Immune responses to mycoplasma infections of the respiratory tract.

Mycoplasmas are capable of causing respiratory disease in a number of species of animals. The pathogenicity of the mycoplasma species ranges from those that cause major disease outbreaks and economic loss to what might be considered the more highly evolved and successful parasites at the other end of the spectrum that survive for long periods in the host without being recognised and evicted. This prolonged colonisation of mucous membranes which is typical of many mycoplasmas is related to certain unique features of the mycoplasma and its interaction with the hosts immune system. An initial step in infection is the attachment of the mycoplasma to the epithelial lining of the respiratory tract. Lack of cell wall confers plasticity and may engender the intimate association of mycoplasma and host cell that has been noted. This in turn may favour persistence of the extracellular parasite. Before the specific immune response is produced avoidance of the non-specific immune mechanisms would clearly aid survival. Both passive (capsules) and active (toxic effects) mechanisms of avoiding phagocytosis have been proposed. Both humoral and cell mediated responses are generated by mycoplasma infections. The serum antibody response follows the usual course IgM, G and A. The indications of cell mediated immunity that have been reported include; delayed type hypersensitivity reactions, lymphocyte transformation responses and inhibition of macrophage migration. The concept that the pathological lesions are in a large part due to host reactivity is well accepted. The lung lesions may contain infiltrating and dividing lymphocytes some of which are producing specific antibody. Evidence for the lung lesion in some animals being partly due to the hosts cell mediated response has also been produced. The local immune response appears to be of greater relevance to immunity to infection than the systemic response, in general the association between local antibody and immunity is much better than for serum antibody. Of particular note is the high contribution of local IgG production, particularly in the lower respiratory tract. Attempts are now being made to use this increased understanding to produce effective killed vaccines that produce immune responses in the lung. Such studies will hopefully lead to the development of 'killed' vaccines that are effective. It can be urged that mycoplasmas would be less pathogenic if they did not produce an inflammatory response and some species have been shown to have an immunosuppressive effect. Such a property could affect the lesion, and hence pathogenicity, and also aid mycoplasma persistence.(ABSTRACT TRUNCATED AT 400 WORDS)