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Background. Control of vancomycin-resistant Enterococcus fuecium (VRE) in European hospitals is hampered because of widespread asymptomatie carriage of VRE by healthy Europeans. In 2000, our hospital (The University Medical Center Utrecht, Utrecht, The Netherlands) was confronted with a large outbreak of VRE. Intervention. On the basis of genotyping (by pulsed-field gel electrophoresis), epidemic and nonepidemic VRE strains were distinguished, and infection-control measures were exclusively targeted toward epidemic VRE. The outbreak was retrospectively divided into 3 periods of different infection-control measures. Compliance with use of alcohol-based hand rubs was enforced during all periods. Period I involved active surveillance, isolation of carriers, and cohorting (duration, 4 months); preemptive isolation of high-risk patients for VRE colonization was added in period II (7 months); and cohorting and preemptive isolation were abandoned in period III (18 months). Methods. When the outbreak was identified, 27 patients in 6 wards were colonized; 93% were colonized with an epidemic VRE strain. Detection rates of nonepidemic VRE were 3.5%, 3.0%, and 2.9% among 683, 810, and 977 screened patients in periods I, II, and III, respectively, comparable to a prevalence of 2% (95% confidence interval [CI], 1%-3.5%) among 600 nonhospitalized persons. The relative risks of detecting epidemic VRE in periods II and III, compared with period I, were 0.67 (95% CI, 0.41-1.10) for period II and 0.02 (95% CI, 0.002- 0.6) for period III. Infection-control measures were withheld for patients colonized with nonepidemic VRE (76 [54%] of 140 patients with a test result positive for VRE). Use of alcohol-based hand rubs increased by 31%-275% in outbreak wards. Conclusion. Genotyping-targeted infection control, isolation of VRE carriers, enhancement of hand-hygiene compliance, and preemptive isolation successfully controlled nosocomial spread of epidemic VRE infection. [ABSTRACT FROM AUTHOR]

Vancomycin-resistant enterococci (VRE) have emerged as important nosocomial pathogens, initially in the USA, but now also in Europe, where hospital outbreaks are being reported with increasing frequency, although the incidence of VRE infections remains extremely low in most European countries. The recently demonstrated in-human transmission of vancomycin resistance from VRE to methicillin-resistantStaphylococcus aureus(MRSA) in two American patients underscores the potential danger of a coexisting reservoir of both pathogens. As MRSA is already endemic in many European hospital settings, prevention of endemicity with VRE seems relevant, but should be balanced against the costs associated with the implementation of effective strategies. The presence of a large community reservoir of VRE in Europe could hamper the feasibility of infection control strategies. Although the prevalence of colonisation amongst healthy subjects has apparently decreased after the ban on avoparcin use in the agricultural industry, a large proportion of admitted patients are still potential sources of VRE transmission. With no risk profile available to identify these carriers, effective screening, followed by barrier precautions for carriers, seems to be impossible. Recent studies, however, have suggested that hospital outbreaks are almost exclusively caused by specific genogroups of VRE that can be characterised phenotypically and genotypically (e.g., co-resistance to ampicillin and the presence of the variantespgene). Based on our own experience, we propose that VRE infection control programmes should be restricted to patients colonised with these VRE strains. If such a strain is cultured from a clinical sample, surveillance amongst contact patients is recommended and barrier precautions should be implemented in the case of documented spread. [ABSTRACT FROM AUTHOR]