Vancomycin-Resistant Enterococcus (VRE)

Vancomycin-resistant Enterococcus (VRE) refers to strains of Enterococcus bacteria -- primarily Enterococcus faecium and Enterococcus faecalis -- that have acquired genetic mutations or mobile genetic elements (plasmids and transposons) conferring resistance to vancomycin, a glycopeptide antibiotic traditionally considered a last-resort treatment for gram-positive infections. Enterococci are gram-positive, facultatively anaerobic cocci that normally colonize the gastrointestinal tract, female genital tract, and oral cavity as part of the normal flora. These organisms are intrinsically resistant to many commonly used antibiotics, including cephalosporins, aminoglycosides (low-level), and clindamycin. Vancomycin resistance develops through acquisition of the vanA or vanB gene clusters, which alter the target site (D-alanyl-D-alanine terminus) on the bacterial cell wall precursor peptidoglycan, replacing the terminal D-alanine with D-lactate. This modification reduces vancomycin binding affinity by approximately 1000-fold, rendering the antibiotic ineffective. VRE causes healthcare-associated infections including urinary tract infections, bacteremia, wound infections, intra-abdominal infections, and rarely endocarditis. VRE can survive on environmental surfaces (bed rails, doorknobs, stethoscopes, blood pressure cuffs) for days to weeks, facilitating transmission in healthcare settings. Transmission occurs primarily through direct contact with colonized or infected patients, or through...