Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Centre for Immunology and Infectious Disease, Blizard Institute of Cell and Molecular Science, 4 Newark Street, London E1 2AT, UK.
Int J Antimicrob Agents. 2010 Apr;35(4):342-6. doi: 10.1016/j.ijantimicag.2009.12.015. Epub 2010 Feb 9.
Development of multiple antibiotic resistance in Streptococcus pneumoniae typically involves either mutation or transformation at several well-separated chromosomal loci. We postulated that this series of genetic events would be more likely to occur in organisms with deficient DNA repair mechanisms. Investigation of 27 antibiotic-resistant or -susceptible clinical isolates of S. pneumoniae revealed a broad range of mutation frequencies, but no isolate was as mutable as a mismatch repair (MMR)-deficient laboratory isolate. No correlation was observed between antibiotic resistance and higher mutation frequency. Examination of a further 180 clinical isolates using a newly developed rapid screen method also failed to identify any isolates with a mutation frequency as high as the MMR-deficient control strain. We argue that there is currently no clear evidence of a distinct population of mutators among clinical pneumococci.
肺炎链球菌中多重抗生素耐药性的发展通常涉及几个分离良好的染色体基因座的突变或转化。我们假设，在 DNA 修复机制有缺陷的生物中，这一系列遗传事件更有可能发生。对 27 株抗生素耐药或敏感的肺炎链球菌临床分离株的研究显示，突变频率差异很大，但没有一个分离株像错配修复（MMR）缺陷的实验室分离株那样容易突变。抗生素耐药性与更高的突变频率之间没有相关性。使用新开发的快速筛选方法对另外 180 株临床分离株进行的检查也未能鉴定出任何突变频率与 MMR 缺陷对照菌株一样高的分离株。我们认为，目前没有明确的证据表明临床肺炎球菌中有一个独特的突变体种群。
