Candidemia in the Surgical Intensive Care Unit

contribute to atherogenesis is supported by the results of several epidemiologic studies, which suggest that Helicobacter pylori [5], cytomegalovirus (CMV) [6], herpes simplex virus (HSV) [7], and Chlamydia pneumoniae [8] may have atherogenic effects. However, existing epidemiologic data about the association of some of these pathogens with atherosclerosis are conflicting [9]. Moreover, recently published data [10] support the hypothesis that atherosclerosis has an immunopathological component; these data render it improbable that a single infectious agent should assume particular importance in the initiation or progression of atherogenesis. Our data for 218 consecutive patients (119 men and 99 women; mean age, 64.6 years [range, 29–83 years]) who underwent coronary angiography support the hypothesis of Witkin et al. [1], that “triggers” such as IL-1RA gene polymorphisms or additional exposure to other pathogens could influence the effect of infectious agents on the development of CAD. Blood samples obtained from all subjects were tested for serologic markers of 6 infectious pathogens (C. pneumoniae, hepatitis A virus, H. pylori, CMV, and influenza virus types A and B). We examined the possible association between seropositivity for a particular microbial agent and angiographically proven coronary artery disease (defined as 1 coronary artery with stenosis 150%-diameter). Analysis of serologic markers for all 6 microbial agents demonstrated that seropositivity for a single pathogen was not a predictor of risk for CAD. In contrast, the number of infectious pathogens to which individuals have been exposed (i.e., the “infectious burden”) correlated with the prevalence of CAD. A total of 48.8% of patients with CAD and 31.2% of patients without CAD tested positive for 4 of the 6 serologic markers ( ); 21.3% of P p .02 patients with CAD and 9% of patients without CAD tested positive for 5 of the 6 serologic markers ( ). Therefore, P p .03 our data support the hypothesis of Witkin et al. [1] that some “triggers” such as cytokine-receptor gene polymorphisms or additional exposure to other pathogens could influence a patient’s susceptibility to the atherogenic effect of infection with a particular pathogen.