Contagious Bovine Pleuropneumonia (CBPP)

Contagious Bovine Pleuropneumonia (CBPP) is primarily a disease of cattle caused species of Mycoplasma.

Contagious Bovine Pleuropneumonia (CBPP) is characterized by fever, agalactia, anorexia, depression, coughing, thoracic pain, back arched back, dyspnoea, expiratory grunt, pleuritic friction rubs, dull areas of lung, edema of throat and dewlap.

Contagious Bovine Pleuropneumonia (CBPP) in a Calf

Etiology

CBPP is caused by Mycoplasma mycoides susbspecies mycoides small colony ( MmmSc). Six closely related members of this species affects cattle, sheep and goats but it is not spread to other species. The organism is pleomorphic. The organism can be grown in a special media and embryonated hens eggs.

Epidemiology

Prevalence of infection

It is reported to be endemic in most parts of Africa.

Economic impacts

It is the most economically important disease in cattle in Africa and has been imposed directly due to mortality, decreased milk yield, vaccination, disease surveillance and research program, and less due to quarantine, loss of trade, and fatal nature of the disease.
Indirectly, the losses occurs via loss of weight, working ability, delayed marketing, decreased fertility, long quarantine period, loss of trade and fatal nature of the disease.

Predisposing factors

The disease is mainly influenced by the environment including disinfectants, heat, and drying but the organism unable to survive in the environment without a host.
Stress due to starvation, exhaustion, inter current disease can cause the sequestrum to break down and convert the animals into and active cases.
The infected animals carry potential organism for at least 3 years period.

Sources of infection

Large number of viable organism are passed through urine.
The organsm is isolated from semen, preputial washings, milk, urine frozen embryos of cows and bulls.
Placenta and urine are infective for a long period.
Chronic carriers are less infective than clinical cases.
In Asia, CBPP has been reported in India, Bangaladesh, Myanmar.
Sporadic outbreaks have been recognized in Middle East was attributed to importation of cattle from Africa.

Transmission

Direct and repeated contacts between sick and healthy animals.
Inhalation of infective droplets from active or carrier animals is the principal route of infection.
Though the distance one meter between animal is usually considered to be sufficient, but the disease is reported to spread over 45m distance.
Aerosol and indirect transmission occurs.

Host Susceptible

Cattle are the only species predominantly affected by the organism. However, natural infection also occurs in a wide variety of animals such as buffalo, yak, bison, reindeer, and antelopes.
In sheep and goats infection causes local cellulitis without pulmonary movement.
No difference in susceptibility of Bos Taurus and Bos Indicus cattle.

Pathogenesis

Cattle may need at least 8 months period (longer incubation period) before they infected and to show the signs and so require longer period of quarantine.

The disease spread principally through inhalation of infected droplets. The organism possess carbohydrate cell capsule and produce hydrogen peroxide. It develops an acute lobar pneumonia, pleurisy and invades the lungs of cattle to cause mycoplasmemia resulting in localization in numerous other sites including kidneys, brain, leads to high morbidity and mortality.

Thrombosis in pulmonary vessels prior to the development of pneumonic lesions and there is no general increase in blood coagulability and no generalised tendency to spontaneous thrombosis.

Galactan is associated with pathogenicity of the organism but its mode of action is uncertain. Galacan can cause necrosis, and a connective tissue response in cattle similar to the sequestrum in chronically infected animals.

Following infection the organism is isolated from bulls semen. Death results from anoxia and toxaemia.

Clinical Signs

Per Acute Form

Affected cattle may die in a week after the onset of respiratory distress.

Acute form

The incubation period is 3-6 weeks and may exceeds 6 months sometimes.
It is characterized by sudden onset of high fever 40 degree celcius, a fall in milk yield, anorexia and cessation of rumination.
Severe depression, animals stand apart or lag behind other group.
Cough at the initial period during exercise, thoracic pain, disinclined to move, standing with the elbow out, arched back, extended head, shallow and rapid respiration with expiratory grunting.
Pain evinced on percussion of chest.
Auscultation reveals a pleuritic friction, sounds in early stages, dullness, fluid sounds, moist gurgling, noise in later stages of infection.
Edematous swelling of throat, and dewlap, swelling on large movable joints, in calves valvular endocariditis, myocarditis noticed
In fatal cases death occurs at a variable course from several days to 3 weeks.

Chronic and Sub Acute Form

Recovered animals may be clinically normal but in some animals inactive sequestrum forms in the lung with a necrotic centre of sufficient size to produce toxaemia causing unthriftiness.
A chronic cough, mild respiratory distress.
During exercise this sequestra commonly break down when the animal is exposed to environmental stress and cause an acute attack of disease.

Necropsy Findings

Lesions limited to thoracic cavity, lungs and the lesion is unilateral.
The pleural cavity contain large quantity of clear, yellow brown fluid containing pieces of fibrin.
This fluid is ideal for culture of the organism.
Caseous fibrinous deposits are present on the parietal and visceral surfaces of the lungs.
The interlobular septae are prominently distended with amber colored fluid surrounding distended lymphatics.
This fluid distinctly outlines the lobules which vary in color with red, gray or yellow hepatisation.
Consolidation of lungs with a typically marbled appearance is characteristic.
In chronic or advance case a sequestrum of necrotic lung varying size from 1-10 cam in diameter. Which may be surrounded by a fibrinous capsule.
The sequestrum rupture and are drained by a bronchus. This could be a source for aerosol infection to cattle, this may pave way for epidemics in closed herds.
In calves exudative peritonitis, arthritis, bursitis and fibrinous arthritis of carpal and tarsal joints present.

Diagnosis

Based on clinical signs and necropsy findings.
Isolation and identification of organism.
Molecular diagnosis by PCR
Latex Agglutination Test
Complement Fixation Test (CFT)
Slide floculation and rapid slide agglutination test

Sample Collection

Blood
Serum
Nasal discharge
Pleural fluid
Pulmonary tissue

Differential Diagnosis

Foot and Mouth Disease
Rinderpest
Haemorrhagic Septicemia
Theileriosis
Ephemeral fever
Pulmonary abscesses
Farcy
Actinobacillosis
Echinococcus (Hydatidosis)

Prevention

Vaccination of in contact cattle.
Vaccination of healthy cattle
Disposal of sick cattle in an epidemic outbreak.
Revaccination of cattle at risk.

Control

Disposal of all sick and contacted animals.
At herd level, removal of sources of infection by identification of infected animals and their removal.
It is necessary to do at least two negative tests at 2 months intervals before the herd is classified as free from infection and vaccination of all animals at risk.
Maintenance of hygiene and vaccination is effective.
OIE (The office International Des Epizootics planed to eradicate the infection in stages).
- First stage: Declaration of provisional freedom from diseases by increasing the surveillance including monitoring, inspection and vaccination. After two years the country can declare second stage of freedom from the disease.
- Second stage: No clinical disease, no vaccination and an adequate surveillance. The disease reporting system and effective measures to prevent introduction of disease. Following next two years, declare freedom from infection.
- Third stage: Continueous monitoring. All cases would be reported and vaccination would not be permitted. Then declare freedom of infection.