The epidemiology and control of VRE: still struggling to come of age.

Enterococci have caused infections in hospitalized patients for many decades. Given that they were part of the normal flora of the gastrointestinal (GI) tract and that they frequently appeared as part of the flora in infections related to fecal contamination, they originally were considered endogenous pathogens of little nosocomial import. This view began to change with the appearance of enterococci resistant to vancomycin in Europe in 1988.1 Vancomycin resistance appeared subsequent to earlier reports of enterococci resistant to pencillin2 and aminoglycosides,3,4 raising the concern that infections caused by vancomycin-resistant enterococci (VRE) might be difficult, if not impossible, to treat. A 1993 report5 from the National Nosocomial Infection Surveillance system at the Centers for Disease Control and Prevention (CDC) indicated that VRE had appeared in the United States and had increased from 0.3% of nosocomial enterococci in 1989 to 7.9%. The change was even more dramatic for enterococcal isolates in intensive care units, where VRE had increased in the same period from 0.4% to 13.6%, a 34-fold increase in the 4-year period. During the period covered by that report, six VRE outbreaks were reported in the literature.6-11 In 1994, three more publications described outbreaks of VRE.12-14 These studies during the first 5 years of the VRE epidemic (19891994) began to define the epidemiology of VRE colonization and infection and led to the following conclusions: ● VRE colonize or infect very ill and immunocompromised patients (intensive care, oncology, and transplant patients). ● The GI tract is the most important reservoir. ● VRE contaminate patients’ environments. ● Environmental contamination is increased when patients have diarrhea. ● VRE may be transmitted by medical instruments. ● Prolonged hospital stay increases the risk for acquiring VRE. ● Exposure to cephalosporins and vancomycin may increase the risk of colonization by VRE. ● Close proximity to a VRE-positive patient and being cared for by a nurse caring for a VRE-positive patient increases the risk for acquisition of VRE. ● Resistance in VRE is transferable. ● Although not frank pathogens, VRE can cause invasive disease associated with morbidity and possibly mortality. Presently, the rising epidemic of VRE, the limited or absent therapeutic options for treating serious VRE infections, and a concern that the resistance genes in VRE might be transferred to other gram-positive microorganisms such as Staphylococcus aureus led the CDC to publish recommendations from the Hospital Infection Control Practices Advisory Committee for preventing the spread of vancomycin resistance.15 These recommendations were developed using data from studies published during the first 5 years of the VRE epidemic. The recommendations provided guidelines for the prudent use of vancomycin, recommended educational programs for hospital staff regarding the epidemiology and control of VRE, defined the role of the hospital microbiology laboratory, and outlined an approach for the prevention and control of VRE. Recommendations for control included culture surveys to identify patients colonized with VRE, barrier precautions, environmental decontamination, and establishment of a mechanism to ensure that VRE carriers were placed on Isolation Precautions immediately on readmission to the hospital. Since publication of these recommendations, VRE have continued to spread, and the epidemic has not been controlled. In the second 5 years of the epidemic (1994 to the present), only modest additional contributions have been made to our understanding of the epidemiology and control of VRE. Compared to the case-control studies published between 1989 and 1994, case-control studies published in