Cattoir V, Poirel L, Nordmann P
Service de Bactériologie-Virologie, Hôpital de Bicêtre, Assistance Publique/Hôpitaux de Paris, Faculté de Médecine Paris-Sud, Université Paris XI, France.
Clin Microbiol Infect. 2007 Sep;13(9):940-3. doi: 10.1111/j.1469-0691.2007.01778.x. Epub 2007 Jul 12.
Plasmid-mediated quinolone resistance is being reported increasingly worldwide among isolates of enterobacteria. This resistance is mostly associated with Qnr-like determinants that confer resistance to quinolones, e.g., nalidixic acid, and reduced susceptibility to fluoroquinolones. This study investigated whether amino-acid substitutions in QnrA1 and QnrS1 determinants might be responsible for an enhancement of resistance to quinolones and, particularly, to fluoroquinolones. However, random and site-directed mutagenesis failed to identify any single amino-acid substitution that could be responsible for higher levels of resistance to quinolones or fluoroquinolones, indicating that the selection of such mutants in vivo is probably a rare event.
质粒介导的喹诺酮耐药性在全球范围内的肠杆菌分离株中报告得越来越多。这种耐药性大多与赋予对喹诺酮类药物(如萘啶酸)耐药性以及降低对氟喹诺酮类药物敏感性的Qnr样决定簇有关。本研究调查了QnrA1和QnrS1决定簇中的氨基酸替换是否可能导致对喹诺酮类药物尤其是氟喹诺酮类药物耐药性的增强。然而,随机诱变和定点诱变均未能鉴定出任何可导致对喹诺酮类或氟喹诺酮类药物产生更高水平耐药性的单个氨基酸替换,这表明在体内选择此类突变体可能是罕见事件。