Course Title: Large Animal Medicine-II

Course Code: VMS-421

Anthrax
Anthrax is a peracute disease of animals, characterized clinically by septicemia and sudden death.
Etiology
Bacillus anthracis, a spore forming bacteria when exposed to air. It is resistant to normal termperature and
disinfectant. So, carcass of anthrax affected animal should not be necropsied during postportem examation.
Ames strain of anthrax bacteria used in USA as biological weapon in 2001. Vollum strain also suitable as
bioweapon. Spore can viable in soil for 60 years in a rubber stopped bottle.
Epidemiology
Usually all animals are susceptible to anthrax. Livestock, human and elephant are more susceptible as compared
with others. Goat and horses are less susceptible. Dog, cat and alzerian sheep are resistant. Birds seem to be
resistant to anthrax.
Transmission
Ingestion: contaminated feed and water
Inhalation: spore can be transmitted through air
Biting: Biting flies and other insect harbor anthrax organism
Predisposing factors
• Major climate change such as heavy rainfall after prolong drought and flooding, warm and humid weather
• Close grazing of tough scratchy feed in dry times, which causing a abrasion of oral mucosa
• Grazing on heavily contaminated water holes
Sex: Bulls are more susceptible to infections than cows
Age: Lamb and calves are rarely affected
Pathogenesis
Edema factor: inactivate macrophage
Lethal factor: activate macrophage and produce proinflammatroy cytokines (TNF-α, IL-1β). Death due to shock
and renal failure
Clinical findings
a. Peracute form
• Animal become die without showing any symptoms within 1-2 hr
• High fever up to 1070 F, convulsion and dyspnea
• Unclotted blood release through natural opening
b. Acute form
• High fever, dyspnea, weakness, bloat
• Edema around the neck and navel
• Blood discharge through natural opening
• Pregnant animal may aborted
Diagnosis
• History: Incubation period (1-5 days), sudden death, no history of vaccination, outbreak commonly associated
with contaminated area
• Clinical findings:……
• Necropsy findings: swollen lymphnode, enlarged spleen, putrefy quickly
• Laboratory examination: ear vein or tail vein is preferred for diagnostic specimen, bacterial isolation and
identification, laboratory animal inoculation test, serological test (Ascoli ppt test)
Differential diagnosis
• Lightning strike: History of storms and singeing of hair
• Peracute blackleg: restricted to young animals, crepitating swelling
• Leptospirosis: sporadic, hemoglobinuria
• Bacillary hemoglobinuria: Infarct liver
• Snake biting: Local swelling, fang marks
Treatment
• Penicillin and oxytetracycline is sensitive to anthrax orgnanism
➢ Cattle: 5 to 10 million units. Adm. Two equal part at 12 hrs interval for the first 2 days
➢ In severe ill animals: Crystalline penicillin should be administered intraveinously
• Hyperimmune serum 100-250 ml intraveinously in conjunction with daily antibiotic if available
Prevention and control:
• Hygienic measure
▪ Dead animal should be avoided from postmortem examination
▪ Plugging natural opening following death of animal
▪ Buried under 2 meter depth with calcium oxide (quick lime)
▪ Animal house should be properly washed with 10% NaOH/5% Lysol/10% formalin
▪ Special embargo should be put on importation of bone meal or other animal feed
▪ Bedding or other contaminated material should be buried or burned properly
• Vaccination
▪ Cattle: Anthrax spore vaccine 1 ml s.c
▪ Sheep/goat: 0.5 ml s.c beneath the tail

Blackleg /Black quarter/ Quarter evil/ Quarter ill/ Soil borne infection
Black quarter is an acute infectious disease of ruminants caused by Clostridium chauvoei and characterized by
emphysematous swelling in the heavy muscles, severe toxemia and high mortality rate.
Etiology:
Clostridium chauvoei. The organism is killed by 3% disinfectant and may survive in soil for many years.
Epidemiology
Distribution: worldwide distributed
Species: It’s a disease of ruminants, but cattle are usually affected with the disease.
Source of infection: The causative organism naturally presents in the intestinal tract and remain viable in the
soil for many years.
Age: Young and growing cattle are mostly affected. Usually 6 months- 2 years age group is susceptible with
the disease.
Season: Summer and autumn seasons are prone to the disease
Transmission: Ingesion

Pass through the wall of gastrointestinal tract

Gain access into the blood stream

Deposited in the muscles and other tissues

Risk factor: Muscle trauma associated with transportation, herding and handling allow
bacterial proliferation in traumatic injury
Economic importance: It has been reported that 0.04% cattle were affected with BQ in
Bangladesh and mortality rate 50.79% in affected animals.
Clinical findings
Peracute: Animal will die suddenly without showing any premonitory signs,sometimes anorexia,
fever (104-1070 F), tympany, dry muzzle, nasal discharge may observed. Animal will die within 12-36 hrs of infection
Acute: High temperature, marked lameness due to pronounced muscle swelling, crepitating
sound audible on palpation of the affected region, skin discoloration of the affected area and gas escapes from the
diseased muscles, sometimes slough off muscle from the affected region in case of recovered animals from the disease.
It takes 1-2 month to become fully recovered from disease condition.
Diagnosis
• History: Age- 6 months to 2 years age
• Laboratory diagnosis:
▪ Gram’s staining: Gram + ve anaerobic rod shaped bacteria
▪ Anaerobic culture showing characteristic colony of bacteria
▪ Biochemical examination
▪ Immunodiagnostic test
Treatment
▪ Treatment should be provided immediately with observed clinical signs
▪ Anti BQ serum 100-200ml IV is effective , if available
▪ Anitibiotic: Penicillin 10,000 iu/kg, At first crystalline penicillin IV followed by procaine penicillin half dose
IM in affected muscles and rest dose IM in healthy muscles twice daily for 5-7 days
▪ Antihistaminic drugs
▪ Analgesics
Prevention
Hygienic measures
▪ Dead animals should be disposed properly by burning or deep burial method with quick lime to avoid soil
contamination
▪ Contaminated ground should be disinfected with 3% formalin
▪ Vaccination: Formalin killed, Alum ppt bacterin from local strain of Clostridium chauvoei is most effective
Cattle: > 6 months 5 ml SC, Sheep: > 3 months 3 ml SC. Immunity persists for 6 months and repeated after 6
months.

Hemorrhagic Septicemia/ Acute Pasteurellosis

HS is an acute and highly fatal septicemic disease of cattle and water buffaloes. The disease is characterized
clinically by high fever, edematous swelling of throat region, asphyxia and high mortality.
Etiology: Pateurella multocida is a gram negative bipolar organism
Epidemiology
Worldwide distributed. But cattle and buffalo having severe outbreak in south asian region. The disease also has
been reported in camel, bison, elephants, horses etc.
Season: HS may occur in any time of the year. Outbreaks most often appear in rainy season. Because, infectious
organism survive in moist soil and water source.
Transmission: Ingestion, inhalation
Risk factor: Malnutrition, unhygienic condition, parasitic infestation, prolong transfortation without feed and water,
hard working, long time wetting in rainy water, cold environment
Economic importance: 5% cattle and buffalo act as carrier in endemic region. Affected buffaloes having three times
mortality than cattle.

Pathogenesis:
Normally P. multocida localize in the upper respiratory tract (nasopharynx)

Stress condition let the organism get down

Inhaled organism into the alveoli and inflammation of lung (pneumonia)

When organism localized in GIT tract, inflammation of intestine usually occur

Diarrhoea

Ingestion and inhalation: Bacterimia and septicemia

Damage capillaries leads to edema and swelling the throat region

Asphyxia due to respiratory distress

Treatment:
▪ Treatment should be started as early as possible
▪ Anti HS serum 100-250 ml IV at a time
▪ Antibiotic or Sulphonamide drug
▪ Antihistaminic drug
Prevention and Control:
Hygienic measures
▪ Isolation of affected animal and separated from healthy animals
▪ Avoid the stress of animals
▪ Quarantine of new animals
Vaccination
Three types of vaccine usually used for prevention-i) Plain bacterin ii) Alum-type precipitated bacterin iii)
Oil-adjuvant bacterin
In well managed herds: Calves vaccinate at 3-6 months of age, boosted annually
Free range cattle: Vaccinate animals prior to rainy season
 Brucellosis/Bang’s disease/ Malta fever/ Undulant fever
Brucellosis is an infectious disease of man and animals, caused by bacteria genus Brucella sp. The disease is
characterized primarily by abortion at last trimester of pregnancy and subsequent infertility. In human, the disease
referred as undulant fever or malta fever and in cattle it is called as Bang’s disease.
Etiology
Brucella abortus cattle
Brucella melitensis sheep/goat, it’s a most virulent species in man.
Brucella ovis sheep
Brucella suis pig
Gram negative coccobacilli organism.
Epidemiology
• Worldwide distribution
• Species susceptibility: cattle , sheep, goat , swine are very much susceptible
• Sex: Both male and female are susceptible
• Transmission: Ingestion, direct or indirect contact
• Source of infection: aborted fetus, secreted materials from abortion, contaminated milk
• Economic importance
▪ Decrease milk yield, abortion and subsequent infertility
▪ Increase time interval between calving and milk production
▪ Culling due to infertility
▪ Metritis due to retained placenta
▪ Zoonotic importance
▪ In Bangladesh , approximately 60 million money losses in every year from Brucellosis
Zoonotic significance:
▪ Drinking under boiled milk increase the susceptibility of disease
▪ Limited evidence of man to man transmission
▪ Farmers, veterinarian and butcher are very much susceptible to infection
▪ Malta fever in human
▪ Infertility in man due to orchitis
Pathogenesis
Bacteria enter in the body

Phagocytosed by neutrophil

Then, enter into the lymphnode and localized in different organ through blood circulation

Bull: orchitis, epididymitis, diseases in the accessory genital organ

Cow: Fetus erythritol in pregnant animals helps to multiply the organisms

Lesion on the inter cotyledonary space

Acute ulcerative endomentritis

Late abortion
In non pregnant animals: Usually organisms localized in the udder and uterus. If animal become pregnant, in
that case abortion and infertility occur.
Clinical findings
• Late abortion, retained placenta
• If fetus alive, it may weak, immature and become die within few hours
• Orchitis, epididymitis
Prevention and control
➢ Test and slaughter method
▪ Detection and isolation of affected animal
▪ Killing the affected animal and properly disposed the carcass using burning and burial method
➢ Segretion
 ▪Isolation of affected animal from healthy individuals
▪Quarentine method should be performed for imported animals for thirty days
➢ Hygienic measures
▪ Aborted fetus, uterine or placental discharge/secretions should be properly disposed
▪ Contaminated environment should be properly disinfected
▪ Clinician or animal caretaker hand should be cleaned with antiseptic solution
➢ Vaccination
▪ Brucella abortus strain 19 live vaccine. Vaccinate at 4-8 months of age S.C. Immunity persist for 2 years.

