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目的探讨铜绿假单胞菌对碳青霉烯类药物的耐药机制。方法收集2008年11月至2009年4月我院临床分离的铜绿假单胞菌31株,根据药敏结果分为碳青霉烯类耐药组(21株)和碳青霉烯类敏感组(10株)。另设1株标准株ATCC 27853,用亚胺培南-EDTA(乙二胺四乙酸)抑制试验检测菌株是否产生金属酶,采用PCR法检测各菌株的外膜孔道蛋白oprD2基因,探讨铜绿假单胞菌对碳青霉烯类抗生素耐药机制。结果21株耐药株有7株产生金属酶;21株耐药株经oprD2基因扩增,15株阴性,6株阳性,10株敏感株全部阳性。统计学检验结果表明,碳青霉烯类耐药组与敏感组oprD2基因阳性率的差异有极显著性(P(0.01)。结论oprD2基因缺失和金属酶是本院铜绿假单胞菌对碳青霉烯类抗生素耐药的重要机制。
Objective To investigate the mechanism of drug resistance of carbapenem-resistant Pseudomonas aeruginosa. Methods 31 strains of Pseudomonas aeruginosa isolated in our hospital from November 2008 to April 2009 were collected and divided into carbapenem-resistant group (21 strains) and carbapenem-sensitive group (10 strains). A standard strain ATCC 27853 was also set up to detect the presence of metalloenzymes with imipenem-EDTA (ethylenediaminetetraacetic acid) inhibition test. The oprD2 gene of the outer membrane of each strain was detected by PCR, Resistant mechanism of carbapenem antibiotics to. Results Seven strains of 21 drug-resistant strains produced metalloenzyme. 21 strains of drug-resistant strains were amplified by oprD2 gene, 15 were negative, 6 were positive, and 10 were all positive. Statistical analysis showed that there was a significant difference in the positive rate of oprD2 between carbapenem-resistant group and susceptible group (P (0.01) .Conclusion The deletion of oprD2 gene and the metalloenzyme is the main cause of Pseudomonas aeruginosa An important mechanism of penem antibiotic resistance.