Journal
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
Volume 53, Issue 6, Pages 2475-2482Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/AAC.01432-08
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- Cubist Pharmaceuticals
- National Institute of Allergy and Infectious Disease [AI069087]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI069087] Funding Source: NIH RePORTER
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Mutation of the staphylococcal accessory regulator (sarA) in Staphylococcus aureus limits but does not abolish the capacity of the organism to form a biofilm. As a first step toward determining whether this limitation is therapeutically relevant, we carried out in vitro studies comparing the relative susceptibility of an S. aureus clinical isolate (UAMS-1) and its isogenic sarA mutant (UAMS-929) in the specific context of a catheter-associated biofilm. The antibiotics tested were daptomycin, linezolid, and vancomycin, all of which were evaluated by using concentrations based on the MIC defined as the breakpoint for a susceptible strain of S. aureus (<= 1.0, <= 2.0, and <= 4.0 mu g/ml for daptomycin, vancomycin, and linezolid, respectively). Mutation of sarA had no significant impact on the MIC of UAMS-1 for any of the targeted antibiotics, as defined by Etest antimicrobial susceptibility testing. However, mutation of sarA did result in a significant increase in antimicrobial susceptibility to all targeted antibiotics when they were tested in the specific context of a biofilm. Additionally, whether susceptibility was assessed by using UAMS-1 or its sarA mutant, daptomycin was found to be more effective against established S. aureus biofilms than either linezolid or vancomycin.
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