Tuberculosis
TB is a chronic wasting disease of animals, characterized clinically by tubercle formation on the affected organ.
Etiology
Mycobacterium tuberculosis is an acid fast organism. Cattle might be act as carrier of disease.
Mycobacterium bovis. Cattle and human
Mycobacterium avium Bird. Human, horse and pig can be affected
Epidemiology
▪ Worldwide distribution
▪ Species: Human, cattle, buffalo, sheep, goat and others animals are also susceptible to disease. TB is an
important disease of dairy cattle. Usually exotic breed cattle are more susceptible than indigenous cattle. In
Bangladesh, it has been reported that 0.62% indigenous and 5.9% cross breed cattle are affected with
tuberculosis.
▪ Sources of infection: contaminated milk, respiratory discharge, contaminated feed and water, exhaled air,
sputum, urine, vaginal discharges and discharges from lymph nodes.
▪ Transmission: Ingestion, inhalation and coitus
▪ Public health significance: Drinking under boiled milk, close contanct and contaminated feed and water.
▪ Economic importance: Test and slaughtering of affected animals, reduce milk production 10-25%
▪ It can occurs throughout the body
Pathogenesis:
Ingestion and inhalation

Organism migrates to the nearby lymph node and phagocytosed by neutrophil

Multiply bacteria in neutrophil

Destroy neutrophil

Release toxin from neutrophil

Macrophage engulfs dead neutrophil and bacteria. Multiplication of epitheloid cell around the dead neutrophil

Tubercle formation

Clinical findings
• Incubation period- 6 months to years
• Clinical findings depends on extent and location of lesions
• General sign include progressive emaciation, lethargy, weakness, anorexia and low grade fluctuating fever
• Involvement of gastrointestinal tract manifested by intermittent diarrhea and constipation in some cases
• In advanced case, lymph nodes are greatly enlarged and causing obstruction of GI tract, respiratory tract and
blood vessels. It may drainage out discharge outside
• Respiratory tract: Broncho pneumonia, emaciation, intermittent coughing, moist cough and dyspnea
• Infected bull or contaminated semen make uterine infection
• Tuberculous mastitis: affected udder showing hard , painless enlargement, milk become watery and greenish
yellow
Diagnosis
▪ History and clinical findings
▪ Laboratory diagnosis
• Culture and staining
• Tuberculin test
 a) Single intradermal test: Inject PPD (0.1ml) s.c at caudal fold of tail or mid neck region

Examine the injected site after 72 hrs of injection

Skin thickness at least 5 mm

b) Short thermal test
c) Stormont test
d) Comparative test
Treatment
Treatment sometimes attempted using human drugs such as Isoniazide, Streptomycin and Para aminosalicylic
Prevention and Control
1. Test and slaughter method
• This technique is not applicable for poor country
• Isolation of affected animal from healthy animals
• Attendant of affected animal should be isolated from healthy animal
2. Quarantine
3. Hygienic measures
• Feeder and water trough should be washed with 5% phenol/cresol
• Contaminated milk should be avoid drinking to calf
4. Vaccination: There is no effective vaccine for animal
BCG vaccine for human is used for animal: 50-100 ml S.C –mildly effective

Jhone’s disease/ Paratuberculosis

It is a disease of domestic animals caused by bacteria Mycobacterium paratuberculosis. The disease is
characterized clinically by emaciation, chronic diarrhea, and intestinal wall become thickened and corrugated.
Etiology: Mycobacterium avium paratuberculosis, formally known M. paratuberculosis
Epidemiology:
• Worldwide distributed
• Age: The susceptibility of organism increases resistance with age. Animals usually infected under 30 days of
age, but clinical signs rarely develop in cattle under two years of age
• Predisposing factors
▪Infective dose
▪Age
▪Alkaline soil increase the susceptibility of disease
▪Stress (parturition, transportation, nutritional deficiencies or excess and immunosuppressive agents)
• Transmission:
▪Ingestion (feed, water & colostrum)
▪Intrauterine infection
Pathogenesis
• Non-pregnant

Multiply in the mucosa and sub-mucosa

Decrease nutrient absorption

Prolong diarrhea causes hypoproteinemia and muscle wasting

• Pregnant

Macrophage engulfs bacteria and enters into the mammary gland

Congenital infection

Clinical findings
• Incubation period: 6 months to 2 years
• Clinical signs are rarely appear before 2 years
 • Chronic or intermittent diarrhea, accompanied by gradual body weight
• Diarrheic feces do not contain blood, mucus or epithelial debris and passed without tenesmus. It does not
respond to astringent therapy
• Animals are alert, temperature and appetite are usually normal
• General signs include unthriftyness, rough hair coat, reduced milk yield, rectal temperature may or may not be
elevated
Necropsy findings: Thickened intestinal wall, mesenteric and ileo-cecal lymphnodes are enlarged and edematous.
Diagnosis
• History
• Clinical findings
• Allergic test (Paratuberculin test/ Johnin test)
Treatment
The organism is more resistant as compared with M. tuberculosis
Stremptomycin 50mg/kg for transient improvement
Dihydrostreptomycin 500 mg/kg I.M
Rifampicin 300 mg with Isoniazide 300 mg orally twice daily
Prevention and Control
1. Management of herd
• Culling the affected animal by hypersensitivity test (Johnin test)
• Examine the affected animal before introduction into farm
• Avoid the mixing of carrier or affected animals with healthy individuals
2. Hygienic measures
• Prevention of further spread of infection
▪ Feeding and water trough should kept in high position from the ground
▪ Stalls and building should be properly washed with disinfectant
3. Vaccination
a. Live vaccine (Vallee’s vaccine): usually used in european country
b. Killed vaccine: calf (1-35 days of age) S.C at a time

Why Paratuberculosis control is very difficult in cattle?

▪ It is very difficult to control and impossible to eradicate Johne’s disease due to asymptomatic carrier, infected
but neither ill or nor shedding enough bacteria to be culturally detectable.
▪ Complete cleaning and restocking of a farm is very difficult

Leptospirosis
Leptospira is a spirochete-double membrane bacterium. Flagella present between inner and outer membrane of
bacteria. The disease Leptospirosis is caused by Leptospira sp. in different animals including mammals, birds,
amphibians and reptiles. It is characterized clinically by septicemia, interstitial nephritis, hemolytic anemia and abortion.

Etiology:
Leptospira interrogans sv pomona- pig
Leptospira interrogans sv hardjo-cattle, human (dairy cattle worker)
Epidemiology
▪ Worldwide distributed
▪ Species susceptibility: cattle, buffalo, sheep, goat, dog, cat etc. Sheep and goat are less susceptible as compared
with cattle. Rat and wild animal act as carrier of the disease. The reservoir hosts are highly susceptible to disease
but they are low pathogenic.
▪ Age: Adult animals are highly susceptible as compared with young
▪ Sources of infection: urine of the infected animals, aborted fetus, uterine secretion , contaminated feed and water
▪ Transmission
•Ingestion
• Direct contact with mucous membrane (buccal cavity , conjunctival mucus membrane)
•Transplacental
•Insemination
•Venereal transmission by coitus
Pathogenesis
Infection

Organism multiply in the liver

Hepatic necrosis (individualization of hepatic cell)/ insufficiency

Organism multiply in the blood

Endotoxin from organsim

Septicemia and intravascular hemolysis

Hemoglobinuria

Human encephalitis
Female animal agalactia, mastitis and late abortion
Male animal orchitis
Man is susceptible to all serovers.

Clinical findings
• Incubation period 2-4 weeks
• Acute: septicemia, high fever, anorexia, hemoglobinuria, anemia, dyspnea, abortion in pregnant animals,
mastitis and still birth
• Chronic : abortion and encephalitis
• Human: headache, arthritis, vomition and myalgia
Diagnosis
• History….
• Clinical findings….
• Laboratory diagnosis:
Treatment
Chlortetracycline and oxytetracycline have been reported to be successful in cattle. Human- Doxycycline 100
mg orally at 12 hrs interval for 5-7 days.
Prevention and control
▪ Hygienic measures
• Prevent the spread of infection from infected or dead animals
• Avoid the entrance of rat or wild animal in the farm
• Prevent the contact of farm animal with wild animal
• Isolation of affected animals and culling them from the farm
▪ Chemoprophylaxis: 800 gram oxytetracycline/ton feed for 8-11 days
▪ Vaccination
• Formalin inactivated bacterin
• Vaccinate the animals at 4-6 months of age and revaccinate annually
• Vaccinate pregnant animals and calves get immunity through colostrums from mother

Enterotoxemia
The disease is caused by different type of toxin released from Clostridium perfringens . Overeating to the
animals increase the susceptibility of disease. So, it is also called overeating disease.
Etiology
Clostridium perfringens type B, C
B- Lamb dysentery, calf enterotoxemia
C-Goat enterotoxemia
Epidemiology
• Worldwide distributed
• Age: Young animals are highly susceptible
• Source of infection: Feces of the infected animals
• Transmission: Feeding contaminated feed and water
Pathogenesis
When animal eat excessive amount of feed

Decrease the tonacity of ileum

Vegetative stage of organism (anaerobic condition of intestine increase the susceptibility of disease)
Diagnosis
• History..
• Clinical findings….
• Laboratory diagnosis..
Treatment
▪ Inject hyperimmune serum 25-50 ml i.v twice daily at a time
▪ Antibiotics or Sulphadimidin
▪ Supportive treatment: Infuse normal saline I.V. Hyperglycemia usually occurs in enterotoxemia. So, Dextrose
saline is contraindicated in affected animals.
Prevention and Control
▪ Optimum balanced diet should be provided to the animals
▪ Avoid excessive feeding to animals
▪ Chemoprophylaxis: Chlortetracycline or Oxytetracycline mixed with feed (22mg/1 kg feed)
▪ Vaccination
• Type B, C Bacterin or toxoid used as vaccine
• Pregnant animal vaccinate in enzootic area
▪ 1st vaccine: 1.5 month before parturition
▪ 2nd vaccine: 2 weeks before parturition
• Young animals get antibody through colostrums

Enlist the clostridial diseases of animals with their causal agents

Component release
Disease Causal agent Host
from bacteria

Botulism Clostridium Botulinum Toxin Birds, animals and man

Black leg C. chauvoei Toxin and gas Ruminants
Malignant edema C. sordelli Toxin and gas Animals and human
Braxy C. septicum Toxin and gas Sheep
Black disease C. novyi Toxin and gas Sheep/Goat
Bacillary
C. hemolyticum Toxin and gas Cattle, Sheep and pig
hemoglobinuria
Enterotoxemia C. perfringens Toxin and gas All animals
Tetanus C. tetani Toxin Animals and human

