Synonyms: Pearly disease,Consumption Scrofula,Phthisis.

Tuberculosis is a chronic, infectious disease of mammals caused by Mycobac­terium tuberculosis and characterized by the development of tubercles and by abscess formation, with resulting caseation and calcification.

ETIOLOGY

Mycobacterium tuberculosis:

Types:

1. Avian.
2. Mammalian.
3. Var. bovis.
4. Var. hominis.

Morphological characteristic:

1. Slender rod – 0.2 to 0.6p: x 1.5 to 4JJ.
2. Coccoid and filamentous shapes are frequently seen.
3. Acid-fast organism and usually Gram-positive.

Growth characteristics:

Grows slowly, reaching maximum in 8 wks.

1. Human type – thick, wrinkled.
2.  Bovine type – sparse, rough, and dry.

Avian type – heavy, smooth, and moist.

1. Crumbly dry mass on surface of media.
2. Aerobic.
3. Bovine strains grow best in acid medium, human strains in alkaline medium.
4. Slightly acidified, glycerin bouillon is rendered more acid in reaction by the growth of human strains while growth is inhibited in bovine strains.

Pathogenicity:

Resistance to physical and chemical agents:

1. Killed by light in 3-10 days.
2. Resists drying -150 days in dry cattle feces.
3. Putrefaction not effective in causing death of organism, survives in cattle lung 167 days.
4. Pasteurization, 143°F for 30 min kills organism.
5. Phenolic compounds 2-3%, sodium orthophenyl-phenate 1% – kills organisms
6. Not sensitive to penicillin but is to streptomycin.

EPIZOOTIOLOGY

Distribution;

Disease present in man and animals in all areas of the world, especially the old world, and thickly populated areas.

Tends to be more prevalent in temperature of cold climates because housing of animals during unfavorable weather is necessary.

Transmission:

Bovine:

• Contamination of feed and water which is ingested. Contamination is from the faeces to the ground and feed. Water is contaminated by the organisms being washed from infected animal’s mouth in the process of drinking.
• Aerosol and dust.

Swine:

• Ingestion of contaminated feed and water when running with the infected bovines.
• Aerosol and dust.
• Ingestion of diseased chickens or contaminated droppings.

Avian:

• Ingestion of contaminated feed and water.
• Aerosol and dust.

Susceptible hosts:

Bovine strain

• Cattle, primarily.
• Man.
• Swine.
• Horses, sheep, goats, and parrots, rarely.
• Experimental animals.

Rabbit – very susceptible.

Guinea pig – not as much as rabbit.

Chicken – not susceptible.

Avian strain

• Domestic fowl and pheasant.
• Ducks, geese, and pigeons are relatively resistant.
• Swine.
• Cattle and sheep, rarely.
• Experimental animals.
• Rabbit – very susceptible.
• Guinea pig resistant.
• Chicken – kills.

Human strain:

• Man.
• Anthropoid apes and monkeys.
• Parrots.
• Cattle, swine, cats and dogs, rarely.
• Experimental animals.
• Guinea pigs are highly susceptible.
• Rabbits are susceptible but rarely succumb.
• Chickens  not susceptible.

Factors influencing susceptibility:

Age:   

• Little influence except that the aged have had more opportunity to come in contact with infection.
• Younger ages of people more susceptible. Effects noted later in life. This is par­ticularly true in relation to the bovine strain.

Sex:

No differences.

Condition:

Little influence, but poor condition increases an existing infection.

Feeding:

• Lack of cleanliness from poor feeding and drinking facilities is dangerous from the standpoint of spreading the disease.
• Milk and dairy by-products are a source of infection for calves.

Housing:

• Crowded facilities are conducive to the spread of the disease.
• Poorly lighted and poorly arranged stables promote spread of tuberculosis.
• Common drinking troughs are dangerous.

SYMPTOMATOLOGY

Bovine tuberculosis:

With few exceptions the course is chronic.

Poor condition.

When disease is extensive, or

1. If respiratory, digestive, or circulatory systems are involved.
2. Temperature is usually normal.
3. Respiratory system is usually the seat of clinical tuberculosis

(a) Dyspnea.-  Increased frequency of breathing. Inspiratory interference from stenosis due to swollen lymph nodes.  Cough from pulmonary lesions- Harsh and dry, becoming soft, moist, and low- Occurs at irregular intervals.- May be easily and repeatedly produced-by pinching the trachea.

