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Epidemiology, prevention and control of vancomycin-resistant enterococci

Author
Deverick J Anderson, MD, MPH
Section Editor
Anthony Harris, MD, MPH
Deputy Editor
Elinor L Baron, MD, DTMH

INTRODUCTION

Vancomycin-resistant enterococci (VRE) are an increasingly common and difficult-to-treat cause of hospital-acquired infection. The epidemiology of VRE and strategies for preventing its spread will be reviewed here. The infection control measures described are applicable to all resistant enterococci.

The mechanisms of vancomycin resistance, infections caused by VRE, and the treatment of VRE are discussed separately. (See "Mechanisms of antibiotic resistance in enterococci" and "Microbiology of enterococci" and "Treatment of enterococcal infections".)

DEFINITIONS

Vancomycin inhibits enterococci by binding to the D-alanyl-D-alanine (D-Ala-D-Ala) terminus of cell wall precursors, compromising the subsequent enzymatic steps in the synthesis of cell wall. High-level resistance to vancomycin is encoded by different clusters of genes referred to as the vancomycin-resistance gene clusters (eg, vanA, vanB, and vanD gene clusters).

The end result is the replacement of D-Ala-D-Ala–ending peptidoglycan precursors with D-alanyl-D-lactate termini, to which vancomycin binds with significantly lower affinity. The replacement of D-alanine by D-lactate, which disrupts one of the five hydrogen bonds required for the interaction of vancomycin with its target, increases the minimum inhibitory concentration (MIC) of vancomycin almost 1000-fold. (See "Mechanisms of antibiotic resistance in enterococci", section on 'Vancomycin resistance'.)

In the 2006 report from the Clinical and Laboratory Standards Institute, the following MIC definitions were used for vancomycin susceptibility and resistance in enterococci [1]:

                      

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Literature review current through: Nov 2016. | This topic last updated: Tue Sep 22 00:00:00 GMT+00:00 2015.
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