Tetanus/Lock jaw
Tetanus is an infectious zoonotic disease affecting almost all mammals caused by toxin, released from
Clostridium tetani and characterized clinically by hyperesthesia, convulsion, stiffness of muscle and death due
to respiratory failure.
Etiology
Clostridium tetani, a gram +ve, anaerobic with terminal spore former organism. Spore can persist in soil for
many years. It is resistant to steam heat at 1000C for 30-60 minute, but destroyed at 1150C for 20 minutes.
Epidemiology
Distribution: Worldwide distributed and prevalent in tropical country.
Species: cattle, buffalo, sheep, goat, camel, horses are most susceptible. Dog, cat and birds are somewhat
resistant
Sources of infection: Fecal material, soil
 Pattern of disease: Tetanus usually sporadic disease, but it can occur as epidemic form in cattle, young pig,
lambs and kids.
Transmission: Through deep punctured wound
Mortality rate: Mortality rate higher in young ruminants and adult cattle have recovery rate
Risk factor: Castration, shearing, docking, vaccination, punctured wound in the hooves of horse, injury to
coronet in cattle during ploughing time
Pathogenesis
Portal of entry of organism through deep punctured wound

Toxin produced from bacteria within 4-8 hours

Neurotoxin/ tetanospasmin absorbed by nerves

Spasmodic, tonic convulsion and death due to asphyxia (fixation of muscles of respiration)
Clinical findings
▪ Incubation period 1-3 week
▪ Stiff gait, prolapse of third eyelid
▪ Difficulty in swallowing, general muscle stiffness in other parts of the body
▪ Regurgitation of feed and water
▪ Secondary aspiration pneumonia is a potential sequel
▪ Animal become dehydrated due to lack of water intake, hypersalivation and profuse sweating
▪ Hyperesthesia, titanic convulsion following external stimuli (So, animal should be keep in dark condition)
Diagnosis
▪ History……
▪ Clinical findings….
▪ Necropsy findings:
• No gross or histopathological changes observed in dead animals. But hyperemia and hemorrhage in lungs
due to asphyxia.
▪ Laboratory diagnosis: Isolation and culture of causative bacteria, the organism can n’t ferment carbohydrate
▪ Differential diagnosis
• Strychnine poisoning (uncommon in farm animals)
• Hypocalcaemic tetany (confined in lactating mares and respond to calcium salt)
• Acute laminitis
• Lactation tetany
Treatment
A) Principle of treatment include
i) Elimination of causative bacteria
• If infection site is found, it should be treated locally. Administered anti toxin serum locally in the wound
and after 1 hour remove debridement from infection site using H 2O2. Direct application of H2O2 in the
wound facilitates absorption of toxin.
• Parenteral and local administration of procaine penicillin @ 25000 IU/kg bw twice daily for 3 to 5 days,
followed by once daily for next 5 days.
• Neutralization of residual toxin: Tetanus antitoxin 1500 IU IM daily for 3 to 5 days
• Relaxation of mucscle: Acetyl promazine 0.05 mg/kg IM twice daily; Xylazine 0.05 to 0.1 mg/kg b.w.
B) Supportive treatment: Animal should be kept in dark, quite and well bedded place
Prvention and control
• Sterilization of instrument before surgical operation such as castration, docking and shearing
• Inject Tetanus Toxoid gives immunity after 2 weeks of vaccination and persist up to 1 year
• Prevention of vaccination in lamb is achieved by vaccinating ewes at last 2-3 weeks of gestation .

Salmonellosis
Salmonellosis is an important disease of all animal species, characterized clinically by i) peracute septicemia ii)
acute enteritis and iii) chronic enteritis.
Etiology
Horse: Salmonella typhimurium, S. newport
Cattle: S. typhimurium (both man and animal), S. Dublin, S. Newport
Gram –ve, pleomorphic, produce potent endotixin and secretory diarrhea within the gut
 Importance: Universal occurrence, all animal species affected, high mortality rate and abortion, public health
significance.
Epidemiology
Worldwide distribution
Age: Particularly neonatal animals are severely affected.
Species: Pigs are most susceptible followed by cattle and horse
Pathogen factor: Organisms are facultative intracellular organisms that survive in the phagolysosome of
macrophage and can evade bactericidal effects of antibody and complement.
Transmission
• Carrier animals- T
• he organism usually persists in lymphnode and tonsil. But can n’t pass with feces.
o Ingestion: contaminated feed and water. Salmonella can survive up to 6 years in dried bovine feces.
Risk factor
• Animal risk factor
▪ Long time transportation
▪ Intercurrent disease
▪ Acute deprivation of feed and water
▪ Parturation
▪ Surgery
▪ Immunity
▪ Age of animals
• Environmental and managemental factor
▪ Intensive pasturue utilization
▪ Pasture contaminated by cowdung, other animal feces and human sewage
▪ House animals are susceptible as compare with grazing animals
▪ Introduction of infection in farm
▪ Contaminated feed stuffs, carrier animals
▪ Free flying birds, wild animals
• Pathogen risk factor
▪ Facultative intracellular organism
▪ Pleomorphism causing antimicrobial resistance
Economic importance
• Loss of money due to diagnosis, treatment and death for clinical diseases
• Cleaning and disinfection
• Reduced feed conversion and weight gain
Clinical findings
Septicemia
• Newborn foal and young pigs upto 4 months are usually affected
• High fever (105-1070 F), dullness, depression and death within 24-48 hr
Acute enteritis (common in adult mammal)
• High fever (104-1060 F)
• Diarrhea, sometimes dysentery
• Feces have putrid smell with blood and mucus
• Abortion in pregnant cows
Chronic enteritis
• Survivors from acute enteritis may remain chronic
• In calves, intermittent diarrhea, occasional passage of blood spot and fibrinous cast
Diagnosis
▪ History
• High morbidity and moderate mortality
• Most common in animals up to 3 months of age
• Enzootic in particular feed-lot farm
▪ Clinical findings….
▪ Laboratory diagnosis
• Determination of leukocyte abnormalities
▪ Marked leucopenia, neutropenia with enteric salmonellosis
▪ Fecal leukocytes on the fibrin tags
 • Confirmatory diagnosis
▪ Isolation and identification of the causative agents
▪ Serological test
Treatment
1. Antimicrobial therapy
• Trimethoprim-sulphonamide is effective as both parenteral and oral therapy. Because it can penetrate
the phagocyte.
❖ Use of antimicrobial for the treatment of clinical salmonellosis is controversial due to the different
response to treatment.
❖ Antibiotic resistance
❖ Carrier of the disease
2. Supportive treatment
• Fluid therapy for shock management
• Astringent preparation for the treatment of diarrhea
• Frequent feeding with small amount of milk advisable.
Prevention and control measures
1. Hygienic management
a) General princinples
• Eliminate stress and environmental contamination
• Colostrum feeding
b) Prevention of introduction of infection
• Animals should be avoid from sources of infection
• Prevention of introduction of infection or carrier animals
• Introduction of animal in farm, which is free from salmonellosis
c) Limitation of spread of infection within a herd
• Isolate the infected animals from healthy individuals and provide vigorous treatment
• Prophylactic use of antimicrobials like oxytetracycline 55 mg/litre
• Feeder and water trough should be avoided from sources of infection
• Proper disinfection of the animal sheds
• The persons who working in infected farm should be concerned on their own health
2. Immunization
• Killed bacterin and live attenuated vaccines are available
• Prenatal vaccine provide immunization of the newborn
• Vaccination of pregnant cattle with formalin killed S. typhimurium vaccine at 2 weeks before parturition
protect their calves against infection

Colibacillosis
Colibacillosis is one of the most common disease of newborn farm animals caused by pathogenic E. coli,
characterized clinically by a) Septicemia, manifested by severe illness and rapid death in severe hours b) Enteric
form manifested by diarrhea, dehydration, acidosis and death.
Etiology
Escherichia coli, Gram –ve, aerobic, rod shape and endotoxin producing bacteria. It has three antigen-somatic (O),
capsular (K) and flagellar (H) antigen.
❖ Enterotoxigenic E. coli colonize in the intestine

Produce toxin which are not invasive and produce enteritis by adherence and colonize on the intestinal wall

Diarrhoea
❖ Necrotoxic E. coli (NTEC) produce cytotoxic necrotizing factor CNF1 and CNF2. NTEC2 restricted to calves
and lambs with diarrhea and septicemia.
❖ Serotype O157H:7 and act as reservoir for cattle. Hemorrhagic colitis usually produced by this serotype. O78-
septicemia in calves and piglets.
Epidemiology
• Distribution: worldwide distributed
• Animal risk factor
▪ Young animals (calves, lambs and kids) are in high risk to the disease
▪ Most common in animals under 3 days of age. It may occur as early as 12-18 hr of birth
 ▪ Enterotoxigenic E. coli found in calves, rarely in adult cattle
▪ Age related resistance developed as the calf become older
▪ Animals which take inadequate amount of colostrums are highly susceptible
• Immunity
Normally newborn are agammaglobinemic, so it need colostrums Ig within hrs of birth to obtain protection.
Colostrum absorption occurs during the first 6-12 hrs of birth and decreases rapidly from 12-24 hrs after birth.
• Environment and management risk factor
▪ Weather condition: High environmental temperature, sudden change of weather, windy and cold
weather etc. increase the risk of outbreak of diarrhea.
▪ Nutritional and feeding method: a) Heat denatured skim milk increases the susceptibility of diarrhea b)
Irregular feeding practice c) General or specific nutritional deficiency-lack of energy, protein or vitamin
A
▪ Standard housing and hygiene: Overcrowding and unhygienic condition increases the susceptibility of
infection.
▪ Source of infection and disease transmission: a) contaminated feed and water with feces, vaginal and
uterine discharge, and coliform mastitis milk b) Transmission by ingestion and direct contact with
nasopharyngeal mucosa (meningitis)
• Pathogen risk factor
▪ K99+ enterotoxigenic E. coli are major virulent strain as compared with other serotype
▪ O78 septicemic E. coli are invasive
▪ Enterotoxigenic form are not invasive
▪ Animals which recovered from disease can suffer from localized infection in different site of the body
(joint, brain)
Pathogenesis
Enterotoxigenic E. coli in intestine

