Pine oil cleaner-resistant Staphylococcus aureus: reduced susceptibility to vancomycin and oxacillin and involvement of SigB.
Pine oil cleaner-resistant Staphylococcus aureus: reduced susceptibility to vancomycin and oxacillin and involvement of SigB.
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耐松油清洁剂的金黄色葡萄球菌：对万古霉素和苯唑西林的敏感性降低以及 SigB 的参与。
DOI：
10.1128/aem.68.11.5417-5421.2002
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发表时间：
2002
影响因子：
4.4
通讯作者：
Gustafson,JohnE
中科院分区：
文献类型：
--
作者：
Price,ChristopherTD;Singh,VineetK;Jayaswal,RadheshyamK;Wilkinson,BrianJ;Gustafson,JohnE
在含有 POC.S 的实验室培养基上分离出对家用松油清洁剂 (POC) 具有抗性的金黄色葡萄球菌菌株 COL 突变体。表达 POC 抗性 (POCr) 表型的金黄色葡萄球菌突变体也表现出对细胞壁活性抗生素万古霉素和苯唑西林的敏感性降低。 POCr表型依赖于S。金黄色葡萄球菌替代转录因子 SigB，因为 sig 失活消除了 POC 耐药性升高的表达以及万古霉素和苯唑西林敏感性的降低。 COLsigB::kan 抑制突变体的分离，其维持 thesigB::kanallele，表明 POCr 表型也可以通过 asigB 独立机制进行较低程度的表达。这些结果支持了越来越多的报告表明，普通消毒剂可以选择对抗生素敏感性降低的细菌。一系列体外筛选的糖肽中间体。与亲本菌株相比，金黄色葡萄球菌 (GISA) 分离株也表现出 POC 敏感性降低。总的来说，我们的证据表明导致 POCr 表型的突变也可能与导致 GISA 表型的机制有关。
Mutants ofStaphylococcus aureusstrain COL resistant to a household pine oil cleaner (POC) were isolated on laboratory media containing POC.S. aureusmutants expressing the POC resistance (POCr) phenotype also demonstrate reduced susceptibility to the cell wall-active antibiotics vancomycin and oxacillin. The POCrphenotype is reliant on theS. aureusalternative transcription factor SigB, since inactivation ofsigBabolished expression of elevated POC resistance and the reductions in vancomycin and oxacillin susceptibilities. The isolation of suppressor mutants of COLsigB::kan, which maintain thesigB::kanallele, indicates that the POCrphenotype can also be expressed to a lesser degree via asigB-independent mechanism. These results bolster a growing body of reports suggesting that common disinfectants can select for bacteria with reduced susceptibilities to antibiotics. A series of in vitro-selected glycopeptide-intermediateS. aureus(GISA) isolates also expressed reductions in POC susceptibility compared to parent strains. Viewed collectively, our evidence suggests that mutations leading to the POCrphenotype may also be involved with the mechanism that leads to the GISA phenotype.