贵阳某医院耐碳青霉烯类肺炎克雷伯菌的分子流行病学分析

目的 研究耐碳青霉烯类肺炎克雷伯菌(carbapenem resistant Klebsiella pneumoniae, CRKP)的耐药性、耐药基因与同源性,为临床用药与院感控制提供依据。方法 收集贵州省人民医院2016年5月-2017年2月临床上分离的50株CRKP,检测其对19种抗菌药的药物敏感性。PCR法扩增碳青霉烯酶基因(blaKPC、blaIMP、blaVIM、blaOXA和blaNDM-1)并对扩增阳性产物进行测序,所得序列与GenBank数据库进行比对,确定耐药基因分型。采用ERIC-PCR法进行同源性检测。结果 50株CRKP均为多重耐药菌。19种抗菌药物中,耐药率低于50%的抗菌药物有多黏菌素0、替加环素4%、米诺环素20%、四环素38%。对复方磺胺甲噁唑的耐药率为60%,对碳青霉烯类、头孢菌素、氨曲南、含酶抑制剂、以及喹诺酮类、氨基糖苷类的耐药率为84%~100%。50株CRKP中,48株(96%)检出碳青霉烯酶基因,其中41株(82%)blaKPC-2、3株(6%)blaIMP-8和4株(8%)blaNDM-1。41株检出KPC-2型碳青霉烯酶的CRKP分为6个基因型(A-F型),其中A型18株、B型6株、C型12株、D型3株、E型、F型各1株。结论 CRKP的耐药率高,主要耐药机制是产KPC-2型碳青霉烯酶,其次是产NDM-1、IMP-8型碳青霉烯酶。CRKP存在科室间、科室内的克隆传播,应加强对CRKP的监测和院感控制。

Molecular epidemiological analysis of carbapenems-resistant Klebsiella pneumoniae in a hospital in Guiyang

Objective To study the drug resistance, resistance genes and the homology of carbapenem-resistant Klebsiella pneumonia (CRKP), and to provide the basis for clinical medication and nosocomial infection control. Methods 50 strains of CRKP were isolated from clinical specimens from Guizhou Provincial People's Hospital from May 2016 to February 2017. Antimicrobial susceptibilities of these strains for 19 kinds of antibiotics were tested. Polymerase chain reaction (PCR) and DNA sequencing were used to detect the resistance genes (blaKPC, blaIMP, blaVIM, blaOXA, and blaNDM-1).The homology was determined by ERIC-PCR. Results All of the 50 strains of CRKP were multidrug-resistant bacteria. Among the 19 antibiotics, there were four with resistance rates lower than 50%, including polymyxin (0), tetracycline (4%), minocycline (20%), and tetracycline (38%). The resistance rate to compound sulfamethoxazole was 60%. The resistance rates to carbapenems, cephalosporins, aztreonam, enzyme inhibitors, quinolones, and aminoglycosides were 84%~100%Among the 50 strains of CRKP, 48 strains (96%) were detected carbapenem genes, of which 41 (82%) were blaKPC-2, 3 (6%) were blaIMP-8, 4 were (8%) blaNDM-1. The 41 strains of CRKP with the blaKPC-2 gene were divided into six genotypes (A~F), of which 18 were A, six were B, 12 were C, three were D, one were E, and one were F. Conclusion The resistance rate of CRKP was high. The main mechanism of drug resistance was KPC-2 type carbapenemase, followed by NDM-1 and IMP-8type carbapenemases.There was clone propagation of CRKP between and inside departments, and thus the monitoring and nosocomial infection control of CRKP should be