摘要
目的研究30株铜绿假单胞菌对喹诺酮类药物的耐药机制。方法用PCR及测序法研究拓扑异构酶Ⅱ和Ⅳ的gyrA、gyrB、parC和parE基因;同时用琼脂稀释法测定环丙沙星、左氧氟沙星的MIC和加入羰基氢氯苯腙(CCCP)后的MIC,以确定存在外排机制。结果菌株中23株(76.7%)有gyrA突变,主要为Thr-83→Ile,第87位突变3株;10株(33.3%)parC基因突变,其中5株为Ser-87→Leu,3株第91位突变;gyrB和parE突变较少见。CCCP能显著降低环丙沙星和左氧氟沙星的MIC。结论铜绿假单胞菌的耐药性日趋严重,两类拓扑异构酶基因突变和外排泵机制是铜绿假单胞菌耐喹诺酮类药物的主要机制。
Objective To study the mechanism of quinolone resistance in Pseudomonas aeruginosa. Methods Polymerase chain reaction （PCR） and DNA sequencing were used to study the mutation of gyrA, gyrB, parC and pareE genes. The minimum inhibitory concentration （MIC） of ciprofloxacin and levofloxacin with or without CCCP were determined by agar dilution method. Results gyrA mutation was identified in 23 （76.7%） strains, mostly Thr-83→Ile. Mutation in codon 87 was found in only 3 strains, parC mutation was identified in 10 （33.3%） strains, with Ser-87→Leu in 5 strains. Mutation in gyrB or parE was relatively infrequent. The MICs of ciprofloxacin and levofloxacin were reduced significantly by adding CCCP. Conclusions The antimicrobial resistance in P. aeruginosa is becoming a more and more serious problem. Mutation of two types of topoisomerases and efflux pump are the main mechanism of quinolone resistance in clinical isolates of P. aeruginosa.
出处
《中国感染与化疗杂志》
CAS
2007年第2期92-95,共4页
Chinese Journal of Infection and Chemotherapy
基金
卫生部北京医院青年基金
关键词
铜绿假单胞菌
喹诺酮类
耐药机制
Pseudomonas aeruginosa
Quinolone
Resistance mechanism
作者简介
许宏涛（1973-），女，主管检验师，硕士，主要从事细菌鉴定和耐药机制研究。通讯作者：许宏涛，E-mail：guoguo040901@163．com。
