Abstract
Multiple antimicrobial resistance in Staphylococcus aureus can result from mutations leading to reduced susceptibility to Pine oil-based cleaners (PS RS) as well as following growth with the non-steroidal anti-inflammatory salicylate. We now define the contributions of the alternative sigma factor ( sigB) and staphylococcal accessory regulator ( sarA) to these mechanisms. We conclude that sarA plays a more prominent role than sigB in overall intrinsic multiple antimicrobial resistance. Both genes have similar effects on intrinsic vancomycin resistance, and the salicylate-inducible mechanism is not sigB- or sarA-dependent. Furthermore, analyses determined that altered expression of sigB and sarA is not responsible for the salicylate-inducible mechanism, and sarA upregulation is associated with the PS RS phenotype.
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