrow dioulders. It measures 25-75 mm x 12mm.
Fascioloides magna: - Recorded in the liver of cattle, sheep, bison, deers, it
measures 23-100 mmxll-26mm.
Dicrocoeium dendritium: - Occurs in the bile duct of sheep, goats, cattle, pigs,
deers, dog, donkey & man.
Incidence: - Occurrence of this disease is worldwide. It is very common in areas
where irrigation channel tanks, ponds, are present in good numbers, because in these
the intermediate host of flukes lives. Because of this fact flukes are not common in
Bidar district. However it is present in
animals purchased from neighboring states like A.P. and Maharashtra and also sheep
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gone for grazing to far of places during summer. All age groups are susceptible, young
ones/ arc more susceptible and severe form of the disease occurs when compared to
adults. It causes severe economic loss which may be due to; 1) Mortality 2) Decrease
in production which may vary from 8-20%. Decrease in milk production.
Transmission:
• Ingestion of metacercariae
• May be also congenital.
Life cycle: - The adult flukes are present in the bile ducts. They lay eggs, these eggs
are passed through the bile into intestine, and thrown out of the body through, the
faeces. These eggs under suitable environmental conditions develop, into miracidium
which penetrate into the intermediate host i.e. snail (Lymnea spp), and develops into
sporocyst. The sporocyst develops into radia and radia gives rise to cercaria. The
cercaria comes out of the snail and forms a cyst around it called metacercaria. These
metacercaria are found attached to leaves of the water plant and floating in water.
When the animals are taken to tanks, ponds and channels for ingesting along with
water metacercaria are also ingested, which goes to the intestine and cyst breaks open
releasing the immature fluke. This Witt reach the bile duct in any one of the following
ways;
1) These can penetrate though the wall of the intestine and get into peritoneal cavity,
then it penetrates through the liver capsule and then migrate through the liver
parenchyma and gets into the bile duct.
2) From the intestine it will get into the portal vein and through this parenchyma it will
get into the liver and migrating through this parenchyma it will reach the bile duct.
In the bile duct they mature and become adults and start laving eggs. The above
life cycle is characteristic of F. hepatica.
F. gigantica - similar to F. hepatica
F. magna - Life cycle is same but in cattle it forms cyst in the liver and hence
the fife cycle may not be completed. But in sheep it is similar to F. hepatica.
Dicrocoelium dendriticum - Here 2 intermediate hosts are present. The first
intermediate host is the snail. Where in miracidium gets into the snail and forms
sporocyst and then cercaria (there is no radia stage from sporocyst) is formed which
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are thrown out of the snails in the form of “slime balls” which are eaten by the ants
(2nd IH) and develops into “Meta cercaria”. Final host gets infected by eating such ants
in the feed. The cercaria is released in the intestine and crawls through the bile duct
opening and migrates through bile into the gall bladder.
Pathogenesis:
Acute Fascioliasis: - The immature flukes burrow and migrate through liver
parenchyma leading to destruction of parenchyma. In addition, they feed on the
hepatic cells. Due to these things damage to the blood vessels results in haemorrhages
and bleeding. If too many immature Hukes are migrating through liver it may cause
sudden death due to the above damages.
Chronic Fasciolisasis: - Due to the migration of immature flukes the hepatic cells are
destroyed and are replaced by fibrous tissue leading to cirrhosis of liver. The small bile
duct undergoes thickening and hardening due to the constant irritation caused by the
flukes. Later on deposition of calcium in the wall of bile ducts can occur. Because of
these things the bile ducts become more prominent and this condition is known as
"piped stem liver".
In fascioliasis, anaemia can occur, and the causes of anaemia are:
1) The flukes suck blood at the rate of 0.2 ml per fluke per day.
2) May be due to haemorrhages and internal bleeding.
3) Suppression of the bone marrow
4) Destruction of the RBCs.
In fascioliasis, obstructive jaundice can occur. Because the conjugated bilirubin
formed in the liver is not excreted into the intestine through the bile, since bile duct is
obstructed by the flukes. Hence, conjugated bilirubin gets into the circulation and
stains the mucosa and serosa yellow coloured.
Due to the liver damage, albumin is not synthesized in good amount leading to
hypoproteinaemia. This result in decrease in the osmotic pressure of blood leading to
seepage of fluid part of blood into the cavities, in s/c tissues especially of
intermandiblar space i.e. Bottle jaw.
Clinical findings:
Acute: - Young claves and lambs can die without showing any clinical signs. In
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some, the signs noticed are, anorexia, pale mucous membranes, dullness,
weakness, edema of the throat and conjunctiva. Upon palpation of the last two
intercostal spaces of the right side, the animal evinces pain and enlargement of the
liver can be noticed. Many will die and can show the symptoms of passing of
blood or bloody discharge from the anus and nasal cavity.
Chronic: - 1) Alternating diarrhoea and constipation, dehydration, weakness,
sunken eyebafls.2) Bottle jaw. 3) Pale mucous membrane; in adults decrease in
milk production. In sheep wool may fall off. Emaciation and some may have
jaundice.
In very chronic cases debility and emaciation is common and the animal
appearing like having skin and bone appearance.
Course: - Acute:-Up to 2 day to- several days, chronic: Months (2, 3, 4 months to 1
year).
Necropsy findings: -
Acute: -Liver is enlarged, haemorrhages and blood clots on the liver and fluke
burrowing tracts most common. Serous fluid in peritoneal cavity. Lot of flukes in
liver.
Chronic: - Liver is small, hard and shrunkened. The bile ducts are prominent, hard
and thickened "pipe stem liver". Lot of flukes in the bile ducts.
Such livers are condemned for human consumption.
Diagnosis:-
1. By clinical signs
2. Faecal examination. The liver fluke ova arc big in size, the opcreulum and
embryonic mass are indistinct. The eggs are yellow coloured.
3. Serological tests. Indirect IPT, Indirect FAT, and ELISA are used.
4. Vanden Berg test: - Direct test will be positive.
5. Urine analysis: -
a) Test for bile pigment is positive.
b) Test for urobilinogen is negative since it is not formed
Differential Diagnosis: -
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(1) Amphistomiasis - By faecal examination - foul smelling faeces, and the ova
having a knob with distinct operculum and embryonic mass.
(2) Salmonellosis:- Fever, diarrhoea, dysentery.
(3) Johne's disease: Nonjresponding chronic diarrhoea, thick pea soup type of faeces.
No fever. By faecal examination one can rule out - no ova.
(4) Parasitic diarrhoea: Faecal examination - reveals the presence of various types
of nematode ova.
Treatment: -
I. To eliminate the flukes administer any one of the following anthetaintie.
1. Carbon tetrachloride (CC14 or CTC) available as 450 ml chemical.
Dose: Calf: l-2mt Adult cattle: 3-5 ml, Lambs: 0.5-4 ml Sheep: 1-3 ml; Dogs: 1-
5 ml.
Route: orally, mixed with butter milk and drench, it. It is effective against native
flukes.
This drug has been administered parenterally i.e. i/m or s/c either alone or
mixing with equal quantity of liquid paraffin.
Dose: - 1 ml/9 kg. b. wt. with a maximum of 30 ml, 10-15 ml/animal i/m.
If the dose is 30 ml give 15 mi at 2 sites.
CTC toxicity: CNS depression, drowsiness, inco-ordination, cardiovascualr collapse. It
is also hepatotoxic. This may be due to administering CTC with fat where it is quickly
absorbed. It may also be related to hypocalcaemia. This toxicity is commonly noticed
in weak and debilitated animals, when such animals are presented, first treat with
calborol and liver extract for 1-2 weeks and then administer CTC. If Nicotinic acid is
available administer 2 gms of nicotinic acid and then after one hour administer CTC.
2. Hexachloroethane:-
1) Aviothane (ICI) 500 gin & 3 kg packet.
2) Fairmethaine - 30 gms, and 1 kg packet.
3) Hexathane (Sarabhai) 30 gm & 500 gm sachet.
Dose: 220 mg / kg. b. wt. (Calf: up to 15 gms. Yearlings to adult: 30 - 45 gms
and Sheep: 5-15 gms.)
Effective on immature flukes.
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3. Hexachlorophene
“Distodin” (Pfizer) available as 100 mg tabs
“Flukin” (AR-Ex) 100 mg tab
Flukin forte (AR-Ex) 1 gm tab
Dose: - 10-20 mg/kg b. wt. All species.
Route: - Orally in a Banana or as electuary or Roti.
4. Nitroxynil - Trodax (M&B) 34% solution, available as 10 ml, 50 ml vial.
Dose: 10 mg/kg. b. wt. Route: s/c. This drug will stain wool and should be
careful enough to prevent it. Also it will stain milk so avoid using in lactating cow.
5. Oxyclozanide - Zanil (Imkemex) it is a 3.4% w/v available as 1 litre container.
Dose: 10-15 mg/kg. b. wt. orally.
Nilzan (Imkemex) it contains Tetramisole - 3%, oxyclozanide 3%, w/v (50ml,
100ml. 1 litre size container)
Dose: 0.33 ml/kg. b. wt.
It is effective against adult worm.
Distodin fluke bolus (pfizev) 1 gm/bolus
6. Hetol @ 125 mg/kg b. wt.
It is effective against adult worm.
7. Freon – Dose: Cattle: 100 mg/kg
Sheep: 330-660 mg/kg
It is effective against adult flukes.
8. Bithional - Cattle: 30-35 mg/kg orally.
9. Phenacetin - 150 mg/kg. for 2 days orally to sheep.
10. Distoject - contains Nitroclofene.
Cattle: 3 mg/kg. i/m.
11. Acedist - 6.5 - 33 mg/kg.
Effective against adults.
12. Clioxanide - 40 mg/kg. Orally- effective against both mature and immature
flukes.
13. Niclofolan - 2-3 mg/kg orally effective against mature flukes, can be used for
i/m route also.
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14. Rafoxanide (Ranide l0 g packets 20% powder) - 7.5 mg/kg orally, also half the
dose s/c.
15. Diamphenitide - 100 mg/kg b. wt. orally - effective against immature flukes.
16. Rafoxanide + Levamisole: Available
17. Albendazole 2.5% suspension i.e. 25 mg/ml used @ 10 mg/kg b. wt., orally.
II. To overcome dehydration, give lactated ringers with dextrose i/v
III. Administer liver extracts like Belamyl, Beekom-L
IV. To overcome anaemia, administer haematinics.
Calf: 3 ml. Heifer - 5 ml.
Adult: 10 ml i/m alternative days for 5 days.
Control:
I. Identify the suffering animals and treat them.
II. To eliminate the source of infection the following is done:
A) to eliminate the snails. To kill the snails various chemicals have been used
which are known as Molluscieides.
1) Copper sulphate: effective at 26 ppm. It can be applied to marshy lands at the
rate of 9 kgs of CuSo4.
2) Frescon - N - trityl - morpholene. 0.25- 0.5 ppm.
3) Sodium pentachlorophenate 6 ppm.
4) Bayluscide (Bayer) 0.35 ppm.
5) Copper pentachlorophenate 4.5 kg/acre.
Characteristics of Molluscicide:
1) It should be very effective at very low concentration.
2) It should be cheap and commonly available.
3) It should not produce adverse/harmful effect to water faunae, animals and
human beings.
It is very difficult to get chemical with the above property hence one or other
draw back will be present.
Lot of work has been done by WHO in African countries by using
molluscicides for the control of snails m Human Schistosomiasis.
B) By rearing of Ducks.
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These fib ducks will eat the snails.

This is highly impracticable because ducks will be used for meat purpose by the
human beings.
C) Hand piecing and destroying of snails. It is practically impossible to eliminate all
the snails and the cost of labour is very high.
D) Biological control: Any one of the following may be tried:
a) Hydrophiius triangularis - water scavenger beetle.
b) Dyticus marginalis.
c) Spherodema rusticum- giant water bug.
d) Lamprophorus tenebrosa - Larva of Firefly.
These will eat snails at the rate of 1-5 snails/day. The practical utility of the
above is questionable because of the chances of above acting as pests to well grown
crops.
AMPHISTOMIASIS
(Immature Amphistomiasis, Intestinal Amphistomiasis, Stomach fluke disease)

It is a parasitic infestation mainly of cattle caused by various genera of
Amphistomes and characterized by severe enteritis.
Cause:
Paramphistomum - P. cervi,
P. orthocodnim
P. gotoi
P. epiditum
Cotylophoron - C. cotylophorum
Calicophoron - C. calicophorum
C. Cylonocotyle - Cey. streptocoelium
Cey. thapari
Gastrothylax - G. cruminifer
Fischoederius - F. clongatus
F. cobaldi
Carmyerius - C. spatiosus
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C. gregarius
Gigantocotyle - G. explanfetum
They are flukes, they measure about 5-13 mm in length X 2-5 mm in breadth.
They are light red in colour. The mature flukes are found in the rumen and the
immature flukes are found in the intestine.
Incidence: World wide. Mainly a disease of cattle and buffalo and also recorded from
sheep and goat. It can cause mortality of 40-60% resulting in good economic loss.
Commonly occurring disease. Severe form of the disease is seen in yearlings but can
occur in any age group and any sex and breed.
Transmission: By ingestion of contaminated feed and water especially of tanks,
ponds and channel water.
Life Cycle: - The adult flukes in the Rumen lay eggs and will be passed through the
faeces. Under suitable environmental conditions further development of egg occurs
and the eggs hatches releasing the miracidium. The miracidium penetrates the snail
like Indoplanorbis exustus, Lymnaea spp. Bulinus sp., Planorbis planorbis and
develops into sporocyst → radia → cercaria. The cercaria comes out of the snail
develops into metacercaria which will be found dn water plants and water. When the
animals ingest water and water plants, the metacercaria goes to intestine. From the
intestine they migrate into the rumen through the oesophageal groove. In the rumen
they develop into adults and start laying eggs.
Pathogenesis: - The immature flukes which are in the intestine are harmful. They
attach to the intestinal mucosa and pluck the mucosa. This results in ulcer formation
and bleeding or haemorrhages. These damages results in diarrhoea → dehydration →
Haemoconcentration → shock → death.
Clinical signs: - Diarrhoea which is profuse, faeces smells foul and contains mucosal
shreds. Symptoms of dehydration, anorexia, depression, bottle jaw, some may collapse
and die. In some loss of weight, weakness, emaciation is seen. Sometimes immature
flukes are passed in the faeces.
Necropsy Findings: - Atrophy of muscles, s/c edema, excess of fluid in peritoneal
cavity, serous atrophy of fat, - due to mal-nutrition, or mal-absorption. Haemorrhages
in small intestine, ulcers and thickening of mucosa of small intestine. Plenty of light
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red coloured adult flukes in the rumen and reticulum.

Diagnosis:-
1) By signs of diarrhoea, foul smelling faeces.
2) Faecal examination, in the early stages eggs are not seen and also we may see
immature flukes in the faeces.
Differential Diagnosis:-
1) Fascioliasis:- Faecal Exam and finding the characteristic ova.
2) Johne's disease: - Thick pea soup like faeces, not responding to treatment.
3) Salmonellosis:- Fever, diarrhoea, dysentery.
Treatment:- Very similar to fascioliasis. To over come etiological agent any one of
the following drugs can be used:
1. Carbon tetrachloride
2. Hexachlorophene Refer Fascioliasis for dose and route of
3. Hexachloroethane. administration
4. Niclosamide - Niclosan, 500 mg tab Niclex - powder (Alved) 75% w/w
Niclex bolus (Alvcd) 1 gm bolus 90 mg/kg, b. wt. Orally.
5. Bithional.
6. Methyridine.
7. Yomesan.
8. Resorantel.
Supportive therapy:
a. Koalin pectin preparation or Astringent mixture.
b. To overcome dehydration - lactated ringers and Dextrose.
Control: - Similar to fascioliasis.
NASAL SCHISTOSOMIASIS (NS)

(Nasal granuloma, snoring Disease)
It is a parasitic disease mainly of cattle caused by a blood fluke i.e.
Schistosoma nasale, and it is characterized by snoring, nasal discharge and nodular or
cauliflower like lesions in the nasal cavity.
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Etiology: - Schistosoma nasale previoulsy known as Schistoma nasalis. It is a blood

fluke. It is found in the nasal veins of the nasal cavity. Males and females are present.
The males measures about 6.3 -11 mm and female 5-11 mm. The male is having a
gynaecophoric canal and in this canal the female is carried during copulation.
Incidence: - It is a disease of the Indian subcontinent i.e. this disease occurs in India,
Pakistan, Srilanka and Burma (Miyanmer). It is a very common disease of our country
and even in Karnataka. It is mainly a disease of cattle and to an extent buffaloes. This
disease has been recorded for the first time in sheep by the AICRP on nasal
schistosomiasis. Bangalore centre. Later on by Tamil Nadu AICRP on NS and latter on
recorded from goats also. Minimum age of infestation in cattle is 6 months, and 11
months in buffalo (and above). There is no variation in breed or sex.
Economic importance: - The economic loss is due to-
1) Reduction in the working capacity of animals.
2) Reduction in milk yield.
3) Mortality due to NS is very low and very rare.
Transmission: - The infective stage of the parasite is the cercaria which actively
penetrates the skin, the oral and nasal mucosa.
Life Cycle: - The adult flukes are present in the nasal veins and lay eggs. These eggs
are passed out of the body through the nasal discharge. These eggs develops under
suitable environmental condition and hatches releasing the miracidium. The miricidim
enters the intermediate hosts i.e. snails - Indoplanorbis exustus and develops into
sporocyst I which gives rise to sporocyst II. This gives rise to cercaria. There is no
matacercaria formation. The cercaria is the infective stage which actively penetrates
the skin or oral mucosa or nasal mucosa when the animal ingests water from tanks,
ponds and channels. Then they enter circulation and through circulation go to Nasal
veins and localize in these veins. They develop into adult flukes and start laying eggs.
Pathogenesis:- The adult worms are harmless. The harmful effects are produced by
the eggs. The egg in the nasal cavity undergoes development and will have miracidium
which secretes proteolytic enzyme which comes out of the pores of egg shell. These
enzymes damage the wall of veins resulting in the rupture of venules/veins. Then the
eggs enters the surrounding tissue and around this there will be, infiltration of
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eosinophils, neutrophils and macrophages. These proteolytic enzymes act on these

cells and bring about degenerative changes of these cells resulting in formation of ray
like structures. This is known as actinobody formation- means pseudotubercle. Later
on lot of neutrophils, lymphocytes and monocytes gets into the site which results in
small abscess formation. Later on ripening of the abscesses occurs leading to braking
open of abscess releasing the ova into the nasal discharge.
To these areas granulation tissues grows and fills up the area resulting in
nodule or cauliflower like lesion. Usually small nodules form, then these coalesce
together to form cauliflower like growths.
Clinical findings:- 1) Nasal discharge - serous, mucous, mucopurulent,
serosanguineous, blood & blood clots also can be seen. 2) Sneezing. 3) Snoring which
can be heard even from a distance and is due to obstruction of nasal passage. 4)
Nodules or cauliflower like lesions in the nasal cavity. This type of lesion may not be
present in some animals but commonly seen in most of the animals. 5) Decrease in
working capacity, decrease in milk production and in advanced cases dyspnoea can be
seen.
Course: - It is a chronic disease and without treatment it is present throughout the life
of animal.
Necropsy findings: - Nodules or cauliflower like lesions in the nasal cavity.
Diagnosis:-
1) By symptoms of snoring, and nasal discharge.
2) By lesions- nodules or cauliflower like lesions, in the nasal cavity.
3) By examination of the nasal discharge and demonstrating the presence of eggs. The
nasal discharge is collected by using an instrument called Vaulkman's Scoup. The
scraping should be done until slight bleeding occurs.
Method: - 1) Direct- place a small quantity of discharge on a slide and add 2 drops of
5-10% Sodium or potassium hydroxide mix the contents and place a coverslip and
examine under the low power of microscope.
2) Indirect: - Transfer the nasal scrapings into a glass centrifuge tube and add 3-5 ml
of 5-10% sodium or potassium hydroxide. Boil the contents and cool it. Centrifuge at
2000 - 3000 rpm for 5 minutes. Discard the supernatant. Mix the sediment and transfer
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a small quantity on a slide and put a coverslip. Examine the slide under the low power
of microscope. If Napoleon hat shaped or Boom rang shaped eggs are seen then it is
positive for nasal granuloma.
3) Intradermal test: - Jagannath et. al. (1988) Veterinary College, Bangalore devised
this test. In this test the antigen from S. japonicum is injected intra dermally at the
base of tail. If erythema and wheal occurs within 10-20 minutes, then it is considered
as positive. Erythema about 0.7 to 2,7 cm in size.
Differential Diagnosis: - NG should be differentiated from Rhinosporidiosis. It is a
disease, which is recorded in foreign countries and commonly Australia, U.S.A. also
in our country. It is caused by fungus called Rhinosporidium seeberi and this disease
is very similar to NG and the double walled endospores are detected in the nasal
discharge.
Treatment: - To eliminate the fluke any one of the following can be used:
1) Anthiomaline (M&B) - Lithium antimony thiomalate 6% available as such and
Anthiomaline (M&B) as a 50 ml vial and cost is about Rs. 907/-
Dose: - 15-20 ml deep i/m administered 3-4 times at an interval of 3 days i.e., twice a
week for 2 weeks. Even can be used on alternate days for 3-4 times. Some
veterinarians have tried i/v route also.
Side effect: - It causes painful swelling at the site of injection which can be overcome
by fomentation.
2) Antimosan (Bayer) - 50, 500 ml container. It contains penta sodium antimony
biscatechol - 3:5 disulphonate.
Dose:- is 20-40 ml/animal, any route i/v, i/m or s/c 3 times at an interval of 3-4 days.
Now available in our country.
3) Neguvon (Bayer) - It is a Ectoparasiticide, powder 1 kg packet but not available in
out-country. This drug has been tried as follows:
i) 30 ma/kg b. wt daily for 8 consecutive days orally as drench. It was toxic.
ii) 40 mg/kg, b. wt. - for 4 consecutive days orally - also toxic.
iii) 40 mg/kg. b. wt. 4 times administered on alternative days was found better.
Here the animals behaved as though they have recovered from this disease i.e.
no nasal discharge, no nodules, no snoring for only 1-3 months and then again
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animals exhibited the clinical signs of the disease.