Increase adenyl cylase enzyme

Convert ATP to cAMP

Increase secretion in the intestine

Diarrhea causes excessive loss of fluid from the body

▪ Hemoconcentration and circulatory shock lead to death

▪ Increase acidosis
▪ Hyperkalemia
▪ Severe hypoglycemia due to reduce rate of conversion of lactic acid to glucose
Clinical findings
1. Coliform septicemia
▪ Animals are weak, depressed, dehydrated and presence of tachycardia
▪ Initially temperature may be high but rapidly to subnormal when animals become severe weak and
moribund stage
▪ Postsepticemic localization may appear in about one week in survival cases (arthritis, meningitis,
panophthalmitis)
▪ Course may vary from 24-96 hr. Survival rate less than 12%
2. Enterotoxigenic colibacillosis
▪ It occurs usually 3 to 5 days of age
▪ Profuse watery to pasty, pale yellow to white color diarrhea
▪ Blood fleck (small spot) and very foul smelling feces
▪ Tail and perineum soiled with feces
▪ Diarrhea causes severe dehydration and acidosis
Diagnosis
▪ History….
▪ Clinical findings…
▪ Laboratory examination
✓ Isolation and identification of causative bacteria by culture and biochemical examination
 ✓ Ferment lactose to rose pink color
✓ Serological test: ELISA. CFT
Differential diagnosis

Sl.
Disease Age Septicemia Diarrhea
no.
1. Enterotoxigenic E. coli 3-5 days +/- +
2. Salmonellosis 5-42 days + +
3. Clos. Perfringens B &C 5-15 days - +
4. Rota viral diarrhea 5-15 days - +
5. Corona viral diarrhea 5-21 days - +
Parvo virus and bovine viral
6. >14 weeks - +
diarrhea
7. Coccidiosis >30 days - +
8. Cryptosporidiosis 5-35 dats - +

Treatment
A. Coliform septicemia
▪ Detection of drug sensitivity: selection of antimicrobials , fluid and
electrolytes therapy
B. Enteric colibacillosis
▪ Fluid and electrolytes therapy
▪ Antimicrobial therapy
▪ Immunoglobulin therapy
▪ Antimotility drugs and intestinal protectant
▪ Alteration of diet
Prevention
1. Reduce the exposure of newborn to the infectious agent
▪ Hygienic management during parturation
▪ Cleaning perineum and udder with antiseptic solution
▪ Isolation of affected animals from healthy individuals
2. Provide maximum non specific resistance
▪ Provide adequate balanced diet to cow
▪ Feeding colostrums to newborn
▪ Adequate space for newborn animals should be provided
3. Vaccination
▪ Pregnant cow
▪ Newborn calf
✓ Vaccinate cow at 2-4 weeks before parturation. In that case calf will receive Ig from dam through milk.
✓ Neonatal calf feeding with K99+ monoclonal Ab
✓ Recombinant vaccine

Mastitis
The term mastitis comes from Greek word mastos-breast, itis-inflammation. Inflammation of the mammary gland
is called mastitis, which is characterized by physical, chemical and bacterial changes in the milk and pathological
changes in the glandular tissue.

Physical-discoloration, presence of clots and flakes

Chemical-Sodium or chloride increased
Pathological-Bacteria and leukocytes are increased in milk (≈ 98-99% WBC + 1-2% epithelial cells)
Changes in glandular tissue: redness, swelling, heat and pain on palpation
Clinical mastitis:
- Swelling, hot, pain and induration (increase fibrous element in tissues)
-Presence of clotted milk and flakes
Subclinical mastitis:
-No palpable abnormalities
-Increase total leukocyte count and bacteria
Etiology
1. Contagious pathogen
Streptococcus agalactiae
Staphylococcus aurus
Mycoplasma sp.
2. Envirnomental pathogen
Strep. uberis
Strep. dysagalactiae
Escherichia coli
3. Mycoplasmal infection
M. bovis
M. bovigenitalium
4. Fungal infection
Trichosporon spp.
Aspergillus fumigates
Candida albicans
4. Algae infection: Prototheca trispora
Epidemiology
• Worldwide distributed including Bangladesh
• Species: All mammals are susceptible
• Stage of lactation: Early first 2 months of lactation
• Age: 3rd lactation in cows, 4th lactation in buffaloes
• Percentage of risk factor
✓ Inadequate milking hygiene (75%)
✓ Equipment malfunction (20%)
✓ Cow factors (5%)
• Sources of infection
▪ Traumatic injury due to injured teat, vigorous sucking of teat and defective milking machine
▪ Environment: Trauma, soil, wash cloths, milker’s hand, milking machine cups due to milking from
infected quarter
• Economic loss
▪ Loss of milk production -70%
▪ Decreased milk yield-7%
▪ Culling of cows due to infected quarter-14%
▪ Treatment cost-8%
▪ Miscellaneous-1%
• Public health significance: Tuberculosis, streptococcosis, brucellosis and antibiotic residue in milk
Pathogenesis
• Invasion-organism passes from the exterior of the teat to milk in teat canal
• Infection-multiply rapidly in mammary tissues and inflammation
• Gram +ve mastitis: Exotoxin release from bacteria and causes death of the duct and alveolar cells

Edema and death of the mammary tissues

• Gram–ve mastitis: Systemic effects from endotoxin. Animals usually die by septicemic shoock.
Clinical findings
a) Peracute mastitis
• Swelling, heat, pain and abnormal secretion from udder
• Serous milk
• Accompained by fever and other systemic signs (depressed, rapid pulse rate and anorexia)
b) Acute mastitis
• Swelling, heat and pain like peracute symptoms
• Clotted blood,pus and flakes in the milk
• Fever, dullness and depression are slight to moderate
• Swollen supra mammary lymph node
c) Sub acute mastitis
• No systemic changes
• Changes in the udder is less observable
 d) Chronic mastitis
• Cow remain infected more than 100 days
• Three or more quarter become infected per lactation
• Watery milk
• Fibrosis of the affected teat
e) Subclinicl mastitis
• High somatic cell count without any visible abnormality of the milk and udder
• No inflammatory reaction detectable
Diagnosis
• History
✓ Herd management
✓ Milking system
✓ Milk hygiene
✓ High somatic cell count (>500,000 neutrophil/ml)
• Clinical findings
✓ Swelling , heat , pain and abnormal secretion from udder
• Laboratory diagnosis
✓ Milk pH : Normal 6.4-6.8 , mastitis milk > 6.9
✓ Chloride test: Increase chloride in milk
✓ Leukocyte detection
▪ White side test: 5 drops milk + 2 drops 4% NaOH-clotted milk detect +ve mastitis
▪ California mastitis test: 2 ml milk + reagent (Alkylaryl sulphate)- Gelly consistency of milk
✓ Bacteriological isolation: Culture and staining
Treatment
• Peracute case
✓ Systemic and intramammary antibiotics therapy
✓ Anti inflammatory drugs
✓ Oral and intravenous fluid therapy
• Acute case
✓ Systemic and intramammary antibiotics for 3 days
• Subacute case
✓ Intramamary antibiotics for 3 days
• Supportive treatment
✓ Streptokinase enzyme has been used to liquefy and discharge pus and blood clot
✓ Corticosteroid injection reduce inflammation
✓ Antihistaminic drugs: Extensive tissue damage and severe inflammation
✓ Application of cold: Crushed ice suspended around the udder which reduce the absorption of toxin
✓ 5% Dextrose saline, if no fever
✓ Oral administration of cobalt to enhance antibiotic activity
✓ Oxytocin for milk letdown
✓ Strip quarter every 2 hrs
Summer mastitis
The disease is common in European country in non lactating heifer and cows at pasture in summer and wet
weather. The disease is most prevalent in summer and rainy season. Severe systemic reaction and abscess
develop in the udder by Actinomyces pyogenes.
Prevention and control measures
✓ To prevent the spread of infections from diseased to healthy animals
▪ Isolation of affected animals and provide treatment
▪ Examine the newly purchased cow at least in two occasion before introduction into a new herd
▪ Reservoir animal should be culled from the herd in case of non satisfactory treatment
▪ Wearing gloves before milking
▪ Isolation of affected animal form healthy cow
▪ At first milking healthy cow followed by mastitis affected cow
▪ Milker’s hand, udder, teat should be properly cleaned with antiseptic solution before milking
✓ Environmental hygiene
▪ Animal house should be properly cleaned two times daily
▪ Avoid overcrowding of animals
▪ After calving, animal house should be cleaned with disinfectant solution
 ▪ Regular feeding of cow with vitamin E, selenium, copper or zinc can prevent the animal from mastitis

Actnomycosis/ Lumphy jaw

Actinomycosis is a chronic suppurative and granulomatous disease of man and animals, caused by Actinomyces
bovis and characterized by rarefying (make thin) osteomyelitis of the bones of the head, particularly maxilla
and mandible and suppurative granulomatous tissue reaction and involves soft tissue of gastrointestinal tract.
Etiology
▪ Gram +ve pleomorphic, anaerobic and non spore forming organism
▪ Organism microscopically appears ‘ray fungus’. Greek word Aktis-ray, Mykes-fungus. Organism from clump
called ‘sulphar granule’.
Epidemiology
▪ Worldwide distributed
▪ Pattern: Sporadic in nature
▪ Species susceptibility: Primarily cattle and secondarily swine and horse
▪ Source: Organisms are normal flora of oral cavity and nasopharyngeal mucosa. So, infections originated from
endogenous source.
▪ Risk factor: Abrasion or penetrating wound of the oral mucosa that allows it to gain access into deeper tissue
Clinical findings
▪ Bone of the maxilla and mandible particularly at the level of central molar teeth.
▪ Swelling of tissues due to proliferation of fibrous connective tissue and leukocyte infiltration making tumor like
mass
▪ Swelling are very hard, immovable and painful to touch
▪ Lesion on the mandible interfere prehension and mastication.
▪ Discharge of pus is sticky, honey like consistency and white-yellow granule
▪ Involvement of soft tissue like esophageal groove, reticulum causing impair digestion
Diagnosis
• History: Eating coarse spiny grass material, eruption of teeth
• Clinical findings: Swelling maxilla and mandible, sulphur granule in the pus
• Laboratory diagnosis: pus diluted with 10% NaOH and gently crushed under cover slip, Gram staining (Gram
+ve, pleomorphic organism)
Treatment
• Surgically removal of pus and prolong chemotherapy
• Ampicillin and amoxicillin have an advantage over penicillin
• Sodium iodide solution 10% 1gm/kg IV; potassium iodide 6-10gm/day for 7-10 days

