Problems and perils of vancomycin resistant enterococci.

Abstract

Enterococci have been a therapeutic challenge for haIfa century; first in the management of endocarditis, then associated with the emergence of resistance to streptomycin and later to all aminoglycosides, and now with the increasing levels of resistance to penicillins. A major leap in the problem of antimicrobial resistance occurred more than a decade ago when vancomycin resistant enterococci (VRE) were first identified. This resulted from the acquisition by Enterococcus faecium of vancomycin resistant genes. Five types of vancomycin resistance have since been described (VanA-VanE) and others also appear to exist. VanA and VanB are caused by complex gene clusters that may be plasmid and/or transposon encoded. As a result of the gene cluster, cell wall precursors in the bacteria are formed that do not allow effective vancomycin binding, thus the action of vancomycin to inhibit cell wall synthesis is prevented. Therapy of infections caused by VRE is difficult, but a number of potentially effective antibiotics are now being tested in humans, including quinupristin/dalfopristin, linezolid, evernimomycin, daptomycin and LY333328. Combinations of antibiotics such as ampicillin with quinupristin/dalfopristin or with imipenem, and newer fluoroquinolones are also being evaluated. Until the time when these drugs become available, we must rely on careful monitoring of microbial transmission in hospitals, and we must utilize multi-faceted approaches to prevent the increase in the number and spread of VRE.