Outbreak of vancomycin-resistant enterococci in a burn unit

Citation
Ps. Falk et al., Outbreak of vancomycin-resistant enterococci in a burn unit, INFECT CONT, 21(9), 2000, pp. 575-582
Citations number
29
Categorie Soggetti
Envirnomentale Medicine & Public Health
Journal title
INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
ISSN journal
0899823X → ACNP
Volume
21
Issue
9
Year of publication
2000
Pages
575 - 582
Database
ISI
SICI code
0899-823X(200009)21:9<575:OOVEIA>2.0.ZU;2-E
Abstract
OBJECTIVE: To investigate and control an outbreak of colonization and infec tion caused by vancomycin-resistant enterococci (VRE) in a burn intensive c are unit (BICU). DESIGN: Epidemiological investigation, including multiple point-prevalence culture surveys of patients and environment, cultures from hands of healthc are workers (HCWs), pulsed-field gel electrophoresis (PFGE) typing of patie nt acid environmental isolates, case-control study, and institution and mon itoring 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 colonize d by VRE, and 4 of these patients developed bacteremia. Of 2,844 environmen tal cultures, 338 (11.9%) were positive, but all hand cultures from HCWs we re negative, PFGE typing indicated that the outbreak was clonal, with VRE i solates from patients differing by less than or equal to 4 bands from the i ndex case. Thirteen of 14 environmental isolates varied by less than or equ al to 4 bands from the pattern of the index case. A case-control study anal yzed by exact logistic regression identified diarrhea (odds ratio [OR], 43. 9; 95% confidence interval [CI95], 5.5-infinity; P=.0001) and administratio n 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 Novem ber 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 f rom the BICU in July 1997, using barrier isolation and a very aggressive en vironmental 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 environment al contamination. Changes in gastrointestinal (GI) tract function (motility ) and administration of medications, other than antibiotics, that have an e ffect on the GI tract may increase the risk of GI tract colonization by VRE in burn patients. Application of barrier isolation and an aggressive envir onmental decontamination program can eradicate VRE from a burn population.