耐亚胺培南鲍曼不动杆菌医院内感染流行的分子机制研究

目的研究耐亚胺培南鲍曼不动杆菌的耐药谱特征及其医院内感染流行和耐药性产生的分子机制,为临床防治提供依据.方法4株耐亚胺培南鲍曼不动杆菌分离自2002年10月至2003年1月外科重症监护病房的感染患者,采用纸片扩散法及E-test进行药物敏感性检测及MIC值测定,肠杆菌科基因组内重复一致序列聚集合酶链反应(ERIC-PCR)进行克隆株的DNA分型,耐药质粒转移及消除试验、等电聚焦电泳、PCR扩增β-内酰胺酶基因及其克隆测序以识别其耐药基因和进行质粒定位.结果4株菌除对头孢哌酮/舒巴坦复合制剂的MIC值较低外,对头孢菌素类、氨基糖甙类和氟喹喏酮类等抗生素均显示出了较高水平的多重耐药性;DNA分型证实为同一克隆株;产OXA-23型碳青霉烯酶和PER-1型超广谱β-内酰胺酶(ESBLs);OXA-23定位在质粒上,PER-1定位在染色体上.结论本组耐亚胺培南鲍曼不动杆菌为多重耐药株,同一克隆株在不同感染个体间的相互传播导致了本次医院内感染的流行,产OXA-23和PER-1型β-内酰胺酶是其耐药性产生的重要原因.

Study on the molecular mechanism of the nosocomial outbreak caused by carbapenem-resistant Acinetobactor baumannii strains

Objective To study the molecular mechanism of the nosocomial outbreak and resistance production of carbapenem-resistant Acinetobacter baumannii strains and identify their charateristics of drug resistance patterns.Methods From October 2002 to January 2003,Carbapenem-resistant Acinetobacter baumannii strains from 4 nosocomial inpatients at surgery intensive care unit(SCU) were collected and tested for drug suseptibility and MIC determination.ERIC-PCR was carried out for DNA typing of clonal strains.Resistance plasmid transfer and curing experiment,isoelectric focusing,PCR for beta-lactamase gene amplification and DNA sequencing was also implemented for resistance-gene identification and its plasmid location.Results 4 carbapenem-resistant strains were multiresistant to beta-lactams,aminoglycosides,and fluoroquinoloes,but sensitive to cefoperazone-sulbactam combinations.Chromosomal DNA homologous analysis indicated that they were the identical clonal strains.These strains produce both OXA-23 carbapenem-hydrolyzing beta-lactamase and PER-1 extended-spectrum beta-lactamase,PER-1 gene was located in the chromosomal DNA of these strains and OXA-23 located at resistance plasmids.Conclusions These carbapenem-resistant Acinetobacter baumannii isolates were also multiresistance strains.One clonal epidemic strain transmitted among inpatients at SCU caused this nosocomial outbreak.The presence of OXA-23 and PER-1 beta-lactamases were involved in the carbapenem resistance of this epidemic nosocomial strains.