AmpC酶介导的铜绿假单胞菌耐药研究

Study on resistance of Pseudomonas aeruginosa mediated by AmpC β-lactamases

目的了解AmpC酶在铜绿假单胞菌对β-内酰胺类抗生素耐药机制中所起的作用。方法选取同一患者治疗前后临床分离株,随机扩增多态性DNA(RAPD)对菌株进行基因分型,微量稀释法测定细菌对头孢他啶的最低抑菌浓度(MIC),头孢西丁三相试验和头孢西丁诱导试验检测AmpC酶产生情况。结果8组铜绿假单胞菌的RAPD分型完全一致,抗生素治疗后分离株对头孢他啶的MIC值较治疗前增加≥8倍,抗生素治疗前分离株头孢西丁三相试验均为阴性,其中6株菌株头孢西丁诱导试验阳性,而治疗后的分离株头孢西丁三相试验均呈阳性。结论β-内酰胺类抗生素治疗失败与AmpC酶被诱导后持续高产有关,对诱导高产酶阳性株引起的感染要避免使用AmpC酶的强诱导剂。

Objective To investigate the production of AmpC β-lactamase and its role in resistance to β-lactam in clinical isolates of Pseudomonas aeruginosa. Methods Pairs ofPseudomonas aeruginosa before and after treatment with antibiotics isolated from the same patient were genotyped by random amplified polymorphic DNA （RAPD）. Minimum inhibitory concentrations （MICs）were determined by micro-dilution broth method. Cefoxitin induced test and cefoxitin 3-dimensional test were performed to detect AmpC β-lactamase. Results RAPD profiles of eight pairs of Pseudomonas aeruginosa were exactly the same. MIC to ceftazidime equal or increased greater than eight times after treatment. Cefoxitin induced test were positive in six strains isolated before treatment. Cefoxitin 3- dimensional test were negative in all strains isolated before treatment but were positive in all strains isolated after treatment. Conclusions Failure of treatment with β-lactams was associated with the overproducing of AmpC β- lactamase. β-1actams that can induced the production of AmpC β-lactamase can not be chosen for infection caused by hyperinducible Pseudomonas aeruginosa strains producing AmpC β-lactamase.