CID 2000;30 (June) Brief Reports 947

1: 16) IgA antibody (62 % of case patients vs. 50 % of control patients; ) and IgM antibody (10 % vs. 0%;).P =.17 P =.02 However, the relationship between AAA and the presence of IgA antibodies was attenuated after adjustment (adjusted OR, 1.17). We found that serological evidence of past infection with C. pneumoniae is positively associated with AAA. However, cautious interpretation of these results is warranted. A re-stricted sample size resulted in imprecise OR estimates. Fur-thermore, the pathological implications of serological evi-dence of C. pneumoniae infection are uncertain. Nevertheless, these ®ndings may lead to important insights into the etiology and pathophysiology of AAA. Infection of aortic tissue by other infectious agents, chie¯y Treponema pallidum, has long been recognized as a cause of AAA. In vitro and animal model studies have shown that the arterial system is a potential target tissue for C. pneumoniae infection [8, 9], and at least 2 studies have demonstrated that AAA tissue often harbors evidence of infection [5, 6]. In addition, a recent study discovered C. pneumoniae ± speci®c T lym-phocytes among in vivo activated cells from AAA tissue, suggesting that C. pneumoniae might be more than an ªin-nocent bystanderº [10]. Further research into the possible etiologic role of C. pneumoniae in aortic aneurysm is warranted