Vancomycin-resistant enterococci were initially reported in 1986 in Europe. In the last two decades enterococci have become recognized as a leading cause of healthcare associated bacteremia, surgical wound infection, and urinary tract infection. According to the National Nosocomial Infection Surveillance System (NNIS), prior to 1990 the occurrence of VRE infections in ICU’s in the U.S. was less than 1% of all enterococcal infections reported; by 1993 the occurrence had risen to 13.6% and ten years later, in 2003, VRE infections had more than doubled to 28.5%. Though the occurrence of VRE in hospitals was typically associated with larger hospital size (more than 200 beds) and university affiliation, hospitals of other sizes have also reported increases in endemic rates and clusters of VRE colonization and infection, indicating the upward trend is not limited by institution size. Data reported to the CDC during 2004 showed that VRE caused about one of every three infections in hospital intensive care units. This increase poses several problems, including the lack of available antimicrobials for therapy, since most VRE are also resistant to multiple other drugs (e.g., aminoglycosides and ampicillin) previously used for the treatment of infections due to these organisms. Many VRE are resistant to all presently available antibiotics. Several case-control and historical-cohort studies show that the risk of death associated with antibiotic-resistant enterococcal bacteremia is several times higher than the risk of death associated with susceptible enterococcal bacteremia.
In addition, evidence suggests the vancomycin-resistant gene (VAN A gene) present in VRE may be transmitted to other gram-positive organisms, such as S. aureus. Though VRE is neither more infectious nor more virulent than susceptible enterococci, it poses a greater challenge because treatment options are limited to combinations of antimicrobials or experimental compounds with unproven efficacy.