That means it produces a temporary curative effect. Recurrence of the
disease was noticed within 1-3 months.
iv) 50 mg/kg, b. wt. - 4 times at an interval of 3 days.
The effect was similar to iii.
v) Topical application (a) the powder was mixed with small quantity of water and
made into a paste and was applied and rubbed to nasal lesion every day for 10
days. (b) An ointment was prepared with vaseline and applied to the lesions
once a day for 10 days. These methods were also toxic to animals.
4) Ambilhar (Ciba) - It contains Niridazole. It is a drug used for Human
schistosomiasis and it was available as tablet Dose: 25-50 mg/kg was not effective, 75
mg/kg/ b. wt. daily for 7 daus was toxic.
Schedule: In one schedule, it was administered twice a day for 2 consecutive days. It
was found to be slightly toxic. Then this schedule was modified and the drug was
administered once a day for 4 consecutive days and this method was not toxic, and the
animals recovered from disease.
5) Sodium antimony tartarate (SAT) : It is available as a chemical in powder form.
Prepare a 2% solution in 10% Dextrose saline.
Dose: 1.5 mg / kg body weight.
Route: Administered as a slow i/v. injection. Draw the solution into a 20 or 30 ml
syringe. Insert the 18 gauge needle into the jugular vein of a cow and fix the needle
check whether the needle is exactly in the vein or not. Then connect the syringe, draw
few ml of blood into the syringe. Inject 2-3 ml slowly, draw few ml of blood into the
syringe. Inject 2-3 ml slowly then, draw few ml of blood into the syringe and again
administer 2-3 ml. Repeat this procedure, until all the solution is injected.
6) Potassium antimony tartarate - available as Tartametic (Ethicare) available as 2%
and 4% solution 25 mi vial.
Dose: - route & schedule of administration is similar to sodium antimony tartarate.
Adverse reaction to Sodium and Potassium antimony tartarate
If by chance perivascular infiltration of the drug occurs then it causes severe
irritation and swelling of the region. The swelling goes on increasing and it appears as
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though another head is growing in that region. This swelling will be hard and mostly
fibrous.
The antimony preparation should not be used in cows which are in advanced
stage of pregnancy even though they are suffering from NS. Because - 1) They are
highly irritant resulting in swelling which may be responsible for fever resulting in
abortion. 2) Delaying the treatment for 3-4 months will not cause the death of the
animal.
7) Praziquantal: @ 5 mg /kg. b. wt. orally, reduced the EPG.
8) Muraleedharan. K and Rajashekar C. (1996). Comparative efficacy of some
Anthelmintics against nasal schistosomiasis in cattle. I.V.J. 73 (3): 265-269.
Oxyclozanide 10 mg/kg b. wt. oral / once a week for 3 weeks – best
Levamisole 7.5 mg/kg s/c once a week for 3 weeks - 2nd best
Rafoxanide 7.5 mg/kg, orally once.
Ivermectin 0.2 mg/kg b. wt. (1 ml/ 50 kg) s/c once.
Lithium Antimony thiomalate 15-20 ml animal i/m once a week for 3 weeks.
Complete cure was not noticed and reduction in EPG and lesions was observed
Control:-
1. Identify the infected animals and treat them.
2. Eliminate the source of infection.
a. Give tap or well water to the animals. Because such water does not
contain the cercaria, it is not possible practically. So store the pond or
tank or channel water for 24-48 hrs and then allow the animals to ingest
the water. This method makes the water free from cercaria because they
will not survive in such condition for 24-48 hours.
b. To eliminate the source of infection, we have to eliminate the
intermediate hosts i.e. snails. This method is very similar to the one
mentioned in fascioliasis.
c. Guppy fish method: - Lebistus reticulatus which is commonly kept in the
aquarium, to keep the water clean because it ingests the excreta. One
guppy fish will ingest 48% of the miracidium in one hour. Thus reducing
the no. of miracidia entering the snail and the no. of cercaria coming out
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of the snail. In addition, one guppy fish will devour 1000 cercaria per
hour. This method was developed by Dr. K, Muraieedharan, Dr. S.
Prasanna Kumar and Dr. K. S. Hegde (1975) who was awarded the Dr.
K. M. Nair's memorial award for the best Research paper published in
IVJ, in 1975. Very easy to breed the guppy fish, very economical, not
harmful.
OTHER, SCHlSTOSOMES OF DOMESTIC ANIMALS

1. Schishosoma bovis: - Occurs in the portal and mesenteric vessels of cattle,
sheep, goats and sitataga in southern Europe, Southern Asia and Africa. The affected
animals become anaemic, lose condition and show alternate diarrhoea and
constipation, gradually wasting away until death takes place. The faeces contains
blood and mucous and the eggs can be found in them in large numbers.
A characteristic feature is the marked grey pigmentation of the lungs and liver.
On microscopic examination there is pigment in the liver and numerous eggs may be
found, surrounded by cellular infiltration and fibrous tissue. The intestine shows the
presence of eggs in its wall in the form of grey clusters or thickenings which are
opaque and grating to the knife. The mucosa usually shows small haemorrhages and
submucosa may be thickened.
2. S. spindale: Occur in the mesentric vein of cattle, goats, sheep and dog in India
and Sumatra.
The eggs are passed in the faces but sometimes also in the urine. The eggs are
elongate, flattened on one side and have terminal spine.
3. S. indicum: Occurs in; theca; portal, pancreatic, pelvic hepatic, and mesenteric
veins of sheep, goats cattle, equines and camels in India. The eggs cause nodules in
various organs and cirrhosis of the liver with debility especially in horses. The eggs
are oval with a terminal spine.
4. S. suis: Occurs in the pig and dog in India. It may be identical with S.
incognitum.
5. S. japonicum: Occurs in the portal and mesenteric vessels of man as well as
cattle, horse, sheep, goat, dog, cat, rabbit and pig in the Far East. The eggs are passed
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in the faeces. They are short, and oval, and may have a small lateral spine or knob.
The main clinical sign is diarrhoea and the faeces contains mucous and blood.
Abscesses in the liver and intestine. Ascites is usually present.
II. NEMATODES
1. ASCARIASIS
(a) CANINE ASCARIASIS
It is one of the common parasitic infestations of all the domestic animals. It is a
parasitic disease of dogs caused by Toxocara canis & Toxascaris leonina &
characterized by signs of pneumonia & enteritis.
Incidence: - Recorded throughout the world. Very common parasitic infestation of
dogs. Puppies are highly susceptible when compared to adults.
Etiology: Toxocara canis: - It is a round large worm. Males measure about 10 cms
& females 18 cms in length, occurs in the small intestine.
Toxascaris leonina:- A long round worm, males 7 cms & females 10 cms. Occurs
in the small intestine
Transmission: - By ingestion of eggs containing second/third stage larvae.
- Transclostral
- Transplacental
Toxocara canis: -
Life Cycle: - The adult worms are present in intestine and they lay eggs. One adult
female worm can lay up to 200,000 eggs in a day and these eggs are passed in the
stool. The eggs develop, under suitable environmental condition. The larva moulds to
become second stage larvae. The eggs containing the second/third stage larva is the
infective stage. The animals when they ingest contaminated feed and water or by
licking skin of animals containing the eggs, swallow this stage. It goes to the intestine
and the egg hatches and releases the second / third stage larva. This larva penetrates
the intestinal mucosa gets into the portal vein and goes to the liver. From the liver it
goes to the heart and enters the circulation. In adult dogs or bitches somatic migration
occurs, where in the third stage larva goes to the various tissues like liver, heart,
kidney, muscles and remains in these tissues. Hence this stage is (3rd stage) tying
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dormant. Further development does not occur in these tissues. When the bitch is in
42nd day of gestation some of the larvae are withdrawn from these tissues into the
circulation. These larvae pass through the placenta and get into the developing Foetus.
They remain in the liver of the foetus. This type of transmission is called as
transplacental transmission.
After the birth of the puppies, some of the larvas are secreted along with the
colostrum. When pups suckle the colostrum, the 3rd stage larvae get into the intestine
and through the portal vein into the liver. This type of transmission is known as
‘Transcolostral transmission’. These larvae go through blood to the heart and through
circulation into the lungs. In the lungs, by rupturing of the capillary, the larvae enter
the alveoli or parenchyma of alveoli. Here they mould to become the 4th stage larvae.
These migrate into the bronchiole and then into bronchi to the trachea. From Trachea,
it goes to the larynx & then to the mouth & reswallowed through the esophagus goes
to the stomach & then to the intestine, hi the intestine, they mould to become the 5th
stage larva & become adults. These develop to become mature worms & the female
starts laying eggs.
The pups under 5 weeks of age if they ingest the eggs containing 2nd stage
larva it goes to the intestine and gets into the portal vein and goes to the liver. From
liver, it goes to the heart and then to the lungs (4th stage). From the alveoli it migrates
to the larynx and then to the mouth and reswallowed. It gets into the stomach and then
goes to the intestine.
If the pups are more than 5 weeks of age and above and if they ingest the eggs
containing me 2nd stage larva, the somatic migration seen in adult dog will be seen in
such pup also.
Toxascaris leonina:
Life Cycle: The eggs containing the 2nd stage larva when it is ingested it goes to the
intestine. Here it hatches and larva comes out. The moulding of larvae takes place
and complete development of worm into the adult occurs in the intestine itself.
Pathogenesis: - Because the larvae are present in the liver and lungs, damage to these
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organs occurs. In the liver, it causes formation of milky white spots and here it is
called white spotted liver. In the lungs, damage to parenchyma occurs with
haemorrhages, pneumonic changes are also seen. In the intestine it causes mild form of
enteritis and also due to the accumulation of large number of adult worms in the form
of bundle will result in intestinal obstruction, intussusception or intestinal perforation
resulting in the death of pups.
Clinical findings: - Some pups may die without showing symptoms, which may be
due to intestinal obstruction. Occasional Vomition, diarrhoea, dehydration- weakness,
emaciation, unthriftiness, rough hair coat, pot belly, and symptoms of pneumonia like
coughing is also seen.
Stunted growth can be seen in pups. Vomition can result in aspiration of the
material into the respiratory system, leading to aspiratory pneumonia.
Nervous signs are also seen; i.e. restlessness, incoordination, etc. These
symptoms may be due to the irritation of the nerve endings of the intestinal mucosa by
the worm.
Necropsy Findings: - Refer to pathogenesis.
Diagnosis: - By faecal examination.
Treatment: - Drug of choice is Piperazine.
Dose:- 100-300 mg/kg. This drug is given orally.
The first dose is given when the pups are 2-3 weeks of age, as the larvae have
developed into the adult worms. Because the drug is effective against mature worms
only. The drug is not effective against immature worms and migrating larvae. Then
repeat the drug at 6 and 8 weeks of are to kill all the worms. The following drugs also
can be used:
1) Chinapodium oil - 0.1 ml/kg b. wt. Orally
2) Diethyl Carbamazine Citrate - 50 mg/kg b. wt. Orally
3) Thiabendazole - 300-500 mg/kg b. wt. Orally
4) Tetramisole - 10 mg/kg b. wt. Orally
5) Pyrental tartrate - 5-7 mg/kg b. wt. Orally
6) Dichlorovas - 12-15 mg/kg
7) Neguvon - 75 mg/kg tid for 2 weeks
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8) Avion/Tetracap - 0.l ml/lb b. wt. Orally

9) Fenbendazole - 5 mg/kg b. wt. Orally.
720 mg/kg b. wt. For 5 days
10) Nitroscanate - 50 mg/kg b. wt
11) Mebendazole - 10 mg/kg bid orally
12) Levamisolewuss - 7.5 mg/kg b. wt. Orally
13) Albendazole - 5-10 mg/kg b. wt. Orally.
SWINE ASCARIASIS
It is caused by Ascaris suum.
Life Cycle: - It is almost similar to Toxocara canis but controversy is there regarding
the transplacental and transcolostral transmission. Here the disease is characterized by
severe dyspnoea which is called 'Thumps'. (Rib cage raising and falling). Here the
disease is characterized by blockage of bile ducts and here obstructive jaundice may be
noticed.
Necropsy findings: - Milky white spotted liver is very characteristic lesion and it is
nothing but a chronic granulomatous inflammation with white necrotic material.
Treatment: -
1) Piperazine (Citrate) - 100-300 mg/kg b. wt. In the feed.
2) Sodium Fluoride - (old drug) 100-150 mg/kg b. wt. In feed.
3) Hygromycine - (old drug) 6000 IU/lb. of feed.
This is extensively used as feed additive and used for the period of 60 days.
4) Levamisole - Effective against both immature and mature worms - 7.5 mg/kg b.
wt., orally or i/m.
5) Tetramisole - 15 mg/kg b. wt., orally. It is effective against both mature and
immature worms.
6) Parbendazole - 30 nig/kg b. wt., orally.
7) Fenbendazole - 5 mg/kg b. wt., orally.
8) Cambendazole - 20 mg/kg b. wt., orally.
9) Morantal tartrate - 5 mg/kg b. wt., orally.
Piperazine compounds available in our Country-
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Piperazine hydrate : Piperazine phosphate : Piperazine citrate

100 mg : 104 mg : 120 mg
(More effective)
Mechanism of action of Piperazine: -
It is having a narcotizing effect on worms. It may be necessary to administer
purgative
like MgSO4 after 1-2 hours of administration of Piperazine.
Piperazine Compounds: -
1) Helmacid Liquid (Glindia): It is a 45% solution of piperazine hydrate.
Container size: 115 ml and 450 ml bottle. Dose:- 4-5 ml /10 kg b. wt. In all spp.
Of large animals. 1 ml/5 kg b. wt. In dogs and cats. Better to avoid piperazine in
cats as it may cause adverse effects:
2) Helmacid Tablets: Piperazine hydrate 260 mg/tab.
3) Helmacid with Senna granules: It produces laxative and purgative effect also.
Available as 10 gm sachet.
4) Antepar (Burrough's Wellcome): 40% piperazine citrate solution Container
size: l00 mg and 450 ml bottle.
5) Antepar Tablets: Contains 500 mg of piperazine per tablet.
6) Piperex (Sarabhai): 35 and 225 gms containers available. Along with this 9 gm
spoon is also available.
7) Verban Liquid. (Cynamid): 56.3% solution of Piperazine hexahydrate. 120 ml,
450 ml, bottles and 4.5 liter jar available.
8) Vermex Liquid (Pfizer): This contains Piperazine hexahydrate. 100 ml, 500 ml,
4.5 liters containers available. 165 mg/ml.
9) Helmavet (Minumix Pharmaceuticals): 45% piperazine hydrate solution 100 ml
and 500 ml bottles.
10) Piperazine Liquid (HAL): 450 mg/ml. It contains piperazine 45%, 500 and 4.5
liter jar available.
Many other companies also- prepares this product
Toxocave Cati:- occurs in the small intestine of the cat and wild felidae.
Ingestion of eggs containing infective second stage larvae.
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Life cycle is almost similar to T. Canis.

Mouse may act as intermediate host – 2nd stage larvae.
Second stage larvae may be found in the tissue of earthworms, cockroaches,
chickens, sheep and other animals fed infective eggs.
Visceral larva migreys – Mainly caused by the larvae of T. Canis through the larval
stages of T. leonine, T. Cati, Capillaria hepatica (of rodents) and lagochilascais minor
(of wild felines) etc have also been incriminated. Characterized by the chronic
granulomatous lesions in or inner organs of children like liver, lungs , brain,
sometimes eye, somatic maven.
4. BOVINE ASCARIASIS
Bovine ascariasis is caused by Toxocara vitulorum. (Neoascar is vitulorum).
They occur in small intestine of calves of cattle and buffaloes. They cause the severe
form of the disease in young caves of 1-4 months of age. Buffalo calves suffer from
severe form of the disease when compared to cattle calves. Now a days it is considered
as the number one cause of calf mortality in buffalo calves, causing considerable
economic loss to the dairy farmers. Mortality can range from 25 to 50%.
Etiology: - It is caused by Taxocara vitulorum (Neoascaris vitulorum). The males
measure up to 25 cm x 5 mm and the females 30 cms x 6 mm. The cuticle is not as
thick as that of other large ascarids and these worms therefore have soft, translucent
appearance. The eggs are subglobular, provided with a finely pitted albuminous layer
and measure 75-95 by 60-75µ.
Transmission: It is very similar to that of Toxocara canis. Transplacental and
transcolostral is very common and-it may vary from place to place. In Bidar it appears
to be transplacental transmission, which playing a major role.
Life cycle: It is also very similar to that of T. canis.
Pathogenesis: This is also very similar to that of T. canis. It appears that worm load
plays an important role. It appears that liver may be significantly affected. Depending
on these above factors, clinical signs vary from one buffalo calf to the other. The
changes can be mild, moderate and very severe.
In advanced cases intestinal obstruction due to forming of bundles by the adult worms
in the intestine can lead to death of the calf. The exact reason vet not known, however
330
the possibility of toxemia playing a major role cannot be ruled out.

Clinical findings: Depending on the severity, three forms of the disease are observed:
1. Mild form (Grade I): The buffalo calf will be in a standing position and will not
exhibit much of the clinical signs. Here at the most, one can observe mild
diarrhoea.
2. Moderate form (Grade II): In this form, the buffalo calf will be slightly anorexic,
slightly weak, rough hair coat, pot belly and slightly depressed. Slight to
moderate diarrhoea may be present. Slight loss of weight may also occur.
Worms can be noticed in the faeces.
3. Severe form (Grade III): In this form, the buffalo calf will be recumbent,
anorectic, markedly depressed, weak and subnormal temperature is very
characteristic. Usually the animal has not passed the faeces from 1-3 days
indicative of constipation. In addition conjunctival mucous membranes are
congested, shallow respiration and weak heart beats occurs. The faeces will be
pasty, brown in colour and slightly foul smelling.
Necropsy findings: These are very similar to Toxocara canis. In advanced cases, the
entire length of the intestine especially colon will be filled with worms.
Diagnosis:
2. Faecal examination.
3. Examination of colostrum and milk up to a period of 15-20 days can reveal the 3rd
stage larvae.
Treatment: Mild and moderate form of Ascariasis responds well to anthelmintic
treatment. Supportive therapy may not be required. However, severe form of
Ascariasis requires anthelmintic as well as supportive treatment. Even inspite of
vigorous supportive therapy, many of the buffalo calves will succumb to severe form
of Ascariasis.
The following anthehnintics can be used:
1. Piperazine @ 100-300 mg/kg body wt., orally.
2. Tetramisole @ 15 mg/kg body wt., orally.
3. Levamisole @ 7.5 mg/kg body wt., orally, S/C, I/M.
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4. Fenbendazole @ 5-10 mg/kg body wt., orally.

5. Albendazole @ 10 mg/kg body wt., orally.
6. Mebendazole @ 10-20 mg/kg body wt., orally.
7. Ivermectin @ 0.2 mg/kg body wt., S/C, orally.
The following supportive therapy can be tried:
1) Fluid therapy: 5% Dextrose, DNS, Lactated Ringer’s solution Aroryte-M can be
administered @ 1-2 bottles, I/V.
2) Camphor-in-oil: Crush 1-2 tablets of camphor and mix it in 5 ml of ground
nut oil and administer 0.5 -1.0 ml S/C and 0.5 -1.0 ml I/M. This may be
beneficial to overcome hypothermia.
Corticosteroids: Dexamethazone @, 0.5-1.0 mg/kg, body wt. I/V. I/M
may help in over coming Toxaemia and hypothermia.
3) Calcium preparations: Administer 20-30 ml of calcium borogluconate or Mifex
(Ca, Mg, P, Dextrose) I/V or S/C. It may be useful hypothermia.
4) Antibacterial agents: May or may not be useful. Use of Gentamicin, Ampicillirt,
Amoxycillin, OTC etc., may be beneficial.
1. Proper disposal of faeces.
2. Administering of an anthelmintic in the advanced stage of gestation is very
essential. Here the drug effective against 3rd stage larvae is required. This will
over come the transplacental and transcolostral transmission. However such
drugs are not available for use in buffaloes and cows.
3. Following regular deworming schedule is a must. Administering of any one of
the anthelmintic mentioned under treatment when the carves are of 1 month, 2
months, 3 months and 4 months of age is very essential. This will save lot of
calves.
ANCYLOSTOMIASIS
It is a disease of dogs caused by Ancylostoma caninum, Uncinaria and Necator
spp characterized by poor growth, anaemia.
Incidence: - It occurs through out the world. All breeds of dogs are equally susceptible
and young ones are highly susceptible when compared to adults.
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Etiology: -
1) Ancylostoma caninum are gray to red coloured worms, females are slightly
longer than males. Males measures about 10-12 mm in length, and females
measures about 14- 16 mm. Both have well-developed buccal capsule and 3
pairs of ventral teeth.
2) Ancylostoma brazilliens: Found in small intestine of dog, cat, foxes and
human beings.
3) Ancylostoma tubaeformis: Found in cats.
4) Ancylostoma duodenale: Common in man and also occurs in dogs and cats.
5) Necator americanus: Common in man.
6) Uncinaria stenocephala: Dogs, cats and foxes.
Transmission: - Infective larvae enter the final host either by penetrating the skin or
by ingestion of contaminated feed and water
Life Cycle: - Life Cycle is direct. The eggs hatch and parasitic larvae are produced in
about a week. There are 2 free-living larvae.
(a) Non parasitic stage larvae which is very sensitive to dessication.
(b) Infective larvae which is capable of entering the body by penetrating the skin.
Second stage larvae (50 larvae infective) penetrate the skin and get in to the
blood, then carried to the heart and later on to lungs. Larva stays in the lung
capillaries for a while become 4th stage larvae and enter the alveoli by
rupturing and penetrating capillaries. Larvae crawls up in respiratory tract
coughed off and men swallowed. It develops and mould after reaching intestine
and becomes adult and lays eggs. An infected pup can pass as many as 5 million
eggs / day.
(2) Sometimes larvae directly get in to the GIT ok becomes adult with out migration
(3) Sometimes larvae in the circulation may get through placenta to the foetus and may
develop prenatal infection, and this is transplacental transmission. This is questioned
by many workers.
(4) Transcolostral transmission: - Larvae in the milk for 20 days after whelping are
recorded.
Pathogenesis: - Migrating larvae does not cause much damage only adult parasites are
333
harmful as they are active blood suckers and cause severe anaemia. The mechanisms
of anaemia are
(1) Sucking of blood by parasites (0. 1 ml / parasite/ day)
(2) Hemorrhages in the intestine, it is observed, mat the parasite produces a type
of anticoagulant which is responsible for haemorrhages. Anaemia does not occur
as
long as iron in body reserve is present. When its reserve is depleted it results in
microcytic hypochromic anaemia.
(3) Malabsorption: - Impaired absorption of iron from the intestine.
(4) Disturbances in hemopoiesis (Not confirmed).
Clinical findings: - Puppies may die without showing any symptoms. At the age of 2-
3 weeks it remain alive, shows the signs of severe anaemia and coma. Other dogs show
anemia, weakness, pale visible mucous membranes, increase in heart rate, emaciation,
ascites (hypoproteinaemia), dry skin, stunted growth, mild diarrhoea, melaena (black
coloured faeces), and itching of skin.
Necropsy findings: - Anaemia, cachexia is well marked, pale visible mucous
membranes, ascites. Intestine is swollen, haemorrhages, lot of worms embedded in its
lumen. Red-bite marks of intestine are very important lesions.
Diagnosis: -
(1) Faecal examination. Egg may appear in different shape. It should be
differentiated from coccidial oocyst and Dipylidium caninum egg. Coccidial
oocysts are very small where as Dipylidium egg/blood capsule is very large.
(2) Occult blood test - positive.
Differential Diagnosis: - Disease should be differentiated from the diseases which
causes anaemia, like:
(1) Acute leptospirosis: High fever, haemoglobinuria, jaundice, demonstration of
organism in urine.
(2) Chronic nephritis: Normocytic normochromic anaemia.
(3) Coccidiosis: Dysentery and oocyst in the faeces.
(4) Canine babesiosis: High fever, haemoglobinuria, demonstration of organism
inside the RBCs.
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(5) Canine Ehrlichiosis: Detection of organism in the cytoplasm of mono nuclear

cells.
Treatment: -
(1) Disophenol (2, 6, Di-iodo 4-nitro phenol) is available as Ancylol 10 ml Vial, 1 ml
contains 45 mg.
Dose is 1 ml /4.5 kg body weight/(10 mg/kg. b. wt. and 0.2-2 ml/dog s/c).
(2) Tetrachloro ethylene (Tetracap) 0.2 ml/kg orally. Should be administered after
overnight fasting. Administer a saline purgative (MgSo4 + NaCl) after the
administration of Tetracap.
(3) Bephenium hydroxy naphthoate (Alcopar, Burroughs wellcome) is administered
@ 15-20 mg/kg and repeat after 6-10 days.
(4) Thdabendazole: 300-500 mg/kg orally.
(5) Mebendazole 22 mg/kg, daily, orally for 5 days.
(6) Pyrental: 6-15 mg/kg, orally commonly used in human beings.
(7) Albendazoie 5-10 mg/kg body weight.
(8) Panacur 50 - 100 mg/kg. body weight orally.
(9) Nitroscanate 50 mg/kg. body weight (New drug) orally.
Supportive treatment: - To over come anaemia -
1) Blood transfusion is done in severe anaemia.
2) Haematinics like Imferon and Ferrous sulphate are used.
To over come metabolic acidosis and dehydration give sodium bicarbonate and
lactated Ringer's solution.
Control:
(1) Keep the floor dry.
(2) Treat the floor with sodium borate at the rate of 10 lbs/100 sq. feet or 1% sodium
hypochlorite solution. This treatment kills the larvae or exposes the sheath of egg
so that larvae cannot survive in the environment Sodium borax should not be
applied to the lawns.
(3) Proper disposal of stool.
(4) The following vaccines have been tried:
a. Killed.
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b. X-irradiated vaccine.
c. Attenuated vaccine (5, fluro uracil can be used).
(5) Admn. of fenbendazole every day 15 days before whelping and 5-7 days after
whelping / 40th day of gestation to 14 days after whelping @ 50 mg/kg, b. wt.
orally.
HOOKWORMS OF SHEEP AND GOAT

