CAJ | 학술논문

目的了解对碳青霉烯类抗菌药物耐药大肠埃希菌的耐药机制及与内源性感染的关系.方法将临床分离的来源于同一患者血培养和粪便培养的大肠埃希菌2株,采用浓度梯度法(E-test)测定亚胺培南、美罗培南的最低抑菌浓度(MIC)值,纸片扩散法测定其他16种抗菌药物的敏感性,等电聚焦电泳(IEF)检测所产生的β-内酰胺酶,PCR及序列分析确定其基因型,接合试验和Southern杂交进行耐药基因定位,脉冲场凝胶电泳(PFGE)分析2株菌株的同源性.结果亚胺培南、美罗培南对2株大肠埃希菌的MIC值均≥32 mg/L,均产KPC-2(等电点值为6.7)和SHV-12(等电点值为8.2).blaKPC-2基因位于可转移的54 kb质粒上.PFGE显示2株大肠埃希菌为同一克隆株.结论 2株大肠埃希菌的耐药性及染色体DNA酶切图谱均一致,该患者大肠埃希菌败血症极可能是肠道的大肠埃希菌移位引起的内源性感染.
목적 료해대탄청매희류항균약물내약대장애희균적내약궤제급여내원성감염적관계.방법 장림상분리적래원우동일환자혈배양화분편배양적대장애희균2주,채용농도제도법(E-test)측정아알배남、미라배남적최저억균농도(MIC)치,지편확산법측정기타16충항균약물적민감성,등전취초전영(IEF)검측소산생적β-내선알매,PCR급서렬분석학정기기인형,접합시험화Southern잡교진행내약기인정위,맥충장응효전영(PFGE)분석2주균주적동원성.결과 아알배남、미라배남대2주대장애희균적MIC치균≥32 mg/L,균산KPC-2(등전점치위6.7)화SHV-12(등전점치위8.2).blaKPC-2기인위우가전이적54 kb질립상.PFGE현시2주대장애희균위동일극륭주.결론 2주대장애희균적내약성급염색체DNA매절도보균일치,해환자대장애희균패혈증겁가능시장도적대장애희균이위인기적내원성감염.
Objective To investigate the resistant mechanism of carbapenem-resistant Escherichia coli and its relationship with endogenous infection. Methods Two carbapenem-resistant Escherichia coli strains were isolated from blood and stool of a same patient, respectively. The minimal inhibition concentrations (MIC) of the two isolates against imipenem and meropenem were determined by E-test. The susceptibility against other antimicrobial agents were done by disc diffusion method. Isoelectric focusing electrophoresis (IEF), polymerase chain reaction (PCR) amplification,cloning and sequencing, conjugation, Southern blotting were carried out to analyze the encoding gene of β-lactamases. Homology analysis of the two strains was done by pulsed field gel electrophoresis (PFGE). Results MIC against imipenem and meropenem of the two strains were both≥32 mg/L.Both strains produced KPC-2 (pI 6.7) and SHV-12 (pI 8.2) β-lactamases. blaKPC2gene was located on a 54 kb transferable plasmid. PFGE showed that the two Escherichia coli strains were derived from the same clone. Conclusions The resistance and enzyme digestion map of chromosome DNA of the two Escherichia coli strains are coincident. The Escherichia coli septicemia of this patient is probably an endogenous infection caused by the immigration of Escherichia coli from the gut.