Pumbwe L, Everett M J, Hancock R E, Piddock L J
Department of Infection, Medical School, University of Birmingham, UK.
FEMS Microbiol Lett. 1996 Sep 15;143(1):25-8. doi: 10.1111/j.1574-6968.1996.tb08456.x.
A clinical isolate of Pseudomonas aeruginosa G48, became resistant during fluoroquinolone treatment giving rise to the post-therapy isolate, G49. To determine whether mutation in gyrA gave rise to fluoroquinolone resistance, G49 was transformed with a plasmid encoding gyrA (pNJR3-2); this reduced the MIC of fluoroquinolones for G49 two-fold. DNA sequencing of gyrA of G49 demonstrated a mutation at Thr-83, substituting with isoleucine. The outer membrane of G49 was shown to lack OprF, suggesting that loss of this protein may be involved in the multiple antibiotic resistance phenotype; however, when G49 was transformed with a plasmid encoding oprF (pRW5), expression of oprF was shown to have no effect upon the phenotype.
铜绿假单胞菌临床分离株G48在氟喹诺酮治疗期间产生耐药性,形成了治疗后的分离株G49。为了确定gyrA基因突变是否导致氟喹诺酮耐药,用编码gyrA的质粒(pNJR3-2)转化G49;这使G49对氟喹诺酮的最低抑菌浓度降低了两倍。对G49的gyrA进行DNA测序,结果显示第83位苏氨酸发生突变,被异亮氨酸取代。结果表明,G49的外膜缺乏外膜孔蛋白F(OprF),这表明该蛋白的缺失可能与多重耐药表型有关;然而,当用编码oprF的质粒(pRW5)转化G49时,oprF的表达对该表型没有影响。