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Antimicrobial Agents and Chemotherapy, August 2003, p. 2492-2498, Vol. 47, No. 8
0066-4804/03/$08.00+0 DOI: 10.1128/AAC.47.8.2492-2498.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Di Olden,1 Stephen Pearson,3 Clare Franklin,4 Denis Spelman,4 Barrie Mayall,3 Paul D. R. Johnson,1,
and M. Lindsay Grayson1,2,
Department of Infectious Diseases, Monash Medical Centre, Clayton,1 Department of Epidemiology and Preventive Medicine, Monash University, Melbourne,2 Department of Microbiology, Austin & Repatriation Medical Centre, Heidelberg,3 Microbiology Department, Alfred Hospital, Prahran, Victoria, Australia4
Received 26 August 2002/ Returned for modification 13 January 2003/ Accepted 7 May 2003
Accurate assessment of the risk factors for colonization with vancomycin-resistant enterococci (VRE) among high-risk patients is often confounded by nosocomial VRE transmission. We undertook a 15-month prospective cohort study of adults admitted to high-risk units (hematology, renal, transplant, and intensive care) in three teaching hospitals that used identical strict infection control and isolation procedures for VRE to minimize nosocomial spread. Rectal swab specimens for culture were regularly obtained, and the results were compared with patient demographic factors and antibiotic exposure data. Compliance with screening was defined as "optimal" (100% compliance) or "acceptable" (minor protocol violations were allowed, but a negative rectal swab specimen culture was required within 1 week of becoming colonized with VRE). Colonization with VRE was detected in 1.56% (66 of 4,215) of admissions (0.45% at admission and 0.83% after admission; the acquisition time was uncertain for 0.28%), representing 1.91% of patients. No patients developed infection with VRE. The subsequent rate of new acquisition of VRE was 1.4/1,000 patient days. Renal units had the highest rate (3.23/1,000 patient days; 95% confidence interval [CI], 1.54 to 6.77/1,000 patient days). vanB Enterococcus faecium was the most common species (71%), but other species included vanB Enterococcus faecalis (21%), vanA E. faecium (6%), and vanA E. faecalis (2%). The majority of isolates were nonclonal by pulsed-field gel electrophoresis analysis. Multivariate analysis of risk factors in patients with an acceptable screening suggested that being managed by a renal unit (hazard ratio [HR] compared to the results for patients managed in an intensive care unit, 4.6; 95% CI, 1.2 to 17.0 [P = 0.02]) and recent administration of either ticarcillin-clavulanic acid (HR, 3.6; 95% CI, 1.1 to 11.6 [P = 0.03]) or carbapenems (HR, 2.8; 95% CI, 1.0, 8.0 [P = 0.05]), but not vancomycin or broad-spectrum cephalosporins, were associated with acquisition of VRE. The relatively low rates of colonization with VRE, the polyclonal nature of most isolates, and the possible association with the use of broad-spectrum antibiotics are consistent with either the endogenous emergence of VRE or the amplification of previously undetectable colonization with VRE among high-risk patients managed under conditions in which the risk of nosocomial acquisition was minimized.
Present address: Infectious Diseases and Microbiology Departments, Austin & Repatriation Medical Centre, Studley Rd., Heidelberg, VIC 3084, Australia.
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