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目的了解南昌大学第二附属医院质粒介导的耐氟喹诺酮类药物大肠埃希菌的流行情况和耐药机制。方法收集该院2009年1月至2011年12月常规培养的耐左氧氟沙星的大肠埃希菌株100株,提取DNA后PCR扩增qnrA、qnrB、qnrC、qnrD、qnrS、aac(6’)-Ib和qepA基因,并对aac(6’)-Ib阳性产物测序比对。结果 (1)7株细菌检测出qnr基因,其中qnrA2株,qnrS 5株,1株qnrS和qnrA同时阳性,qnrB、qnrC和qnrD均未检出。(2)5株检测出aac(6’)-Ib基因,测序结果经BLAST比对均为野生型,未发现aac(6’)-Ib-cr基因。(3)所有菌株均未检测出qepA基因。结论该院的氟喹诺酮类抗菌药的耐药机制主要还是靶位突变和细胞膜通透性改变导致的,但7%的质粒介导的耐药基因的检出率也提醒我们要密切关注质粒介导的耐药情况。
Objective To understand the prevalence and drug resistance mechanism of plasmid-mediated fluoroquinolone-resistant Escherichia coli in the Second Affiliated Hospital of Nanchang University. Methods 100 strains of Escherichia coli resistant to levofloxacin were routinely collected from January 2009 to December 2011 in our hospital. DNA was extracted and qnrA, qnrB, qnrC, qnrD, qnrS, aac (6 ’) - Ib qepA gene and sequence alignment of aac (6 ’) - Ib positive product. Results (1) The qnr gene was detected in seven strains of bacteria. Among them, qnrA2, qnrS, qnrS and qnrA were all positive and qnrB, qnrC and qnrD were not detected. (2) Five strains of aac (6 ’) - Ib were detected. The results of BLAST were wild type and no aac (6’) - Ib-cr gene was found. (3) No qepA gene was detected in all the strains. Conclusion The mechanism of fluoroquinolone antibacterial resistance in this hospital is mainly caused by the change of target site and cell membrane permeability. However, the detection rate of 7% of plasmid-mediated drug resistance genes also reminds us to pay close attention to plasmid Drug-resistant situation.