Contagious Caprine Pleuropneumonia

Introduction

Contagious caprine pleuropneumonia (CCPP) is a cause of major economic losses to goat production in at least 30 countries in Africa and Asia containing a total goat population of more than 300 million.
This condition is caused by Mycoplasma capricolum subsp. capricolum and occasionally M. mycoides subsp. capri or M. mycoides subsp. mycoides. It is a member of the Mycoplasma mycoides cluster which includes M. mycoides subsp. mycoides SC (MmmSC), M. mycoides subsp. mycoides LC (MmmLC), M. mycoides subsp. capri (Mmc), M. capricolum subsp. capricolum (Mcca) and Mycoplasma species bovine group 7 (Bg7), an uncharacterized bovine isolate, which causes other diseases of ruminants. CCPP is a significant disease of goats in Africa, the Middle East and Western Asia, and is characterized primarily by its contagious nature. The disease causes interstitial, fibrinous pleuropneumonia, interlobular oedema and hepatization of the lung causing high mortality rates of up to 80% and morbidity rates of up to 100%.
The most important distinguishing features of CCPP, with respect to the other goat respiratory mycoplasmoses, were defined by Hutcheon and are quoted as follows: the disease is readily contagious to susceptible goats; sheep and cattle are not affected by disease; local oedematous reactions do not occur in goats when infective inoculum is given subcutaneously (Hutcheon, 1889).
In natural infections, transmission of the disease is by aerosol. The environment as a whole plays an important role in the appearance, evolution and severity of CCPP. Due to the high sensitivity of mycoplasmas to the external environment, close contact is essential between infected and naive animals for transmission to take place, and, overcrowding and confinement favours close contact and circulation of mycoplasmas. Stress factors due to malnutrition and transport over long distances can predispose the animal to disease. In Africa where extensive and traditional husbandry is practised, pathogens spread when animals meet at watering points and grazing areas.

Signalment

CCPP affects only goats, of any breed, sex or age worldwide. Younger animals tend to suffer more severe clinical signs than adults.

Clinical Signs

The animal may appear generally depressed, dull, weak and lethargic. The animal will be pyrexic and have signs of weight loss of reduced weight gain. If the animal is in milk then milk yield will be severely reduced. Sometimes the disease may manifest as sudden death only.
Respiratory signs include bilateral nasal discharge, dyspnoea, tachypnoea and coughing. Some goats may appear to be in severe respiratory distress.

Pathology

The gross pathological lesions are localized exclusively to lung and pleura and are often unilateral. Affected lungs can be totally hepatized, and have a port wine colour (Thiaucourt and Bölske, 1996). A lung section shows a fine granular texture with various colours, but usually without any thickening of the interlobular septa. There is often an abundant pleural exudate and conspicuous pleuritis. The pleural exudates can solidify and form a gelatinous covering sometimes over the whole lung. In acute cases, the pleural cavity contains an excess of straw-coloured fluid with fibrin flocculations (Kaliner and MacOwan, 1976; Wesonga et al., 1993). In chronic cases there is a black discolouration of the lung tissue and sequestration of the necrotic lung areas. Adhesions between the lung and the pleura are very common and often very thick (MacOwan and Minette, 1977). Histological examination of the lung tissues may show acute serofibrinous to chronic fibrino-necrotic pleuropneumonia with infiltrates of serofibrinous fluid and inflammatory cells, mainly neutrophils, in the alveoli, bronchioles, interstitial septae and subpleural connective tissue. Intralobular oedema is more prominent but interlobular oedema has also been reported. Peribronchial and perbronchiolar lymphoid hyperplasia with mononuclear cell infiltration is also present (MacOwan and Minette, 1976; Kibor, 1990; Wesonga et al., 1998; Msami et al., 1998).

Diagnosis

In the field, diagnosis of mycoplasma pneumonia cannot be established on clinical signs or on postmortem examinations alone. In outbreaks of classical acute CCPP, the high mortality and typical early thoracic lesions in goats are highly indicative of M. capricolum subsp. capripneumoniae infection, but all cases of caprine mycoplasmosis need additional laboratory tests to establish a presumptive diagnosis.