Actinobacillosis
Actinobacillosis is chronic infectious disease caused by Actinobacillus lignieresii, and characterized by lesion
consists of multiple, hard and granulomatous abscess in soft tissues of the head, upper alimentary tract and
associated lymph nodes.
Etiology
Gram-ve, coccobacillary organism. It appears single or short chain sulphur granules.
Epidemiology
• Worldwide distributed
• Species susceptibility: cattle, sheep, pigs, horses etc.
• Pattern: Sporadic in nature
• Sources of infection: normal flora of gastrointestinal tract,discharges from saliva, feces, contaminated feed and
water
• Treansmission: Ingestion
Clinical findings
• Glossal actinobacillosis
✓ Tongue is swollen and hard
✓ Unable to prehension and mastication
✓ Excessive salivation
✓ Nodules and ulcer formation on the tongue
✓ Active inflammation replaced by fibrous tissue
• Lymphadenitis
✓ Visible and palpable enlargement of retropharyngeal and sub-maxillary lymph nodes
 ✓ Loud snoring respiration
✓ Ruptured enlarge lymphnode release thin odorous pus
✓ Center of the nodule showing minute granule
Diagnosis
History: Injury of the oral cavity due to feeding coarse material, sharp grass and hay
Clinical findings
Laboratory diagnosis: Culture and staining (Grm+ve), biochemical test
Treatment
• Topical and systemic iodide administration
• Parenteral antibiotic therapy

Foot-rot/ Interdigital Necrobacillosis/ Foul in the foot

Foot-rot is an infectious bacterial disease of animals especially cattle, sheep and goat which is characterized by
inflammation of the sensitive tissues of the feet and severe lameness.
Etiology
Fusobacterium necrophorum
Spherophours necrophorum
Bacteroides noduses
Epidemiology
• Worldwide distribution
• Age: All age groups are susceptible but common in adult
• Breed: Exotic breed cattle are more susceptible than zebu cattle
• Climate factor: Wet humid weather, rainy season,
• Sources of transmission: Discharges from the affected feet
• Transmission: Abrasion to the skin of feet.
Clinical findings
• Moderate fever
• Lameness of the affected foot
• Anerexia
• Foul smelling discharges from the affected foot
• Decrease milk production
• Sometimes hoof may slough off due to untreated cases
Diagnosis
• History
• Clinical findings
• Laboratory diagnosis: Gram staining
Treatment
• Topical application:Foot bathing with copper sulphate (5%), formalin (2%) or zinc sulphate solution (10%) may
be applied by brush to the lesion and it will give excellent result
• Systemic treatment : Antibiotic, antihistaminic and anti inflammatory drugs
Prevention and Control measures
• Foot bathing with copper sulphate 5% or formaline 5%. Cattle walk through foot bath twice daily can eliminate
lesion.
• Chemoprophylaxis (Organic iodide/ Oxytetracycline)
• Hygienic management of the animal shed.

Strangles/Equine Distemper
It is an acute highly infectious disease of horse caused by Streptococcus equi and characterized by inflammation
of the upper respiratory tract and associated lymphnodes with abscessation. It causes enlarged lymphnodes
between jawbones, which strangle the respiration. Hence, the name for the disease is strangles.
Epidemiology
The disease was worldwide distributed. The disease has been recognized as early as 1700s
Pattern: Endemic in domesticated horse population in worldwide.
Age: Any age group of horse can be affected with the disease
Immune response: Immature animals have lower immune response with the disease. So, they have higher
susceptibility to disease as compared with adults.
 Risk factor: poor nutrition, overcrowding, cold weather, poor ventilation, prolong transformation, pre existing
disease etc.
Economic importance
✓ Diseased animal cannot used for training purpose
✓ Reduced performance time, breeding rate
✓ Treatment cost and troublesome control measures
Transmission
✓ Contaminated pastures, barns, weather, feeding trough
✓ Direct contact
Source of infection: Nasal secretion, pus from infected site
Clinical findings
✓ Incubation period 3 to 21 days. Clinical signs persist for 3 to 7 days, but it may persist up to 2 weeks
✓ Clinical signs depends on severity of infection
✓ Common signs includes inappetance, fever, listlessness (nasal discharge), swelling lymph nodes around the head
and neck
✓ In most severe cases, swelling lymph node causes abnormal respiratory noise.
✓ To relive pressure on throat, affected horse showing stretched neck
✓ Mild case: lethargic, malaise
✓ Severe case: Swelling lymph node, painful condition to touch and drainage pus from lymph node
✓ Possible complication includes asphaxia due to swollen lymph nodes, guttural pouch filled with pus, purpura
hemorrhagica, heart disease
Diagnosis
✓ History, Clinical findings
✓ Laboratory diagnosis

Treatment
✓ Drainage out of pus from abscess and washing with antiseptic solution
✓ Penicillin is effective for treatment. Penicillin 15000 IU/kg i.m; Tetracycline 5-10 mg/kg
Prevention and control
In the outbreak area, horse can be segregated in to three groups
a) Those affected with the disease should be treated, but not vaccinated
b) Horse with no known contact should be vaccinated
c) Horses known to have been contact should be observed for 7 to 10 days. If no fever and clinical findings,
then vaccinate the horse
✓ Quarantine and restrict the movement of horse for 8 weeks
✓ Disinfection of stalls, water bucket, feeding and water trough
✓ Sanitize any equipment exposed to the infected animals
✓ Vaccination: Provide immunity for 6 months to 1 year. Booster vaccination to maintain adequate
protection.

Glanders
Glanders is a highly contagious and fatal disease of equidae family with zoonotic potential, caused by infection
with the bacterium Burkholderia mallei and characterized by nodular lesions of the lungs and other organs as
well as ulcerative lesions on the skin and mucous membrane of the nasal passage.
Epidemiology
Distribution: Once upon a time glanders was distributed throughout the world. Now it has been eradicated from
the world through screening programme (Test and slaughter method). The countries include North America,
Australia and most of the European countries are free from glanders. It is now limited to parts of Africa, Middle
East and Asia.
Species: Solipeds (single hoof) are mostly susceptible to disease. It includes horse, donkey, mule etc. Carnivores
are susceptible to disease, if they consume glandered meat. Sheep, cattle, swine are restricted to infection.
Human: Nodular eruption on the face, legs, arm, nasal mucosa and metastatic pneumonia may occur
Transmission: Ingestion of contaminated feed and water, direct contact with mucous membrane and inhalation
Sources of infection: Nasal discharge or exudates, discharges from the ulcerated skin
Clinical findings
Acute: High temperature up to 1060 F, thick muco-purulent nasal discharge, death due to septicemia. Acute
phage of the disease mostly confined in donkey.
 Chronic: Debilitating condition, nodular ulcerative lesion on the skin and nasal mucosa, enlargement of lymph
node, ulcerative lesions are usually replaced by stellate scar
Forms of glanders
Nasal form
✓ Unilateral or bilateral nasal discharge, yellowish-green exudates from nostril
✓ Nodules and ulcer on the nasal mucosa
✓ Nasal ulcer heal as stellate scar
Cutaneous form (Farcy)
✓ Multiple nodules may develop on the skin of the legs or other parts of the body
✓ Nodules may rupture and leave as ulcer and discharges yellowish exudates
✓ Nodular lesion on liver and spleen
✓ 95% mortality in untreated cases within 3 weeks
Pulmonary form
✓ Lesions on the lungs may develop with nasal and cutaneous lesions
✓ Nodules are gray, white and firm surrounded by hemorrhagic zone
✓ Discharges from ruptured nodule
✓ Dyspnea, severe coughing
✓ Liver and spleen also affected with the disease
Diagnosis
✓ History
✓ Clinical findings
✓ Laboratory diagnosis: Mallein test-sensitive and specific clinical test for glanders, serological test-CFT, ELISA
✓ Differential diagnosis
• Strangles: Bilateral nasal discharge. Unilateral discharge in ganders cases
• Enzootic lymphangitis: Histoplasma farciminosum causing characteristic nodule on the skin
• Ulcerative lymphangitis: Corynebacterium pseudotuberculosis causing dermatitis and abscess
formation
Treatment
• Tetracycline, ciprofloxacin, gentamycin and sulphonamide drugs are sensitive to this orgnasims
• Sulphonamide drugs are traditionally used in human glanders cases
• Destroyed affected animal is the best choice to avoid the spreed of infection
Prevention and control measures
• Hygienic measures
• Quarantine
• Restriction of movement of affected animals
• Avoid the contact of affected animals with healthy ones

Foot and mouth disease (FMD), Apthous fever or Tiger heart disease/
Vesicular Aphtha
Foot and mouth disease is a highly contagious acute disease of all cloven footed animals caused by Aphthovirus
and characterized clinically by fever and vesicular eruption in the mouth and feet.
Etiology
Genus: Aphthovirus
Family:Picornaviridae
There are seven serotypes of FMD. A, O, C, Asia-1 and Southern African Territories (SAT-1,2,3) are available
in the different parts of the world. In our country A, O, Asia-1 serotypes are prevalent in FMD endemic region.
Sometime C type also appeared in some part of the country.
Epidemiology
Geographical distribution: FMD is endemic in parts of Asia, Africa, middle east, South America and parts of
Europe.
Host range: Cloven-footed domestic and wild animals are primarily affected.
Source of virus: saliva, feces, urine, milk and semen.
Transmission:
• Direct or indirect contact
• Animate or inanimate vector
• Inhalation
• Ingestion
Economic importance
• High communicable disease
• Decrease in milk and meat production
• Most of the cattle don’t gain their normal weight and milk production in lactating cows.
• Embargo in imported animal products causing loss of money
Clinical findings
• Incubation period is 2 to 21 days
• Fever (103-1050F), dullness, anorexia and decrease milk production
• Vesicles on the buccal and nasal mucous membrane including mouth, tongue, lips followed by appearance of
blister between claws and coronary band
• Infection on the feet may lead to stamping or kicking of the feet, reluctant to move
• Mortality less than 1% , but young animals may die due to myocarditis
• Mortality very high in young animals
Diagnosis
• History
• Clinical findings
• Laboratory examination: virus isolation and identification (culture, serological test, PCR)
Treatment
• There is no specific treatment due to viral etiology
• Washing mouth with 0.01% PPM/2 %alum / 2% Borax with honey or isotonic sodium bicarbonate solution
• In case of foot lesion 0.1% PPM or commercial washing solution specific for FMD
• Sulphadimine or broad-spectrum antibiotic against secondary bacterial infection.
Prevention and Control measures
• Hygienic management
✓ Isolation of affected animals and provide treatment
✓ Animal shed should be properly washed with disinfectant solution
✓ Restriction of movement of affected animals
✓ Quarentine measures for the newly imported animals from other country or market place
• Immunoprophylaxis: Monovalent vaccine-3 ml, Bivalent -6 ml, Trivalent-9 ml. Initial vaccination at 4 months
of age and revaccinate at 6 months interval subcutaneously.

