Glycopeptide-resistant enterococci: deciphering virulence, resistance and epidemicity

Abstract

Since their first discovery, glycopeptide-resistant enterococci have emerged as important nosocomial pathogens first in the US, followed by the rest of the world. In this review the most recent findings that relate to enterococcal epidemiology, virulence and glycopeptide-resistance maintenance will be discussed. Frequent horizontal gene transfer and recombination, resulting in high-level genome plasticity, facilitating rapid responsiveness of enterococci to changing environmental conditions may have contributed to the worldwide emergence. For Enterococcus faecium this has resulted in the development of a distinct genetic subspecies, clonal complex 17, responsible for the majority of glycopeptide-resistant enterococci-related hospital burden. Preliminary data also suggest that such high-risk enterococcal clonal complexes may exist within Enterococcus faecalis. The last 2 years have not only disclosed novel determinants implicated in enterococcal pathogenesis, but also showed that enterococci are able to sense their environment and regulate virulence gene expression accordingly. Linkage of glycopeptide resistance in enterococci to plasmid maintenance systems holds a doomed perspective for controlling antibiotic resistance emergence. Recent developments have improved our understanding of enterococcal population structure, pathogenesis and glycopeptide-resistance maintenance. This may contribute to the development of novel intervention strategies to prevent enterococcal infections and contain the spread of glycopeptide-resistant enterococci.