(b) Auscultation may reveal louder vesicular sounds in one lung.-  Rales occur frequently.

I Percussion – Areas of dullness – Pain occurs –    Induces cough.

Udder

     (a) Swelling of supramammary lymph nodes

     (b) Nodular, circumscribed, or diffuse swellings.    

     I Milk secretion may cease.

(5) Palpable lymph nodes show enlargement.

     (a) Retropharyngeal.

     (b) Submaxillary.

      I Precrural.

     (d) Supramammary.

     (e) Mediastinal nodes when enlarged cause tympany of the rumen.

(6) Genital involvement.

     (a) Rarely occurs, but when present any part of the genital tract may be involved, causing sterility.

     (b) Avian type may cause abortion.

(7) Central nervous system involvement.

     (a) Paresis.

     (b) Hyperesthesia.

     I Motor irritation.

     (d) Maniacal symptoms, rarely.

(8) Intestinal symptoms.

     (a) Diarrhea.

     (b) Emaciation.   

     I Chronic bloat after feeding following enlarged mediastinal lymph nodes.

     (d) Rectal examination may reveal roughened peritoneum and enlarged mesenteric lymph nodes.   

(9) Liver abscesses.

     (a) Pain on percussion.

Porcine tuberculosis:

The great majority of cases remain unrecognized until discovered at time of slaughter.

The chronic course of the disease and the relatively short life of swine account for lack of observable symptoms.

Unthriftiness, nodular swelling of the neck region, digestive disturbance, enlargements of bones and joints, and pulmonary symptoms have been observed.

Poultry:

1. Ravenous appetite and general emaciation – feel breastbone (going light),
2. Pale wattles and comb, swollen joints and culars.
3. Eyes usually bright.
4. Lameness in one or both legs.
5. Birds extensively infected usually more than one year old.
6. Birds seldom suffer from tuberculosis of the lung.
7. Avian-type tubercle bacilli viable in soil for as long as 4 years and in buried fowl car­cula more than 2 years.

Canine and feline:

1. May be infected by human or bovine types.
2. Lesions resemble neoplasms; often grayish-white and are circumscribed.
3. Rarely observed due to the gradual eradication of the disease in cattle.

PATHOLOGY

Pathogenesis:

Organisms enter on feed, water, dust.

1. Digestive tract.
2. Respiratory tract.
3. Wound infection.
4. Congenital.

Organisms are ingested by leucocytes.

Multiplication occurs in leucocytes.

Leucocytes with the organism localize in the lymph nodes.

1. Submaxillary lymph nodes.
2. Mesenteric lymph nodes.
3. Pulmonary lymph nodes.
4. May localize primarily in tissue other than lymph nodes.

Formation of tubercles.

1. Started by the leucocyte reaction and reticulo-endothelial cell reaction. Lymphocytes appear “giant cell” forms.
2. Encapsulated by fibrous connective tissue which is produced by fibroblasts.
3. Reticulo-endothelial granulation tissue occurs.

Necrosis.

1. Caseation to liquefaction.
2. From center to periphery.
3. Causes extension of tubercles.
4. Necrosis through a blood vessel may result in generalized tuberculosis.

Progressive tuberculosis.

1. Multiplication.
2. At old lesion.
3. At new site.

Calcification of tubercle.

Death of animal.

Cause of symptoms.

(1) Destruction of tissue.

(2) Absorption of products of necrosis.

         (a) A tissue toxemia.

(3) A part becomes dysfunctional.

(4) Secondary complications cause death.

(5) Hemorrhage as from pulmonary tuberculosis causes death.

Postmortem lesions:

a. The tubercle.

(I) At first, barely visible, gray, translucent nodule.

(2) When plain, visible to naked eye:

            (a) Yellow in cattle, sheep, goats, and swine.

            (b) White in horses and carnivores.

(3) Tubercles fuse to form tuberculous masses.

            (a) Dry and cheesy – caseous lesions.

            (b) Gritty if calcification is present – (caseocalcareous lesions).

            I Pearly disease.

(4) Generally considered impossible to differentiate from other granulomatous neo­plasms by gross pathology.

b. Location of lesions.

(I) Cattle:

          (a) Lungs and pleura.

          (b) Liver, spleen, and peritoneum.

          I Regional lymph nodes.

          (d) Skin and bones, occasionally.

(2) Swine:

         (a) Cervical lymph nodes.

