铜绿假单胞菌临床分离株中的 nfxC 型喹诺酮耐药性
nfxC-type quinolone resistance in a clinical isolate of Pseudomonas aeruginosa.
作者信息
Fukuda H, Hosaka M, Iyobe S, Gotoh N, Nishino T, Hirai K
机构信息
Central Research Laboratories, Kyorin Pharmaceutical Co., Ltd., Tochigi-ken, Japan.
出版信息
Antimicrob Agents Chemother. 1995 Mar;39(3):790-2. doi: 10.1128/AAC.39.3.790.
Abstract
Quinolone resistance gene nqr-T91 in a clinical isolate of Pseudomonas aeruginosa P1481 was cotransducible with catA1 in P. aeruginosa PAO. The nqr-T91 transductant, PKH-T91, was resistant to norfloxacin, imipenem, and chloramphenicol and showed less norfloxacin accumulation than the parent strain did. Loss of the 46-kDa outer membrane protein (D2) and an increase in the 50-kDa outer membrane protein in PKH-T91 were observed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Lipopolysaccharides in the transductant were also changed. These alterations were considered to be related to lower levels of norfloxacin accumulation in PKH-T91. These genetic and biochemical properties suggested that an nfxC type of quinolone-resistant mutation occurred in a clinical isolate of P. aeruginosa P1481.
摘要
铜绿假单胞菌临床分离株P1481中的喹诺酮耐药基因nqr-T91可与铜绿假单胞菌PAO中的catA1共转导。nqr-T91转导子PKH-T91对诺氟沙星、亚胺培南和氯霉素耐药，并且与亲本菌株相比，其诺氟沙星蓄积量较少。通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳观察到PKH-T91中46 kDa外膜蛋白（D2）缺失，50 kDa外膜蛋白增加。转导子中的脂多糖也发生了变化。这些改变被认为与PKH-T91中较低水平的诺氟沙星蓄积有关。这些遗传和生化特性表明，在铜绿假单胞菌临床分离株P1481中发生了nfxC型喹诺酮耐药突变。
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