(1) Bunostomum trigonocephalum: - Common one is which is present in small
intestine of sheep and goats and it is similar to Ancylostomiasis.
Treatment: - Thiabendazole 75 mg/kg, orally. All other broad spectrum anthelmintics
used for Strongyle sp. are used here also.
(2) Gaigeria pachyscelis: - Similar to Bunostomum and found in sheep and goat of
India and Africa.
HOOK WORMS OF CATTLE

Bunostomum phlebotornum: - Similar to Ancylostomes. Mainly occurs in cattle and
rarely in sheep and goat.
Treatment: - Thiabendazole 50-110 mg/kg, Orally.
All other broad spectrum anthelmintics used for Strongyle sp can be used here
also.
CANINE SPIRQCERCQSIS
Caused by Spirocerca lupi and characterized by the development of nodules in the
oesophagus, stomach and aorta of dogs, fox, wolf and jackals.
Etiology: - Spirocerca lupi - it is a nematode, it is bright red in colour and spiral in
shape and, male measures about 30-50 mm and females 50-80 mm.
Transmission: - Ingestion of intermediate host i.e. coprophagus beetles and also due
to numerous transport hosts (paratenic host) like amphibians, reptiles and birds.
Infective stage is the 3rd stage larvae.
Life cycle: - The embryonated eggs are laid in the oesophagus or stomach and are
passed in the faeces. These eggs are ingested by Coprophagus beetle and in the beetles,
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larva are encysted in the tracheal rings (L3). These beetles are ingested by the transport
host i.e., mainly by birds i.e. chickens. When the dog eats the beetles or transport host
the larva (L3) gets into the stomach and penetrates the wall of the stomach and reaches
the gastric and gastro epiploic artery. Through the wall of these arteries they get into
the coeliac artery and then migrate to the aorta. They may remain in aorta or they may
bypass the connective tissue through tunnel like structures between the nodule of aorta
and oesophagus and gets into wall of the oesophagus and then into the stomach. When
they are in the oesophagus or stomach ttiey become adults and then start laying eggs.
Pathogenesis: - Migrating larvae produces haemorrhages, inflammatory reaction,
purulent streaks or abscesses and these heal up and lead to stenosis of aorta.
Later on, chronic granulomatous inflammation sets in leading to formation of
nodules in the oesophagus and stomach. These nodules can unite together to form
pedunculated mass. Due to this, difficulty in ingestion of food, and also repeated
vomition occurs.
Nodules can break open abruptly leading to massive internal bleeding which is
often fatal.
Sequelae:
1) May cause oesophageal sarcoma.
2) Hypertrophic pulmonary osteo arthropathy.
Some larvae can get into long bones -—thickening of bones.
3) Pyaernic nephritis.
4) Spondylitis of adjacent thoracic vertebrae (cervical spondyiosis)
5) Aplastic anaemia.
Clinical findings: - Depends on place of nodules:
Stomach - persistent vomition and no food remaining in the stomach.
Oesophagus - Comes in the way of deglutition and also due to pressure on trachea,
difficulty in respiration. Loss of weight emaciation, weakness, and in oesophageal
sarcoma. Animal will die of severe emaciation.
Sometimes sudden death - due to rupture of nodules present in pulmonary aorta
-thoracic cavity filled with lot of blood.
In prolonged cases, there may be enlargement of long bones.
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Necropsy findings: - Nodules in stomach, oesophagus and aorta. If the aorta is

ruptured then clotted blood is found in thoracic cavity.
Diagnosis:-
1) By Symptoms of persistent vomition weakness and emaciation.
2) Faecal examination: Eggs are small, capsule shaped, oval, containing larva.
3) X-ray of longbones- pulmonary osteoarthropathy.
Treatment:-
(I) Dieihyl carbamazine citrate- Drug of choice since long time and administered @ 25
mg/kg body weight orally for 4-10 days. The preparations available are-
1) Hetrazan (Lederle) l00 mg/tab.
2) Lorcid (Vets Pharma) - 400 mg/tab.
3) Caricide
4) Banocide
(II) Disophenol (Ancylol) -1 ml/4.5kg bod}' weight s/c is effective.
(III) Recently levamisole and albendazole have been found to be effective.
(IV) Avermectins: Also has been used.
(V) “Surgical therapy is also not of much use”.
Prevention and control: Control of intermediate hosts may be of use in prevention of
the spirocercal infection.
CANINE HEART WORMS

It is a parasitic disease of dogs, cats, foxes and wolves caused by Dirofilaria
immitis and is characterized by malfunctioning of the right side of the heart, leading to
passive venous congestion, ascites and hydrothorax.
Etiology: It is caused by the filarial worm, Dirofilaria immitis. The male worms are
12-16 cms and the female worms are 25-30 cms in length.
Incidence: Heart worms have been recorded through out the world in dogs, cats,
foxes wolves etc. It can occur in any age group.
Transmission: The third stage larva is the infective stage and is transmitted by the bite
of all the three types of mosquitoes namely Anopheles, Culex and Aedis.
Life cycle: The adult worms are found in the right atrium, right ventricle and
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pulmonary artery. The adult female lays the first stage larva known as the microfilaria.
The larvae get into the circulation and will be found in the peripheral blood. When the
mosquito sucks the blood the first stage larvae get into the mosquito and further
development takes place. This larva moulds twice to become the third stage larva
which is the infective stage. When such mosquitoes suck the blood from a dog, they
introduce the third stage larvae. In the subcutaneous tissue and muscular tissue further
development of larvae occurs for a while. Then they get into the blood and through
circulation these larvae are carried to the right side of the heart. Within 1-2 months
they become adults.
Pathogenesis: The larvae in the subcutaneous tissue cause dermatitis and itching. The
larvae and the adult worms in the heart causes the blood flow from right auricle to
right ventricle to pulmonary artery to lungs will become irregular and there will be
back flow of blood leading to passive venous congestion which is characterized by.
ascites, anasarca, etc. The worms cause rugose or villose endarteritis of the
pulmonary artery resulting in the formation of the thrombus. This can cause
infarction, necrosis and fibrosis.
Clinical findings: In some animals sudden death can occur which may be due to infra
vascular haemorrhages and there may be renal haemosiderosis.
Commonly the disease is characterized by chronic cough which will be
exaggcratd exercise. Weakness, pot belly, rapid breathing and upon exercise the dog
may collapse and A Upon auscultation heart murmurs can be heard. ECG will indicate
inverted T wave.
Necropsy findings: Acites, hydrothorax, hypertrophy and enlargement of the right
side of the heart and lot of adult worms are seen.
Diagnosis:
1. By symptoms / clinical signs.
2. By blood examination: Any one or all the methods mentioned below can be used to
demonstrate the microfilaria in me blood of dogs collected during the evening and
night:
a) Direct method: Place a drop of blood on a slide and place a coverslip and
examine under the low power of the microscope. The moving larvae can be
339
demonstrated.
b) Make a blood smear and stain with Giemsa and examine under the
microscope to demonstrate ‘S’ shaped larvae.
c) Modified Knotf s method: Place 1 ml of blood in a centrifuge tube and then
add 9 ml of 2% formaline and mix the contents. Then centrifuge for 5-10
minutes at 1000-1500 RPM. Discard the supernatant and mix the sediment.
Place a drop of the sediment on a slide and add a drop of 1: 1000 Methylene
blue solutions and mix the contents. Then place a coverslip and examine
under the microscope for the blue coloured larvae.
3. Serological test: ELISA has been used.
Treatment: To eliminate die worms, various drugs have been used. Since the drugs
have to be used for a prolonged period of time, it will end in toxicity or adverse
reaction. Any one of the following drugs can be used:
1. Thiacetarsamide sodium (Caparsolate): It contains 20% arsenic and is available as a
powder. Make a 1% solution and administer at the rate of 1.0 mg/lb body weight as a
slow i/v injection, b.i.d. for 2 days. It's effect is only on the adult worms and does not
have any effect on the microfilariae.
It is the drug of choice for heart worms and is not available in our country.
Note:
1. Perivascular infiltration is highly irritant and will result in huge swelling.
2. To overcome the toxicity, administer the antidote. The antidote is Dirnercaprol
(BAL) and it should be administered at the rate of 4 mg/lb body weight per day in
4 divided doses. Also corticosteroids can be administered.
3. Diethyl carbamazirte citrate: Administer @ 25 mg/kg body weight per dose,
orally, t. i.d. for 3-5 weeks.
The effect of the drug is only on the microfilaria. It sensitizes the microfilaria
so that it is readily phagocytized by the macrophages.
4. Antimosan (Bayer): This is an old drug now not available in our country. The
schedule to be followed is :
a) First course is for 6 days @ 0.5 ml/10 kg weighing dog, slow i/v, i/m, s/c daily.
b) Give a break for 7 days.
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c) Start a second course@ 1.0 ml dairy for 6 days.

d) Give a break for 7 days.
e) Start the third course @ 1.5 ml daily for 6 days.
The drug temporarily sterilizes the female worm.
Only the cumulative effect is fatal to the worm.
5. Levamisole: Recent studies have given highly encouraging results in treating heart
worms with levamisole. 11 mg/kg, b. wt. orally 5-6 days.
Levamisole: 6 Mg/kg b. wt. Orally.
Control: All the efforts should be made to eliminate the intermediate host i.e, the
mosquitoes. Various ectoparasiticides should be used to eliminate the mosquitoes.
VERMINOUS PNEUMONIA OF CATTLE

(Lung worm infestation, verminous bronchitis, Husk, Hoose)
It is a parasitic disease of cattle caused by Dictyocaulus viviparus and is
characterized by pneumonia.
Etiology: It is a round worm and the males measure about 5 - 5.5 cms and the females
about 6-8 cms in length.
Incidence: Reputed from many parts of the world. It is very common in U.K. and
U.S.A. In our country it is commonly recorded in hilly areas. This worm is highly host
specific as only the cattle are affected. Cattle of all the age group can be affected but
calves of 4-10 months of age are commonly affected with the severe form of the
disease. Commonly seen in warm, wet summer months.
Transmission: is by ingestion of contaminated feed and water. The infective stage is
the third stage larva.
Life cycle: The adult worms are present in the bronchioles and alveoli and they lay
eggs. These eggs are coughed up and reswallowed. Then they pass through the g.i.
tract and while passing through the eggs are hatched and the first stage larvae will be
passed in the faeces. Under moist environmental conditions, the larvae develops and
moulds twice to become the third stage larvae and this is the infective stage.
When the animal ingests the infective stage, it will get into the small intestine.
Then they will penetrate the intestinal wall and get into the mesenteric lymph nodes.
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Here the third stage larva mould to become the 4th stage larva. Then it gets into the
lymphatics and goes to the heart and then into the lungs. In lungs they get into the
alveoli and develop into the mature worm and starts laying eggs.
Pathogenesis: The migrating larvae damage the intestine and lungs and haemorrhages
are seen. When they will be in the bronchi, there will be inflammation resulting in
accumulation of neutrophils and eosinophils leading to the obstruction of the air
passages and emphysema develops. Damage to the intestine can result in diarrhoea.
Clinical findings: This condition can be acute or sub-acute one.
1. Acute type: This type commonly occurs in adult cattle. Calves also can be affected.
Initially there will be fever of 104 -105°F, nasal discharge, increase in heart and
respiratory rate, the breathing will be shallow and hurried. Coughing which will be
loose and husky. There will be increase in vesicular murmurs and bronchial tone.
Because of emphysema, crackling sounds can be heard. There will be marked
reduction in the body weight. Later on there will
Administer corticosteroids like Dexamethasone @ 10 mg/calf or 20 mg/adult,
i/m.
Control:
2. Avoid grazing of animals on wet pastures.
3. Vaccinate the animal with any one of the following :
a) X-ray irradiated vaccine: This vaccine is prepared by IVRI, Izathnagar, UP. This
vaccine contains the third stage larvae of the lung worm exposed to the X-rays. It is
administered orally at an interval of 6 days twice. The larvae gets into the intestine
and then into mesenteric lymph nodes and stays there. Here it triggers the immune
response. It gives 90 -100 % protection.
b) Triethylene malamine attenuated vaccine: This vaccine contains the third stage
larvae exposed to this chemical. Thus me larvae lost its pathogenicity. To preserve
this vaccine is difficult and hence not commonly used when compared to the first
vaccine.
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VERMINOUS PNEUMONIA OF SHEEP AND GOATS

Etiology: It is due to:
1. Dictyocaulus filaria which is very similar to D. viviparus
2. Mullerius capillaris.
3. Protostrongylus rufescense.
For number 2 and 3 the life cycle is indirect and needs snails and slugs as
intermediate host. They cause nodules in the lung parenchyma.
Treatment: It is very similar to cattle.
VERMINOUS PNEUMONIA IN PIG

Etiology:
1. Metastrongylus apri.
2. Metastrongylus salmi.
3. Metastrongylus pudendotectus.
Life cycle: is indirect, as earth worms act as intermdiate host.
These lungworms transmit hog cholera and swine influenza viruses.
Treatment: is very similar to cattle.
VERMINOUS PNEUMONIA IN HORSES AND DONKEYS

Etiology: Dictyocaulus arnfieldi which is very similar to D. viviparus.
It occurs commonly in donkeys when compared to horses. It produces mild
form of the disease.
Recently the following drugs have been used for the treatment of lung worms in
all the species of domestic animals, and are found to be very effective:
1. Ivermectin : Used @ 0.2 mg/kg body weight, s/c.
2. Fenbendazole : Used @ 5-7.5 mg/kg body weight, orally.
3. Albendazole : Used @ 5-10 mg/kg body weight, orally.
4. Oxibendazole : 2.5-5.0 mg/kg body weight, orally.
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PARASITIC GASTROENTERITIS
(Parasitic Diarrhoea)
It is a parasitic infestation of almost all the domestic animals caused by various
species of Trichostrongylus, Ostertagia, Nematodirus, Cooperia etc., and it is
charactered by gastroenteritis.
Etiology: Cattle Sheep & Goats

Name of the parasite Abomasum, Small intestine Abomasum,Small
intestine
I. Trichostrongvlus sp.
Trichostrongylus axei + - + -
T. colubriformes - + + -
T. longtspicuiaris - + - +
II. Ostertagia sp.
O. ostertagi - - + -
O. circumcincta - - + -
O. trifurcata - - + -
III. Cooperia sp.

C. punctata - + - +
C. onchophora - + - +
C. pectinata - + - -
C. curticei - - - +
IV. Nematodirus sp.
N. spathiger - + - +
N. battus - + - +
N. filicoffis - + - +
N. helvetianus - + - -
These worms are nematodes and they are short and thick worms.
Incidence: - Present throughout die world. They cause severe economic loss which
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may be due to-

(1) Stunted growth - they utilize the nutrients.
(2) Mortality.
(3) Anaemia (Trichostrongylus) not so severe.
Young ones are highly susceptible and severe form of disease is seen.
Transmission: - It is due to ingestion of contaminated feed and water which contains
3rd stage larva.
Life cycle: - The adult worms are present either in abomasum or small intestine and
lay eggs. They are passed in the faeces and under suitable environmental conditions,
the larvae develop and mould twice to become the 3rd stage larva. These are ingested
by the animals which go to abomasum or small intestine and develop into the adults.
Pathogenesis: - Some of the larvae can get into the gastric glands and may destroy
them. Hence the hydrochloric acid secretion is reduced. The normal pH of abomasal
fluid is 2.5-4.5 and in this condition there will be increase^ in PH and it may be around
6. Due to this change, indigestion occurs. Also formation of pepsin is reduced
resulting in improper digestion of proteins. Some of the pepsinogen get into blood and
its level increases in the blood.
These worms also cause abomasitis and enteritis which results in increased
motility of gastro intestinal tract.
All the above changes cause diarrhoea → dehydration → haemoconcentration.
Because of these changes, there will be hypoproteinaemia i.e., total plasma
proteins (TTP) will be decreased from its normal value of 7-7.5 gms9'o to 4-5 gm %.
This results in anasarca. Ostertagia also can cause mircoscopic nodules in the gastro-
intestinal tract.
Clinical findings: - Diarrhoea and the faeces may be dark green in colour and may or
may not be foul smelling. Rough hair coat, anasarca, stunted growth, decrease in gain
in weight, weakness and emaciation, are seen.
Constant mortality in a dairy farm can be seen which is very important.
Necropsy findings: - Abomasitis, enteritis and presence of large number of worms.
Diagnosis: -
1. By symptoms /clinical signs.
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2. By faecal examination. By morphological characteristics of eggs it is very

difficult to identify the worms into various genera and hence they are classified
as
strongyle ova.
3. Biochemical, TPP - 4-5 gm%
Blood pepsinogen level is increased.
(1) Colibacillosis - Young ones under 2 wks, fever and chalky white diarrhoea.
(2) Salmonellosis - Any age group, usually young ones, fever, diarrhoea and
dysentery.
(3) Viral gastroenteritis - R.P. and B.V.D. Oral lesions, fever, diarrhoea and
dysentery.
(4) Parasitic - Fascioliasis, Amphistomiasis, Coccidiosis. Faecal examination
reveals the characteristic ova, or oocyst.
(5) Johne's disease - No fever, thick pea soup like diarrhoea and not responding to
treatment and it is a chronic disease.
Treatment: - I. To overcome the gastro-intestinal parasites any of the following broad
spectrum anthelmintics can be given.
I. Phenothiazine: Chemical name is Thiodiphenyl amine.
Also known as Dr. Roger's product. It is a very old product, used extensively
for a long period of time. Now a days it is not commonly used even though it is cheap.
It is available as "Phenovis" (EEL) 95% dispersible powder 58% 3 kg tin (Rs. 300/-).
It is a green powder.
Dose: - Cattle - 10 gm/45 kg bodyweight with a maximum of 79 gms/animal
and administered orally. Sheep and goats: 5-20 gms depending on the size of animal.
Horse: - 3-5 gms/45 kg, body weight orally - through naso-gastric tube or as an
electuary.
Metabolism: - Half of the drug administered remains in the gastro-intestinal tract and
produces its effect. The other half of the drug gets converted into phenothiazine
sulphoxide by the action of certain enzymes in the mucosa of gastro-intestinal tract
and gets absorbed. It goes to the liver and converted into leucophenothiazone and
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leucothional. These go to the kidney and get filtered in the urine. Then they get
oxidised and forms into phenothiazone and thional. These oxidised products are brown
colouring dyes which imparts brown or reddish brown colour to the urine.
Phenothiazine sulphoxide can get into the anterior chamber of eye and when it
is exposed to ultraviolet rays i.e., sunlight, it causes keratitis, ulceration, blindness
within 36 hous. Such type of reaction can occur in non pigmented skin leading to
photosensitisatt'on. Eventhough it has been extensively used for long period of time,
now a days it is not commonly used because;
(1) Photosensitisation - Keratitis, dermatitis.
(2) In anaemic and debilitated animals it has been shown to cause lysis of RBCs.
(3) In advanced stage of pregnancy, it may cause abortion.
(4) In sheep, when this drug is administered, due to spilling of urine on the wool, the
colour of wool is changed to brown or reddish brown which is very difficult to
remove.
4. Osteopetrosis:
This condition can appear at any tone after one month of age but commonly
seen to 12 weeks of age. In this condition the long bones of the limb are most
commonly affected. There will be uniform or irregular thickening of diaphysis or
metaphysic and the bones are increased in size. In advanced cases, the term ''boot like
shanks” has been used. The periosteum is thickened and bone is spongy and in the
initial stages can be cut easily.
Histophathologically, we see increased number of osteoblast and osteocytes.
Diagnosis:
1) By-necropsy findings.
2) By culturing of the virus - liver, spleen.
3) Serological test - COFAL test commonly used. Virus neutralization, FAT and
ELISA can be used.
Differential diagnosis
Feature Marek’s disease Lymphoid leucosis
1 Type of virus Herpes virus Retrovirus
2 Incidence Frequently above 5% Rarely above 5%
3 Age 6 weeks or older Not less thatn 16 weeks
4 Symptom Frequently paralysis Non specific
5 CNS involvement Yes No
6 Macroscopic lesions
- Neural enlargement Frequent Absent
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- Bursa of fabricious Diffused enlargement or Nodular tumors

