ABSTRACT
Introduction The worldwide spread of methicillin-resistant Staphylococcus aureus (MRSA) during the 1980s and 1990s led to increasing reliance on the glycopeptides vancomycin and teicoplanin as the only agents displaying reliable activity against these strains. In 1988, high-level vancomycin resistance was first reported in enterococci (vancomycinresistant enterococcus, [VREJ) 11 and throughout the 1990s it was feared that, with the increasing selective pressure due to high vancomycin use in hospitals and the increasing prevalence of both VRE and MRSA, vancomycin resistance would transfer from VRE into MRSA. In fact, when vancomycin resistance was first reported in a clinical strain of S. aureus in 1997 it had low-level resistance, due to a mechanism different from that seen in enterococci 121. Such vancomycin-intermediateS. aureus (VISA) have subsequently been discovered in many countries around the world, although they remain rare 131. Soon after the emergence of VISA, Hiramatsu described strains that are sensitive to vancomycin by conventional testing but have a subpopulation which can survive in the presence of higher vancomycin concentrations 141. These so-called heterogeneous vancomycin-intermediateS. aureus (h VISA) appear to have a similar mechanism of resistance to VISA and have now been reported from all over the world, at rates varying from 0 to 20o/o of all MRSA 131.
