Direct detection of Chlamydia pneumoniae in atherosclerotic plaques

Abstract

Chlamydia pneumoniae has recently been established as a third species of the obligate intracellular Chlamydiae. Respiratory epithelium was identified as its primary target and the pathogen is now recognized as an important cause of mild community-acquired pneumonia, pharyngitis, and bronchitis [5,8, 12]. C. pneumoniae is characterized by an extraordinarily high seroprevalence: seroepidemiological surveys indicate virtually everybody to be infected with the organism at least once during lifetime and reinfections to be common [12]. Nevertheless, it has been extremely difficult to recover viable isolates from the site of infection. In fact, this difficulty in adapting primary isolates to the artificial conditions of cell culture has been the reason why this extremely frequent bacterial pathogen has not been identified earlier than 1986 [8]. As chlamydiae are quite notorious for causing persistent disease with severe tissue destruction, concern on sequelae from recurrent chlamydial infection is justified [32]. In this respect, coronary artery disease has been related to prior or persistent C. pneumoniae infection [28-30]. Based on antichlamydial IgG elevation and the presence of immune complexes containing chlamydial lipopolysaccharide in coronary heart disease patients, C. pneumoniae infection was suggested as an independent cardiovascular risk factor in studies from Finland [28, 29]. These results proved reproducible wherever the attempt was made [18, 22, 31]. However, these indirect statistical associations cannot provide evidence of causality.