Emergence and spread of vancomycin resistance among enterococci in Europe.

G. Werner*, T. M. Coque, A. M. Hammerum, R. Hope, W. Hryniewicz, A. Johnson, I. Klare, K. G. Kristinsson, R. Leclercq, C. H. Lester, M. Lillie, C. Novais, B. Olsson-Liljequist, L. V. Peixe, E. Sadowy, G. S. Simonsen, J. Top, J. Vuopio-Varkila, R. J. Willems, W. WitteN. Woodford

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

375 Citations (Scopus)


Nowadays, six types of acquired vancomycin resistance in enterococci are known; however, only VanA and to a lesser extent VanB are widely prevalent. Various genes encode acquired vancomycin resistance and these are typically associated with mobile genetic elements which allow resistance to spread clonally and laterally. The major reservoir of acquired vancomycin resistance is Enterococcus faecium; vancomycin-resistant Enterococcus faecalis are still rare. Population analysis of E. faecium has revealed a distinct subpopulation of hospital-acquired strain types, which can be differentiated by molecular typing methods (MLVA, MLST) from human commensal and animal strains. Hospital-acquired E. faecium have additional genomic content (accessory genome) including several factors known or supposed to be virulence-associated. Acquired ampicillin resistance is a major phenotypic marker of hospital-acquired E. faecium in Europe and experience has shown that it often precedes increasing rates of VRE with a delay of several years. Several factors are known to promote VRE colonisation and transmission; however, despite having populations with similar predispositions and preconditions, rates of VRE vary all over Europe.

Original languageEnglish
JournalEuro surveillance : bulletin européen sur les maladies transmissibles = European communicable disease bulletin
Issue number47
Publication statusPublished - 20 Nov 2008


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