Jesse T W, Englen M D, Pittenger-Alley L G, Fedorka-Cray P J
Bacterial Epidemiology and Antimicrobial Resistance Research Unit, U.S. Department of Agriculture, Agricultural Research Service, Athens, GA 30605-2720, USA.
J Appl Microbiol. 2006 Apr;100(4):682-8. doi: 10.1111/j.1365-2672.2005.02796.x.
The aim of this study was to identify point mutations in the gyrA quinolone resistance determining region (QRDR) of Campylobacter coli (n = 27) and Campylobacter jejuni (n = 26) that confer nalidixic acid (NAL) resistance without conferring resistance to ciprofloxacin (CIP).
Point mutations in the QRDR of gyrA from C. coli and C. jejuni isolates were identified by direct sequencing. All isolates (n = 14) with minimum inhibitory concentrations (MICs) >or=4 microg ml(-1) for CIP and >or=32 microg ml(-1) for NAL possessed a missense mutation leading to substitution of Ile for Thr at codon 86. Three isolates with a missense mutation leading to a Thr86Ala substitution had MICs <4 mug ml(-1) for CIP and >or=32 microg ml(-1) for NAL.
These data confirm previous findings that Thr86Ile mutations confer resistance to both CIP and NAL. However, resistance to NAL alone was conferred by a single Thr86Ala mutation.
Resistance to NAL alone arises independently from CIP resistance. In addition, the role of other previously described point mutations in quinolone resistance is discussed.
本研究旨在鉴定空肠弯曲菌(n = 26)和结肠弯曲菌(n = 27)的gyrA喹诺酮耐药决定区(QRDR)中的点突变,这些突变赋予对萘啶酸(NAL)的耐药性而不赋予对环丙沙星(CIP)的耐药性。
通过直接测序鉴定来自结肠弯曲菌和空肠弯曲菌分离株的gyrA的QRDR中的点突变。所有对CIP的最低抑菌浓度(MIC)≥4μg/ml且对NAL的MIC≥32μg/ml的分离株(n = 14)都具有错义突变,导致第86位密码子的异亮氨酸替代苏氨酸。三株具有导致Thr86Ala替代的错义突变的分离株对CIP的MIC<4μg/ml,对NAL的MIC≥32μg/ml。
这些数据证实了先前的发现,即Thr86Ile突变赋予对CIP和NAL的耐药性。然而,单独对NAL的耐药性由单个Thr86Ala突变赋予。
单独对NAL的耐药性独立于对CIP的耐药性产生。此外,还讨论了其他先前描述的点突变在喹诺酮耐药性中的作用。