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The relation between Chlamydia pneumoniae and atherosclerosis.

A causative role of infection in the pathogenesis of atherosclerosis was first proposed in 1908 by Sir William Osler.' Although originally this view was not widely accepted, there is now renewed interest in the contributions made by common chronic infections to the pathogenesis and progression of coronary artery disease (CAD). The modemr "response to injury" model of atherosclerosis acknowledges that infection may initiate and perpetuate endothelial damage2 but the contribution of other mechanisms-metabolic, inflammatory, or haemostatic-also needs to be considered. The latest infective agent to be implicated in atherosclerosis is Chlamydia pneumoniae, a Gram negative obligate respiratory pathogen. C pneumoniae is a common cause of bronchitis and pneumonia, but infection is usually subclinical and follows a benign course. Up to 60% of the population have serological evidence of previous infection and individuals are probably infected several times throughout their lives or harbour chronic infection. Because culture of the organism is difficult, confirmation of infection often requires a systemic antibody response to be identified.3