Vancomycin-Resistant Enterococci

Abstract

Objective To review vancomycin resistance in enterococci ( Enterococcus faecalis and Enterococcus faecium) with respect to history, epidemiology, mechanism of resistance, and management. Data Sources A MEDLINE, IDIS, and current journal search of English-language articles on vancomycin-resistant enterococci (VRE) published between 1982 and 1994 was conducted. Study Selection Studies and reports pertaining to vancomycin-resistant E.faecalis and E. faecium were evaluated. Case reports, cohort, epidemiologic, in vitro and in vivo studies were evaluated. Data Extraction Reports in which vancomycin minimum inhibitory concentrations were 32 μg/mL or more were evaluated. Data Synthesis Large outbreaks of VRE infection have occurred as a result of nosocomial spread. Such outbreaks have required intensive infection control procedures to limit the spread of VRE. Vancomycin resistance in E. faecalis and E. faecium has been subdivided into phenotypes, VanA and VanB. The mechanism of vancomycin resistance is caused by the production of depsipeptide D-Ala-D-Lac, which replaces D-Ala-D-Ala in the peptidoglycan pathway, thereby preventing the binding of vancomycin to D-Ala-D-Ala in the peptidoglycan cell wall. The vanA gene is associated with a transpositional element (Tn1546) that can be transferred via conjugation while most data suggest that vanB has an endogenous origin. Education, aggressive infection control practices, surveillance programs, and appropriate use of vancomycin are necessary to respond to the VRE problem. Conclusions The prevalence of VRE has increased significantly in recent years and has become a worldwide problem. Several factors, such as prior exposure to vancomycin and antibiotics (e.g., cephalosporins, antianaerobic agents), physical location in the hospital, immunosuppression, prolonged hospital stay, and VRE gastrointestinal colonization are associated with VRE infection and colonization. Antibiotic treatment of serious VRE infection depends on the phenotype. Optimal treatment of the VanA phenotype is unknown; the VanB phenotype may be treated with teicoplanin and an aminoglycoside.