vancomycinresistant

Vancomycin resistance refers to bacterial strains that are not inhibited by vancomycin, a glycopeptide antibiotic used to treat serious Gram-positive infections. The most clinically relevant vancomycin-resistant pathogens are vancomycin-resistant enterococci (VRE), but vancomycin-resistant Staphylococcus aureus (VRSA) and vancomycin-intermediate resistant S. aureus (VISA) have also been reported. Vancomycin resistance can arise through alteration of the drug’s binding site in the cell wall precursors, most commonly substitution of D-Ala-D-Lac for D-Ala-D-Ala, reducing drug affinity. Genes encoding these changes, such as vanA and vanB, are often carried on mobile genetic elements and can spread between bacteria. In VISA, resistance can be associated with thickened cell walls leading to reduced drug penetration.

Clinical impact includes limited treatment options and higher morbidity, particularly in healthcare settings where VRE is common. Infections may include bloodstream, urinary tract, intra-abdominal, and wound infections. Diagnosis relies on culture and antimicrobial susceptibility testing to determine vancomycin minimum inhibitory concentrations (MIC); molecular tests can detect van gene determinants.

Treatment choices depend on the organism and resistance mechanism. For VRE, options such as linezolid or daptomycin are frequently used, with variable activity by species and local resistance patterns. VRSA remains rare and may require combination therapy and susceptibility-directed regimens. Infection prevention is critical and includes contact precautions, hand hygiene, environmental cleaning, and antimicrobial stewardship to minimize selective pressure.

Historical notes: first clinical reports of vancomycin resistance in enterococci emerged in the late 1980s, with sporadic VRSA cases reported since the early 2000s. Ongoing surveillance tracks resistance trends and guides policy.