- Tumors in skin & muscles atrophy Usually absent
preoventriculus May be present
7 Lymphoid proliferating in Yes No
skin & feather follicle
8 Microscopic lesions
- Neural involvement Yes No
- Liver tumors bursa of Often perivascular Focal or diffused
fabricious Inter follicular tumor & Focal or diffused intra
atrophy of follicles follicular tumor
9 Origin of tumor T-cells B-cells
10 Cytology of tumor Pleomorphoic lymphoid cells Lymphoblast
including lymphoblast, small,
medium and large
lymphocytes and reticulum
cells
11 Availability of vaccine Available Not available
Treatment: No treatment is available.
Control: Very difficult to control this disease because

i) Good vaccines are not available. Good hygienic measures are not useful as
mode of transmission is transovarian.
ii) Selective breeding appears to be helpful in controlling this disease but it is
expensive. In this method, efforts will be made to mate a known genotype
by using the Mandelian laws to obtain a stock of chicks which will be
resistant to Lymphoid leucosis.
a. The cow’s milk should not be used for human consumption for 3 days after
administration.
b. This drug should not be administered to pregnant ewes during the first two
months of gestation, because it can cause teratogenic effect.
5. Albendazole:
Available as "Analgon suspension" (Wockhardt) 70 ml bottle, 1 litre, 4.5 litre, 25
litres can.
25 mg of albendazole/ml of suspension
Albomar (Glindia) - suspension
30 ml, 120 ml, 2500 ml suspension. It is a 2.5 % suspension.
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Albomar - powder 250 gms and 50 gms. It is a 15% powder Valbazan (SKF)
available as 30 gm sachet powder and tabs 150 mg/tab and 600 mg/bolus.
Dose: 5-10 mg/kg, b. wt. Orally. Broad spectrum anthelmintic, effective against
strongyles, flukes, and tapeworms.
6. Oxybendazole
Dose: 10 mg/kg b. wt., orally.
3. Imidazothiazoles:
a) Tetramisole: Available as "Nirverm" (ICI) It is a 30% powder (out of 100 gm
powder 30 gm active ingredient). 10 gms and 100 gm container.
Dose: 15 mg/kg, b. wt.
35 -50 mg of Nifverm/kg b. wt., It is a powder which readily dissolves in water
hence
administer as drench.
Broad spectrum anthelmintic and very safe drug in all the large animals.
It is also an immunopotentiating drug and it potentiates the CMI response. There
are no contraindications in sheep and goat. It is a d-form (dextro rotatory).
b) Levamisole: It is a 1-form of tetramisole i.e., lew rotatory.
Available as Helmonil (Alved, Madras) powder 30% powder. 10 gms, 50 gms, l00
gms and 1 kg tin.
Helmonil tablets – 150 mg/tab
Helmonil bolus
Helmonil injectable 10 ml, 30 ml vial 182 mg of levamisole Hcl/ml of inj. solution
Kalmisole (KAL) - 75 mg/ml. Dose: 7.5 mg/kg, b. wt., Orally or i/m or s/c.
It is also having immunopotentiating effect. It is used in human being, sheep, goat
and all species. It is also used along with vaccine especially in Clostridium
chauvoei, Cl. septicum, etc. It potentiates the CMI response and also it increases
the humoral imrqne response. It is also used along with H.S. vaccine and got good
response.
"Lemasol" (Ranbaxy) available as 10% powder, 20 gm and 100 gm. Available as
50 ml vial, 75 mg/ml.
"Wormal" soluble powder (Microlabs) 20 gm, 50 gm, 500 gm. 30% powder, 300
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mg of levamisole Hcl/gm of powder.

This is also quite safe in large animals but not extensively used in dogs
because it causes side effects like vomition, tremors, salivation, bone marrow
disturbances.
Mechanism of action:
Levamisole blocks the metabolic pathway responsible for formation of
ATP. It produces muscarinic and nicotinic like effect.
4. Tetrahydropyrimidines:
(a) Pyrantel tartarate:
This drug causes nicotinic like effect. Here acetyl choline gets accumulated
and hence paralysis of worm occurs.
(b.) Morantal citrate (Broad spectrum)
"Banminth IT (Pfizer) available as 4% solution, container size 100 ml. 500
ml, 4.5 litre.
Available as tablets. 118.8 mg/tab.
Available as Banminth forte bolus- 1.188 gm/bolus.
Dose: 10 mg/kg, b. wt. or tab/20 kg, b. wt. or one bolus / 200 kg, b. wt.
Contraindication: This drug should not be administered within 72 hours
after the administration of CCl4 other wise, severe mortality will occur
Broad spectrum means - These anthelmintics are effective against various species
of Trichostrongylus, Haemonchus, Bunostomum, Trichuris, Ostertagia, Cooperia,
Nematodirus.
All are not effective against Ascaris but few anthelmintics, like
Fenbendazole, Albendazole, Levamisole are effective against Ascaris of dog,
swine, cattle and buffalo.
5. Ivermectin inj. (Ivoma 1 ml, .7 ml, 20 ml and oral suspension (Dynamic pharma)
1% w/v -cattle 1 ml/50 kg s/c
Broad spectrum anthelmintic sheep 0.5 ml/25 kg
Also for ticks, lice, nites.
6. Thiophanate wettable powder (M&B) -Thiophanate 70% w/w 10g, l00 g, 1 kg.
Effective against mature and immature worms and also ovicidal.
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Dose: 70 mg/kg b, wt., orally.

Schedule of dewoming:
1st dose at 1 -2 months of age.
2nd dose at 2-3 weeks after the first dose.
Repeat once in 3 months until they are one year of age. The first dose is given
at 1-2 months of age because by that period the adult worms will be found in the g.i.
tract. Majority of the anmelmintics are effective against mature worms. The second
dose is given after 2-3 weeks because the immature worms were not eliminated by (he
anthelmintic and by allowing 2-3 weeks these worms will become mature, so that, they
are also eliminated.
For the animals which are one year and above regular deworming is done once
in 3-6 months.
If an adult animal is suffering from parasitic infestation, the anthelmintic is
administered twice at an interval of 2-3 weeks. This schedule holds good for both
Trematodes and nematodes.
II. To overcome anaemia, administer haematinics.
III. To overcome dehydration and metabolic acidosis give lactated ringers i/v.
IV. To overcome hypoproteinaemia give protein rich feed and if necessary
administer Hermin (Alembic) it contains essential aminoacids. 200 ml bottle
Dose: As much as possible.
To over come hypogtycaemia and supply energy administer 1-2 bottles of 5-
10% dextrose i/v.
V. To reduce diarrhoea, administer "Neblon" or Kaolinpectin preparation.
VI. Give mineral vitamin mixture for 3-4 weeks; Lactivet, Nuvimin forte - old
name
Supplivite - M (sarabhai).
These animals suffering from heavy parasitic infestation will take many weeks
to return to normal condition after treatment.
Control: -
1. Rotational grazing. Here the grazing land (pasture) is divided into different
plots.
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Animals were grazed in the first plot for few days and then moved on to the
second plot. This is done to cover all the plots. This will eliminate the source of
infection.
2. Management practices like –
(a) Avoid overcrowding.
(b) Proper disposal of faeces.
(c) Keep water and feed troughs above ground level.
(d) Maintain high plane of nutrition.
(e) Keep the barn dry.
3. Follow regular deworming schedule.
4. Vaccination ~ x-ray irradiated vaccines have been tried, but commercially not
available.
HAEMONCHOSIS
It is a severe parasitic infestation of cattle, sheep and a goat caused by
Haemonchus sp. and is characterized by anaemia and anasarca.
Etiology: -
(1) Haemonchus contortus
(2) Haemonchus placei:
Both found in the abomasum of cattle, sheep and goats. They are short, thick
round worms-about 1-2.5 cm in length. They are called as "Barber's pole" worms.
They suck lot of blood from abomasum which is similar to the hook worm -
anaemia, weakness, emaciation, pale mucous membrane, and lack in growth rate.
Symptoms of anaemia is seen, and in chronic cases the animals will be very much
emaciated i.e., skin and bones. The PCV and TRC will be very low.
Transmission: Life cycle, diagnosis, treatment and control is very similar to parasitic
diarrhoea
EQUINE STRONGYLOSIS
It is a parasitic infestation of horses caused by various species of Strongylus.
Triodontophorus and Trichonema and characterized by anaemic and colicy signs and
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debility.
Etiology: Strongylus vutgaris, Strongylus edentatus and Strongylus equinus and are
known as large strongyles which suck blood. Triodontophorus and Trichonema are
called small strongyles which will not suck blood.
Strongylus vulgaris: Since it is a very common parasite, its details are given below:
Transmission: is by ingestion of 3rd stage larvae.
Life cycle: The adults are found in the caecum and colon and lay eggs. These are
passed in the faeces. Under suitable environmental conditions, the larvae develop and
moulds twice to become 3rd stage larvae. Upon ingestion, it goes to the intestine and
penetrates the mucosa and gets into the mesenteric arteries. They will enter the tunica
intema of the artery and crawls through this artery and goes to the aorta. It may be
circulated to renal hepatic, cerebral and coronary artery. Latter they will come back to
caecum and colon and become adults and start laying eggs.
Pathogenesis:
3. They cause arteritis.
4. They produce aneurysms and even nodules. Because of this, the lumen of the
blood vessels is decreased and blood supply to the part of the intestine is decreased.
Latter on the blood supply may be completely stopped, leading to necrosis of intestine
resulting in toxaemia and death. It occurs but not always the case.
Because of 1 and 2, the animal will exhibit colicy sings. In some animals,
rupturing of the nodules resulting in massive internal bleeding and death can occur.
Clinical findings: Very common disease in horses and it is world wide in distribution.
Anaemic (pale mucous membranes, increase in heart and respiratory rates) and colicy
(stamping, kicking the abdomen rolling) signs are commonly seen, especially
perspiration, diarrhoea and edema of the ventral abdomen, Toxaemic signs like high
fever initially and subnormal temperature latter on, cyanotic mucous membrane and
muddy red mucous membrane, if too severe. Necropsy finding: llions mentioned under
pathogenesis are seen
Diagnosis:
1. By faecal examination-presence of ova.
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2. By symptoms: If any horse with colicy signs is present then suspect for
strongyles.
Treatment: To remove the worms administer any one of following:
Thiabendazole 1- 100-300 mg/kg, orally most commonly used drug.
Mebendazole - 10 mg/kg b. wt., orally
Cpmbendazole - 25 mg/kg, b. wt.
Fenbendzole - 30-60 mg/kg, b. wt.
Morantal citrate - 10 mg/kg, b. wt
Ivermectin 0.2 mg/kg, b. wt s/c orally very effective.
The drugs are administered orally either by;
(1) stomach tube-commonly used method
(2) Electuary.
(3) Drenching-not commonly done, only experienced attenders will do it
rarely.
(4) By using oral dosing guns/syringe most commonly used method in
foreign countries.
Other principles of treatments are similar to parasitic diarrhoea. Treatment of
colic should be given.
Control: Similar to parasitic diarrhoea can be adopted regular deworming 3-6 times in
a year proper disposal effaces is very much essential.
TAPE WORMS OF DOGS AND CATS

Many types of tapeworms affect domestic animals and it is very common in
dogs and cats. Among them Dipylidium caninum and Echinococcus granulosus are
very common. Incidence: Tapeworms have been recorded through out the world
occurs commonly in young animals usually they cause mild form of the disease and
sometimes it can be severe too. Etiology: The tapeworms are flat and tape like and
can measure from few mms to few cms to few meters in length. They contain the
scolex, neck and strobila. The strobila is full of proglottids and the immature ones are
near the scolex or neck and the mature ones are farther away from the neck. The
mature proglottids contain the egg or egg capsules.
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The commonly occurring tapeworms of dogs and cats and their particulars are
given in the table.
Transmission: is by ingestion of the part of the or the entire intermediate host
containing the various type of larval stages like cysticercoid, cysticercus, coenurus,
hydatid cyst etc. the intermediate hosts can be fleas, fish and various domestic
animals.
Life cycle: The adult tape worms are present in the g.i. tract especially of the intestines
of dogs and cats. The matured segment which is ripened may be passed or while
passing through the g.i tract gets ruptured and releases the eggs in the stool. The
oncosphere develops and the eggs containing this are ingested by the intermediate
host. They go to the intestine and gets ruptured releasing the oncosphere which will get
into the blood and through the circulation gets localised in various visceral organs like
fiver, lungs, muscles, it develops to give rise to proglottids which gets matured and
then gets detached. These contain many ova which are passed in the stool.
Cysticercoid: - A small vesicle, practically without a cavity and one head -
invertebrates
Cysticercus: - A bladder worm with a large vesicle and one head.
Coenurus: - Usually a large cyst, containing fluid with a number of heads developing
on a wall.
Hydatid cyst or Echinococcus: - Large cysts with fluid -> brood capsule which
contains heads.
Pathogenesis: In the final host i.e. dogs and cats, the tapeworms usually are not very
harmful they can cause irritation and mild congestion of the intestinal mucosa. They
utilize the nutrients of the host for their development and deprives the host of essential
nutrients resulting in weakness, loss of weight and debility.
They cause harmful effect in the intermediate host. They damage and even
destroy the affected ones. The symptoms depend on the type of organ affected. The
human beings also can be affected as they are intermediate host for some of the
tapeworms of dogs and cats.
Clinical findings: General unthriftiness, malaise, irritability, capricious appetite,
shaggy coat, colic, mild diarrhoea and occasionally emaciation and epileptiform fits.
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Abdominal irritation may be present indicated by nodding and biting at the belly by
the animals.
The proglottids that may be evacuated irritate the anus and so the animals drag
themselves on the ground sitting on their buttocks i.e., scooting which is a very'
characteristic symptom of tape worm infection. Another important finding is the
passing of boiled rice grain like structures in the stool.
Diagnosis:
1. By symptoms/clinical signs.
2. Faecal examination: (a) Detection of segments in the stool - place a segment on the
slide and put a drop of water and tease the segment with the help of pins to release the
ova or egg capsule from the segment, (b) Do the routine faecal sedimentation method
for the presence of eggs or egg capsules.
By looking at the morphological characteristics of the eggs, one can identify
some of the tape worms. The characteristic of the onchosphere is the presence of
three pairs of hooks.
Treatment: Many drugs have been used for the elimination of tapeworms. Some
drugs are effective against the entire tape worm and some are against the strobila for
which repeated medication is required. Some drugs require the help of a laxative or a
purgative to evacuate the paralyzed worms from the intestines.
Most of the drugs are effective against the adult worms present in the intestines
and very few are effective against the stages present in the intermediate host. As
such, the stages present in the intermediate host have to be removed surgically or else
such animals have to be euthanized. The following drugs have been used:
1. Anthelin
2. Bunamidine hydrochloride: It is nothing but N, N- dibutyl 4-hexyloxy
naphthamidine HCl and is available as Scolaban tablets. It is used @ 25-50 mg/kg
body weight after fasting the animal for 3-4 hours. The tablet should not be
crushed.
3. Arecoline hydrobromide: It is administered @. 1 mg/kg body weight after starving
the animal for 12 hours. It paralyses the worms and increases the peristalsis of the
g.i. tract.
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The adverse reactions can be emesis and exaggerated catharsis and to overcome
this, the antidote is Atropine sulphate @ 0.045 mg/kg body weight.
It is not used in cats as it causes excessive bronchial secretion.
4. Bithional
5. Dichlorophene (2,2' -methylene bis - (4-chlorophenol) was previously available as
Dicestal, Distophene, Cestophene as 500 mg tablets and is not available now. Its
mechanism of action is very similar to that of Niclosamide, It was used @ 0.3
gm/kg for dogs and 0.1-0.2 gm kg for cats.
6. Diuredosan is used @ 25-50 mg'Tcg body weight as a single dose and is not
available in our country.
7. Hexachlorophene was available as Distodin and Flukin tabs and was administered
@ 10 mg kg body weight. Now it is banned through out the world.
8. Mebendazole is available as Mebex etc., containing 100 mg of this substance in a
tablet. It is administered «gi 22 mg/kg body weight.
9. Nemural.
10. Nitroscanate: It is administered (ft. 50 mg/kg body wt.
11. Praziquantel: Since it is 100% effective against E. granulosus it is the drug of
choice and regularly used in dogs to prevent hydatidosis in human beings and
animals. It is administered (a) 5 mg/kg body weight orally, s/c or i/m. Droncit tabs
50 mg tabs.
12. Niclosamide: It is the most commonly used drug for the elimination of tapeworms
of
domestic animals. It is available in the market as:
a) Niclex powder 75 % w/w (Alved co.)
b) Niclex tablets and bolus (Alved co.)
c) Niclosan tablets - each tablet containing 500 mg of niclosamide.
Dose: Dogs and Cats: 100 -150 mg /kg body weight. Cattle, Sheep and Goats:
50-150 mg /kg body weight.
Note:
1. After over night fasting this drug should be administered.
2. Administer a purgative 2 hours after the administration of niclosamide to
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expell the killed worms.

Mechanism of action: Inhibition of absorption of glucose by the tapeworms and
uncoupling of the oxidative phosphorylation process in the mitochondria of
cestodes leading to blocking of Kreb's cycle, which leads to accumulation of
lactic acid and death of the tapeworm.
It is also known as Yomesan and Mansonil in other countries.
It is used for the treatment of Dipylidrum caninum, Taenia saginata,
Taenia solium, Dipyhbothrium latum and Moneizia sp,
13. Wopell (Indian Herbs): It is a herbal preparation and is available in 100 g and 1 kg
packets.
Dose: 0.6 gm/kg body weight, orally.
Adverse reactions :Vomition. diarrhoea.
14. Taenil (Indian Herbs) : Similar to wopell.
Schedule of deworming:
1st dose: at 2-3 months of age.
2nd dose : 2-3 weeks after the 1st dose.
Subsequent doses : Once in 3 months.
Developing stage of tapeworm of dogs and cats causing disease in intermediate
hosts:
1. Gid or Sturdy or Staggers in Ruminants.
Taenia multiceps or Multiceps multiceps is a tapeworm present in the intestine
of dogs. The eggs are passed in the faeces of dogs and they develop into
oncosphere in the soil. These are ingested by the sheep, goat and cattle and they
go to the intestine. The egg ruptures and releases the oncosphere which
penetrate the intestinal mucosa and get into
they pick up the earthworms, the larvae goes to the intestine. Those larvae enters the
lung either by penetrating the duodenum and then the lungs or by penetrating the
duodenum gets into the portal vein and goes into the heart and from the heart into the
lungs. By breaking opening of the capillaries in the lungs, they enter the alveolus, then
into the bronchioles and then crawl up and gets into the trachea. In the trachea, they
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further develop and becomes the adult and attaches to the mucosa of the trachea and in
this condition they will be found throughout their life.
Because of this condition, they cause severe irritation and inflammation which
results in coughing. Because of the presence of large number of worms in the trachea,
blocking of the trachea occurs resulting in laboured breathing which is due to parasite
that is why it is known as 'gapes'.
The affected birds will be having coughing, anorexia, depression and
repeatedly throwing of head to throw out the blocking mass. The birds will
be having laboured breathing i.e. dyspnoea which is characterized by stretching of
neck and breathing through the opened beaks.
Treatment :
1. Thiabendazole - 0.5% in mash for 9-20 days.
2. Mebendazole - for prevention 0.006% in the feed.
for therapy 0.0125% in the feed.
3. Cambendazole - 50 mg/kg for 2 days.
4. Levamisole - 0.04% in the feed for 2 days or 2
gms/gallon of water for a day and then once in a month is
effective.
Treatment of Ascariasis of poultry:
1. Piperazine can be given in the feed @ 0.2-0.4% and in water 0.1-0.2% and
for a single bird 50-100 mg/bird. This is effective against Ascardia galli.
2. Phenothiazine is effective against Heterakis gallinarum
3. Combination of piperazine and phenothiazine eliminates both the worms.
Piperazine - 0.11% → administered in the feed.
Phenothiazine - 0.50% → administered in the feed.
4. Tetramisole - is effective against A. galli, H. gallinarum and Capillaria sp. @
40 mg/kg body weight.
5. Levamisole @ 30 mg/kg body weight or 0.3-0.6% in drinking water is effective
against both the worms.
6. Pyrantel tartarate - 15-20 mg/kg body weight.
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CESTODES OF POULTRY
Various species of tapeworms affects the poultry and these are quite common.
The list of cestodes and their characteristics are given in the table.
Incidence: They are world wide in their distribution and commonly seen in domestic
fowls.
Transmission: Is by the ingestion of the intermediate host.
Life Cycle: The adult tapeworms are present in the intestine of the birds and they lay
eggs. The eggs are passed in the faeces and they develop under suitable environmental
conditions. Inside the egg the oncosphere develops. These are ingested by
the intermediate hosts. The eggs hatch and release the oncosphere which further
develop into a cysticercoid which is nothing but a small cyst like structure having one
scolex and very little fluid. These may
be found in the g. i. tract or body cavity of the intermediate host. When the bird ingest
the intermediate host, evagination of the scolex occurs which is attached to the mucosa
of the intestine. From the neck, the proglottids develop and ripen. The adult tapeworm
starts laying the eggs or the ripened proglottids are detached and while passing through
the g. i. tract get ruptured and the eggs are passed in the faeces.
Pathogenesis: They may cause moderate to severe catarrhal enteritis. Rai11ietina
echinobothrida can cause the development of nodules in the intestine.
Symptoms: Weakness, slight reduction in the gaining of body weight and slight
anaemia are commonly seen. Also mild to moderate diarrhoea with excess mucous and
mucosal shreds can be seen. Very few birds will be emaciated.
Post mortem findings: Upon opening of the intestine, big tapeworms can be readily
seen, where as minute or very small or microscopic tapeworms like Davainea and
Amoebotaenia are not readily visible to the naked eye. However, mild to moderate
catarrhal enteritis with fluidy intestinal contents can be seen. In R. echinobothrida
these are not seen.
Diagnosis: is by faecal examination. Some of the eggs are having characteristic
features and by utilizing these, they can be identified into different genera.
Also it can be diagnosed by teasing of the segments. Place ripened segments on
a glass slide, put 1 or 2 drops of water and by using 2 ball point pins, tease the
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segments. After removing the solid part, place a cover slip and examine under the low
power of the microscope.
The diagrams of ova of commonly occurring cestodes and nematodes of poultry
are given in the chart.
Treatment: To eliminate the tapeworms administer any one of the following.
1. Niclosamide @ 0.5 gms/kg body weight.
2. Mixture of Tin sulphate, tin phosphate and tin oxalate at the ratio of 5:3:2
can be administered @ 1 gm/kg body wt.
3. Di-n-butyl-dilaurate (Butynorate) @ 75-125 mg/bird administered in a
capsule.
4. Nemural @ 12 mg/kg and Dicestal (Dichlorophen) 1.2 gm/kg b.
wt. have been used, but not available in our country.
Administer the above drugs orally and repeat after 3 wks.

