Hiramatsu Keiichi, Kayayama Yuki, Matsuo Miki, Aiba Yoshifumi, Saito Michie, Hishinuma Tomomi, Iwamoto Akira
Juntendo University Research Center for Infection Control Science, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Juntendo University Research Center for Infection Control Science, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
J Glob Antimicrob Resist. 2014 Dec;2(4):213-224. doi: 10.1016/j.jgar.2014.04.006. Epub 2014 Jun 7.
Vancomycin-intermediate Staphylococcus aureus (VISA) and its precursor hetero-VISA (hVISA) were discovered almost 20 years ago and have continued to be a stumbling block in the chemotherapy of methicillin-resistant S. aureus (MRSA). Unlike vancomycin resistance mediated by the van gene in enterococci and staphylococci, VISA is generated by accumulation of mutations. It displays diverse and intriguing genetic mechanisms underlying its resistance phenotype. Here we make a brief note on our recent understanding of the genetics of hVISA, VISA and the newly discovered phenotype 'slow VISA' (sVISA).
万古霉素中介金黄色葡萄球菌（VISA）及其前体异质性VISA（hVISA）大约在20年前被发现，至今仍是耐甲氧西林金黄色葡萄球菌（MRSA）化疗中的一个绊脚石。与肠球菌和葡萄球菌中由van基因介导的万古霉素耐药性不同，VISA是由突变积累产生的。它的耐药表型背后存在多种有趣的遗传机制。在此，我们简要介绍一下我们对hVISA、VISA以及新发现的“缓慢VISA”（sVISA）表型遗传学的最新认识。
