Higgins P G, Fluit A C, Milatovic D, Verhoef J, Schmitz F-J
Institute of Medical Microbiology, Immunology and Hygiene, University of Cologne, Goldenfelstrasse 19-21, 50935 Cologne, Germany.
Int J Antimicrob Agents. 2003 May;21(5):409-13. doi: 10.1016/s0924-8579(03)00009-8.
The target enzymes GyrA and ParC and two efflux pump regulatory genes mexR and nfxB were analysed to determine changes associated with fluoroquinolone resistance in Pseudomonas aeruginosa. Both low- and high-level ciprofloxacin resistance was associated with a Thr-83Ile substitution in GyrA. A ParC Ser-80Leu substitution was found in highly resistant isolates in tandem with the Thr-83Ile substitution in GyrA. Mutations in the efflux regulatory genes were associated with resistance only when in tandem with a mutation in GyrA or ParC. These data show that the main mechanism of fluoroquinolone resistance in P. aeruginosa is mediated primarily through mutations in GyrA, and that mutations in ParC and the efflux regulatory genes are secondary.
对靶标酶GyrA和ParC以及两个外排泵调节基因mexR和nfxB进行分析，以确定与铜绿假单胞菌对氟喹诺酮类药物耐药性相关的变化。低水平和高水平环丙沙星耐药性均与GyrA中的Thr-83Ile替换有关。在高度耐药菌株中发现ParC的Ser-80Leu替换与GyrA中的Thr-83Ile替换同时存在。外排调节基因中的突变仅在与GyrA或ParC中的突变同时存在时才与耐药性相关。这些数据表明，铜绿假单胞菌对氟喹诺酮类药物耐药的主要机制主要是由GyrA中的突变介导的，而ParC和外排调节基因中的突变是次要的。