An 'in the field' diagnostic procedure is the latex agglutination test (LAT) (Rurangirwa et al 1987b). This test is based on a polysaccharide isolated from Mccp (Rurangirwa et al 1987a) which is used to sensitise latex beads. The sensitised latex beads are then used to detect serum antibodies from goats infected with CCPP (Rurangirwa et al 1987b). The specificity of LAT was assessed using WM25 monoclonal antibody which is specific for Mccp (Rurangirwa et al 1987c; Belton et al 1994) and reacts with the polysaccharide (Rurangirwa et al 1992). The specificity of LAT was further confirmed by evaluating specific growth inhibiting rabbit antisera to various mycoplasma isolates (Rurangirwa et al 1987c). The sensitised latex beads are stable at 4°C, room temperature and 37°C for over one year. Thus the long shelf-life of the beads at different temperatures makes it possible to prepare large amounts which can be stored until used. The latex agglutination test is an excellent procedure for the diagnosis of CCPP and can be run in two minutes on samples of whole blood or serum, requires no sophisticated equipment or storage facilities and is adaptable to any laboratory or field conditions - an example of a pen-side diagnostic test. The test is carried out by mixing a drop of the sensitised beads with a drop of blood or serum from the suspected animal on a glass slide for one minute and the results read visually and recorded as positive or negative. LAT combined with presenting clinical signs and necropsy indicating fibrinous pleuropneumonia is confirmatory of Mccp associated CCPP.
Definite diagnosis is made by the isolation of M. capricolum subsp. capripneumoniae from clinical samples, usually lung tissue and may be a long and difficult process. The success of isolation depends primarily on the attention that is given to sample collection.
The growth inhibition (GI) test is the simplest and most specific, but the least sensitive of the tests available. It depends on the direct inhibition of mycoplasma growth on solid media by specific hyperimmune serum, and detects primary surface antigens (Dighero et al., 1970).
The direct and indirect fluorescent antibody tests are among the most effective, simple and rapid serological methods of identification for most mycoplasma (Rosendal and Black, 1972). Several forms have been described, the most commonly used one is the indirect fluorescent antibody (IFA) test which is applied to unfixed colonies on agar.
The complement fixation test (CFT) and the indirect haemagglutination test (IHA) are serological methods of diagnosis, as is the ELISA. These have varying degrees of efficacy.
Until recently, isolation was the only way to confirm the presence of CCPP. Diagnostic systems based on PCR have been developed for the rapid detection, identification and differentiation of members of the M. mycoides cluster and the specific identification of M. capricolum subsp. capripneumoniae (Bashiruddin et al., 1994; Hotzel et al., 1996).

The diagnosis of outbreaks of CCPP is complicated by other infectious agents causing similar syndromes. Pleuropneumonic disease resembling Mccp-associated CCPP can also be produced by Mycoplasma mycoides subsp. capri (Mmc) and caprine variants of M. mycoides subsp. mycoides (Mmm). Mmc was originally considered to be the cause of CCPP, but its full importance as a pathogen of goats has now become doubtful, both because of the discovery of the Mccp and because many isolates previously classified as Mmc have subsequently been found to be caprine variants of Mmm. Mmc has been isolated from several countries in Africa and Asia, and from Australia. The disease reproduced experimentally with Mmc is largely restricted to the thoracic cavity, with or without a septicaemic phase and death. In contrast, caprine variants of Mmm generally causes a syndrome which may include not only pleuropneumonia but also mastitis, polyarthritis, keratoconjunctivitis, acute septicaemic death, sometimes with symptoms of the central nervous system, and abortion. Mmm is a major cause of disease in goats in USA, France, Israel and India. Experimentally, the disease caused by Mccp differs from that produced by Mmc and Mmm in: being readily contagious and fatal to susceptible goats; not affecting sheep or cattle; not producing local oedematous reactions when injected subcutaneously; and being characterised histo-pathologically by an interstitial, intralobular oedema of the lung, compared with the thickening of the interlobular septa which is seen with Mmc and Mmm (Kaliner and MacOwan 1976). Pasteurella haemolytica (both biotypes A and T) and P. multocida have also been associated with pleuropneumonia in goats, although experimental evidence of their pathogenicity in this host is meagre.

Treatment and Control

The macrolides (erythromycin, spiramysin, and tylosin), tetracyclines and quinolones are active against M. capricolum subsp. capripneumoniae.
Control measures include prevention of mixing and good hygiene. Movement restrictions and slaughtering infected animals are recommended for countries that are newly infected.

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References

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