VISA and hVISA in hospitals

Staphylococcus aureus is noted for its clinical spectrum of disease ranging from asymptomatic colonisation to overwhelming sepsis and death and for its ability to become resistant to antibiotics. Resistance to beta-lactams, methicillin resistance, was first described 50 years ago, becoming a clinical problem in hospitals in the 1970s and the community in the 1990s. MRSA strains that originated in hospitals are usually also resistant to most of the non-beta-lactams as well, leaving vancomycin as the main parenteral drug to treat serious MRSA infections, with the role of new drugs like daptomycin and linezolid not well defined. MRSA strains can exhibit low-level resistance to vancomycin (vancomycin-intermediate S. aureus [VISA]), probably due to a thickened cell wall, which results in the trapping of vancomycin away from the active site of the septum in dividing cells. Detecting this resistance is difficult as multiple genetic pathways lead to this resistance, obviating a molecular test, forcing reliance on phenotypic tests, all of which have issues with sensitivity, specificity and cost. Mortality of bloodstream infection correlates with vancomycin MIC so in this situation the MIC should be determined by Etest or microbroth dilution especially if endocarditis is present. Detection of resistant subpopulations (heterogeneous vancomycin-intermediate S. aureus [hVISA]) can be done with the expensive and time-consuming population analysis profile (PAP) but it is unclear if this confers additional therapeutic information.