1. Good managemental practices.
2. Eliminate the int. host by spraying the ectoparasiticides.
PROTOZOAN DISEASES OF POULTRY

COCCIDIOSIS
It is a protozoan disease of poultry caused by various species of Eimeria and is
characterized by sudden onset, diarrhoea, dysentery, weakness and mild to very heavy
mortality rate.
Incidence: It occurs through out the world. The species of the birds affected are
domestic fowls, turkeys, ducks, geese, pheasants, G. fowl etc. Any age group can be
affected but commonly occurs in a severe form in young ones. It causes severe
economic loss which may be due to:
1. Mortality rate which may vary from 5-20%
2. Reduction in gain in weight which is commonly seen in sub-clinical
form of coccidiosis where in feed conversion rate is decreased.
It can cause an economic loss of 60-120 million dollars throuhgout the world
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and in addition, another 150 million dollars, due to use of prophylactic agents in the
feed and water.
Etiology :
These protozoans belong to the :
Phylum : Apicomplexa
Genus : Eimeria
Species : There are 9 species of Eimeria affecting the poultry and
they are :
E. tenella
E. acervulina Most Pathogenic
E. necatrix
E. brunetti E. maxima E. traecox
E. hagani, E. mitis E. mivati
Eimeria is characterized by having a oocyst which contains 4 sporocysts and
each sporocyst containing 2 sporozoites.
The bird after exposure to one species will be immune
to that particular species, thus indicating that there is no
cross protection.
The birds exposed to marek's disease virus will be highly susceptible to
coccidiosis because such birds will be in the state of immuno-suppression because T-
cells are affected.
Transmission: is by the ingestion of feed and water containing the
sporulated oocysts.
Life cycle: The oocysts are passed in the faeces. These undergo further
development under suitable environmental conditions arid gives rise to
sporulated oocysts. When these are ingested by the birds they go to the g.i. tract and by
the action of Trypsin, rupturing of the oocyst occurs releasing these sporozoites which
penetrate the intestinal epithelial cells and invades the mucosa. These develops into
Schizont 1 and by repreated binary fission merozoites are formed which are released
by the rupturing of the epithelial cells. These merozoites invades other epithelial cells
and develops into Schizont 2. Binary fission occurs and again merozoites are produced
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and released by rupturing of epithelial cells. These further invade the other epithelial
cells and develop and give rise to microgametocyte and
macrogametocyte. These give rise to microgamete and macrogamete respectively.
The microgamete fuses with the macrogamete and give rise to zygote which develops
into the oocyst.
Pathogenesis: The pathogenesis depends on the following factors :
1. The number of sporulated oocysts ingested by the bird.
2. The species of Eimeria involved.
3. Nutritional status of the bird.
4. Management practices.
5. Concurrent diseases.
Depending on the above factors, inflammation of the various parts of
the intestine occurs. It can be mild to severe catarrhal enteritis or haemorrhagic
enteritis
Clinical Findings : Sudden onset, diarrhoea, dysentery, where in the
droppings may have blood clots or fresh blood or sometimes only blood.
Weakness, depression, huddling of together of the birds and anaemic
signs like pale combs and wattles and conjuctiva, increase in heart and
respiratory rates can be seen. Finally it will end in death of the bird.
In sub-clinical form, the symptoms are not seen and only the loss
in gain in weight can be seen.
Post mortem findings :
1. E. acervulina: The entire intestine may be affected but
commonly the duodenum is affected. Whitish lesion varying from
discrete, small, round or elongated lesions, l-2 mm to ladder like streaks.
2. E. praecox : It affects the duodenum, usually without lesions and the
intestine may contain mucoid exudate.
3. E. necatrix : Commonly it affects the middle part of the small intestine.
The serous surface is covered with whitish focal lesions and haemorrhagic spots. The
intestinal contents consist of blood and mucous.
4. E. maxima : The middle portion of intestine is distended and
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mucoid intestinal content may be tinged with blood. The exudate may be pink. A few
pin point haemorrhages may be seen on the serous surface and the intestinal wall is
thickened.
5. E. brunetti : It affects the lower half of intestine and causes damage in
the area below the yolk diverticulum. Intestinal wall may be pink and few
haemorrhagic lesions will be visible on the serous surface.
6. E. mivati : It affects the lower intestine where in the intestinal wall is
thickened and intestinal contents will be reddish mucoid in nature.
7. E. tenella : It affects the caecum causing 'caecal coccidiosis'. Pin
point haemorrhagic and whitish spots occur on the serous surface. The caeca is filled
with fluid, coagulated blood or necrotic material.
8. E. mitis : No lesions and mucoid exudate may be seen in duodenum.
9. E. hagani: Pin head haemorrhages i.e. petichial haemorrhages in the
duodenum.
Diagnosis :
1. By symptoms of diarrhoea and dysentery.
2. Faecal examination to demonstrate the presence of
oocysts.
Depending on the part of intestine affected and the type of occyst demonstrated
with its measurements, the type of Eimeria involved will be identified.
Treatment: For the prevention and treatment of coccidiosis one of the following
drugs can be used:
I. Nitrofurazone Compounds :
1. Avicox (Micro Labs) 5 kg and 25 Kg drumjand contains :
Nltrofurazone 25%
Furazolidone 3.6%
2. Bio cox (Ag Vet) similar to Avicox.
3. Bifuran tablet (SKF) and it contains :
Nitrofurazone 100.0 mg
Furazolidone 14.5 mg
4. Bifuran feed suplement (SKF) is similar to Avicox.
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5. Binit supplement (Glaxo) 1/kg bag

Similar to Avicox + Vitamin K 0.2%
6. Coxysol (Alved) is similar to Avicox.
7. Coxysol A-K soluble powder - similar to Avicox +
Vitamin A 2000 IU + Vit. K3 2 mg/gm.
8. Dozone premix (Sarabhai) is similar to Avicox.
9. Furanitro tab (Piya) - it contains :
similar to Bifuran tablets.
10. Kox. care feed supplement (Vesper) - It contains :
Nitrofurazone 4.6%
Vitamin K 0.5%
11. Mifuran feed suplement (Medicine India) is similar to
Avicox.
12. Poultryfuran (Aries) is similar to Avicox
13. Vetsfuran (Vets Pharma) is similar to Avicox.
14. Vetsfuran tablets (Vets Pharma) is similar to Bifuran
tablets.
15. Vet furan - K tab (Vets Pharma) it contains :
Nitrofurazone 110 rag
Furazolidone 16 mg
Vit K3 1 mg
Dose : In the feed - for treatment : 0.11% for 5 days
for prevention : 0.0055%
Feed supplement : 500 gms of the product per tonne of
feed for 1-14 weeks
II. Clopidol ;
1. Amfedol FS (Ranbaxy), 1 and 5 kg drum.
It contains 25 gms of clopidol / 100 gins of powder.
2. Clopidox powder (Micro Labs) - is similar to Amfedol.
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3. Coccidium premix (Wockhardt) - is similar to Amfedol.

4. Coccidol premix (Ventri) - is similar to Amfedol.
5 Coxymix premix (Ag Vet) - is similar to Amfedol.
6. Coyden - 25 powder (MJ Pharma) is similar to 1
7. Klop premix (Sarabhai) is similar to No. l.
8. Regecoccine premix (Art-Feed).
Dose : In feed for prevention : 0.0125%
500 gms of Amfedol / ton of feed.
III. Amprolium compounds :
1. Amprolium soluble powder (Merind) 600 gms container.
It contains 20% Amprolium HCl.
2. Amprol
For treatment : 0.012-0.024% for 3-5 days in Drinking
water and afterwards 0.006% for 1-2 weeks.
For prevention : 30 gms of Amprolium soluble powder
per 100 litres of drinking water.
IV. Binitro -o-toulamide :
1. Coccivin premix (Sarabhai) 1 and 10 kgs.
25% of this is present.
2. Coxidot powder (MJ Pharma) 10 kgs; 25% powder
3. Coxyban premix (Ag Vet) 25% powder.
4. Dot feed additives (Aries) 25%
5. Dotci feed supplement (Blue cross) 25% powder.
6. Ethcoxi premix (Concept) 25%
7. Veldot feed additive (Ventri) 25%
8. Zonamix powder (piya) 25%
Dose : For prevention : l kg/2-3 tons of feed upto 8th week of age.
1 kg/3-6 tons of feed from 9-14
weeks of age.
V. Tetracycline preparations :
1. Codrinal powder (Hoechst) 20 gms bottle along with a spoon. Each
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grame of Codrinal contains: .

Tetracycline HCl 0.05 gm
Sod. salt of p-toluene sulphonyl -beta-
methoxy - ethyl urethane 0.55 gm
Crystalline Lactose 0.375 gm
Sodium bi sulphate 0.025 gm
Dose: 1 gm (1/2 spoon) / litre of water – Prevention.
4 gm (1 spoon) / litre of water – Curative.
Stunted growth can be seen in pups. Vomition can result in aspiration of the
material into the respiratory system, leading to aspiratory pneumonia.
Nervous signs are also seen; i.e. restlessness, incoordination, etc. These
symptoms may be due to the irritation of the nerve endings of the intestinal mucosa by
the worm.
Necropsy Findings: - Refer to pathogenesis.
Diagnosis: - By faecal examination.
Treatment: - Drug of choice is Piperazine.
Dose:- 100-300 mg/kg. This drug is given orally.
The first dose is given when the pups are 2-3 weeks of age, as the larvae have
developed into the adult worms. Because the drug is effective against mature worms
only. The drug is not effective against immature worms and migrating larvae. Then
repeat the drug at 6 and 8 weeks of are to kill all the worms. The following drugs also
can be used:
14) Chinapodium oil - 0.1 ml/kg b. wt. Orally
15) Diethyl Carbamazine Citrate - 50 mg/kg b. wt. Orally
16) Thiabendazole - 300-500 mg/kg b. wt. Orally
17) Tetramisole - 10 mg/kg b. wt. Orally
18) Pyrental tartrate - 5-7 mg/kg b. wt. Orally
19) Dichlorovas - 12-15 mg/kg
20) Neguvon - 75 mg/kg tid for 2 weeks
21) Avion/Tetracap - 0.l ml/lb b. wt. Orally
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22) Fenbendazole - 5 mg/kg b. wt. Orally.

720 mg/kg b. wt. For 5 days
23) Nitroscanate - 50 mg/kg b. wt
24) Mebendazole - 10 mg/kg bid orally
25) Levamisolewuss - 7.5 mg/kg b. wt. Orally
26) Albendazole - 5-10 mg/kg b. wt. Orally.
SWINE ASCARIASIS
It is caused by Ascaris suum.
Life Cycle: - It is almost similar to Toxocara canis but controversy is there regarding
the transplacental and transcolostral transmission. Here the disease is characterized by
severe dyspnoea which is called 'Thumps'. (Rib cage raising and falling). Here the
disease is characterized by blockage of bile ducts and here obstructive jaundice may be
noticed.
Necropsy findings: - Milky white spotted liver is very characteristic lesion and it is
nothing but a chronic granulomatous inflammation with white necrotic material.
Treatment: -
10) Piperazine (Citrate) - 100-300 mg/kg b. wt. In the feed.
11) Sodium Fluoride - (old drug) 100-150 mg/kg b. wt. In feed.
12) Hygromycine - (old drug) 6000 IU/lb. of feed.
This is extensively used as feed additive and used for the period of 60 days.
13) Levamisole - Effective against both immature and mature worms - 7.5 mg/kg b.
wt., orally or i/m.
14) Tetramisole - 15 mg/kg b. wt., orally. It is effective against both mature and
immature worms.
15) Parbendazole - 30 nig/kg b. wt., orally.
16) Fenbendazole - 5 mg/kg b. wt., orally.
17) Cambendazole - 20 mg/kg b. wt., orally.
18) Morantal tartrate - 5 mg/kg b. wt., orally.
Piperazine compounds available in our Country-
Piperazine hydrate : Piperazine phosphate : Piperazine citrate
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100 mg : 104 mg : 120 mg

(More effective)
Mechanism of action of Piperazine: -
It is having a narcotizing effect on worms. It may be necessary to administer
purgative
like MgSO4 after 1-2 hours of administration of Piperazine.
Piperazine Compounds: -
11) Helmacid Liquid (Glindia): It is a 45% solution of piperazine hydrate.
Container size: 115 ml and 450 ml bottle. Dose:- 4-5 ml /10 kg b. wt. In all spp.
Of large animals. 1 ml/5 kg b. wt. In dogs and cats. Better to avoid piperazine in
cats as it may cause adverse effects:
12) Helmacid Tablets: Piperazine hydrate 260 mg/tab.
13) Helmacid with Senna granules: It produces laxative and purgative effect also.
Available as 10 gm sachet.
14) Antepar (Burrough's Wellcome): 40% piperazine citrate solution Container
size: l00 mg and 450 ml bottle.
15) Antepar Tablets: Contains 500 mg of piperazine per tablet.
16) Piperex (Sarabhai): 35 and 225 gms containers available. Along with this 9 gm
spoon is also available.
17) Verban Liquid. (Cynamid): 56.3% solution of Piperazine hexahydrate. 120 ml,
450 ml, bottles and 4.5 liter jar available.
18) Vermex Liquid (Pfizer): This contains Piperazine hexahydrate. 100 ml, 500 ml,
4.5 liters containers available. 165 mg/ml.
19) Helmavet (Minumix Pharmaceuticals): 45% piperazine hydrate solution 100 ml
and 500 ml bottles.
20) Piperazine Liquid (HAL): 450 mg/ml. It contains piperazine 45%, 500 and 4.5
liter jar available.
Many other companies also- prepares this product
Toxocave Cati:- occurs in the small intestine of the cat and wild felidae.
Ingestion of eggs containing infective second stage larvae.
Life cycle is almost similar to T. Canis.
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Mouse may act as intermediate host – 2nd stage larvae.

Second stage larvae may be found in the tissue of earthworms, cockroaches,
chickens, sheep and other animals fed infective eggs.
Visceral larva migreys – Mainly caused by the larvae of T. Canis through the larval
stages of T. leonine, T. Cati, Capillaria hepatica (of rodents) and lagochilascais minor
(of wild felines) etc have also been incriminated. Characterized by the chronic
granulomatous lesions in or inner organs of children like liver, lungs , brain,
sometimes eye, somatic maven.
4. BOVINE ASCARIASIS
Bovine ascariasis is caused by Toxocara vitulorum. (Neoascar is vitulorum).
They occur in small intestine of calves of cattle and buffaloes. They cause the severe
form of the disease in young caves of 1-4 months of age. Buffalo calves suffer from
severe form of the disease when compared to cattle calves. Now a days it is considered
as the number one cause of calf mortality in buffalo calves, causing considerable
economic loss to the dairy farmers. Mortality can range from 25 to 50%.
Etiology: - It is caused by Taxocara vitulorum (Neoascaris vitulorum). The males
measure up to 25 cm x 5 mm and the females 30 cms x 6 mm. The cuticle is not as
thick as that of other large ascarids and these worms therefore have soft, translucent
appearance. The eggs are subglobular, provided with a finely pitted albuminous layer
and measure 75-95 by 60-75µ.
Transmission: It is very similar to that of Toxocara canis. Transplacental and
transcolostral is very common and-it may vary from place to place. In Bidar it appears
to be transplacental transmission, which playing a major role.
Life cycle: It is also very similar to that of T. canis.
Pathogenesis: This is also very similar to that of T. canis. It appears that worm load
plays an important role. It appears that liver may be significantly affected. Depending
on these above factors, clinical signs vary from one buffalo calf to the other. The
changes can be mild, moderate and very severe.
In advanced cases intestinal obstruction due to forming of bundles by the adult worms
in the intestine can lead to death of the calf. The exact reason vet not known, however
the possibility of toxemia playing a major role cannot be ruled out.
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Clinical findings: Depending on the severity, three forms of the disease are observed:
1. Mild form (Grade I): The buffalo calf will be in a standing position and will not
exhibit much of the clinical signs. Here at the most, one can observe mild
diarrhoea.
2. Moderate form (Grade II): In this form, the buffalo calf will be slightly anorexic,
slightly weak, rough hair coat, pot belly and slightly depressed. Slight to
moderate diarrhoea may be present. Slight loss of weight may also occur.
Worms can be noticed in the faeces.
3. Severe form (Grade III): In this form, the buffalo calf will be recumbent,
anorectic, markedly depressed, weak and subnormal temperature is very
characteristic. Usually the animal has not passed the faeces from 1-3 days
indicative of constipation. In addition conjunctival mucous membranes are
congested, shallow respiration and weak heart beats occurs. The faeces will be
pasty, brown in colour and slightly foul smelling.
Necropsy findings: These are very similar to Toxocara canis. In advanced cases, the
entire length of the intestine especially colon will be filled with worms.
Diagnosis:
2. Faecal examination.
3. Examination of colostrum and milk up to a period of 15-20 days can reveal the 3rd
stage larvae.
Treatment: Mild and moderate form of Ascariasis responds well to anthelmintic
treatment. Supportive therapy may not be required. However, severe form of
Ascariasis requires anthelmintic as well as supportive treatment. Even inspite of
vigorous supportive therapy, many of the buffalo calves will succumb to severe form
of Ascariasis.
The following anthehnintics can be used:
8. Piperazine @ 100-300 mg/kg body wt., orally.
9. Tetramisole @ 15 mg/kg body wt., orally.
10. Levamisole @ 7.5 mg/kg body wt., orally, S/C, I/M.
11. Fenbendazole @ 5-10 mg/kg body wt., orally.
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12. Albendazole @ 10 mg/kg body wt., orally.

13. Mebendazole @ 10-20 mg/kg body wt., orally.
14. Ivermectin @ 0.2 mg/kg body wt., S/C, orally.
The following supportive therapy can be tried:
5) Fluid therapy: 5% Dextrose, DNS, Lactated Ringer’s solution Aroryte-M can be
administered @ 1-2 bottles, I/V.
6) Camphor-in-oil: Crush 1-2 tablets of camphor and mix it in 5 ml of ground
nut oil and administer 0.5 -1.0 ml S/C and 0.5 -1.0 ml I/M. This may be
beneficial to overcome hypothermia.
Corticosteroids: Dexamethazone @, 0.5-1.0 mg/kg, body wt. I/V. I/M
may help in over coming Toxaemia and hypothermia.
7) Calcium preparations: Administer 20-30 ml of calcium borogluconate or Mifex
(Ca, Mg, P, Dextrose) I/V or S/C. It may be useful hypothermia.
8) Antibacterial agents: May or may not be useful. Use of Gentamicin, Ampicillirt,
Amoxycillin, OTC etc., may be beneficial.
5. Administering of an anthelmintic in the advanced stage of gestation is very
essential. Here the drug effective against 3rd stage larvae is required. This will
over come the transplacental and transcolostral transmission. However such
drugs are not available for use in buffaloes and cows.
6. Following regular deworming schedule is a must. Administering of any one of
the anthelmintic mentioned under treatment when the carves are of 1 month, 2
months, 3 months and 4 months of age is very essential. This will save lot of
calves.
ANCYLOSTOMIASIS
It is a disease of dogs caused by Ancylostoma caninum, Uncinaria and Necator
spp characterized by poor growth, anaemia.
Incidence: - It occurs through out the world. All breeds of dogs are equally susceptible
and young ones are highly susceptible when compared to adults.
Etiology: -
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7) Ancylostoma caninum are gray to red coloured worms, females are slightly
longer than males. Males measures about 10-12 mm in length, and females
measures about 14- 16 mm. Both have well-developed buccal capsule and 3
pairs of ventral teeth.
8) Ancylostoma brazilliens: Found in small intestine of dog, cat, foxes and
human beings.
9) Ancylostoma tubaeformis: Found in cats.
10) Ancylostoma duodenale: Common in man and also occurs in dogs and cats.
11) Necator americanus: Common in man.
12) Uncinaria stenocephala: Dogs, cats and foxes.
Transmission: - Infective larvae enter the final host either by penetrating the skin or
by ingestion of contaminated feed and water
Life Cycle: - Life Cycle is direct. The eggs hatch and parasitic larvae are produced in
about a week. There are 2 free-living larvae.
(c) Non parasitic stage larvae which is very sensitive to dessication.
(d) Infective larvae which is capable of entering the body by penetrating the skin.
Second stage larvae (50 larvae infective) penetrate the skin and get in to the
blood, then carried to the heart and later on to lungs. Larva stays in the lung
capillaries for a while become 4th stage larvae and enter the alveoli by
rupturing and penetrating capillaries. Larvae crawls up in respiratory tract
coughed off and men swallowed. It develops and mould after reaching intestine
and becomes adult and lays eggs. An infected pup can pass as many as 5 million
eggs / day.
(2) Sometimes larvae directly get in to the GIT ok becomes adult with out migration
(3) Sometimes larvae in the circulation may get through placenta to the foetus and may
develop prenatal infection, and this is transplacental transmission. This is questioned
by many workers.
(4) Transcolostral transmission: - Larvae in the milk for 20 days after whelping are
recorded.
Pathogenesis: - Migrating larvae does not cause much damage only adult parasites are
harmful as they are active blood suckers and cause severe anaemia. The mechanisms
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of anaemia are
(5) Sucking of blood by parasites (0. 1 ml / parasite/ day)
(6) Hemorrhages in the intestine, it is observed, mat the parasite produces a type
of anticoagulant which is responsible for haemorrhages. Anaemia does not occur
as
long as iron in body reserve is present. When its reserve is depleted it results in
microcytic hypochromic anaemia.
(7) Malabsorption: - Impaired absorption of iron from the intestine.
(8) Disturbances in hemopoiesis (Not confirmed).
Clinical findings: - Puppies may die without showing any symptoms. At the age of 2-
3 weeks it remain alive, shows the signs of severe anaemia and coma. Other dogs show
anemia, weakness, pale visible mucous membranes, increase in heart rate, emaciation,
ascites (hypoproteinaemia), dry skin, stunted growth, mild diarrhoea, melaena (black
coloured faeces), and itching of skin.
Necropsy findings: - Anaemia, cachexia is well marked, pale visible mucous
membranes, ascites. Intestine is swollen, haemorrhages, lot of worms embedded in its
lumen. Red-bite marks of intestine are very important lesions.
Diagnosis: -
(1) Faecal examination. Egg may appear in different shape. It should be
differentiated from coccidial oocyst and Dipylidium caninum egg. Coccidial
oocysts are very small where as Dipylidium egg/blood capsule is very large.
(2) Occult blood test - positive.
Differential Diagnosis: - Disease should be differentiated from the diseases which
causes anaemia, like:
(6) Acute leptospirosis: High fever, haemoglobinuria, jaundice, demonstration of
organism in urine.
(7) Chronic nephritis: Normocytic normochromic anaemia.
(8) Coccidiosis: Dysentery and oocyst in the faeces.
(9) Canine babesiosis: High fever, haemoglobinuria, demonstration of organism
inside the RBCs.
(10) Canine Ehrlichiosis: Detection of organism in the cytoplasm of mono
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nuclear cells.
Treatment: -
1) Disophenol (2, 6, Di-iodo 4-nitro phenol) is available as Ancylol 10 ml Vial, 1
ml contains 45 mg.
2) Dose is 1 ml /4.5 kg body weight/(10 mg/kg. b. wt. and 0.2-2 ml/dog s/c).
3) Tetrachloro ethylene (Tetracap) 0.2 ml/kg orally. Should be administered after
overnight fasting. Administer a saline purgative (MgSo4 + NaCl) after the
administration of Tetracap.
4) Bephenium hydroxy naphthoate (Alcopar, Burroughs wellcome) is
administered @ 15-20 mg/kg and repeat after 6-10 days.
5) Thdabendazole: 300-500 mg/kg orally.
6) Mebendazole 22 mg/kg, daily, orally for 5 days.
7) Pyrental: 6-15 mg/kg, orally commonly used in human beings.
8) Albendazoie 5-10 mg/kg body weight.
9) Panacur 50 - 100 mg/kg. body weight orally.
10) Nitroscanate 50 mg/kg. body weight (New drug) orally.
Supportive treatment: - To over come anaemia -
3) Blood transfusion is done in severe anaemia.
4) Haematinics like Imferon and Ferrous sulphate are used.
To over come metabolic acidosis and dehydration give sodium bicarbonate and
lactated Ringer's solution.
Control:
(1) Keep the floor dry.
(2) Treat the floor with sodium borate at the rate of 10 lbs/100 sq. feet or 1% sodium
hypochlorite solution. This treatment kills the larvae or exposes the sheath of egg
so that larvae cannot survive in the environment Sodium borax should not be
applied to the lawns.
(3) Proper disposal of stool.
(4) The following vaccines have been tried:
a. Killed.
b. X-irradiated vaccine.
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c. Attenuated vaccine (5, fluro uracil can be used).

