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JAC Advance Access published online on September 23, 2008

Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkn390
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

High acquisition and environmental contamination rates of CC17 ampicillin-resistant Enterococcus faecium in a Dutch hospital

Marieke J. A. de Regt1,*, Lotte E. van der Wagen1, Janetta Top1, Hetty E. M. Blok1, Titia E. M. Hopmans1, Adriaan W. Dekker2, Ronald J. Hené3, Peter D. Siersema4, Rob J. L. Willems1 and Marc J.M. Bonten1,5

1 Department of Medical Microbiology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands 2 Department of Haematology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands 3 Department of Nephrology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands 4 Department of Gastroenterology and Hepatology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands 5 Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands

Received 11 July 2008; returned 5 August 2008; revised 12 August 2008; accepted 18 August 2008


* Correspondence address. Department of Medical Microbiology, University Medical Centre Utrecht, G04.614, PO Box 85500, 3508 GA Utrecht, The Netherlands. Tel: +31-88-7555006; Fax: +31-88-7555426; E-mail: m.deregt{at}umcutrecht.nl

Background: Enterococcus faecium has rapidly emerged as a nosocomial pathogen worldwide, and the majority of these isolates belong to clonal complex-17 (CC17). In Europe, CC17 isolates are usually ampicillin-resistant, but most are still vancomycin-sensitive. We aimed to study ampicillin-resistant E. faecium (ARE) epidemiology in our hospital.

Methods: In a 3 month study, 210 of 358 admissions (59%) to haematology and gastroenterology/nephrology were screened for rectal ARE colonization on admission (<48 h) and 148 of 210 (70%) also at discharge (<72 h). In a second (3 month) study, environmental swabs from eight predetermined sites were obtained from ARE-colonized haematology patients once weekly. All ARE isolates were genotyped by multiple-locus variable-number tandem repeat analysis (MLVA).

Results: ARE admission prevalence was 10% and 16% and acquisition rates were 39% and 15% in haematology and gastroenterology/nephrology, respectively. Carriage on admission was associated with previous admission <1 year (OR 5.0, 95% CI 1.8–14.0) and acquisition with β-lactam (OR 2.7, 95% CI 1.1–6.7) and quinolone use (OR 3.1, 95% CI 1.1–8.2). Five of the 57 (9%) colonized patients developed invasive ARE infections. Genotyping revealed 12 genotypes (all CC17) with two MLVA types responsible for 94% of acquisitions. In 18 of the 19 colonized patients, the environment was contaminated with ARE. Sites most often contaminated were the toilet seat (43%), over-bed table (34%) and television remote control (28%).

Conclusions: CC17 ARE epidemiology is characterized by high admission (10% to 16%), acquisition (15% to 39%) and environmental contamination (22%) rates, resulting from cross-transmission, readmission and antibiotic pressure. A multifaceted infection control approach will be needed to curtail further spread.

Key Words: VRE , epidemiology , nosocomial infections


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