Mycoplasma capricolum subsp. capricolum

Introduction

This bacteria is also known as: M. capricolum

Mycoplasma capricolum
Phylum	Firmicutes
Class	Mollicutes
Order	Mycoplasmatales
Family	Mycoplasmataceae
Genus	Mycoplasma
Species	M.capricolum

M.capricolum subsp. capricolum is a species of the Mycoplasmas genus. It causes the serious and economically devastating condition in goats and sheep in Africa and Asia called Contagious Caprine Pleuropneumonia. The bacteria was previously known as Mycoplasm F38, before its specificity was known and it was renamed according to the species it pathogenised.

M. capricolum subsp. capripneumoniae is a member of the Mycoplasma mycoides cluster which are a phylogenetically related grouping of ruminant mycoplasmas and include M.capricolum subsp. capricolum, M. mycoides subsp. mycoides SC, M. mycoides subsp. mycoides LC, M. mycoides subsp. capri, and Bg7. The phenotypic and genetic traits shared in this group have their basis in conventional biochemical and immunological tests such as colony size and growth characteristics, substrate utilization, isozyme patterns, protein profiles and DNA hybridization studies (Rodwell, 1982; Salih and Rosenbusch, 1983; Cottew et al., 1987). A close relationship between M. capricolum subsp. capripneumoniae and M. capricolum subsp. capricolum was found by DNA probes and sequence comparison of members of the M. mycoides cluster but a probe capable of distinguishing between them was developed indicating that they were differences between the species (Taylor et al., 1992). Comparisons of sequences of a putative membrane protein from these strains also showed a close relationship between M. capricolum subsp. capripneumoniae and M.capricolum subsp. capricolum which together with Bg7 formed a subcluster distinct from the M. mycoides subspecies (Thiaucourt et al., 2000).

Phylogenetic groupings have been made by close examination of the sequences from both operons of 16S rRNA from many mycoplasmas and confirm the position of M. capricolum subsp. capripneumoniae within the M. mycoides cluster which is in the spiroplasma group (Weisburg et al., 1989; Bascuñana et al., 1994; Pettersson et al., 1996a; Pettersson et al., 1996b; Pettersson et al., 1998). Intraspecific variations in these genes from M. capricolum subsp. capripneumoniae strains from diverse geographic areas have shown the existence of two evolutionary lines, and this has also been the finding from molecular typing by the AFLP (amplified fragment length polymorphism) method (Kokotovic et al., 2000). Analyses of the 16sRNA genes from a narrower ranging group of strains have also shown sequence differences, and collectively, the number of differences between these strains was found to be greater that the number of differences used to distinguish between species of mycoplasmas. Nevertheless, 16S rRNA gene sequence analysis may be a useful epidemiological tool for M. capricolum subsp. capripneumoniae (Heldtander et al., 2001).

The polysaccharide capsule of M. capricolum subsp. capripneumoniae may have a similar role to that described for M. mycoides subsp. mycoides SC in contagious bovine pleuropneumonia (CBPP) (Rurangirwa et al., 1987). The galactan capsules are generally considered to promote pathogenicity either directly by toxic effects, or by promoting resistance to phagocytosis (Rosenbusch and Minion, 1992).

There is very little information on the pathogenic mechanisms of M. capricolum subsp. capripneumoniae, although some hypothesis can be drawn from comparison with other mycoplasmoses and especially with CBPP (Thiaucourt and Bölske, 1996). A striking feature of CCPP is the host and tissue specificity of the causative agent, as lesions are produced only in goat lungs. Some mycoplasmas have adhesins, but no such component has yet been described for M. capricolum subsp. capripneumoniae. Although M. capricolum subsp. capripneumoniae is present in high quantities in affected lungs, there is no dissemination to other organs. This may be due to a specific reaction of the lung tissue towards a mycoplasmal component that leads to an exacerbated inflammatory response (Thiaucourt and Bölske, 1996).

== Clinical Signs The disease causes acute onset pleuropneumonia with pyrexia, weight loss and agalactia. The disease is notifiable to the World Organisation for Animal Health (OIE).

Diagnosis

M.capricolum can be identified by growth inhibition disc tests. There are inactivated vaccines available.

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

Macrolides, tetracyclines and quinolones are active against this organism.

References

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Images

Picture Title Caption Copyright CCPP Diagnostic Media Mycoplasma capricolum subsp. capripneumoniae strain F38 colonies after 7 days of incubation on CCPP Diagnostic Media (Mycoplasma Experience, Reigate, UK) showing dark pigmentation and red crystalline deposits. Mycoplasma Experience, Reigate, UK

Date of report: 07/04/2011

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