(5) Admn. of fenbendazole every day 15 days before whelping and 5-7 days after
whelping / 40th day of gestation to 14 days after whelping @ 50 mg/kg, b. wt.
orally.
HOOKWORMS OF SHEEP AMD GOAT

(1) Bunostomum trigonocephalum: - Common one is which is present in small
intestine of sheep and goats and it is similar to Ancylostomiasis.
Treatment: - Thiabendazole 75 mg/kg, orally. All other broad spectrum anthelmintics
used for Strongyle sp. are used here also.
(2) Gaigeria pachyscelis: - Similar to Bunostomum and found in sheep and goat of
India and Africa.
HOOK WORMS OF CATTLE

Bunostomum phlebotornum: - Similar to Ancylostomes. Mainly occurs in cattle and
rarely in sheep and goat.
Treatment: - Thiabendazole 50-110 mg/kg, Orally.
All other broad spectrum anthelmintics used for Strongyle sp can be used here
also.
CANINE SPIRQCERCQSIS
Caused by Spirocerca lupi and characterized by the development of nodules in the
oesophagus, stomach and aorta of dogs, fox, wolf and jackals.
Etiology: - Spirocerca lupi - it is a nematode, it is bright red in colour and spiral in
shape and, male measures about 30-50 mm and females 50-80 mm.
Transmission: - Ingestion of intermediate host i.e. coprophagus beetles and also due
to numerous transport hosts (paratenic host) like amphibians, reptiles and birds.
Infective stage is the 3rd stage larvae.
Life cycle: - The embryonated eggs are laid in the oesophagus or stomach and are
passed in the faeces. These eggs are ingested by Coprophagus beetle and in the beetles,
larva are encysted in the tracheal rings (L3). These beetles are ingested by the transport
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host i.e., mainly by birds i.e. chickens. When the dog eats the beetles or transport host
the larva (L3) gets into the stomach and penetrates the wall of the stomach and reaches
the gastric and gastro epiploic artery. Through the wall of these arteries they get into
the coeliac artery and then migrate to the aorta. They may remain in aorta or they may
bypass the connective tissue through tunnel like structures between the nodule of aorta
and oesophagus and gets into wall of the oesophagus and then into the stomach. When
they are in the oesophagus or stomach ttiey become adults and then start laying eggs.
Pathogenesis: - Migrating larvae produces haemorrhages, inflammatory reaction,
purulent streaks or abscesses and these heal up and lead to stenosis of aorta.
Later on, chronic granulomatous inflammation sets in leading to formation of
nodules in the oesophagus and stomach. These nodules can unite together to form
pedunculated mass. Due to this, difficulty in ingestion of food, and also repeated
vomition occurs.
Nodules can break open abruptly leading to massive internal bleeding which is
often fatal.
Sequelae:
3) May cause oesophageal sarcoma.
4) Hypertrophic pulmonary osteo arthropathy.
Some larvae can get into long bones -—thickening of bones.
6) Pyaernic nephritis.
7) Spondylitis of adjacent thoracic vertebrae (cervical spondyiosis)
8) Aplastic anaemia.
Clinical findings: - Depends on place of nodules:
Stomach - persistent vomition and no food remaining in the stomach.
Oesophagus - Comes in the way of deglutition and also due to pressure on trachea,
difficulty in respiration. Loss of weight emaciation, weakness, and in oesophageal
sarcoma. Animal will die of severe emaciation.
Sometimes sudden death - due to rupture of nodules present in pulmonary aorta
-thoracic cavity filled with lot of blood.
In prolonged cases, there may be enlargement of long bones.
Necropsy findings: - Nodules in stomach, oesophagus and aorta. If the aorta is
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ruptured then clotted blood is found in thoracic cavity.

Diagnosis:-
4) By Symptoms of persistent vomition weakness and emaciation.
5) Faecal examination: Eggs are small, capsule shaped, oval, containing larva.
6) X-ray of longbones- pulmonary osteoarthropathy.
Treatment:-
(I) Dieihyl carbamazine citrate- Drug of choice since long time and administered @ 25
mg/kg body weight orally for 4-10 days. The preparations available are-
5) Hetrazan (Lederle) l00 mg/tab.
6) Lorcid (Vets Pharma) - 400 mg/tab.
7) Caricide
8) Banocide
(II) Disophenol (Ancylol) -1 ml/4.5kg bod}' weight s/c is effective.
(III) Recently levamisole and albendazole have been found to be effective.
(IV) Avermectins: Also has been used.
(V) “Surgical therapy is also not of much use”.
Prevention and control: Control of intermediate hosts may be of use in prevention of
the spirocercal infection.
CANINE HEART WORMS

It is a parasitic disease of dogs, cats, foxes and wolves caused by Dirofilaria
immitis and is characterized by malfunctioning of the right side of the heart, leading to
passive venous congestion, ascites and hydrothorax.
Etiology: It is caused by the filarial worm, Dirofilaria immitis. The male worms are
12-16 cms and the female worms are 25-30 cms in length.
Incidence: Heart worms have been recorded through out the world in dogs, cats,
foxes wolves etc. It can occur in any age group.
Transmission: The third stage larva is the infective stage and is transmitted by the bite
of all the three types of mosquitoes namely Anopheles, Culex and Aedis.
Life cycle: The adult worms are found in the right atrium, right ventricle and
pulmonary artery. The adult female lays the first stage larva known as the microfilaria.
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The larvae get into the circulation and will be found in the peripheral blood. When the
mosquito sucks the blood the first stage larvae get into the mosquito and further
development takes place. This larva moulds twice to become the third stage larva
which is the infective stage. When such mosquitoes suck the blood from a dog, they
introduce the third stage larvae. In the subcutaneous tissue and muscular tissue further
development of larvae occurs for a while. Then they get into the blood and through
circulation these larvae are carried to the right side of the heart. Within 1-2 months
they become adults.
Pathogenesis: The larvae in the subcutaneous tissue cause dermatitis and itching. The
larvae and the adult worms in the heart causes the blood flow from right auricle to
right ventricle to pulmonary artery to lungs will become irregular and there will be
back flow of blood leading to passive venous congestion which is characterized by.
ascites, anasarca, etc. The worms cause rugose or villose endarteritis of the
pulmonary artery resulting in the formation of the thrombus. This can cause
infarction, necrosis and fibrosis.
Clinical findings: In some animals sudden death can occur which may be due to infra
vascular haemorrhages and there may be renal haemosiderosis.
Commonly the disease is characterized by chronic cough which will be
exaggcratd exercise. Weakness, pot belly, rapid breathing and upon exercise the dog
may collapse and A Upon auscultation heart murmurs can be heard. ECG will indicate
inverted T wave.
Necropsy findings: Acites, hydrothorax, hypertrophy and enlargement of the right
side of the heart and lot of adult worms are seen.
Diagnosis:
1. By symptoms / clinical signs.
2. By blood examination: Any one or all the methods mentioned below can be used to
demonstrate the microfilaria in me blood of dogs collected during the evening and
night:
a) Direct method: Place a drop of blood on a slide and place a coverslip and
examine under the low power of the microscope. The moving larvae can be
demonstrated.
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b) Make a blood smear and stain with Giemsa and examine under the
microscope to demonstrate ‘S’ shaped larvae.
c) Modified Knotf s method: Place 1 ml of blood in a centrifuge tube and then
add 9 ml of 2% formaline and mix the contents. Then centrifuge for 5-10
minutes at 1000-1500 RPM. Discard the supernatant and mix the sediment.
Place a drop of the sediment on a slide and add a drop of 1: 1000 Methylene
blue solutions and mix the contents. Then place a coverslip and examine
under the microscope for the blue coloured larvae.
3. Serological test: ELISA has been used.
Treatment: To eliminate die worms, various drugs have been used. Since the drugs
have to be used for a prolonged period of time, it will end in toxicity or adverse
reaction. Any one of the following drugs can be used:
1. Thiacetarsamide sodium (Caparsolate): It contains 20% arsenic and is available as a
powder. Make a 1% solution and administer at the rate of 1.0 mg/lb body weight as a
slow i/v injection, b.i.d. for 2 days. It's effect is only on the adult worms and does not
have any effect on the microfilariae.
It is the drug of choice for heart worms and is not available in our country.
Note:
5. Perivascular infiltration is highly irritant and will result in huge swelling.
6. To overcome the toxicity, administer the antidote. The antidote is Dirnercaprol
(BAL) and it should be administered at the rate of 4 mg/lb body weight per day in
4 divided doses. Also corticosteroids can be administered.
7. Diethyl carbamazirte citrate: Administer @ 25 mg/kg body weight per dose,
orally, t. i.d. for 3-5 weeks.
The effect of the drug is only on the microfilaria. It sensitizes the microfilaria
so that it is readily phagocytized by the macrophages.
8. Antimosan (Bayer): This is an old drug now not available in our country. The
schedule to be followed is :
f) First course is for 6 days @ 0.5 ml/10 kg weighing dog, slow i/v, i/m, s/c daily.
g) Give a break for 7 days.
h) Start a second course@ 1.0 ml dairy for 6 days.
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i) Give a break for 7 days.

j) Start the third course @ 1.5 ml daily for 6 days.
The drug temporarily sterilizes the female worm.
Only the cumulative effect is fatal to the worm.
5. Levamisole: Recent studies have given highly encouraging results in treating heart
worms with levamisole. 11 mg/kg, b. wt. orally 5-6 days.
Levamisole: 6 Mg/kg b. wt. Orally.
Control: All the efforts should be made to eliminate the intermediate host i.e, the
mosquitoes. Various ectoparasiticides should be used to eliminate the mosquitoes.
VERMINOUS PNEUMONIA OF CATTLE

(Lung worm infestation, verminous bronchitis, Husk, Hoose)
It is a parasitic disease of cattle caused by Dictyocaulus viviparus and is
characterized by pneumonia.
Etiology: It is a round worm and the males measure about 5 - 5.5 cms and the females
about 6-8 cms in length.
Incidence: Reputed from many parts of the world. It is very common in U.K. and
U.S.A. In our country it is commonly recorded in hilly areas. This worm is highly host
specific as only the cattle are affected. Cattle of all the age group can be affected but
calves of 4-10 months of age are commonly affected with the severe form of the
disease. Commonly seen in warm, wet summer months.
Transmission: is by ingestion of contaminated feed and water. The infective stage is
the third stage larva.
Life cycle: The adult worms are present in the bronchioles and alveoli and they lay
eggs. These eggs are coughed up and reswallowed. Then they pass through the g.i.
tract and while passing through the eggs are hatched and the first stage larvae will be
passed in the faeces. Under moist environmental conditions, the larvae develops and
moulds twice to become the third stage larvae and this is the infective stage.
When the animal ingests the infective stage, it will get into the small intestine.
Then they will penetrate the intestinal wall and get into the mesenteric lymph nodes.
Here the third stage larva mould to become the 4th stage larva. Then it gets into the
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lymphatics and goes to the heart and then into the lungs. In lungs they get into the
alveoli and develop into the mature worm and starts laying eggs.
Pathogenesis: The migrating larvae damage the intestine and lungs and haemorrhages
are seen. When they will be in the bronchi, there will be inflammation resulting in
accumulation of neutrophils and eosinophils leading to the obstruction of the air
passages and emphysema develops. Damage to the intestine can result in diarrhoea.
Clinical findings: This condition can be acute or sub-acute one.
1. Acute type: This type commonly occurs in adult cattle. Calves also can be affected.
Initially there will be fever of 104 -105°F, nasal discharge, increase in heart and
respiratory rate, the breathing will be shallow and hurried. Coughing which will be
loose and husky. There will be increase in vesicular murmurs and bronchial tone.
Because of emphysema, crackling sounds can be heard. There will be marked
reduction in the body weight. Later on there will
Administer corticosteroids like Dexamethasone @ 10 mg/calf or 20 mg/adult,
i/m.
Control:
5. Avoid grazing of animals on wet pastures.
6. Vaccinate the animal with any one of the following :
a) X-ray irradiated vaccine: This vaccine is prepared by IVRI, Izathnagar, UP. This
vaccine contains the third stage larvae of the lung worm exposed to the X-rays. It is
administered orally at an interval of 6 days twice. The larvae gets into the intestine
and then into mesenteric lymph nodes and stays there. Here it triggers the immune
response. It gives 90 -100 % protection.
b) Triethylene malamine attenuated vaccine: This vaccine contains the third stage
larvae exposed to this chemical. Thus me larvae lost its pathogenicity. To preserve
this vaccine is difficult and hence not commonly used when compared to the first
vaccine.
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VERMINOUS PNEUMONIA OF SHEEP AND GOATS

Etiology: It is due to:
4. Dictyocaulus filaria which is very similar to D. viviparus
5. Mullerius capillaris.
6. Protostrongylus rufescense.
For number 2 and 3 the life cycle is indirect and needs snails and slugs as
intermediate host. They cause nodules in the lung parenchyma.
Treatment: It is very similar to cattle.
VERMINOUS PNEUMONIA IN PIG

Etiology:
1. Metastrongylus apri.
2. Metastrongylus salmi.
3. Metastrongylus pudendotectus.
Life cycle: is indirect, as earth worms act as intermdiate host.
These lungworms transmit hog cholera and swine influenza viruses.
VERMINOUS PNEUMONIA IN HORSES AND DONKEYS

Etiology: Dictyocaulus arnfieldi which is very similar to D. viviparus.
It occurs commonly in donkeys when compared to horses. It produces mild
form of the disease.
Recently the following drugs have been used for the treatment of lung worms in
all the species of domestic animals, and are found to be very effective:
5. Ivermectin : Used @ 0.2 mg/kg body weight, s/c.
6. Fenbendazole : Used @ 5-7.5 mg/kg body weight, orally.
7. Albendazole : Used @ 5-10 mg/kg body weight, orally.
8. Oxibendazole : 2.5-5.0 mg/kg body weight, orally.
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PARASITIC GASTROENTERITIS
(Parasitic Diarrhoea)
It is a parasitic infestation of almost all the domestic animals caused by various
species of Trichostrongylus, Ostertagia, Nematodirus, Cooperia etc., and it is
charactered by gastroenteritis.
Etiology: Cattle Sheep & Goats

Name of the parasite Abomasum, Small intestine Abomasum,Small
intestine
I. Trichostrongvlus sp.
Trichostrongylus axei + - + -
T. colubriformes - + + -
T. longtspicuiaris - + - +
II. Ostertagia sp.
O. ostertagi - - + -
O. circumcincta - - + -
O. trifurcata - - + -
III. Cooperia sp.

C. punctata - + - +
C. onchophora - + - +
C. pectinata - + - -
C. curticei - - - +
IV. Nematodirus sp.
N. spathiger - + - +
N. battus - + - +
N. filicoffis - + - +
N. helvetianus - + - -
These worms are nematodes and they are short and thick worms.
Incidence: - Present throughout die world. They cause severe economic loss which
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may be due to-

(4) Stunted growth - they utilize the nutrients.
(5) Mortality.
(6) Anaemia (Trichostrongylus) not so severe.
Young ones are highly susceptible and severe form of disease is seen.
Transmission: - It is due to ingestion of contaminated feed and water which contains
3rd stage larva.
Life cycle: - The adult worms are present either in abomasum or small intestine and
lay eggs. They are passed in the faeces and under suitable environmental conditions,
the larvae develop and mould twice to become the 3rd stage larva. These are ingested
by the animals which go to abomasum or small intestine and develop into the adults.
Pathogenesis: - Some of the larvae can get into the gastric glands and may destroy
them. Hence the hydrochloric acid secretion is reduced. The normal pH of abomasal
fluid is 2.5-4.5 and in this condition there will be increase^ in PH and it may be around
6. Due to this change, indigestion occurs. Also formation of pepsin is reduced
resulting in improper digestion of proteins. Some of the pepsinogen get into blood and
its level increases in the blood.
These worms also cause abomasitis and enteritis which results in increased
motility of gastro intestinal tract.
All the above changes cause diarrhoea → dehydration → haemoconcentration.
Because of these changes, there will be hypoproteinaemia i.e., total plasma
proteins (TTP) will be decreased from its normal value of 7-7.5 gms9'o to 4-5 gm %.
This results in anasarca. Ostertagia also can cause mircoscopic nodules in the gastro-
intestinal tract.
Clinical findings: - Diarrhoea and the faeces may be dark green in colour and may or
may not be foul smelling. Rough hair coat, anasarca, stunted growth, decrease in gain
in weight, weakness and emaciation, are seen.
Constant mortality in a dairy farm can be seen which is very important.
Necropsy findings: - Abomasitis, enteritis and presence of large number of worms.
Diagnosis: -
4. By symptoms /clinical signs.
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5. By faecal examination. By morphological characteristics of eggs it is very

difficult to identify the worms into various genera and hence they are classified
as
strongyle ova.
6. Biochemical, TPP - 4-5 gm%
Blood pepsinogen level is increased.
(6) Colibacillosis - Young ones under 2 wks, fever and chalky white diarrhoea.
(7) Salmonellosis - Any age group, usually young ones, fever, diarrhoea and
dysentery.
(8) Viral gastroenteritis - R.P. and B.V.D. Oral lesions, fever, diarrhoea and
dysentery.
(9) Parasitic - Fascioliasis, Amphistomiasis, Coccidiosis. Faecal examination
reveals the characteristic ova, or oocyst.
(10)Johne's disease - No fever, thick pea soup like diarrhoea and not responding to
treatment and it is a chronic disease.
Treatment: - I. To overcome the gastro-intestinal parasites any of the following broad
spectrum anthelmintics can be given.
I. Phenothiazine: Chemical name is Thiodiphenyl amine.
Also known as Dr. Roger's product. It is a very old product, used extensively
for a long period of time. Now a days it is not commonly used even though it is cheap.
It is available as "Phenovis" (EEL) 95% dispersible powder 58% 3 kg tin (Rs. 300/-).
It is a green powder.
Dose: - Cattle - 10 gm/45 kg bodyweight with a maximum of 79 gms/animal
and administered orally. Sheep and goats: 5-20 gms depending on the size of animal.
Horse: - 3-5 gms/45 kg, body weight orally - through naso-gastric tube or as an
electuary.
Metabolism: - Half of the drug administered remains in the gastro-intestinal tract and
produces its effect. The other half of the drug gets converted into phenothiazine
sulphoxide by the action of certain enzymes in the mucosa of gastro-intestinal tract
and gets absorbed. It goes to the liver and converted into leucophenothiazone and
386
leucothional. These go to the kidney and get filtered in the urine. Then they get
oxidised and forms into phenothiazone and thional. These oxidised products are brown
colouring dyes which imparts brown or reddish brown colour to the urine.
Phenothiazine sulphoxide can get into the anterior chamber of eye and when it
is exposed to ultraviolet rays i.e., sunlight, it causes keratitis, ulceration, blindness
within 36 hous. Such type of reaction can occur in non pigmented skin leading to
photosensitisatt'on. Eventhough it has been extensively used for long period of time,
now a days it is not commonly used because;
(5) Photosensitisation - Keratitis, dermatitis.
(6) In anaemic and debilitated animals it has been shown to cause lysis of RBCs.
(7) In advanced stage of pregnancy, it may cause abortion.
(8) In sheep, when this drug is administered, due to spilling of urine on the wool, the
colour of wool is changed to brown or reddish brown which is very difficult to
remove.
c. The cow’s milk should not be used for human consumption for 3 days after
administration.
d. This drug should not be administered to pregnant ewes during the first two
months of gestation, because it can cause teratogenic effect.
5. Albendazole:
Available as "Analgon suspension" (Wockhardt) 70 ml bottle, 1 litre, 4.5 litre, 25
litres can.
25 mg of albendazole/ml of suspension
Albomar (Glindia) - suspension
30 ml, 120 ml, 2500 ml suspension. It is a 2.5 % suspension.
Albomar - powder 250 gms and 50 gms. It is a 15% powder Valbazan (SKF)
available as 30 gm sachet powder and tabs 150 mg/tab and 600 mg/bolus.
Dose: 5-10 mg/kg, b. wt. Orally. Broad spectrum anthelmintic, effective against
strongyles, flukes, and tapeworms.
6. Oxybendazole
Dose: 10 mg/kg b. wt., orally.
387
3. Imidazothiazoles:
a) Tetramisole: Available as "Nirverm" (ICI) It is a 30% powder (out of 100 gm
powder 30 gm active ingredient). 10 gms and 100 gm container.
Dose: 15 mg/kg, b. wt.
35 -50 mg of Nifverm/kg b. wt., It is a powder which readily dissolves in water
hence
administer as drench.
Broad spectrum anthelmintic and very safe drug in all the large animals.
It is also an immunopotentiating drug and it potentiates the CMI response. There
are no contraindications in sheep and goat. It is a d-form (dextro rotatory).
b) Levamisole: It is a 1-form of tetramisole i.e., lew rotatory.
Available as Helmonil (Alved, Madras) powder 30% powder. 10 gms, 50 gms, l00
gms and 1 kg tin.
Helmonil tablets – 150 mg/tab
Helmonil bolus
Helmonil injectable 10 ml, 30 ml vial 182 mg of levamisole Hcl/ml of inj. solution
Kalmisole (KAL) - 75 mg/ml. Dose: 7.5 mg/kg, b. wt., Orally or i/m or s/c.
It is also having immunopotentiating effect. It is used in human being, sheep, goat
and all species. It is also used along with vaccine especially in Clostridium
chauvoei, Cl. septicum, etc. It potentiates the CMI response and also it increases
the humoral imrqne response. It is also used along with H.S. vaccine and got good
response.
"Lemasol" (Ranbaxy) available as 10% powder, 20 gm and 100 gm. Available as
50 ml vial, 75 mg/ml.
"Wormal" soluble powder (Microlabs) 20 gm, 50 gm, 500 gm. 30% powder, 300
mg of levamisole Hcl/gm of powder.
This is also quite safe in large animals but not extensively used in dogs
because it causes side effects like vomition, tremors, salivation, bone marrow
disturbances.
Mechanism of action:
Levamisole blocks the metabolic pathway responsible for formation of
388
ATP. It produces muscarinic and nicotinic like effect.

