Abstract
Methicillin-resistant Staphylococcus aureus (MRSA) with decreased susceptibility to glycopeptides can be categorized as first, heteroresistant to vancomycin (hVISA); second, with intermediate susceptibility to vancomycin (VISA); and third, fully resistant to vancomycin (VRSA). Whereas the hVISA and VISA isolates are characterized by increased cell wall thickness, activated cell wall synthesis and reduced autolysis, VRSA harbor the vanA gene cluster resulting in a remodeled peptidoglycan. Nonsusceptibility to daptomycin has been associated with changes in the structure and function of the cell envelope and surface charge. Linezolid resistance in MRSA is often associated with mutations in the 23S rRNA, although resistance mediated by an acquired gene (cfr encoding a 23S rRNA methyltransferase) has now been documented in several continents and in outbreak settings.
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