Bovine papillomatosis/ Wart

Papillomatosis is the inflammatory reaction on the skin by papilloma virus in all species of domestic animals.
But cattle are most commonly affected.
Etiology: Papilloma virus
Epidemiology
• Worldwide distributed
• Species: cattle , sheep, goat, horse and human
• Age: Young animals less than 2 years of age are usually affected
• Infection site: neck, legs, back and abdomen are more usual site of infection. Because these sites are usually
abraded and virus can get entrance for infection
• Sources of infection: Keratinized epithelium of the wart tissue. The epithelium shed from wart can readily
contaminated fomites such as fences, stanchions and stable.
Clinical findings
• Warts can occur anywhere of the body
• Commonly seen in the head and neck
• Shape of the wart is pea-sized lumps to large orange sized balls on stalk
Diagnosis
• History
• Clinical findings
Treatment
• Autohemotherapy
• Autogenous vaccine
• Systemic injection with lithium thiomalate
• Cryosurgery with liquid nitrogen (-1960F)
Procedure of autogenous vaccine preparation
• Approximately 2 gram wart tissues should be collected from the body of the affected animal after cleaning the
sites with the help of sharp knife.
• The wart tissues should be made into small piece s with a sterile scissors and then prepare a paste with the help
of morter and pestle in buffered glycerol (50% glycerol-saline) and prepare 10% suspension in glycerol-saline
• Centrifuge the suspension at 3000 rpm for 20 minutes and then supernatant to be collected
• The virulent virus should be inactivated with formalin (0.4% 1-2 drops formalin in 20 ml suspension)
• Then added antibiotic solution (penicillin + streptomycin) to make the vaccine sterile
• Inject 5 ml S.C at 7 days interval in 3 occasions

Bovine viral diarrhea-Mucosal disease

Bovine viral diarrhea is one of the most devastating diseases of cattle. It causes death of large animals when it
attacks on herd. The disease is characterized clinically by severe diarrhea, ulceration of muzzle, nasal and oral
cavities, fever, leucopenia, reduction in milk secretion, cessation of rumination and abortion.
• The lesions resemble to rinderpest
Etiology: Bovine viral diarrhea virus. BVD is closely related to Hog cholera in pig and Border disease in sheep
Epidemiology
• Worldwide distributed
• Age group: All age groups are susceptible. But frequently found in cattle with 6 months to 2 years. Colostral
antibody can protect calves for 3 to 6 months after birth
• Sources of infection: Feces, secretion from nose and mouth, fomites (foot wear, clothing, musk etc.)
Clinical findings
• High fever (104-1060F)
• Yellowish discharge from nose and eyes. Erosion and ulceration of the muzzle and buccal cavity
• Diarrhea contain mucous and blood
• Sometimes pneumonia present due to secondary bacterial infection
• Abortion in pregnant animals
• If fetus survive, congenital defects are usually seen
Diagnosis
• History
• Clinical findings
• Laboratory findings
✓ Leukopenia
✓ Serological test, PCR
Treatment
• There is no specific treatment due to viral etiology
• Antibiotic or Sulphonamide drugs
• Fluid and electrolytes therapy
Prevention
• Hygienic management: Sound management practice eliminate persistently infected cattle
• Vaccination: Vaccinate in pregnant animals causing passive immunity in pregnant animals.

Bovine malignant catarrh/ Malignant catarrh/ Malignant catarrhal fever

Malignant catarrhal fever is a generalized viral disease characterized clinically by high fever, profuse nasal
discharge, ophtalmia, lymphadenopathy, leucopenia, sometimes diarrhea and CNS signs are also evident.
Etiology: MCF virus
Epidemiology
• Worldwide distributed
• Cattle, buffaloes and wild ruminants are most commonly affected
• Transmission: Inhalation and ingestion
Clinical findings
• Head and eye form (common form)
✓ High fever, nasal and ocular discharges progressing from serous to mucopurulent and purulent
discharges
✓ Stomatitis
✓ Ophtalmia includes lacrimation, purulent exudation, photophobia, hyperemia and blindness
 ✓ Corneal opacity results to blindness
Diagnosis
✓ History
✓ Clinical findings
✓ Laboratory examination
Treatment
✓ There is no specific treatment due to viral etiology
✓ Antibiotics/ Sulphonamide drugs
✓ Fluid and electrolytes therapy
Control
✓ Cattle should be separated from reservoir host (wild ruminants and small ruminants)

Cowpox and Buffalo pox

Cowpox is a benign contagious viral disease on the skin of cattle which is characterized clinically by the
presence of typical pox lesions on the teat and udder.
Etiolgoy: Cowpox virus. The virus of cowpox is closely related to vaccinia and smallpox virus.
Epidemiology
✓ Worldwide distributed especially in western Europe.
✓ Transmission: Usually transmitted by milking machine and hand of the attendants. The disease might be
mechanically transmitted by insect biting.
Clinical findings
✓ Incubation period 3 to 7 days
✓ After mild fever, papules appear around the teat and udder
✓ Erythema with localized edema occurs at the site of future pock development
✓ The vesicle rapidly progress to pustule then rupture and scab development within few days
✓ Ulceration on the teat and udder is common.
✓ Healing complete within 4 weeks
Diagnosis
✓ History
✓ Clinical findings
✓ Differential diagnosis
• Cowpox: In human severe localized or generalized skin lesions.
• Pseudocowpox (Milker’s nodules): Localized skin lesions on the hand of man
Treatment
• No specific treatment
• Topical steroid ointment with anesthetic and antibiotics
• Systemic antibiotic, antihistaminic drug and pain killer drugs can be used
Prevention and Control
• Quarentine and examine the newly purchased livestock at least 14 days before introduction into new herd.
• Isolation of infected cows and provide treatment
• Ensuring the treatment of cows from any abraded skin lesions
• Washing teat with antiseptic solution before and after milking

Bovine ephemeral fever/ Three-day sickness/ Bovine epizootic fever/

Three-day stiff sickness
Bovine ephemeral fever is an arthropod-transmitted, non-contagious viral disease of cattle and water buffaloes,
characterized clinically by sudden onset of high fever with short duration, depression, stiffness and lameness
with high morbidity and low mortality.
Etiology
It is an Arbovirus spread by blood sucking insects. The virus is antigenically similar to other viruses non-
pathogenic for cattle.
Epidemiology
• Worldwide distributed. The disease was first described in South Africa. It is usually known to exist in tropical,
sub-tropical and temperate countries of the world.
• Host range: The disease observed only in cattle and water buffalo
• Age: Calves less than 6 months of age least affected. But fat bull and cows are usually affected
• Morbidity-80%, Mortality:1-2 %
Transmission
Insect bite (Culicoides mosquito)
Clinical findings
• High fever with short duration usually lasting only 1 to 2 days
• Stiffness with a shifting lameness affecting one or more legs
• Increase respiratory rate
• Less of appetite
• Decrease milk yield
• Swelling lymphnodes
Diagnosis
• History
• Clinical findings
Treatment
• There is no specific treatment due to viral etiology
• Palliative treatment with sodium salicylates may benefit in muscle stiffness
• Non-specific therapy: reduce fever and alleviate joint pain (Paracetamol, Ketoprofen or phenylbutazone may be
used)
Control
• Live attenuated vaccine: Two initial course 2 to 4 weeks apart and revaccinate annually. Dose: 2 ml S.C at the
neck region.

Rinderpest (Cattle plague)

Rinderpest is an acute infectious and contagious viral disease of domestic animals. It is characterized clinically
by high fever, ulceration in the buccal cavity and diarrhea. According to FAO 2011, the disease was fully wiped
out from the world following small pox.
Etiology
Paramyxoviridae, morbillivirus genus
The disease has antigenic similarities with canine distemper and measles virus. The disease also similar to PPR
Epidemiology
Virus was first isolated from India. Initially Australia, Newzealand, Japan and Phillipine eradicate the disease
In 2011, the disease eradicated from the world
Susceptibility: Ruminants and pigs are highly susceptible. The disease appears as epidemic form in cattle and
buffalo. In sheep and goat, the disease also reported as epidemic form.
Transmission: Contaminated feed and water, direct contact, ingestion, inhalation and insect biting
Clinical findings
✓ Incubation period 6-9 days
✓ High fever and salivation
✓ Redness of the mucous membrane
✓ High respiratory and pulse rate
✓ Erosion and ulceration in the buccal cavity
✓ Bloody diarrhea
✓ Dermatitis in chronic stage of the disease
Diagnosis
✓ History and clinical findings
✓ Laboratory examination: Leukocyte count below 4000/µl
✓ Post mortem lesions: Zebra stripe lesion on intestine
Treatment
✓ Antibiotics for secondary bacterial infection
✓ Fluid and electrolytes therapy due to severe bloody diarrhea
✓ Antidiarrheal drugs: Loperamide
✓ Astringent mixture
Prevention and control measures
✓ Rinderpest recovered cattle produce longterm immunity. If calf get colostrum from recovered mother can
protect the disease up to 4-8 months
✓ Hygienic measures
• Affected animals should be separated from healthy ones
• Provide treatment to the sick animals
 • Animal house should be properly washed with disinfectant solution
• Avoid importation of animals form affected region
✓ Vaccination
• Serum simultaneous vaccine
Inject 0.2 ml blood from infected animal S.C at one side and hyperimmune serum another side of the
neck
Disadvantages: Healthy animal can get infection
• Goat tissue prepared vaccine: Cattle 1 ml , Buffalo 0.5 ml S.C
Disadvantages: Exotic breed cattle cannot immunize with this vaccine.
• Lapinized vaccine: Cattle 2 ml S.C. Rabbit passage vaccine
Disadvantages: Indigenous cattle are not sensitive to this vaccine
• Avianized vaccine
• Tissue culture vaccine: Effective for cattle, buffalo, sheep and goat
Cattle 1 ml S.C-protect up to 10 years
• Measles vaccine: Effective for calf and adult cattle.

