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伊朗德黑兰地区烧伤患者分离的铜绿假单胞菌临床分离株中碳青霉烯类耐药机制的研究。

Determination of carbapenem resistance mechanism in clinical isolates of Pseudomonas aeruginosa isolated from burn patients, in Tehran, Iran.

机构信息

Department of Microbiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Student Research Committee, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.

出版信息

J Epidemiol Glob Health. 2017 Sep;7(3):155-159. doi: 10.1016/j.jegh.2017.04.002. Epub 2017 Apr 29.

Abstract

Carbapenems are the most important therapeutic options that effect against serious infections caused by multidrug resistant Pseudomonas aeruginosa (MDR-PA) isolates. Carbapenems resistant isolates of P. aeruginosa are increasing worldwide. The aim of this study was to determine the carbapenem resistance mechanisms in clinical P. aeruginosa isolates from burn patients, in Tehran, Iran. A total of 53 non-duplicated isolates of carbapenem-resistant P. aeruginosa were collected from burn patients. The presence of carbapenemase genes were determined by PCR. AmpC overproducer isolates were detected by phenotypic method. The mutation and transcription level of oprD were determined by PCR-sequencing and quantitative Real-time PCR (RT-PCR), respectively. Twenty-seven (50.9%) isolates were positive for carbapenemase (bla=25 and bla=2) and showed high-level resistance to imipenem and meropenem. Twenty-eight isolates were AmpC overproducers. All isolates had a mutation in the oprD gene and down-regulation of oprD was found in 56.6% of MDR-PA isolates. Although the presence of carbapenemase is the common mechanism of resistant to carbapenem, but carbapenem resistance was found by oprD mutation-driven and the AmpC overproducing isolates in Tehran, Iran.

摘要

碳青霉烯类是治疗多重耐药铜绿假单胞菌(MDR-PA)引起的严重感染的最重要的治疗选择。全球范围内,耐碳青霉烯类铜绿假单胞菌的分离株正在不断增加。本研究旨在确定来自伊朗德黑兰烧伤患者的临床铜绿假单胞菌分离株中碳青霉烯类耐药的机制。从烧伤患者中收集了 53 株非重复的耐碳青霉烯类铜绿假单胞菌分离株。通过 PCR 检测碳青霉烯酶基因的存在。通过表型方法检测 AmpC 过表达分离株。通过 PCR 测序和定量实时 PCR(RT-PCR)分别确定 oprD 的突变和转录水平。27 株(50.9%)分离株对碳青霉烯类(bla=25 和 bla=2)呈阳性,对亚胺培南和美罗培南表现出高水平耐药。28 株为 AmpC 过表达株。所有分离株 oprD 基因均发生突变,56.6%的 MDR-PA 分离株 oprD 下调。尽管碳青霉烯酶的存在是对碳青霉烯类耐药的常见机制,但在伊朗德黑兰发现了 oprD 突变驱动的碳青霉烯类耐药和 AmpC 过表达分离株。

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