Vancomycin-resistant enterococci: an ongoing challenge for infection control.

Enterococci are part of the normal human flora. Enterococcus faecalis und Enterococcus faecium are the most common species isolated from human infections. Vancomycinresistant enterococci (VRE) have emerged as a major cause of nosocomial infection as early as 1986 [1]. 10 years later, >15% of nosocomial enterococcal infections in United States hospitals were due to VRE, and even higher in intensive care units. E. faecium is the most commonly identified species identified. Enterococci are inherently resistant to many antibiotics, in particular to all cephalosporins. Today, >80% of all strains of E. faecium are ampicillinresistant in Switzerland (www.anresis.ch), and approximately 5% are VRE. In contrast, E. faecalis remains susceptible to ampicillin in 97%, and detection of VRE among E. faecalis is rare. VRE belong to the multiresistant pathogens that rapidly spread and are difficult to treat [1, 2] Inducible vancomycin resistance in enterococci is due to a sophisticated mechanism that combines synthesis of cell wall peptidoglycan precursors with low affinity for glycopeptides and elimination of the normal target precursors. Similar to other multiresistant pathogens, VRE was observed in Europe, and in 1994, VRE were first isolated in Switzerland [3, 4]. Vancomycin resistance is seen in addition to E. faecium and E. faecalis, but also has been recognised in E. raffinosus, E. avium, E. durans, and several other enterococcal species. Several genes, including vanA, vanB, vanC, vanD, and vanE, contribute to resistance to vancomycin in enterococci. Multiple epidemics have been described with VRE, predominantly with genotype vanA. Phenotype VanA and VanB are common in the USA, but phenotype Van C appears to be more prevalent in Europe (table) [5, 6]. The emergence and spread of VRE VanC in Europe is related to the use of the growth promoter avoparcin in animal husbandry. Avoparcin is a glycopeptide produced by Streptomyces candidus, closely related to vancomycin. It was banned in 1997, and subsequently, VRE VanC decreased in European hospitals. Knowledge of the type of resistance is critical for infection control purposes: vanA or vanB genes are transferable and can spread from organism to organism.