Rabies
Rabies is an acute encephalitic viral disease of man and warm blooded animals, characterized clinically by
excitement, furious and paralysis.
Etiology
Rhabdoviridae- Lyssa virus. In 1804, Louis Pasteur discovered the virus.
Epidemiology
Distribution: Worldwide distributed. Australia, Newzealand, Britain, Hawoai and scandanavian countries are
free from rabies in the world. The most susceptible countries are located in Asia and Africa.
Transmission: Biting by rabid animals
Season: Dog mating season, summer, winter
Pathogenesis: Biting by rabid animals

Proliferation of virus in the striated muscle

Virus transmits through the neuromuscular junction and enters into the brain

Virus release through trigeminal, olfactory and glossopharyngeal nerve

Clinical findings
• Initial stage: Mild fever, anorexia, reduce milk yield, salivation and harsh voice
• Excitement: Biting, sexual excitement in bull, crazy behavior, lifting tail
• Paralytic form: Paralysis
Treatment
• No treatment should be tried after appearing clinical signs
• Immediately after exposure washing the wound with alkaline soap solution
• Post exposure vaccine
Species Day 1st Day 7 Day 21
Dogs, cats, sheep and goats 2 ml at two sites 1 ml at one site 1 ml at one site

Calves , horses, donkeys and camels 3 ml at two sites 2 ml at two sites 2 ml at two sites

Cows, buffaloes and elephants 4 ml at four sites 3 ml at two sites 3 ml at two sites

Preventive measures
• Prevent the animals from rabid animal biting
✓ Licensing pet animals (dog, cat)
✓ Street dog should be kill
✓ Serum monitoring of dog
✓ Animal should be avoid from biting by wild animal
• Vaccination
✓ Inactivated vaccine: Semple phenolized vaccine
 ✓ Attenuated vaccine
LEP-40-50 times passage of embryonated egg of hen-Dog
HEP-more than 180 times passage-Cattle, sheep, goat and monkey
Immunity persists for one year and revaccinates annually I.M
• Tissue culture vaccine: Fibroblast, DK, BHK1
Immunity persists in cattle and horse/dog as 3 and 2 years, respectively
• Inactivated Rabies virus vaccine (Rabisin)

Age of 1st dose Booster

Born to non-immunized mother Born to immunized mother
Carnivores 4weeks 11 weeks 3 years
Herbivores 2 months 6 months 3 years

Dermatomycosis/ Dermatophytosis/Ringworm
• The term Dermatomycosis derived from Greek word Derma-skin, mykes-fungus and osis-condition. It means
fungal infection on the skin.
• The term Dermatophytosis, Greek work Derma-skin, Phyton-fungus
• Ringworm: Contagious skin infection by fungus characterized by circular scaly patches.
It is an infection of keratinized tissue (skin, hair and claws) by one of the three genera of fungus collectively called
dermatophytes. Epidermophyton, Microsporum and Trichophyton cause dermatomycosis on the skin. The organisms
usually invade hair follicles and keratinized epithelial cells.
Etiology
Cattle: Tr. Verrucosum , Tr. Mentagrophytes- long chain spore
M. gypseum-mosaic pattern spore
Epidemiology
• Worldwide distributed
• All domestic animals species are susceptible
• Age: Young are susceptible than adult
• Management and climate factor: overcrowding condition, high humidity , hot weather and rainy season
• Transmission to man: Tr. mentagrophytes from rodent, M. canis from dog and cat and Tr. verrucosum from
cattle.
• Transmission: Direct or indirect contact (beeding materials, grooming kits, harness etc.)
Clinical findings
• Roughly circular gray-white crust
• In early stage, the surface below the crust is moist. But in advance stage scab detached from the skin and
pityriasis (dandruf) and alopecia appear on the skin
• Itching usually doesn’t occur due to involvement of organism in hair fibers and keratinized epithelial tissue.
Diagnosis
• History
• Clinical findings
• Laboratory diagnosis
✓ Skin scraping test with 10% NaOH or KOH
✓ Wood’s lamp test (Microsporum sp will fluoresce under microscope)
Treatment
• Topical treatment
✓ At first crust should be removed by soft wire brush which is medicated with medicine and
rubbed vigorously. A weak solution of Iodine 7% and salicylic acid 2% should be applied on
the skin on alternate day for 10 days
✓ Whitefield’s ointment (Salicyclic acid 3%, Benzoic acid 5% and Vaseline up to 100%)
✓ Use commercial miconazole, clotrimazole or econazole for 7 days
• Systemic treatment
✓ Sodium iodide 10% solution
✓ Griseofulvin 5-10 mg/kg twice daily for 2 weeks
✓ Ivermectin injection 0.2 mg/kg S.C and repeat same dose after 21 days.
Control
✓ Isolation and treatment of infected animals
✓ Separate grooming tools and feeding utensils
 ✓ Cleaning and disinfection of stables with phenol 2.5 to 5%, Formaldehyde 2% or caustic soda 1%.
✓ Provide vitamin A, E and zinc supplement in diet of young animals.

Babesiosis/ Red water fever/ Cattle tick fever

The disease infects wide variety of vertebrate species, including domestic and wild animals as well as man the disease
is characterized clinically by high fever, destruction of erythrocytes lead to hemoglobinuria, anemia, jaundice, CNS
involvement and death in severe cases.

Etiology Tick
Babesia bigemina-cattle-Boophilus annulatus
B. bovis-cattle- Boophilus annulatus
B. divergens-cattle/human-Ixodes ricinus
B. major-cattle-Hemaphysalis punctata

Epidemiology
Geographical distribution: Worldwide distribution that correspond the distribution to the vector ticks.
Host susceptibility: Cattle are the principal host. Water and African buffalo may also become infected.
Breed: Exotic breed cattle are very much susceptible than indigenous cattle.
Transmission:
• Biting by insect
• Contaminated needle and instrument can transmit physically
Immunity and Susceptibility
• Repeated infection leads to permanent immunity
• If the illness is treated urgently, protozoa can n’t produce antibody. So, no immunity produces in the body.
• In case of repeated infection, Babesia survives in the host for 6 months, then disappears and host again
susceptible with protozoa.
• Age: Inverse age resistance
• Premunition: Immunity persists until the presence of organism in the body.
• Stress: Parturition, starvation or intercurrent disease
• Seasonal factor: It can occur all the season of the year. Mostly prevalent in summer season.
• Economic importance
▪ 50% mortality in enzootic cattle
▪ Loss of meat and milk production
▪ Infertility, weight loss and abortion
Clinical findings
▪ Incubation period 2-3 weeks
▪ Hemoglobinuria
▪ High fever 103-1070 F
▪ Anemia and icterus
▪ Abortion in pregnant female

Treatment
▪ Diminazene diaceturate. 3.5-12 mg/kg body weight. Administered 1 gm mixed with 10 ml distilled water
intramuscularly at a time.
▪ Imidocarb dipropionate. Inject 1.2 mg/kg b.w S.C at a time
▪ Alum 15 gm+ Boric acid 15gm mixed with 250 ml water orally
▪ Supportive treatment : Hematinic preparation orally or parenterally
Prevention and Control
▪ Effective quarantine to the imported cattle prevent the introduction of tick
▪ Eradication of bovine babesiosis from the area depends upon eradication of vector tick
▪ Limitation of prevalence of tick infestation: Tick control by application of acaricides, chemotherapy to kill
babesia in cattle.
▪ Vaccination
➢ Vaccination with live protozoa- Whole blood contained attenuated babesia
➢ Irradiated vaccine
➢ Recombinant vaccine
▪ Chemoprophylaxis: Imidocard dipropionate or Diminazene diaceturate
▪ Tick resistant cattle: Ability of cattle limits the number of survival of tick
Bovine tropical theileriosis
Bovine tropical theileriosis is an important tick-borne hemoprotozoan disease, caused by Theileria annulata
and characterized clinically by fever, lymphnode enlargement, anemia and jaundice.
Etiology
Theileria annulata transmitted by tick Hyalomma anatolicum
Epidemiology
✓ Distribution of the disease depends on the presence or absence of tick
✓ Sources: Cattle and buffaloes are mainly susceptible
✓ Age: All age groups of exotic and crossbred cattle are susceptible. Young zebu cattle are also susceptible. But
adult zebu cattle showing subclinical infection
✓ Seasonal variation: Most of the causes occur in summer and rainy season due to higher activity of vector ticks
in these months
✓ Transmission: Biting tick (Transtadial transmission)
✓ Economic importance:
• Serious losses occur when exotic cattle are introduced in enzootic areas from outside
• Treatment cost, decrease milk production
• Mortality 10% due to T. annulata infection has been reported.
Clinical findings
• Incubation period 1 to 3 weeks (variation of incubation time depends on virulence of organism, breed of animal
and infective dose)
• Fever (104-1070F)
• Fever followed by cessation of rumination, serous nasal discharge and lacrimaion
• Swelling of superficial lymphnode
• Hemoglobinuria
• Rapid heart rate and respiration due to anemia
• Emaciation
• Death may appear within 8 to 15 days
• Cerebral theileriosis causes circling disease
• Later stage: anemia, jaundice, death, subcutaneous nodule over the body
Diagnosis
• History
• Clinical findings
• Laboratory diagnosis: Giemsa staining, Leukopenia in later stage (4 to 5 thousand/mm3)
Treatment
Various drugs or combination of drugs have been tried
• Oxytetracycline hydrochloride 5-10 mg/kg b.W IM for 5 days plus Diminazene diaceturate 12-15 mg/kg IM on
alternate day for 3 injections
• Only Diminazene diaceturate 12 mg/kg I.M on alternate day for 3 injections.
• Parvaquone 10mg/kg weight IM at 48 hrs apart good result at early stage of injection
• Supportive treatment: Antihistaminics treatment to ameliorate symptom
• Choline, liverextract and vitamin B12 were used against anemia.
Control
• Exotic and crossbred cattle should be away from indigenous stock
• Management of exotic cattle in tick proof shed
• Proper management and cleanliness of the herd
• Immunoprophylaxis: Immunization of calves below 2 months of age provides partial protection.

Anaplasmosis
The disease caused by Anaplasma sp in man and animals. The disease is characterized clinically by severe
dibility, anemia and jaundice.
Eitology
Anaplasma marginale-cattle and wild ruminants
Anaplasma central-cattle
Epidemiolgy
Distribution: Common in tropical and sub-tropical regions. The disease is sporadic in nature in temperate
regions.
Source of infection: Carrier animals are act as source of infection.
Transmission: Transmitted by biting insects, transplacental and iatrogenic ways.
Age: Infection between 6 months to 3 years of age has higher risk of infection.
Breed: Exotic and indigenous both have equal susceptibility
Pathogenesis
Infect mature erythrocyte

Multiply in erythrocyte

Parasitized erythrocytes are removed by phagocytosis in reticuloendothelial system with release of inflammatory
mediator causing fever
• Erythrocyte destruction and anemia
• No hemoglobinuria
• Pregnant animals become aborted
Diagnosis
• History
• Clinical findings
• Loboratory diagnosis : Culture, staining and serological test
Treatment
• Tetracycline and imidocarb are most commonly used chemotherapeutic drugs for the treatment of
anaplasmosis
• Blood transfusion in actute case
Prevention and Control
• Dipping animals in acaricides at enzootic area can control the ticks, fly and other insects.
• Serological testing
• Properly disinfected the surgical instruments, needle can prevent from iatrogenic transmission
• Elimination of carrier animals
• Vaccination
✓ Killed vaccine: A. marginale with adjuvant vehicle. Two dose of vaccine should be administered. 1 st
dose vaccine and 2nd dose should be vaccinated before vector season.
✓ Live vaccine: Single vaccination in enzootic area and immunity reinforced by repeated exposure.

