Many species of Mycoplasma are involved in the pathogenesis of pneumonic syndromes in small ruminants. The common species include Mycoplasma mycoides subspecies mycoides (large colony type), Mycoplasma mycoides subspecies capri, Mycoplasma arginini, Mycoplasma ovipneumoniae, Mycoplasma agalactiae and Mycoplasma capricolum. Contagious caprine pleuropneumonia (CCPP) is a distinct disease entity caused by Mycoplasma biotype F 38. Mycoplasma mycoides subspecies capri is also still being considered as a cause of a mild form of CCPP.
Epidemiology
The sero-prevalence of Mycoplasma spp in goats in south-eastern Nigeria has been found to be 92 % and M. ovipneumoniae, M. agalactiae and M. arginini have been isolated from pneumonic lungs in goats and sheep in different parts of Nigeria. M. arginini, M. mycoides subspecies capri, M. ovipneumoniae and Mycoplasma F strain 38 have been isolated from pneumonic lungs of small ruminants in the Sudan. Mycoplasma F strain 38 and M. mycoides subspecies capri have been isolated from goats in Kenya and Ethiopia while M. mycoides subspecies mycoides (large colony type), M mycoides subspecies capri, M. ovipneumoniae, M. capricolum, M. arginini and M. agalactiae have been isolated from pneumonic lungs of goats in Tanzania.
Mycoplasma spp are labile organisms which are easily destroyed by heat, dehydration, sunlight and common disinfectants and therefore they do not survive for a long time outside the body of the animal. Sources of the infection are the clinically sick and carrier animals and infection occurs by inhalation of infective aerosols. Overcrowding in animal sheds, communal grazing land, water points, markets and dips facilitates rapid spread of the infection within and between herds. Stress factors such as heavy rainfall, cold weather and malnutrition which compromise the immune system of the animal can activate latent infection in carrier animals which start to shed the organisms. A long term carrier state may occur. Nomadic practices facilitate the spread of the disease, as so is stock raiding which is common in East African countries.
Clinical features
The pathogenesis of mycoplasmal pneumonia is similar to pneumonic pasteurellosis, as so are the clinical signs and pathological features. The incubation period may be as short as 3-6 days or as long as 3-4 weeks in natural field infections. CCPP is a highly contagious disease of goats and it is characterised by depression, fever (41.6-41.7°C), anorexia, dyspnoea, coughing, abdominal respiration, reluctance to move, bleating, extension of the neck, frothy or mucopurulent nasal discharges and subcutaneous oedema on the chest and abdomen. Stringy salivation may be observed before death. Death may occur within 2 days of the onset of the clinical signs. Morbidity may reach 100 % and mortality ranges from 60% to 100%. Similar features are manifested by acute pleuropneumonia caused by other Mycoplasma spp. Mycoplasma biotype F 38 does not cause disease in sheep or cattle. In endemic areas animals may suffer a chronic disease which is characterised by catarrhal nasal discharges, debility, emaciation and sometimes enteritis. Recovered animals serve as carriers. The syndrome produced by M. mycoides capri causes a less contagious septicaemic disease characterised by inappetence, respiratory distress, low morbidity and mortality rates. The disease may be acute or subacute and may involve the respiratory, alimentary and reproductive systems.
Pathological features
In early stages, acute CCPP is characterised by formation of yellow nodules and congestion around the nodules. Congestion, consolidation and marbling of the lungs together with fibrinous pleurisy, pleural effusion and distension of the interlobular septae are prominent features. The chronic disease is characterised by thickening of visceral pleura and fibrinous adhesion to the chest wall. No sequestrae are formed as in the case of contagious bovine pleuropneumonia. Histopathologically, Mycoplasma F 38 infection is characterised by intralobular oedema while M. mycoides subspecies capri is characterised by interlobular oedema.
Diagnosis
A provisional diagnosis of CCPP can be based on the epidemiology, clinical and pathological features. The causative organisms can be demonstrated in impression smears or cultures of materials from lung lesions, mediastinal lymph nodes and pleural fluid on Mycoplasma media such as Modified Hayflick and Newings's tryptose B. Serological methods of diagnosis include complement fixation, ELISA and agar gel immunodiffusion. Latex agglutination test is very useful in field diagnosis of CCPP. Monoclonal antibodies are also employed in the diagnosis of CCPP. CCPP has to be differentiated from pneumonia caused by M. mycoides subspecies mycoides (larger colony type), M. mycoides subspecies capri, M. capricolum and pneumonic pasteurellosis. Other diseases to be considered in the differential diagnosis of CCPP include pasteurellosis, verminous pneumonia, PPR and other viral pneumonias.
Treatment and Control
Tylosin (11 mg/kg) is effective in the treatment of CCPP when used in early stages of the disease. Oxytetracycline (15 mg/kg), tiamulin, chloramphenicol and penicillin-streptomycin can also be used. Separation and treatment of the affected animals will minimise the spread of the disease. Susceptible naive animals should be vaccinated before being moved to endemic areas. A saponified inactivated Mycoplasma strain F 38 vaccine has been found to be effective in the control of the disease.
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