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Outbreak of Vancomycin‐Resistant Enterococci in a Burn Unit
Pamela S. Falk , MPH, Janice Winnike , BSN, Carla Woodmansee , MT(ASCP), M. Desai , MD and C. Glen Mayhall , MD
Infection Control and Hospital Epidemiology
Vol. 21, No. 9 (September 2000), pp. 575-582
Published by: Cambridge University Press on behalf of The Society for Healthcare Epidemiology of America
Stable URL: http://www.jstor.org/stable/10.1086/501806
Page Count: 8
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OBJECTIVE. To investigate and control an outbreak of colonization and infection caused by vancomycin‐resistant enterococci (VRE) in a burn intensive care unit (BICU). DESIGN. Epidemiological investigation, including multiple point‐prevalence culture surveys of patients and environment, cultures from hands of healthcare workers (HCWs), pulsed‐field gel electrophoresis (PFGE) typing of patient and environmental isolates, case‐control study, and institution and monitoring of control measures. SETTING. BICU in an 800‐bed university medical center in Galveston, Texas. RESULTS. Between June 6, 1996, and July 14, 1997, 21 patients were colonized by VRE, and 4 of these patients developed bacteremia. Of 2,844 environmental cultures, 338 (11.9%) were positive, but all hand cultures from HCWs were negative. PFGE typing indicated that the outbreak was clonal, with VRE isolates from patients differing by ≤4 bands from the index case. Thirteen of 14 environmental isolates varied by ≤4 bands from the pattern of the index case. A case‐control study analyzed by exact logistic regression identified diarrhea (odds ratio [OR], 43.9; 95% confidence interval [CI95], 5.5‐infinity; P=.0001) and administration of an antacid (OR, 24.2; CI95, 2.9‐infinity; P=.002) as independent risk factors for acquisition of VRE. During a 5‐week period in October and November 1996, all patient and 317 environmental cultures were negative for VRE. The outbreak recurred from a contaminated electrocardiogram lead that had not been identified during the prior 5 weeks. VRE were finally eradicated from the BICU in July 1997, using barrier isolation and a very aggressive environmental decontamination program. CONCLUSIONS. A VRE outbreak in a BICU over 13 months was caused by a single clone. After apparent eradication of VRE from a BICU, recrudescence of the outbreak occurred, evidently from a small inapparent source of environmental contamination. Changes in gastrointestinal (GI) tract function (motility) and administration of medications, other than antibiotics, that have an effect on the GI tract may increase the risk of GI tract colonization by VRE in burn patients. Application of barrier isolation and an aggressive environmental decontamination program can eradicate VRE from a burn population.
© 2000 by The Society for Healthcare Epidemiology of America. All rights reserved.