         (b) Bronchial lymph nodes.

         I Portal and mesenteric lymph nodes.

        (d) Liver, lungs, and spleen.

(3) Fowls:

        (a) Liver, spleen, intestines. Lungs, bones, joints,peritoneum, kidneys, and ovaries.

Differential diagnosis

• Parasitic nodules
• neoplastic masses
• fat necrosis
• coccidioidomycosis
• histoplasmosis
• actinobacillosis

DIAGNOSIS

Intradermal test:

Intradermal tuberculin 0.1 mI. is injected into dermis of animal.

     (a) Cattle:

  1) Thin skin of the’caudal fold Md/or vulva.

  2) Cervical region

     (b) Swine:

1) Ear skin and/or vulva.

I Chicken:

  1) Wattle.

Positive reaction in 48-72 hrs. (72 official), small firm swelling at the point of in­jection.

Ophthalmic test:

(1) Concentrated tuberculin is placed into the conjunctival sac of the eye with a camel’s­

     hair brush or with a medicine dropper.

  (a) Ophthalmic-tuberculin discs may be used.

  (b) Two applications of tuberculin are required.

1) First application is for purpose of sensitization.

2) Second application is given 2 to 3 days later for purpose of diagnosis. Close observation required for 8 hrs. following last application.

(2) Positive reaction.

(a) Marked inflammation of the conjunctiva.

(b) Profuse lacrimation.

I Mucopurulent culars.

(3) Rarely used except for retest.

Stormont test:

(1) 0.1 mI. of P.P.D. is injected into the skin of the cervical region.

(2) On 7th day original site is reinjected.

(3) Increase in skin thickness of 5 mm. or more 24 hrs. after 2nd injection is a positive      result.

PROGNOSIS

1. If tuberculous rate of a herd or area is high, the mortality may be as high as 15% in areas of world where disease is uncontrolled.

TREATMENT

     1. Of no consequence

PROPHYLAXIS

1. Immunity:

a. Little development of immunity from having the disease.

b. Immunizing agents have been sought with little success; current ones are:

(1) B.C.G. (Bacillus of Calmette and Guerin).

(a) A dissociated strain which is relatively avirulent. It does not produce lesions. (b) It is used as pre-immunization in early life.

 (2) Vole Tubercle Bacillus.

(a) Isolated from the vole in Great Britain.

(b) Considered to be as satisfactory as B.C.G.

2. Sanitation:

a. Addition of diseased animal into a herd is hazardous.

b. The ARS requires a thorough cleanup with the use of disinfectants after an infected animal is discovered in a cattle herd.

PUBLIC HEALTH RELATIONSHIPS

1. Bovine tubercle bacillus.

a. A public health problem in man.

(1) Transmitted through contaminated milk and milk products.

(2) Children under 16 years of age are most susceptible

Contagious bovine pleuropneumonia

ETIOLOGY

Classification of the causative agent

Mycoplasma mycoides subsp. Mycoides SC (bovine biotype)

Mycoplasmas are microorganisms deprived of cell walls and are, therefore, a) pleomorphic and b) resistant to antibiotics of the beta-lactamine group, such as penicillin

Growth of the mycoplasma is relatively fastidious and requires special media rich in cholesterol (addition of serum).

There is only one antigenic type

Resistance in the environment and to chemicals

Mycoplasma mycoides subsp. Mycoides (SC) is not resistant in the environment and transmission requires close contact

Temperature:     In saline solution –      susceptible to 45°C/120 min and/or 47°C/2 min

In lymph – susceptible to 45°C/240 min and/or 60°C/2 min

It is: Inactivated by acid and alkaline pH

Susceptible: to ether, mercuric chloride (0.01%), calciumhydroxide, phenol (1%/3min),and

formaldehyde solution (0.5%/30 seconds)

Survival:  Survives well in frozen tissues

EPIDEMIOLOGY

Hosts

Cattle (Bos cular), zebu (Bos indicus) and water buffalo (Bubalus bubalis).

