Chlamydia pneumoniae, asthma, and COPD: what is the evidence?

Reading this article will familiarize the reader with (1) the unique chlamydial intracellular life cycle and the propensity for human chlamydial infections to become persistent and to result in immunopathologic (inflammatory) damage in target organs and (2) current evidence linking Chlamydia pneumoniae (Cpn) infection to obstructive lung diseases (asthma and chronic obstructive pulmonary disease, COPD). Potential therapeutic implications of the Cpn-asthma association are also discussed.

All Medline articles (January 1985 to March 1999) that cross-referenced the exploded MESH headings "lung diseases, obstructive" and "Chlamydia pneumoniae" (N = 76). Additional referenced articles, published abstracts, book chapters, and conference proceedings were also utilized.

(1) Case reports and case series that identified Cpn infection in asthma and/or COPD and (2) epidemiologic studies of markers for Cpn infection in asthma and/or COPD that included one or more control groups.

Of 18 controlled epidemiologic studies (over 4000 cases/controls), 15 found significant associations between Cpn infection and asthma using organism detection (polymerase chain reaction (PCR) testing (n = 2 studies) or fluorescent antigen testing (n = 1)), Cpn-specific secretory IgA (sIgA) antibody testing (n = 1), and/or specific serum IgE (n = 2), IgA (n = 4), IgG (n = 3) or other antibody criteria (n = 7). Eight case reports and 13 case series of Cpn infection in asthma (over 100 patients) also include descriptions of improvement or complete disappearance of asthma symptoms after prolonged antibiotic therapy directed against Cpn. Significant associations with COPD (over 1000 cases/controls) were reported in 5 of 6 studies. Results of treating chronic chlamydial infections in COPD patients have not been reported.

Although the full clinical significance of these Cpn-obstructive lung disease associations remains to be established, reports of asthma improvement after treatment of Cpn infection deserve further investigation. Clinicians who manage asthma should be aware of this information since it may help to manage difficult cases. The hypothesis that Cpn infection in COPD can amplify smoking-associated inflammation and worsen fixed obstruction also deserves further study.