Third-Generation Cephalosporins and Vancomycin as Risk Factors for Postoperative Vancomycin-Resistant Enterococcus Infection

Abstract

S INCE THE late 1980s, group D enterococcus (GDEN), including Enterococcus faecalis and Enterococcus faecium, has emerged as an important nosocomial pathogen. Once thought to be a nonpathogen or a copathogen, GDEN has been shown to have the virulence factors necessary to cause infections in varied patient populations. Strains of GDEN resistant to multiple antibiotics have been studied as clinically problematic pathogens in surgical patients. Increased incidence of vancomycin-resistant enterococcus (VRE) has been identified as a serious complication in recipients of solid organ transplants. Throughout the emergence of GDEN as a recognized pathogen, antibiotic use has been cited consistently as a significant risk factor for infection. As antibiotic resistance among enterococci developed and VRE became endemic in many institutions, vancomycin hydrochloride and third-generation cephalosporins (3CGs) have been associated repeatedly with acquisition of VRE. The most commonly held theory on the mechanism by which broad-spectrum antibiotics such as 3GCs select for VRE is a disruption of the patient’s endogenous intestinal microbial flora. This disruption allows for accelerated growth of opportunistic pathogens, such as enterococci. Fairview-University Medical Center, in Minneapolis, Minn, is a large (.300bed) tertiary care teaching hospital. A marked increase in the number of surgical patients with VRE beginning on September 3, 1993, prompted the design of a 1:1 matched case-control study to investigate 3GC use as a risk factor for infection with VRE. By matching patients with VRE infections and those with vancomycinsensitive enterococcus (VSE) infections, we sought to identify the risk factors specific for infection with VRE as opposed to infection with enterococci in general. PAPER