Wild bovids and camels are resistant

Transmission

1.  Aerial, mostly by direct contact: droplets emitted by coughing animals, saliva, and urine. Transmission up to several cularsi has been suspected under favourable climatic conditions
2. Transplacental infection can occur
3. Inapparent carriers are a major source of infection
4. Cattle movement is important in the spread of the disease

Virulent material

Lungs, pleuropneumonia lymph and possibly brain, liver, kidneys, lymph nodes, uterus, fetus and fetal membranes, and urine

Occurrence

For detailed information on occurrence, see recent issues of World Animal Health and the OIE Bulletin

DIAGNOSIS

Incubation period is 1-3 months (sometimes longer)

During an outbreak of natural disease, only 33% of animals present symptoms (hyperacute or acute forms), 46% are infected but have no symptoms (subclinical forms) and 21% seem to be resistant

Clinical diagnosis

In adults

1. Moderate fever with respiratory, pulmonary and pleuretic symptoms: polypnoea, characteristic attitude (elbows turned out, arched back, head extended), cough (at first dry, slight, and not fitful, becoming moist)
2. When the animal gets up or after exercise, breathing becomes laboured and grunting can be heard
3. At percussion, dull sounds can be noticed in the low areas of the thorax

In calves

1. Pulmonary tropism is not the general rule, and infected calves present arthritis with swelling of the joints
2. Co-existence of pulmonary symptoms in adults and arthritis in young animals should alert the clinician to a diagnosis of CBPP

Lesions

1. Important amount of yellow or turbid culars in the pleural cavity (up to 30 litres) that coagulates to form large fibrinous clots
2. Fibrinous pleurisy: thickening and inflammation of the pleura with fibrous deposits
3.  Interlobular oedema, marbled appearance due to hepatisation and consolidation at different stages of evolution usually confined to one lung
4.  Sequestrae with fibrous capsule surrounding grey necrotic tissue in recovered animals

Differential diagnosis

Acute form

   1. East Coast fever
   2. Acute bovine pasteurellosis
   3. Bronchopneumonia and pleuropneumonia resulting from mixed infections

Chronic form

   1. Hydatid cyst
   2. Actinobacillosis and tuberculosis, bovine farcy

Laboratory diagnosis

Procedures

Identification of the agent

   1. Isolation of pathogen and identification by metabolic and growth inhibition tests
   2. MF-dot
   3. Polymerase chain reaction

Serological tests

1. Complement fixation (prescribed test in the Manual). This test should be used only at herd level and never for individual diagnosis
2. Competitive ELISA (under validation by International Atomic Energy Agency and several reference laboratories), and haemagglutination
3. Agglutination test can be used as penside test in active outbreaks at the herd level

Samples

1. Lung lesions, pleural fluids, lymph nodes, lung tissue culars – frozen for isolation of the organism
2. Acute and convalescent sera

PREVENTION AND CONTROL

No efficient treatment. Antibiotic treatment should be prohibited

Sanitary prophylaxis

1. In disease-free areas: quarantine, serological tests (complement fixation) and slaughtering of all animals of the herd in which positive animals have been found
2. Control of cattle movements is the most efficient way of limiting the spread of CBPP

Medical prophylaxis

   1. In infected areas: a CBPP vaccine containing T1 strain is widely used
   2. A CBPP-rinderpest combined vaccine is sometimes used

Surveillance

Recommended Standards for Epidemiological Surveillance for Contagious Bovine Pleuropneumonia were drawn up by an OIE Ad hoc Group on 7-9 June 1993. After revision, these standards were approved by the International Committee during the 63rd General Session

Peste des petits ruminants (PPR)

ETIOLOGY

Classification of the causative agent

Virus family   Paramyxoviridae,

Genus   Morbillivirus.

Antigenically close to rinderpest virus

Resistance to physical and chemical action

Temperature: Some virus may resist 60°C/60 min

pH: Stable between pH 4.0 and 10.0

Chemicals: Susceptible to alcohol, ether, detergents

Disinfectants:  Susceptible to most disinfectants, e.g. phenol, sodium hydroxide 2%/24 hours

Survival:Survives for long periods in chilled   and frozen tissues

EPIDEMIOLOGY

   1. Morbidity rate 90% (susceptible population)
   2. Mortality rate 50-80% (susceptible population)

Hosts

1. Sheep and especially goats. To date diagnosed only in captive wild ungulates from families of Gazellinae (dorcas gazelle), Caprinae (Nubian ibex and Laristan sheep) and Hippotraginae (gemsbok)
2. Experimentally the American white-tailed deer (Odocoileus virginianus) is fully susceptible
3. Cattle and pigs develop inapparent infections
4. Breed-linked predisposition in goats

Transmission

   1. Direct contact between animals
   2. No carrier state
   3. Seasonal variations: more frequent outbreaks during the rainy season or the dry cold season

Sources of virus

Tears, nasal discharge, coughed secretions, and all secretions and excretions of incubating and sick animals

Occurrence

PPR occurs in Africa, the Arabian Peninsula, the Middle East and India

DIAGNOSIS

Incubation period is 3-10 days.

