VANCOMYCIN-RESISTANT ENTEROCOCCI

OBJECTIVE: TO review vancomycin resistance in enterococci (Enterococcu s faecalis and Enterococcus faecium) with respect to history, epidemio logy, mechanism of resistance, and management. DATA SOURCES: A MEDLINE , IDIS, and current journal search of English-language articles on van comycin-resistant enterococci (VRE) published between 1982 and 1994 wa s conducted. STUDY SELECTION: Studies and reports pertaining to vancom ycin-resistant E. faecalis and E.faecium were evaluated. Case reports, cohort, epidemiologic, in vitro and in vivo studies were evaluated. D ATA EXTRACTION: Reports in which vancomycin minimum inhibitory concent rations were 32 mu g/mL or more were evaluated. DATA SYNTHESIS: Large outbreaks of VRE infection have occurred as a result of nosocomial spr ead. Such outbreaks have required intensive infection control procedur es to limit the spread of VRE. Vancomycin resistance in E. faecalis an d E. faecium has been subdivided into phenotypes, VanA and VanB. The m echanism of vancomycin resistance is caused by the production of depsi peptide D-Ala-D-Lac, which replaces D-Ala-D-Ala in the peptidoglycan p athway, thereby preventing the binding of vancomycin to D-Ala-D-Ala in the peptidoglycan cell wall. The vanA gene is associated with a trans positional element (Tn1546) that can be transferred via conjugation wh ile most data suggest that vanB has an endogenous origin. Education, a ggressive infection control practices, surveillance programs, and appr opriate use of vancomycin are necessary to respond to the VRE problem. CONCLUSIONS: The prevalence of VRE has increased significantly in rec ent years and has become a worldwide problem. Several factors, such as prior exposure to vancomycin and antibiotics (e.g., cephalosporins, a ntianaerobic agents), physical location in the hospital, immunosuppres sion, prolonged hospital stay, and VRE gastrointestinal colonization a re associated with VRE infection and colonization, Antibiotic treatmen t of serious VRE infection depends on the phenotype. Optimal treatment of the VanA phenotype is unknown; the VanB phenotype may be treated w ith teicoplanin and an aminoglycoside.