Impact of rpoB Mutations on Reduced Vancomycin Susceptibility in Staphylococcus aureus

clinical strains, 27 (71%) possessed a muta-tion(s) in rpoB encoding the -subunit of RNA polymerase. Furthermore, 95.6 % of the rifampin-resistant mutants obtained from 9 methicillin-resistant S. aureus (MRSA) clinical isolates showed decreased vancomycin susceptibilities. These data indicate the involvement of an rpoB mutation in VISA phenotype expression. Staphylococcus aureus is a leading cause of hospital-acquired infections (10, 17). Vancomycin has been the therapy of choice for treating serious infections caused by multidrug-resistant S. aureus since the 1950s. However, the emergence of vancomy-cin-intermediate S. aureus (VISA), hetero-VISA (hVISA) and vancomycin-resistant S. aureus (VRSA) has threatened the rank of vancomycin as the frontline antibiotic in methicillin-resistant S. aureus (MRSA) chemotherapy (1, 8, 9). VISA and hVISA were first described in 1997. Since then the mechanism of resistance has been pursued, which is based on the accumulation of spontaneous chromosomal mutation