4. Tetrahydropyrimidines:
(a) Pyrantel tartarate:
This drug causes nicotinic like effect. Here acetyl choline gets accumulated
and hence paralysis of worm occurs.
(b.) Morantal citrate (Broad spectrum)
"Banminth IT (Pfizer) available as 4% solution, container size 100 ml. 500
ml, 4.5 litre.
Available as tablets. 118.8 mg/tab.
Available as Banminth forte bolus- 1.188 gm/bolus.
Dose: 10 mg/kg, b. wt. or tab/20 kg, b. wt. or one bolus / 200 kg, b. wt.
Contraindication: This drug should not be administered within 72 hours
after the administration of CCl4 other wise, severe mortality will occur
Broad spectrum means - These anthelmintics are effective against various species
of Trichostrongylus, Haemonchus, Bunostomum, Trichuris, Ostertagia, Cooperia,
Nematodirus.
All are not effective against Ascaris but few anthelmintics, like
Fenbendazole, Albendazole, Levamisole are effective against Ascaris of dog,
swine, cattle and buffalo.
5. Ivermectin inj. (Ivoma 1 ml, .7 ml, 20 ml and oral suspension (Dynamic pharma)
1% w/v -cattle 1 ml/50 kg s/c
Broad spectrum anthelmintic sheep 0.5 ml/25 kg
Also for ticks, lice, nites.
6. Thiophanate wettable powder (M&B) -Thiophanate 70% w/w 10g, l00 g, 1 kg.
Effective against mature and immature worms and also ovicidal.
Dose: 70 mg/kg b, wt., orally.
Schedule of dewoming:
1st dose at 1 -2 months of age.
2nd dose at 2-3 weeks after the first dose.
Repeat once in 3 months until they are one year of age. The first dose is given
at 1-2 months of age because by that period the adult worms will be found in the g.i.
389
tract. Majority of the anmelmintics are effective against mature worms. The second
dose is given after 2-3 weeks because the immature worms were not eliminated by (he
anthelmintic and by allowing 2-3 weeks these worms will become mature, so that, they
are also eliminated.
For the animals which are one year and above regular deworming is done once
in 3-6 months.
If an adult animal is suffering from parasitic infestation, the anthelmintic is
administered twice at an interval of 2-3 weeks. This schedule holds good for both
Trematodes and nematodes.
VII. To overcome anaemia, administer haematinics.
VIII. To overcome dehydration and metabolic acidosis give lactated ringers i/v.
IX. To overcome hypoproteinaemia give protein rich feed and if necessary
administer Hermin (Alembic) it contains essential aminoacids. 200 ml bottle
Dose: As much as possible.
To over come hypogtycaemia and supply energy administer 1-2 bottles of 5-
10% dextrose i/v.
X. To reduce diarrhoea, administer "Neblon" or Kaolinpectin preparation.
XI. Give mineral vitamin mixture for 3-4 weeks; Lactivet, Nuvimin forte - old
name
Supplivite - M (sarabhai).
These animals suffering from heavy parasitic infestation will take many weeks
to return to normal condition after treatment.
Control: -
5. Rotational grazing. Here the grazing land (pasture) is divided into different
plots.
Animals were grazed in the first plot for few days and then moved on to the
second plot. This is done to cover all the plots. This will eliminate the source of
infection.
6. Management practices like –
(f) Avoid overcrowding.
(g) Proper disposal of faeces.
390
(h) Keep water and feed troughs above ground level.

(i) Maintain high plane of nutrition.
(j) Keep the barn dry.
7. Follow regular deworming schedule.
8. Vaccination ~ x-ray irradiated vaccines have been tried, but commercially not
available.
HAEMONCHOSIS
It is a severe parasitic infestation of cattle, sheep and a goat caused by
Haemonchus sp. and is characterized by anaemia and anasarca.
Etiology: -
(1) Haemonchus contortus
(2) Haemonchus placei:
Both found in the abomasum of cattle, sheep and goats. They are short, thick
round worms-about 1-2.5 cm in length. They are called as "Barber's pole" worms.
They suck lot of blood from abomasum which is similar to the hook worm -
anaemia, weakness, emaciation, pale mucous membrane, and lack in growth rate.
Symptoms of anaemia is seen, and in chronic cases the animals will be very much
emaciated i.e., skin and bones. The PCV and TRC will be very low.
Transmission: Life cycle, diagnosis, treatment and control is very similar to parasitic
diarrhoea
EQUINE STRONGYLOSIS
It is a parasitic infestation of horses caused by various species of Strongylus.
Triodontophorus and Trichonema and characterized by anaemic and colicy signs and
debility.
Etiology: Strongylus vutgaris, Strongylus edentatus and Strongylus equinus and are
known as large strongyles which suck blood. Triodontophorus and Trichonema are
called small strongyles which will not suck blood.
Strongylus vulgaris: Since it is a very common parasite, its details are given below:
Transmission: is by ingestion of 3rd stage larvae.
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Life cycle: The adults are found in the caecum and colon and lay eggs. These are
passed in the faeces. Under suitable environmental conditions, the larvae develop and
moulds twice to become 3rd stage larvae. Upon ingestion, it goes to the intestine and
penetrates the mucosa and gets into the mesenteric arteries. They will enter the tunica
intema of the artery and crawls through this artery and goes to the aorta. It may be
circulated to renal hepatic, cerebral and coronary artery. Latter they will come back to
caecum and colon and become adults and start laying eggs.
Pathogenesis:
6. They cause arteritis.
7. They produce aneurysms and even nodules. Because of this, the lumen of the
blood vessels is decreased and blood supply to the part of the intestine is decreased.
Latter on the blood supply may be completely stopped, leading to necrosis of intestine
resulting in toxaemia and death. It occurs but not always the case.
Because of 1 and 2, the animal will exhibit colicy sings. In some animals,
rupturing of the nodules resulting in massive internal bleeding and death can occur.
Clinical findings: Very common disease in horses and it is world wide in distribution.
Anaemic (pale mucous membranes, increase in heart and respiratory rates) and colicy
(stamping, kicking the abdomen rolling) signs are commonly seen, especially
perspiration, diarrhoea and edema of the ventral abdomen, Toxaemic signs like high
fever initially and subnormal temperature latter on, cyanotic mucous membrane and
muddy red mucous membrane, if too severe. Necropsy finding: llions mentioned under
pathogenesis are seen
Diagnosis:
1. By faecal examination-presence of ova.
2. By symptoms: If any horse with colicy signs is present then suspect for
strongyles.
Treatment: To remove the worms administer any one of following:
Thiabendazole 1- 100-300 mg/kg, orally most commonly used drug.
Mebendazole - 10 mg/kg b. wt., orally
Cpmbendazole - 25 mg/kg, b. wt.
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Fenbendzole - 30-60 mg/kg, b. wt.

Morantal citrate - 10 mg/kg, b. wt
Ivermectin 0.2 mg/kg, b. wt s/c orally very effective.
The drugs are administered orally either by;
(5) stomach tube-commonly used method
(6) Electuary.
(7) Drenching-not commonly done, only experienced attenders will do it
rarely.
(8) By using oral dosing guns/syringe most commonly used method in
foreign countries.
Other principles of treatments are similar to parasitic diarrhoea. Treatment of
colic should be given.
Control: Similar to parasitic diarrhoea can be adopted regular deworming 3-6 times in
a year proper disposal effaces is very much essential.
TAPE WORMS OF DOGS AND CATS

Many types of tapeworms affect domestic animals and it is very common in
dogs and cats. Among them Dipylidium caninum and Echinococcus granulosus are
very common. Incidence: Tapeworms have been recorded through out the world
occurs commonly in young animals usually they cause mild form of the disease and
sometimes it can be severe too. Etiology: The tapeworms are flat and tape like and
can measure from few mms to few cms to few meters in length. They contain the
scolex, neck and strobila. The strobila is full of proglottids and the immature ones are
near the scolex or neck and the mature ones are farther away from the neck. The
mature proglottids contain the egg or egg capsules.
The commonly occurring tapeworms of dogs and cats and their particulars are
given in the table.
Transmission: is by ingestion of the part of the or the entire intermediate host
containing the various type of larval stages like cysticercoid, cysticercus, coenurus,
hydatid cyst etc. the intermediate hosts can be fleas, fish and various domestic
animals.
393
Life cycle: The adult tape worms are present in the g.i. tract especially of the intestines
of dogs and cats. The matured segment which is ripened may be passed or while
passing through the g.i tract gets ruptured and releases the eggs in the stool. The
oncosphere develops and the eggs containing this are ingested by the intermediate
host. They go to the intestine and gets ruptured releasing the oncosphere which will get
into the blood and through the circulation gets localised in various visceral organs like
fiver, lungs, muscles, it develops to give rise to proglottids which gets matured and
then gets detached. These contain many ova which are passed in the stool.
Cysticercoid: - A small vesicle, practically without a cavity and one head -
invertebrates
Cysticercus: - A bladder worm with a large vesicle and one head.
Coenurus: - Usually a large cyst, containing fluid with a number of heads developing
on a wall.
Hydatid cyst or Echinococcus: - Large cysts with fluid -> brood capsule which
contains heads.
Pathogenesis: In the final host i.e. dogs and cats, the tapeworms usually are not very
harmful they can cause irritation and mild congestion of the intestinal mucosa. They
utilize the nutrients of the host for their development and deprives the host of essential
nutrients resulting in weakness, loss of weight and debility.
They cause harmful effect in the intermediate host. They damage and even
destroy the affected ones. The symptoms depend on the type of organ affected. The
human beings also can be affected as they are intermediate host for some of the
tapeworms of dogs and cats.
Clinical findings: General unthriftiness, malaise, irritability, capricious appetite,
shaggy coat, colic, mild diarrhoea and occasionally emaciation and epileptiform fits.
Abdominal irritation may be present indicated by nodding and biting at the belly by
the animals.
The proglottids that may be evacuated irritate the anus and so the animals drag
themselves on the ground sitting on their buttocks i.e., scooting which is a very'
characteristic symptom of tape worm infection. Another important finding is the
passing of boiled rice grain like structures in the stool.
394
Diagnosis:
1. By symptoms/clinical signs.
2. Faecal examination: (a) Detection of segments in the stool - place a segment on the
slide and put a drop of water and tease the segment with the help of pins to release the
ova or egg capsule from the segment, (b) Do the routine faecal sedimentation method
for the presence of eggs or egg capsules.
By looking at the morphological characteristics of the eggs, one can identify
some of the tape worms. The characteristic of the onchosphere is the presence of
three pairs of hooks.
Treatment: Many drugs have been used for the elimination of tapeworms. Some
drugs are effective against the entire tape worm and some are against the strobila for
which repeated medication is required. Some drugs require the help of a laxative or a
purgative to evacuate the paralyzed worms from the intestines.
Most of the drugs are effective against the adult worms present in the intestines
and very few are effective against the stages present in the intermediate host. As
such, the stages present in the intermediate host have to be removed surgically or else
such animals have to be euthanized. The following drugs have been used:
13. Anthelin
14. Bunamidine hydrochloride: It is nothing but N, N- dibutyl 4-hexyloxy
naphthamidine HCl and is available as Scolaban tablets. It is used @ 25-50 mg/kg
body weight after fasting the animal for 3-4 hours. The tablet should not be
crushed.
15. Arecoline hydrobromide: It is administered @. 1 mg/kg body weight after starving
the animal for 12 hours. It paralyses the worms and increases the peristalsis of the
g.i. tract.
The adverse reactions can be emesis and exaggerated catharsis and to overcome
this, the antidote is Atropine sulphate @ 0.045 mg/kg body weight.
It is not used in cats as it causes excessive bronchial secretion.
16. Bithional
17. Dichlorophene (2,2' -methylene bis - (4-chlorophenol) was previously available as
Dicestal, Distophene, Cestophene as 500 mg tablets and is not available now. Its
395
mechanism of action is very similar to that of Niclosamide, It was used @ 0.3

gm/kg for dogs and 0.1-0.2 gm kg for cats.
18. Diuredosan is used @ 25-50 mg'Tcg body weight as a single dose and is not
available in our country.
19. Hexachlorophene was available as Distodin and Flukin tabs and was administered
@ 10 mg kg body weight. Now it is banned through out the world.
20. Mebendazole is available as Mebex etc., containing 100 mg of this substance in a
tablet. It is administered «gi 22 mg/kg body weight.
21. Nemural.
22. Nitroscanate: It is administered (ft. 50 mg/kg body wt.
23. Praziquantel: Since it is 100% effective against E. granulosus it is the drug of
choice and regularly used in dogs to prevent hydatidosis in human beings and
animals. It is administered (a) 5 mg/kg body weight orally, s/c or i/m. Droncit tabs
50 mg tabs.
24. Niclosamide: It is the most commonly used drug for the elimination of tapeworms
of
d) Niclex powder 75 % w/w (Alved co.)
e) Niclex tablets and bolus (Alved co.)
f) Niclosan tablets - each tablet containing 500 mg of niclosamide.
Dose: Dogs and Cats: 100 -150 mg /kg body weight. Cattle, Sheep and Goats:
50-150 mg /kg body weight.
Note:
1. After over night fasting this drug should be administered.
uncoupling of the oxidative phosphorylation process in the mitochondria of
cestodes leading to blocking of Kreb's cycle, which leads to accumulation of
lactic acid and death of the tapeworm.
396
It is used for the treatment of Dipylidrum caninum, Taenia saginata,

Taenia solium, Dipyhbothrium latum and Moneizia sp,
13. Wopell (Indian Herbs): It is a herbal preparation and is available in 100 g and 1 kg
packets.
Dose: 0.6 gm/kg body weight, orally.
Adverse reactions :Vomition. diarrhoea.
14. Taenil (Indian Herbs) : Similar to wopell.
1st dose: at 2-3 months of age.
2nd dose : 2-3 weeks after the 1st dose.
hosts:
1. Gid or Sturdy or Staggers in Ruminants.
Taenia multiceps or Multiceps multiceps is a tapeworm present in the intestine of dogs.
The eggs are passed in the faeces of dogs and they develop into oncosphere in the soil.
These are ingested by the sheep, goat and cattle and they go to the intestine. The egg
ruptures and releases the oncosphere which penetrate the intestinal mucosa and get
into they pick up the earthworms, the larvae goes to the intestine. Those larvae enters
the lung either by penetrating the duodenum and then the lungs or by penetrating the
duodenum gets into the portal vein and goes into the heart and from the heart into the
lungs. By breaking opening of the capillaries in the lungs, they enter the alveolus, then
into the bronchioles and then crawl up and gets into the trachea. In the trachea, they
further develop and becomes the adult and attaches to the mucosa of the trachea and in
this condition they will be found throughout their life.
Because of this condition, they cause severe irritation and inflammation which
results in coughing. Because of the presence of large number of worms in the trachea,
blocking of the trachea occurs resulting in laboured breathing which is due to parasite
that is why it is known as 'gapes'.
The affected birds will be having coughing, anorexia, depression and
repeatedly throwing of head to throw out the blocking mass. The birds will
397
be having laboured breathing i.e. dyspnoea which is characterized by stretching of

neck and breathing through the opened beaks.
Treatment :
1. Thiabendazole - 0.5% in mash for 9-20 days.
2. Mebendazole - for prevention 0.006% in the feed.
for therapy 0.0125% in the feed.
3. Cambendazole - 50 mg/kg for 2 days.
4. Levamisole - 0.04% in the feed for 2 days or 2
gms/gallon of water for a day and then once in a month is
effective.
Treatment of Ascariasis of poultry:
4. Piperazine can be given in the feed @ 0.2-0.4% and in water 0.1-0.2% and
for a single bird 50-100 mg/bird. This is effective against Ascardia galli.
5. Phenothiazine is effective against Heterakis gallinarum
6. Combination of piperazine and phenothiazine eliminates both the worms.
Piperazine - 0.11% → administered in the feed.
Phenothiazine - 0.50% → administered in the feed.
7. Tetramisole - is effective against A. galli, H. gallinarum and Capillaria sp. @
40 mg/kg body weight.
8. Levamisole @ 30 mg/kg body weight or 0.3-0.6% in drinking water is effective
against both the worms.
9. Pyrantel tartarate - 15-20 mg/kg body weight.
CESTODES OF POULTRY
Various species of tapeworms affects the poultry and these are quite common.
The list of cestodes and their characteristics are given in the table.
Incidence: They are world wide in their distribution and commonly seen in domestic
fowls.
Transmission: Is by the ingestion of the intermediate host.
Life Cycle: The adult tapeworms are present in the intestine of the birds and they lay
eggs. The eggs are passed in the faeces and they develop under suitable environmental
398
conditions. Inside the egg the oncosphere develops. These are ingested by
the intermediate hosts. The eggs hatch and release the oncosphere which further
develop into a cysticercoid which is nothing but a small cyst like structure having one
scolex and very little fluid. These may
be found in the g. i. tract or body cavity of the intermediate host. When the bird ingest
the intermediate host, evagination of the scolex occurs which is attached to the mucosa
of the intestine. From the neck, the proglottids develop and ripen. The adult tapeworm
starts laying the eggs or the ripened proglottids are detached and while passing through
the g. i. tract get ruptured and the eggs are passed in the faeces.
Pathogenesis: They may cause moderate to severe catarrhal enteritis. Rai11ietina
echinobothrida can cause the development of nodules in the intestine.
Symptoms: Weakness, slight reduction in the gaining of body weight and slight
anaemia are commonly seen. Also mild to moderate diarrhoea with excess mucous and
mucosal shreds can be seen. Very few birds will be emaciated.
Post mortem findings: Upon opening of the intestine, big tapeworms can be readily
seen, where as minute or very small or microscopic tapeworms like Davainea and
Amoebotaenia are not readily visible to the naked eye. However, mild to moderate
catarrhal enteritis with fluidy intestinal contents can be seen. In R. echinobothrida
these are not seen.
Diagnosis: is by faecal examination. Some of the eggs are having characteristic
features and by utilizing these, they can be identified into different genera.
Also it can be diagnosed by teasing of the segments. Place ripened segments on
a glass slide, put 1 or 2 drops of water and by using 2 ball point pins, tease the
segments. After removing the solid part, place a cover slip and examine under the low
power of the microscope.
The diagrams of ova of commonly occurring cestodes and nematodes of poultry
are given in the chart.
Treatment: To eliminate the tapeworms administer any one of the following.
4. Niclosamide @ 0.5 gms/kg body weight.
5. Mixture of Tin sulphate, tin phosphate and tin oxalate at the ratio of 5:3:2
can be administered @ 1 gm/kg body wt.
399
6. Di-n-butyl-dilaurate (Butynorate) @ 75-125 mg/bird administered in a

capsule.
4. Nemural @ 12 mg/kg and Dicestal (Dichlorophen) 1.2 gm/kg b.
wt. have been used, but not available in our country.
Administer the above drugs orally and repeat after 3 wks.

1. Good managemental practices.
2. Eliminate the int. host by spraying the ectoparasiticides.
PROTOZOAN DISEASES OF POULTRY

COCCIDIOSIS
It is a protozoan disease of poultry caused by various species of Eimeria and is
characterized by sudden onset, diarrhoea, dysentery, weakness and mild to very heavy
mortality rate.
Incidence: It occurs through out the world. The species of the birds affected are
domestic fowls, turkeys, ducks, geese, pheasants, G. fowl etc. Any age group can be
affected but commonly occurs in a severe form in young ones. It causes severe
economic loss which may be due to:
1. Mortality rate which may vary from 5-20%
2. Reduction in gain in weight which is commonly seen in sub-clinical
form of coccidiosis where in feed conversion rate is decreased.
It can cause an economic loss of 60-120 million dollars throuhgout the world
and in addition, another 150 million dollars, due to use of prophylactic agents in the
feed and water.
Etiology :
These protozoans belong to the :
Phylum : Apicomplexa
Genus : Eimeria
Species : There are 9 species of Eimeria affecting the poultry and
they are :
400
E. tenella
E. acervulina Most Pathogenic
E. necatrix
E. brunetti E. maxima E. traecox
E. hagani, E. mitis E. mivati
Eimeria is characterized by having a oocyst which contains 4 sporocysts and
each sporocyst containing 2 sporozoites.
The bird after exposure to one species will be immune
to that particular species, thus indicating that there is no
cross protection.
The birds exposed to marek's disease virus will be highly susceptible to
coccidiosis because such birds will be in the state of immuno-suppression because T-
cells are affected.
Transmission: is by the ingestion of feed and water containing the
sporulated oocysts.
Life cycle: The oocysts are passed in the faeces. These undergo further
development under suitable environmental conditions arid gives rise to
sporulated oocysts. When these are ingested by the birds they go to the g.i. tract and by
the action of Trypsin, rupturing of the oocyst occurs releasing these sporozoites which
penetrate the intestinal epithelial cells and invades the mucosa. These develops into
Schizont 1 and by repreated binary fission merozoites are formed which are released
by the rupturing of the epithelial cells. These merozoites invades other epithelial cells
and develops into Schizont 2. Binary fission occurs and again merozoites are produced
and released by rupturing of epithelial cells. These further invade the other epithelial
cells and develop and give rise to microgametocyte and
macrogametocyte. These give rise to microgamete and macrogamete respectively.
The microgamete fuses with the macrogamete and give rise to zygote which develops
into the oocyst.
Pathogenesis: The pathogenesis depends on the following factors :
6. The number of sporulated oocysts ingested by the bird.
7. The species of Eimeria involved.
401
8. Nutritional status of the bird.