Clinical diagnosis

Acute form

1. Sudden rise in body temperature (40-41°C) with effects on the general state: restlessness, dull coat, dry muzzle, depression of appetite
2. Serous nasal discharge becoming mucopurulent and resulting, at times, in a profuse catarrhal culars which crusts over and occludes the nostrils. Respiratory distress
3. Small areas of necrosis on the visible nasal mucous membrane
4. Congestion of conjunctiva, crusting on the medial canthus and sometimes profuse catarrhal conjunctivitis
5. Necrotic stomatitis with halitosis is common
6. Severe non-haemorrhagic culars
7.  Bronchopneumonia evidenced by coughing is a common feature
8. Abortion
9. Dehydration, emaciation, dyspnoea, hypothermia and death within 5-10 days

Per acute form

   1. Frequent in goats

Sub acute and chronic forms

   1. Frequent in some areas because of local breed susceptibility
   2. 10-15 days development with inconsistent symptoms
   3. Pneumopathy

Lesions

• Emaciation, conjunctivitis, erosive stomatitis involving the inside of the lower lips and adjacent gum near the commisures and the free portion of the tongue
• Lesions on the hard palate, pharynx and upper third of the oesophagus in severe cases
• Rumen, reticulum and omasum rarely have lesions
• Small streaks of haemorrhages and sometimes erosions: in the first portion of the duodenum and the terminal ileum
• Extensive necrosis and sometimes severe ulceration of Peyer’s patches
• Congestion around the ileo-caecal valve, at the caeco-colic junction and in the rectum. ‘Zebra stripes’ of congestion in the posterior part of the colon
• Small erosions and petechiae on the nasal mucosa, turbinates, larynx and trachea
• Bronchopneumonia is a constant lesion
• Possibility of pleuritis and hydrothorax
• Congestion and enlargement of spleen
• Congestion, enlargement and oedema of most of the lymph nodes
• Erosive vulvovaginitis may exist

Differential diagnosis

• Rinderpest
• Contagious caprine pleuropneumonia
• Bluetongue
• Pasteurellosis
• Contagious ecthyma
• Foot and mouth disease
• Heartwater
• Coccidiosis
• Mineral poisoning

Laboratory diagnosis

Procedures

Identification of the agent

• Antigen detection
• Agar gel immunodiffusion
• Counter immunoelectrophoresis
• Indirect fluorescent antibody test
• ELISA
• Immunohistopathology
• Virus isolation and identification
• In primary lamb kidney cells or VERO cell line
• Virus cularsisd
• Electron microscopy
• Virus RNA detection
• PPR-specific cDNA probes
• Amplification by polymerase chain reaction (PCR)

Serological tests

Virus cularsisd OIE approved

• Competitive ELISA
• Counter immunoelectrophoresis
• Agar gel immunodiffusion
•  Immunodiffusion inhibition test

Samples

• Swabs of the conjunctival discharges and from the nasal, buccal and rectal mucosae
• Whole blood collected on heparin (blood and anticoagulant should be mixed gently)
• Lymph nodes, especially the mesenteric and bronchial nodes
• Spleen
• Large intestine and lungs

Samples should be transported under refrigeration

PREVENTION AND CONTROL

• No specific treatment
• Antibiotics may prevent secondary pulmonary infections (oxytetracycline, chlortetracycline)

Sanitary prophylaxis

Recommended when the disease appears in previously PPR-free countries.

Medical prophylaxis

• Rinderpest vaccine is commonly used
• A homologous PPR vaccine is also available and is preferable, to avoid confusion when retrospective serological surveys are done
• Both vaccines give strong immunity
• Genetically engineered recombinant vaccines are currently undergoing limited field trials

Sheep pox and goat pox

ETIOLOGY

Classification of the causative agent

Virus family  Poxviridae

 Genus   Capripoxvirus

Resistance to physical and chemical action

Temperature:   Susceptible to 56°C/2 hours; 65°C/30 min

pH:        Susceptible to highly alkaline or acid pH

Chemicals: Sensitive to ether (20%), chloroform, and formalin (1%)

