CAJ | 학술논문

目的明确1株福氏志贺菌RJ506对第3代头孢菌素和氟喹诺酮同时耐药的分子机制.方法通过E-test检测RJ506对各抗菌药物的最低抑菌浓度(MIC),接合试验了解耐药性是否由质粒介导;用聚合酶链反应(PCR)分别扩增染色体和质粒介导的喹诺酮耐药基因并进行序列分析,检测染色体介导耐药的突变位点和质粒介导耐药的基因型;用PCR扩增CTX-M各组超广谱β-内酰胺酶(ESBLs)基因并进行序列分析,检测ESBLs的基因型.结果 RJ506对头孢噻肟和环丙沙星同时耐药,其染色体DNA旋转酶gyrA亚基的83位发现Ser→Leu突变,而gyrB和parC未见突变;该菌株同时含有ESBLs基因blaCTX-M-3和喹诺酮耐药基因qnrS,且分别位于不同的可接合质粒上.结论本实验在国内的志贺菌中检出质粒介导的喹诺酮耐药基因qnrS和CTX-M-3型ESBLs.
목적 명학1주복씨지하균RJ506대제3대두포균소화불규낙동동시내약적분자궤제.방법 통과E-test검측RJ506대각항균약물적최저억균농도(MIC),접합시험료해내약성시부유질립개도;용취합매련반응(PCR)분별확증염색체화질립개도적규낙동내약기인병진행서렬분석,검측염색체개도내약적돌변위점화질립개도내약적기인형;용PCR확증CTX-M각조초엄보β-내선알매(ESBLs)기인병진행서렬분석,검측ESBLs적기인형.결과 RJ506대두포새우화배병사성동시내약,기염색체DNA선전매gyrA아기적83위발현Ser→Leu돌변,이gyrB화parC미견돌변;해균주동시함유ESBLs기인blaCTX-M-3화규낙동내약기인qnrS,차분별위우불동적가접합질립상.결론 본실험재국내적지하균중검출질립개도적규낙동내약기인qnrS화CTX-M-3형ESBLs.
Objective To explore the molecular mechanism of co-resistance to third-generation cephalosporins(cefotaxime and ciprofloxacin) and fluoroquinolones in an isolate of Shigella flexneri RJ506. Methods The minimal inhibitory concentrations (MIC) of Shigella flexneri RJ506 were detected by E-test. The resistance to cefotaxime and ciprofloxacin was determined by conjugation.The mutation of chromosome-mediated resistance and the genotype of plasmid-mediated resistance were determined by polymerase chain reaction (PCR),and chromosome and the resistance gene of plasmid-mediated quinolone were amplified and sequenced.The extended-spectrum β-lactamases (ESBLs) genes and their genotypes were amplified and sequenced by PCR. Results Shigella flexneri RJ506 was resistant to cefotaxime and ciprofloxacin simultaneously and exhibited the Ser83→Leu mutation in gyrA, but there was no mutation in gyrB and parC. The blaCTX-M-3 and qnrS exsisted on two different conjugative plasmids respectively. Conclusions This is a report of a qnrS gene and a blaCTX-M-3 gene in an isolate of Shigella flexneri from China.