Contagious bovine pleura-pneumonia

Contagious bovine pleura-pneumonia (CBPP) is a highly infectious septicemic disease which primarily affects
cattle lung and occasionally joints, caused by Mycoplasma mycoides subsp. mycoides and characterized by
acute lobar pneumonia and pleurisy.
Etiology
CBPP is caused by Mycoplasma mycoides subsp. mycoides. The orgranism is not resistant in environment and
transmission requires close contact. The agent has no cell wall.
Epidemiology
• CBPP is worldwide distributed. But it has been eradicated from South Africa, USA and Australia
• The disease was most prevalent in Zebu and cross bred cattle. But rare in water buffaloes
Breed: European breeds are tend to be more susceptible than indigenous African breed
Age: Young animals are more susceptible than adult
Transmission: Usual route is inhalation. Transplacental transmission also occurs in susceptible animals. Relatively
close contact is required for transmission. Recovered animals act as carrier of agents. Stressors on carrier animals
make them active to infectious agents.
Sources: coughing of animals, saliva and urine
Clinical findings
• In natural infection, the incubation period of the disease might be 20-123 days .
• Moderate fever 105oF, depressed and inappetantace
• Coughing followed by evidence of thoracic pain due to pleurisy
 • Animals stand with abducted elbow in an attempt to decrease thoracic pain and increase chest capacity
• Auscultation of the lung reveal wide variety of sounds, depending on infection of pulmonary parenchyma
• In calves, pneumonia accompanied with polyarthritis
• Chronic form is characterized by ill-thrift and recurrent low grade fever
• Forced exercise may precipitate coughing
Diagnosis
• History and clinical findings
• Necropsy findings: Extensive marked inflammation with associated pleura, consolidated lungs
• Laboratory examination: Serological test
Treatment:
• Oxytetracycline:2-5 mg/kg b.w. IM daily for 5 days
• Tylosin tartrate: 10mg/kg at 12 hrs interval for 6 IM injection
Prevention and Control
• Sanitary prophylaxis: Quarantine and slaughter of all test positive animals, controlling the movement of
affected cattle to healthy herd area
• Chemoprophylaxis
• Immunoprophylaxis

Parasitic diseases
Hepatic fascioliasis (Liver fluke disease)
Acute fascioliosis in cattle characterized by sudden death. Chronic liver fluke disease is characterized by
progressive emaciation, diarrhea, anemia and submandiblar edema.
Etiology
Fasciola hepatica: virulent in cold country due to presence of Lymnaea trancutula
Fasciola giganticaa: Asia and Africa due to presence of snail L. auricularia
Epidemiology
✓ Worldwide distribution
✓ Species: Almost all domestic ruminants are susceptible.
✓ Source: Feces of the chronically infected animals
✓ Intermediate host: Suitable host and snails are required for infection
✓ ≥ 100C is suitable for breeding snail
Pathogenesis
Damage of the liver parenchyma by migration of immature fluke Liver damage and hemorrhage

Secondary infection in damaged liver by Clos. novi, which causes black disease (Head region)
✓ Damage bile ducts by adult fluke and hemorrhagic activity
✓ Cholangitis and fibrosis
✓ Blood loss .05 to 1.0 ml/fluke
✓ Proline release from fluke depress bone marrow
Clinical findings
✓ Prepatent period
✓ Acute: Ingestion of metacercaria (>200), onset of clinical signs 2-6 weeks after ingestion, loss of blood causes
anemia, pale mucus membrane and submandibular edema
✓ Subacute: Ingest 500-1500 metacercaria, clinical signs develops 6-10 weeks after ingestion, pale mucus
membrane, submandibular edema
✓ Chronic: Ingestion of 200-500 metacercaria, signs develop 4-5 months later after ingestion, edema
Diagnosis
✓ History
✓ Clinical findings
✓ Laboratory examination: eggs-yellowish brown, morula at the periphery region
Treatment
✓ Triclabendazole :10 mg/kg
✓ Nitroxynil, oxyclozanide, albendazole, hexachlorophene are also effective against fascioliasis
Control
✓ Reduction of snail population: Chemical agents-Copper sulphate, Sodium pentachlorphenate, Biological
control-duck
✓ Use of anthelmintic: Strategic and tactical control
✓ Chemoprophylaxis
✓ Vaccination

Paramphistomiasis/ Intestinal Amphistomiasis

Immature stage of parasite causes severe enteritis and fetid diarrhea
Paramphistomum cervi
P. microbothrium

Most common rumen fluke

Celynocotyl scoliocoelium- Indentified as the cause of death in buffalo in BD
Epidemiology
✓ Little importance in Europe and America
✓ Occasionally causing diseases in warmer region
✓ 46 to 68% prevalence in BD
✓ All ages of domestic and wild ruminants grazing near water pool
✓ Adult act as reservoir
✓ Water snail Planorbis act as intermediate host.
Pathogenesis
Enteritis in duodenum-diarrhea, dehydration, ulceration and edema
Clinical findings
✓ Severe enteritis-fetid diarrhea
✓ Edema, pale mucosa
✓ Death usually occur 15 to 20 days of infection
Diagnosis
History, Clinical findings, laboratory examination
Treatment
✓ Oxyclozanide
✓ Hexachlorophene
Control
✓ Drainage of low-lying area
✓ After flooding season, metacercaria remain in pasture for 2-3 months and infective for susceptible host. So
animals should be kept away from source of infection.

Ascariasis
Etiology
Toxocara vitulorum
Parascaris equorum
Newborn animals get infection through colostrm. So, day old calves are susceptible to infection.
Clinical findings
PPP:6-8 week
✓ Coughing
✓ Increase breathing
✓ Nasal discharge
✓ Cachexia
✓ Intestinal obstruction
✓ Alternate diarrhea and constipation
Pathogenesis:L-1, L-2 (egg contained larvae) Larva 2 release in the intestine

Liver L3 go to blood

Lung, trachea and bronchi causing coughing

L-4 in Intestine causes diarrhea
Treatment
✓ Piperazine
✓ Fenbendazole
✓ Levamisole
Control
✓ Adm. anthelmintic 7-14 days of age , second dose after 2 weeks of 1st dose

Coccidiosis
Coccidiosis is contagious enteritis in all domestic animals caused by the infection with both Eimeria and
Isospora spp and characterized by diarrhea and dysentery with anemia and chronic form by inferior growth
rates and production.
Etiology
Cattle: E. zuernii and E. bovis
Epidemiology
• Worldwide distributed to all animals
• Coccidiosis is host specific and there is no cross immunity between species of coccidia
• Young calves, lambs, kids, piglets and foals are generally affected but adults are rarely infected with the
protozoa
• The morbidity rate of coccidiosis is very high but the rate of clinical infection is very low (5 to 10%)
• Weaned calves are usually affected due to feeding on the ground
• Risk factor: Overcrowded, winter season, concurrent infections, low immune status, dirty condition on the
animal sheds are increase the susceptibility of infection
• Ingestion: oro-fecal transmission is usual route for infection
Pathogenesis:
• Villous atrophy: reduction of intestinal surface interfere absorption of water and nutrients
• Protein-losing enteropathy: strong acidic intestinal wall that accompanied by protein loss and impair nutrient
absorption
Clinical findings
• Incubation period of coccidian depends on the species. In calves usually 16-30 days
• Temperature usually normal or subnormal
• Hemorrhagic diarrhea , feces may contain mucus and strands of sloughed intestinal mucosa
• Fresh unclotted blood dribbling through anus
• Perineum and tail soiled with blood stained feces
• Animals might be anorexic, dehydrated and anemic
• In addition of diarrhea, the animals show tremor, tetany and blindness
Diagnosis
• History
• Clinical findings
• Laboratory examination: oocyst found under microscope, staining oocytst
Treatment
• Sulphonamides (eg.Sulphadimidin) are commonly used for the treatment of coccidiosis in ruminants and their
concurrent antibacterial activity can limit the secondary bacterial infection
• Amrolium anticoccidial drug is still used for the treatment of coccidiosis in ruminants
• Supportive therapy: Fluid and electrolytes therapy
Control
• Reduction of the number of sporulated oocyts
✓ The clinically infected animals should be isolated and provide appropriate treatment
✓ Avoiding overcrowding of animals
✓ In penned animals, feces should be removed daily and pens should be kept dry
✓ Use feeding trough to avoid contamination of fecal materials
• Reduction of stress
✓ Provide sound management to avoid stress factors
✓ Overcrowding should be avoided
✓ High energy diet should be provided during stress period
 Cryptosporidiosis
Cryptosporidiosis is an important zoonotic protozoan disease of the neonatal farm animals especially calves
caused by Cryptosporidium parvum and characterized clinically by varying degree of diarrhea. Zoonotic
infection in human causes severe diarrhea in immunologically compromised people (AIDS patients)
Etiology
Cryptosporidium parvum infection in cattle calves
Epidemiology
✓ Worldwide distributed
✓ Neonatal farm animals are usually infected with the disease
✓ Age susceptibility:5 to 15 days calves
✓ Source of infection: Feces
✓ Transmission: Oro-fecal transmission
✓ The oocyts are resistant to environmental condition and can survive in cool and moist weather
✓ Risk factor: stress, concurrent infection, unhygienic condition, malnutrition, winter months, some domestic
and pet animals act as reservoir of infection etc.
Clinical findings
✓ Acute diarrhea in calves 1 to 3 weeks of age
✓ Depression and anorexia followed by profuse, yellowish-white color diarrhea,dehydration
✓ The presistant diarrhea causes loss of body weight , emaciation and death
Diagnosis
✓ History
✓ Clinical findings
✓ Laboratory examination: Feces examination under microscope , Ziehl-Neelsen staining for the detection of
pathogen
✓ The cryptosporidiosis could be differentiated from corona virus, rotavirus and enterotoxigenic E. coli and
salmonella
Treatment
✓ Halofuginone @60-120µg/kg b.w for 7 days
✓ Sulphaquinoxaline 4-8 gram daily for 7 days
✓ Fluid and electrolytes therapy for supportive treatment
Control
✓ To minimize the oro-fecal transmission
• Animal shed should be cleaned with proper disinfectant solution
• Affected calf should be separated from healthy ones and provide treatment
• Affected animal attendants also should be treated with proper drugs. Otherwise they might be storehouse of
infection.
• The oocyts are resistant to common disinfectants. So animal shed should be cleaned with 5% ammonia or
10% formalin
• Rat , mice and flies population should be controlled to avoid the risk of infection
✓ Immunoprophylaxis
• Hyperimmune bovine colostrums can reduce the severity of diarrhea and period of oocyst excretion.
• Vaccination with C. parvum given orally after birth provides partial protection of susceptible calves.

Edited by…
SK Kamruzzaman
DVM 17th Batch