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Over the past two decades, vancomycin has been considered the antibiotic of choice for methicillin-resistant Staphylococcus aureus (MRSA) infections. Indeed, multidrug-resistant clones of MRSA for which the only available effective antibacterial agent is vancomycin have recently been identified. Recent reports describing the therapeutic failure of vancomycin for MRSA infections have aroused considerable concern regarding the emergence of MRSA strains for which there will be no effective therapy.1–3 The mechanism of reduced susceptibility in these staphylococcal strains has not been identified, although data indicate that it is not the same as the vancomycin-resistance mechanism in enterococcal strains.4 We describe here . . .
Sieradzki et al. (Thu,) studied this question.