Wang Hui, Sun Hong-li, Ning Yong-zhong, Yang Qi-wen, Chen Min-jun, Zhu Yuan-jue, Xu Ying-chun, Xie Xiu-li
Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, China.
Zhonghua Yi Xue Za Zhi. 2006 Jan 3;86(1):17-22.
To investigate the molecular mechanism of multiple-drug and pan-drug resistance among Acinetobacter species.
Non-repetitive 90 carbapenem-resistant strains of Acinetobacter species were collected in Beijing, Guangzhou, and Fuzhou 1999-2004. The homology of the isolates was determined by both pulsed field gel electrophoresis and randomly amplified polymorphic DNA typing. Seven representative clones were selected from the 90 strains of Acinetobacter isolated from different hospitals to be used for further study. Analytical isoelectric focusing was used to measure the isoelectric point of the beta-lactamase. Plasmid DNA was extracted and purified Genes of different beta-lactamase, including bla(TEM--), bla(SHV-), bla(PER-), blaI(MP-), bla(VIM-), and bla(OXA-) genes, in these clone strains were amplified and sequenced. PCR was used to analyze the integrons.
The P clone strain isolated during an outbreak of pan-drug-resistant Acinetobacter species in Peking Union Medical College Hospital 2004 was not susceptible to most common antimicrobial agents tested. The 7 representative clones produced multiple beta-lactamases: TEM-1, high-level AmpC, SHV-type, OXA-23 carbapenemase and IMP-8 and metalloenzyme respectively. One clone produced PER-1 enzyme. These 7 clone strains were resistant to most beta-lactams (including carbapenems), erythromycin, chloramphenicol, and rifampin. Two clone strains were susceptible to cefoperazone/sulbactam and amikacin while 4 clone strains susceptible to levofloxacin. All of the 7 clones were susceptible to minocycline and colistin. Five different integrons were found, harboring the genes mediating the resistance to aminoglycosides, rifampin, chloramphenicol, and carbapenems (bla(IMP-8)).
The molecular bases of multiple-drug or pan-drug resistance in Acinetobacter species include production of OXA-23 carbapenemase or IMP type metalloenzyme and integrons with different resistance gene cassettes. Pan-drug-resistant Acinetobacter species are susceptible to old antimicrobials agents, such as colistin and minocycline.
探讨不动杆菌属多重耐药及泛耐药的分子机制。
于1999 - 2004年在北京、广州和福州收集90株非重复性的耐碳青霉烯不动杆菌属菌株。通过脉冲场凝胶电泳和随机扩增多态性DNA分型确定分离株的同源性。从不同医院分离的90株不动杆菌中选取7个代表性克隆用于进一步研究。采用分析等电聚焦法测定β-内酰胺酶的等电点。提取并纯化质粒DNA，对这些克隆菌株中不同β-内酰胺酶的基因，包括bla(TEM--)、bla(SHV-)、bla(PER-)、blaI(MP-)、bla(VIM-)和bla(OXA-)基因进行扩增和测序。采用聚合酶链反应（PCR）分析整合子。
2004年在北京协和医院爆发的泛耐药不动杆菌属疫情期间分离出的P克隆菌株对大多数测试的常见抗菌药物不敏感。这7个代表性克隆产生多种β-内酰胺酶：分别为TEM-1、高水平AmpC、SHV型、OXA-23碳青霉烯酶和IMP-8及金属酶。1个克隆产生PER-1酶。这7个克隆菌株对大多数β-内酰胺类药物（包括碳青霉烯类）、红霉素、氯霉素和利福平耐药。2个克隆菌株对头孢哌酮/舒巴坦和阿米卡星敏感，4个克隆菌株对左氧氟沙星敏感。所有7个克隆对米诺环素和黏菌素敏感。发现5种不同的整合子，携带介导对氨基糖苷类、利福平、氯霉素和碳青霉烯类（bla(IMP-8)）耐药的基因。
不动杆菌属多重耐药或泛耐药的分子基础包括产生OXA-23碳青霉烯酶或IMP型金属酶以及带有不同耐药基因盒的整合子。泛耐药不动杆菌属对黏菌素和米诺环素等老一代抗菌药物敏感。
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