Kawai Mako, Yamada Sakuo, Ishidoshiro Ai, Oyamada Yoshihiro, Ito Hideaki, Yamagishi Jun-Ichi
Microbiological Control Laboratories, Technology Research and Development Center, Dainippon Sumitomo Pharma Co. Ltd, 5-51 Ebie 1-chome Fukushima-ku, Osaka 553-0001, Japan.
Department of Clinical Nutrition, Kawasaki University of Medical Welfare, 288 Matsushima, Kurashiki, Okayama 701-0193, Japan.
J Med Microbiol. 2009 Mar;58(Pt 3):331-336. doi: 10.1099/jmm.0.004184-0.
Acriflavine resistance in the clinical meticillin-resistant Staphylococcus aureus isolate KT24 was found not to be mediated by multidrug efflux pumps encoded by qacA/B, smr, qacE, qacG, qacH, qacJ or norA. Early uptake and accumulation of ethidium bromide in MRSA KT24 was significantly lower than that in a susceptible strain, although the efflux rates were similar. Therefore, a permeability barrier in MRSA KT24 may be the conceivable mechanism of acriflavine resistance. Interestingly, it was found that MRSA KT24 had a significantly thickened cell wall, and that cell-wall thickness increased gradually during bacterial growth. In contrast, cell size and surface area in MRSA KT24 were not different from those in the susceptible strain. Moreover, MRSA KT24 exposure to sub-MIC concentrations of acriflavine resulted in a thicker cell wall. These results indicate that cell-wall thickness may be responsible for acriflavine resistance in S. aureus.
临床耐甲氧西林金黄色葡萄球菌分离株KT24对吖啶黄的耐药性并非由qacA/B、smr、qacE、qacG、qacH、qacJ或norA编码的多药外排泵介导。尽管吖啶黄在耐甲氧西林金黄色葡萄球菌KT24中的外排率与敏感菌株相似，但其对溴化乙锭的早期摄取和积累显著低于敏感菌株。因此，耐甲氧西林金黄色葡萄球菌KT24中的通透性屏障可能是其对吖啶黄耐药的一种可能机制。有趣的是，发现耐甲氧西林金黄色葡萄球菌KT24的细胞壁明显增厚，且在细菌生长过程中细胞壁厚度逐渐增加。相比之下，耐甲氧西林金黄色葡萄球菌KT24的细胞大小和表面积与敏感菌株并无差异。此外，耐甲氧西林金黄色葡萄球菌KT24暴露于亚抑菌浓度的吖啶黄会导致细胞壁更厚。这些结果表明，细胞壁厚度可能是金黄色葡萄球菌对吖啶黄耐药的原因。
