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Although the consequences of chlamydial infection may be severe, comparatively little is known about how chlamydiae produce disease. Most of what we do know relates to C. trachomatis infection, which has been studied over the longest period, and for which reasonable experimental model systems are available. However in recent years there has been increasing interest in the mechanisms possibly linking C. pneumoniae and chronic disease.

The most severe sequelae of C. trachomatis infection (visual loss in trachoma; ectopic pregnancy or infertility in pelvic inflammatory disease) are caused by fibrosis and scarring due to the repair of tissue damaged by chlamydial-induced inflammation [see: inflammation and repair]. Apart from the major differences between C. trachomatis associated with lymphogranuloma venereum, on the one hand, and trachoma and lower genital tract infection on the other, there is little evidence for major differences in virulence [lay reader: the capacity to cause disease] between different C. trachomatis types. There is, however, evidence that the host immune response may itself contribute significantly to tissue damage (immunopathology) as well as to immunity. The major determinants of the severity of disease, are:

• socio-environmental factors influencing the number of infecting organisms and the likelihood of repeat infection;
• the magnitude of the initial inflammatory response, (which will partly be determined by pro-inflammatory cytokines etc.) [see: induction of inflammation and repair];
• host genetic factors that regulate the immune response and associated repair mechanisms.

Other determinants less clearly understood may include:

• the sensitivity of the infecting strain to interferon gamma and other potentially protective molecules
• the potential for self-induced immune damage to the host arising from chlamydial heat shock proteins or other chlamydial antigens that are similar to, or mimic, host components see heat shock proteins; heat shock proteins and cell mediated immunity;
• the ability of chlamydiae to become sequestered at immunologically privileged or inaccessible sites (e.g. coronary arteries; joints).
• the ability of chlamydiae to cause or prevent apoptosis (cell death).
  

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Index of immunopathology and associated documents.

[MEW] May 2002