9. Management practices.
10. Concurrent diseases.
Depending on the above factors, inflammation of the various parts of
the intestine occurs. It can be mild to severe catarrhal enteritis or haemorrhagic
enteritis
Clinical Findings : Sudden onset, diarrhoea, dysentery, where in the
droppings may have blood clots or fresh blood or sometimes only blood.
Weakness, depression, huddling of together of the birds and anaemic
signs like pale combs and wattles and conjuctiva, increase in heart and
respiratory rates can be seen. Finally it will end in death of the bird.
In sub-clinical form, the symptoms are not seen and only the loss
in gain in weight can be seen.
Post mortem findings :
1. E. acervulina: The entire intestine may be affected but
commonly the duodenum is affected. Whitish lesion varying from
discrete, small, round or elongated lesions, l-2 mm to ladder like
streaks.
2. E. praecox : It affects the duodenum, usually without lesions
and the intestine may contain mucoid exudate.
3. E. necatrix : Commonly it affects the middle part of the small
intestine. The serous surface is covered with whitish focal lesions and
haemorrhagic spots. The intestinal contents consist of blood and mucous.
4. E. maxima : The middle portion of intestine is distended and
mucoid intestinal content may be tinged with blood. The exudate may be pink. A
few pin point haemorrhages may be seen on the serous surface and the intestinal
wall is thickened.
5. E. brunetti : It affects the lower half of intestine and causes
damage in the area below the yolk diverticulum. Intestinal wall may be pink and
few haemorrhagic lesions will be visible on the serous surface.
402
6. E. mivati : It affects the lower intestine where in the intestinal

wall is thickened and intestinal contents will be reddish mucoid in nature.
7. E. tenella : It affects the caecum causing 'caecal
coccidiosis'. Pin point haemorrhagic and whitish spots occur on the serous
surface. The caeca is filled with fluid, coagulated blood or necrotic material.
8. E. mitis : No lesions and mucoid exudate may be seen in
duodenum.
9. E. hagani: Pin head haemorrhages i.e. petichial haemorrhages in
the duodenum.
Diagnosis :
1. By symptoms of diarrhoea and dysentery.
2. Faecal examination to demonstrate the presence of
oocysts.
Depending on the part of intestine affected and the type of occyst
demonstrated with its measurements, the type of Eimeria involved will be identified.
Treatment: For the prevention and treatment of coccidiosis one of the following
drugs can be used:
I. Nitrofurazone Compounds :
1. Avicox (Micro Labs) 5 kg and 25 Kg drumjand contains :
Nltrofurazone 25%
Furazolidone 3.6%
4. Bio cox (Ag Vet) similar to Avicox.
5. Bifuran tablet (SKF) and it contains :
4. Bifuran feed suplement (SKF) is similar to Avicox.
5. Binit supplement (Glaxo) 1/kg bag
Similar to Avicox + Vitamin K 0.2%
8. Coxysol (Alved) is similar to Avicox.
9. Coxysol A-K soluble powder - similar to Avicox +
403
Vitamin A 2000 IU + Vit. K3 2 mg/gm.

10. Dozone premix (Sarabhai) is similar to Avicox.
11. Furanitro tab (Piya) - it contains :
similar to Bifuran tablets.
10. Kox. care feed supplement (Vesper) - It contains :
Nitrofurazone 4.6%
Vitamin K 0.5%
15. Mifuran feed suplement (Medicine India) is similar to
Avicox.
16. Poultryfuran (Aries) is similar to Avicox
17. Vetsfuran (Vets Pharma) is similar to Avicox.
18. Vetsfuran tablets (Vets Pharma) is similar to Bifuran
tablets.
15. Vet furan - K tab (Vets Pharma) it contains :
Nitrofurazone 110 rag
Furazolidone 16 mg
Vit K3 1 mg
Dose : In the feed - for treatment : 0.11% for 5 days
for prevention : 0.0055%
Feed supplement : 500 gms of the product per tonne of
feed for 1-14 weeks
II. Clopidol ;
1. Amfedol FS (Ranbaxy), 1 and 5 kg drum.
It contains 25 gms of clopidol / 100 gins of powder.
5. Clopidox powder (Micro Labs) - is similar to Amfedol.
6. Coccidium premix (Wockhardt) - is similar to Amfedol.
7. Coccidol premix (Ventri) - is similar to Amfedol.
5 Coxymix premix (Ag Vet) - is similar to Amfedol.
9. Coyden - 25 powder (MJ Pharma) is similar to 1
404
10. Klop premix (Sarabhai) is similar to No. l.

11. Regecoccine premix (Art-Feed).
Dose : In feed for prevention : 0.0125%
500 gms of Amfedol / ton of feed.
III. Amprolium compounds :
1. Amprolium soluble powder (Merind) 600 gms container.
It contains 20% Amprolium HCl.
2. Amprol
For treatment : 0.012-0.024% for 3-5 days in Drinking
water and afterwards 0.006% for 1-2 weeks.
For prevention : 30 gms of Amprolium soluble powder
per 100 litres of drinking water.
IV. Binitro -o-toulamide :
1. Coccivin premix (Sarabhai) 1 and 10 kgs.
25% of this is present.
9. Coxidot powder (MJ Pharma) 10 kgs; 25% powder
10. Coxyban premix (Ag Vet) 25% powder.
11. Dot feed additives (Aries) 25%
12. Dotci feed supplement (Blue cross) 25% powder.
13. Ethcoxi premix (Concept) 25%
14. Veldot feed additive (Ventri) 25%
15. Zonamix powder (piya) 25%
Dose : For prevention : l kg/2-3 tons of feed upto 8th week of age.
1 kg/3-6 tons of feed from 9-14
weeks of age.
V. Tetracycline preparations :
1. Codrinal powder (Hoechst) 20 gms bottle along with a spoon. Each
grame of Codrinal contains: .
Tetracycline HCl 0.05 gm
Sod. salt of p-toluene sulphonyl -beta-
methoxy - ethyl urethane 0.55 gm
405
Crystalline Lactose 0.375 gm

Sodium bi sulphate 0.025 gm
Dose: 1 gm (1/2 spoon) / litre of water – Prevention.
4 gm (1 spoon) / litre of water – Curative.
10.Nitroscanate: It is administered % 50 mg/kg body wt.

11.Praztouantel : Since it is 100% effective against E. granulosus it is the drug of
choice and regularly used in dogs to prevent hydatidosis m human beings and animals.
It is administered @ 5 mg/kg body weight orally, s/c or i/m.
Droncit tabs 50 mg tabs.
12. Niclosamide : It is the most commonly used drug for the elimination of tapeworms
of
a)Niclex powder 75 %w/w(Alved co.)
b)Niclex tablets and bolus (Alved co.)
c)Niclosan tablets - each tablet containing 500 mg of niclosamide,
Dose :
Dogs and Cats : 100-150 mg/kg body weight.
Cattle, Sheep and Goats : 5O -150 mg /kg body weight
Note :
1 After over night fasting this drug should be administered.
uncoupling of the oxidative phosphorylation process in the mitochondria of cestodes
leading to blocking of Kreb's cycle, which leads to accumulation of lactic acid and
death of the tapeworm.
It is used for the treatment of Dipylidium caninum, Taenia saginata, Taenia solium,
Dipylobothrium latum and Moneiziasp.
406
13. Wopell (Indian Herbs); It is a herbal preparation and is available in 100 g and
1kg. packets.
Dose: 0.6 gram/kg body weight, orally.
Adverse reactions: Vomintion, diarrhoea.
14. Taenil (Indian Herbs) : Similar to wopell,
1st dose : at 2-3 months of age.
2nd dose : 2-3 weeks after the 1M dose.
hosts:
1. Gid or Sturdy or Staggers in Ruminants:
Taenia multiceps or Multiceps multiceps is a tapeworm present in the intestine of
dogs. The eggs are passed in the faeces of dogs and they develop into oncosphere
in the soil. These are ingested by the sheep, goat and cattle and they go to the
intestine. The egg ruptures and releases the oncosphere which penetrate the
intestinal mucosa and get into the circulation and go and lodges in the CNS. In the
brain 'coenurus cerebralis' is formed. It is a large vesicle containing fluid and more
than one scolex. The disease known as ‘gid or staggers' occurs as a result of the
cyst exerting pressure on the part of the brain which is destroyed in due course of
time. The clinical symptoms exhibited by the animal depends on the part of the
brain affected. Due to the pressure of the cyst, that part of the cranial bone also gets
destroyed and holes in the bones can be seen.
Clinical findings: Turning of the head laterally and circling. Sometimes the head
is bent towards the sternum and may walk blindly and hit any object which comes in
its way. Staggerring gait, paresis or paralysis of the hind quarters also can occur.
Some may have convulsions, may fall down and die.
Diagnosis: 1. By symptoms 2. By x-ray of the skull.
Treatment: There is no treatment and surgical removal of fee cyst may be tried.
2. Echinococcosis or Hydatidosis:
Echinococcus granulosus, a small tapeworm is present in the small intestine of
407
dogs and other carnivores. The eggs are passed in the faeces of dogs and further
development occurs under suitable environmental conditions on the ground. Then
these are ingested by the intermediate hosts like all the domestic animals and even
human beings. These go to the intestine and the egg hatches and releases the
oncosphere which penetrates through the intestinal epithelium and gets into the
blood. Through circulation they go to the lungs and liver and develops into a
'hydatid cyst' which is usually 5-10 cms in diameter and sometimes it can be of the
size of a foot ball bladder. The cyst contains an inner germinal layer from which
'brood capsule' develops. The brood capsule contains many scolices. Many brood
capsules can be present in one hydatid cyst. The brood capsule can be detached and
floating in the cyst and this is known as 'hydatid sand'. Sometimes the hydatid cyst
can be sterile also. The liver and lungs containing the cyst when it is ingested by
the dog, it goes to the intestine and the cyst gets ruptured and the scolices are
released. Each scolex develops into a tapeworm,
Clinical findings: The presence of hydatid cysts in the liver and lungs produces a
disease called 'hydatidosis'. Usually it is asymptomatic, and the disease is diagnosed
during necropsy. Sometimes symptoms of disorders of the respiratory and digestive
system are seen. The animal can be weak, debilitated and emaciated during the
terminal stages.
Diagnosis: 1. During necropsy. 2. Faecal exam: Eggs arc similar to taenia spp.
Cannot be differentiated 3. By X-rays. 4. By serological tests like HAT, CFT,
Casoni's test etc. ELBA, immuno blotting 5. Allergic test.
Treatment: There is no treatment and surgical removal of the cysts may be
beneficial.
Not indicated in I/H
Prevention and control: (1) Since it is a disease of zoonotic importance, the dogs
should be compulsory dewormed with Praziquantel at regular intervals, so that the
source of infection to human beings and other domestic animals is eliminated.
(2)Dogs should not have access to abbattoirs and P.M. rooms.
(3)Affected organs should not be fed to dogs.
408
CESTODES OF SHEEP AND CATTLE

MONEIZIASIS
It is a cestodal infestation of sheep and cattle caused be Moneizia sp. and is
characterized by diarrhoea, loss of weight and emaciation.
Etiology: Moneizia benedini in cattie and M. expansa in sheep, goat and cattle. They
measure about 600 cms in length and 1.6 cms in breadth.
Transmission: is by ingestion of intermediate host i.e., Oribatid mites.
Life cycle: The eggs arc passed in the faeces of the domestic animal and after
development are ingested by the mites. In the mite it develops into a cysticercoid.
When these mites are ingested by the domestic animals, it goes to the small intestine
and develops into a tapeworm.
Clinical Findings: Diarrhoea, loss of weight, weakness, emaciation and sometimes
death can occur. Convulsions may be seen.
Necropsy findings: Catarrhal enteritis and ulcers.
1.By symtoms.
2.By faecal examination one can demonstrate the presence of big triangular shaped ova
containing the pyriform apparatus having a oncosphere.
Treatment: Administer any one of the cestodicidal drug to eliminate the Moneizia sp.
:
1. Lead arsenate is available as Niftape (Emicare). Niltape is a powder and
contains 20% Lead arsenate.
Dose ; 0.5 g per kid or calf under 3 months of age.
1.0 g per lamb over 2 months or calf over 3 months of age. Give in capsules with
fasting.
2. Niclosamide : Available as Niclosan tablets and Nicies powder, tablets,
bolus.
Dose: Cattle : 50 mg/kg body weight
Sheep and goats: 100 mg/kg body weight
Note : 1. Administer after overnight fasting.
2. Give a purgative 2 hours after administration.
3.Albendazole : @ 5-10 mg/kg body weight, orally appears to be 100% effective.
409
4.Cambendazole : @ 20 mg/kg body weight orally.

5.Fenbendazole: It is available as Panacur (Hoechst). It is available as 25% powder
(125 gm container), tablets and bolus.
Dose: 10 mg/kg body weight, orally. It appears to be very effective.
PARASITIC DISEASES OF POULTRY

The parasites of poultry are divided into endo and ecto parasites. Endoparasites are
again divided into nematodes, cestodes, treamatodes and protozoa.
The list of nematodes and its characteristics are given in the table.
Life cycle : The life cycle can be direct, wherein there
is no intermediate host to complete the life cycle. The
birds get the infection by ingesting the contaminated feed
and water which contains the eggs containing the 2nd or 3rd
stage larva.
The life cycle can be indirect also wherein an intermediate host is required to
complete the life cycle. Here the birds get the infection by ingesting the intermediate
host containing the 2nd or 3rd stage larva.
Upon ingestion, they go to the intestine and hatches to release the 3rd stage larva.
These larva will move and go to their site of predilection and moults twice to become
the adults. The adults mature and start laying of eggs which will be passed in the
droppings.
Harmful effects of nematodes :
Ascaridia galli: Reduction in the gain in weight. In heavy infestation there will be
intestinal obstruction leading to death of the chicks,
Heterakis gallinarum : These cause marked inflammation and thickening of the
wall of the caecum. In heavy infestation it can cause formation of nodules in the
mucosa and submucosa. It transmits Histomonas meleaaridis.
Capillaria annulate : These worms burrows into the crop mucosa and causes
thickening of the wall of the crop and enlargement of the glands.
The symptoms are malnutrition, emaciation and severe anaemia. Methyridine
is administered @ 100-150 mg/kg, s/c.
410
Oxyspirura mansoni ; They are the eye worm and makes the birds uneasy and
continuously scratch at the eyes. The' eyes may be watery with severe inflammation.
The nictitating membrane become swollen. The eye lids sometimes become stuck
together because of white cheesy material .
SYNGAMUS TRACHEA
Synqamus trachea is also called 'red worms' as they are red in colour. It is also
known as 'forked worm' because male and female worms are always together and
gives the appearance of the capital alphabet Y. Also known as 'Gapeworms' because
the word gape is used for laboured breathing due to parasites,
The adult worms are found in the trachea and lay eggs and thrown out of the body.
The eggs develop and may hatch and larva can be free in the soil. Either the
embryonated eggs or free larva can be ingested by the earthworms and they go to the
g.i. tract and gets into the body cavity and can penetrate the musculature. In this
condition the larva can survive in the earthworm for about 4 years. The birds when
Taenia solium
It occurs in the small intestine of man, i.e. man is the final host. Sometimes man can be an intermediate
host.
Commonly the intermediate hosts are pig and the dog. Some times domestic animals like sheep,
goat, cattle, horse, dog, bear and donkey may act as intermediate host.
It is of much importance in pigs and as a public health importance in man.
Transmission
Life cycle: The adult worms are present in the small intestine of man and the ripened proglotids are
released and passed in the small intestine of man and the ripened proglotids are released and palled in
the faeces. Under suitable environmental conditions the hexacanth embryo i.e. oncosphere develops.
This is ingested by the intermediate hosts i.e. pigs. It hatches and releases the oncosphere which
penetrates the intestinal mucosa and enters the blood vessel and goes to the liver, then to heart and
through circulation goes to the striated muscles and also lungs, liver, kidney or brain and develops into
CYSTICERCUS CELLULOSAE. By about two months this will be infective and of the size of 20 x10
mm and contains invaginated scolex.
The cysticerci are found chiefly in the muscles of the heart, tongue, forearm, thigh and neck and other
parts of the body.
Man i.e. final host becomes infected with the adult worms by eating raw pork which contains viable
411
cysticerci.
If human beings act as an intermediate host then the cysticerci are found in the subcutaneous tissue, eye
and brain. In the brain they are known as cysticrrcus racemosus.
Clinical signs: Usually clinical signs are absent in pigs. Sometimes increased sensitivity of the snout
paralyses of the tongue or convulsions can occur.
In humans CNS signs which may be rapidly fatal can occur.
Diagnosis:
1. Usually ante mortem diagnosis.
During postmortem cysts of 6 weeks and above can be detected.
2. Serological tests –Cross reactions
Treatment
In humans, yomeson and dichlorophen are effective.
1. Regular deworming of humans in endemic areas.
2. Condemning the pork with cysts.
3. Freezing at 14-18 o F continuously for four days kills the cyst.
4. Heating the pork at 113-122o F kills the cyst.
Taenia saginata
Primary host: Human beings –small intestine
Secondary host: Cattle
Most of the information on T.saginaa is similar to that of T.solium.
In the cattle, CYSTICERCUS BOVIS which is milky white, round or oval and measures about 7-9 x
5.5 mm. Develops commonly in masseter muscle,
Heart, diaphragm, tongue and can be found in any muscles of the body.
A disease of public health importance.
Treatment is similar to T.solium.
Ante mortem diagnosis is some times difficult as cysticercus is not mature.
1. Ingestion of raw beef and under cooked beef should be avoided.
2. Condemning the affected part during meat inspection.
3. Cook all parts of the meat to 135oF or more.
4. Freezing of the meat to -8 to -10o C up to 10 days.
412
Diphyllobothrium latum
Primary hoat:Man,dog,pig ,cat,polar bearand other fish eating animls-small intestine
Secondary host :1st I.H. Cyclops strenuus ,Diaptonus gracilis
2nd I.H. Fresh water fish –Pike ,trout and salmon and perch.
The scolex, instead suckers have narrow ,deep groves weakrer than suckers called bothria.
It measures about 2-10 meters(6-33 feet) and may develop 3000 segments or more. The scolex is elongated shaped. Eggs
are light
Brown in colour and operculated.
A zoonotic disease. And mainly a disease of man.
Life cycle and transmission

The adult worms are present in the small intestine of man, dog, pig, cat, polar bear and other fish eating
animals. And the ripened proglottids or the eggs are passed in the faeces. The eggs develops for several weeks
and gives rise to coracidium which consists of an oncosphere with 6n hooks) covered with a ciliated
embryophore It swims about in the water and dies soon. The life coracidium is ingested by the 1st I.H. like
Cyclops streaus and Diactomus gracilis and in the body cavity develops into a procercoid in 2-3 weeks. This I.H.
with procercoid is ingested by the second I.H. i.e. fresh water fish and develops into to plerocercoid. The final
host becomes infected through eating raw or insufficiently cooked fish. Then this grows into adult worm in about
4 weeks.
Clinical signs:
No clear cut clinical signs in dogs and cats.
In human beings it produces severe anemia. The mechanism involved is the worms competes and utilizes Vit-B12
in the duodenum. Thus the humans are deprived of Vit-B12 and results in pernicious anemia.
Treatment: Quinacrine hydrochloride and Yomenson are effective in human beings. It may be used in dogs.
1. Do the faecal examination of primary host like humans and dogs and deworm them regularly.
2. Do not allow primary host to ingest raw or insufficiently cooked fish.
413

Viral, Bacterial, Protozoal Disease of Animals

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Viral, Bacterial, Protozoal Disease of Animals

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BACTERIAL, VIRAL, FUNGAL AND PARASITIC DISEASES

An infectious disease is a disease which is transmitted with or without actual

An infectious disease can be peracute, acute, subacute, chronic and subclinical.

The animal husbandry activities contribute significantly to the National economy

1. The type of etiological agent(s) involved.

Anthrax is an acute to peracute infectious disease of all domestic animals and

English worker Factor I Factor II Factor III

2. To overcome the pyrexia, administer antipyretics like analgin @ 40 mg/kg body

Prevention and Control:

(a) HAEMORRHAGIC SEPTICAEMIA

It is a septicaemic disease of mainly cattle and buffaloes caused by Pasteurella

b) Transmission: Past. multocida is a natural inhabitant of tonsils and nasopharynx. They

2. Demonstration of the causative agent:

Prevention and Control:

(b) BOVINE RESPIRATORY DISEASE (BRD)

(c) PNEUMONIC PASTEURELLOSIS OF CATTLE

(d) PASTEURELLOSIS OF SHEEP AND GOATS

ii) Septicaemic pasteurellosis:

iii) Systemic Pasteurellosis:

(e) AVIAN PASTEURELLOSIS

It is a contagious disease of domestic and wild-birds caused by Past. multocida

Prevention and Control:

It is an infectious disease of cattle, buffaloes and sheep caused by Clostridium

Prevention and Control:

Braxy is an acute infectious disease of sheep caused by Cl. septicum and is

Prevention and Control:

(iii) MALIGNANT OEDEMA

Prevention and Control:

It is a highly fatal infectious disease of all domestic animals caused by the

Prevention and Control:

3) Entero-toxaemia in calves: It is caused by Cl. perfrigens type B and C. Commonly

4) Haemorrhagic enterotoxaemia of piglets: It is caused by Cl. perfringens type C and

5) Enterotoxaemia of foals: It is caused by an unknown type Cl. perfringens and Cl.

Prevention and Control:

(vi) PULPY KIDNEY DISEASE

It is an acute toxaemia of ruminants especially sheep caused by Clostridium

Prevention and Control -

It is an acute, highly fatal toxaemia of cattle and sheep caused by Clostridium

Prevention and Control:

Prevention and Control:

Mastitis means inflammation of the mammary gland caused by varieties of

vii) Leptospiral mastitis: L. interrogans pomona, L. interrogans hardjo causes mastitis,

v) California Mastitis Test:

b) Pendistrin-SH ointment (Sarabhai) 6,00 ml tubes

c) Broacil mastitis ointment (IDPI,)

e) Terramycin Animal formula for Mastitis (Pfizer) 14.2 gm tube

h) Alciclox (Vet) Inframammary (Alembic)

j) Floclox-L infusion (Ranbaxy) Disposable syringe

k) Pivipol solution (Ar-Ex Lab) 100 ml bottle

l) Rifijet intramammary (Intercare) Disposable syringe

o) Cobactan (Intervet) 8 gm syringe

p) Amilox (Pranov Agro) Similar to Cobactan

Technique of administering intramammary preparation :

Sl.No Antibacterial agent Dose per quarter

02. Slightly non irritating 02. Slightly costlier

2) Use of 5% dextrose intramammarily: Recent studies have indicated that

3) Use of Dimethyl sulfoxide (DMSO) intramammarily: Prepare 90 per cent solution

4) Use of corticosteroids intramammarily: Any corticosteroid can be infused

6) Use of Immunoglobulins intramammarily: Recent studies indicated that 150 mg of

3. To overcome dehydration administer balanced electrolyte solution like Arolyte-M

5. To overcome the effect of histamines administer antihistamines like Avil @ 10-20

e) Chronic granulomatous mastitis: As the affected quarter(s) is almost destroyed, the

3% Silver nitrate solution 30-60 ml.

In addition, 30-60 ml of 10% formaline or 50-100 ml of 1:1000 Potassium