Disinfectants:   Inactivated by phenol (2%) in 15 min. Sensitive to detergents, e.g. sodium dodecyl sulphate

Survival:   Can survive for many years in dried scabs at ambient temperatures. Virus remains viable in wool for 2 months and in premises for as long as  6  months

EPIDEMIOLOGY

• Morbidity rate: Endemic areas 70-90%
• Mortality rate: Endemic areas 5-10%, although can approach 100% in imported animals

Hosts

Sheep and goats (breed-linked predisposition and dependent on strain of capripoxvirus)

Transmission

• Direct contact
• Indirect transmission by contaminated implements vehicles or products (litter, fodder)
• Indirect transmission by insects (mechanical vectors) has been established (minor role)
• Contamination by inhalation, intradermal or subcutaneous inoculation, or by respiratory, transcutaneous and transmucosal routes

Sources of virus

• Cutaneous lesions (crusts, nodules) resulting in aerosols
• Saliva
•  Nasal secretions
•  Faeces

Occurrence

Sheep pox and goat pox are endemic in most of Africa, the Middle East and Asia

DIAGNOSIS

Incubation period is up to 21 days. Following contact, incubation period is approximately 12 days, but is shorter than this following intradermal inoculation by insects

Clinical diagnosis

• Subclinical cases
• Clinical cases vary from mild to severe:
• fever, depression, polypnoea
• conjunctivitis, lacrimation, rhinitis, oedema of eyelids, photophobia
• cutaneous eruption beginning with erythematous areas especially noticeable in hair or wool-free parts of the body, such as the perineum, inguinal area, scrotum, udder, muzzle, eyelids and axillae
• olesions evolve into papules
• Papulo-vesicular form
• Papules become a white-grey colour, desiccate and form crusts that are easy to remove
• Rarely, papules may transform into vesicles. After rupture of vesicles, a thick crust covers the lesions
• Nodular form (‘stone pox’)
• Papules give rise to nodules involving all the layers of the skin and the subcutaneous tissue
• Necrosis and sloughing of the nodules leaves a hairless scar
• In both forms, nodules develop in the lungs causing bronchopneumonia with cough, abundant nasal discharge, depression, anorexia and emaciation
• Animals may recover within 20-30 days
• Death is frequent when complications occur (abortion, which is rare, secondary infections, fly strike, septicaemia, digestive cularsis)

Lesions

• Skin lesions: congestion, haemorrhage, oedema, vasculitis and necrosis. All the layers of epidermis, dermis and sometimes musculature are involved
• Lymph nodes draining infected areas: enlargement (up to eight times normal size), lymphoid proliferation, oedema, congestion, haemorrhage
• Pox lesions: on mucous membranes of the eyes, mouth, nose, pharynx, epiglottis, trachea, on the rumenal and abomasal mucosae, and on the muzzle, nares, in the vulva, prepuce, testicles, udder, and teats. Lesions may coalesce in severe cases
• Lung lesions: severe and extensive pox lesions, focal and uniformly distributed throughout the lungs; congestion, oedema, focal areas of proliferation with necrosis, lobular atelectasis. Enlargement, congestion, oedema and haemorrhages of mediastinal lymph nodes

Differential diagnosis

• Bluetongue
• Peste des petits ruminants
•  Contagious ecthyma
• Photosensitisation
•  Dermatophilosis
•  Insect bites
• Parasitic pneumonia
• Caseous lymphadenitis
• Mange (scrabies)

Laboratory diagnosis

Procedures

Identification of the agent

• Cell inoculation and identification by immunofluorescence staining of intracytoplasmic inclusion bodies
• Inhibition of cytopathic effect using positive serum
• Antigen detection ELISA

Serological tests

• Virus cularsisd
•  Indirect fluorescent antibody test
• Agar gel immunodiffusion
• ELISA

Samples

• Full skin thickness biopsies taken within 1 week of the first appearance of the lesions
• Lesions in the lungs
• Paired sera

PREVENTION AND CONTROL

No treatment

Sanitary prophylaxis

• Isolation of infected herds and sick animals for at least 45 days after recovery
• Slaughtering of infected herd (as far as possible)
• Proper disposal of cadavers and products
• Stringent disinfection
• Quarantine before introduction into herds
• Animal and vehicle movement controls within infected areas

Medical prophylaxis

• There are numerous attenuated virus vaccines delivered by subcutaneous or intradermal route
• The conferred immunity lasts up to 2 years