Enterococci are Gram-positive cocci that have traditionally been considered to possess low pathogenicity, but have recently emerged as an increasingly common cause of nosocomial infection. Enterococcus faecalis is the predominant commensal species in humans and causes approximately 90% of clinical infections, whilst Enterococcus faecium is being isolated with increasing frequency. Most enterococcal infections are endogenous, however cross-infection between hospitalised patients does occur. Vancomycin-resistant enterococci (VRE) were first isolated in Europe in 1986. The evolution and colonisation of VRE in the European community has been associated with the use of the glycopeptide avoparcin as a growth promoter in pigs and poultry.
Vancomycin resistance in VRE results
from one of six
known resistance phenotypes
.
The resistance phenotypes encode a group of genes that enable synthesis of cell-wall precursors with a terminus modified from the usual D-alanyl-D-alanine group:
Glycopeptides such as vancomycin are unable to bind to the altered cell-wall precursor and therefore are unable to interrupt cell-wall synthesis. VanA and VanB resistance are most commonly seen in Enterococcus faecium and Enterococcus faecalis.
Enterococci are intrinsically resistant to many classes of antibiotics including semisynthetic penicillinase-resistant penicillins, cephalosporins, trimethoprim/sulfamethoxazole and clindamycin.
Susceptibility testing is required to tailor antimicrobial therapy.