产 KPC-2 酶 与插入元件破坏孔蛋白基因 的遗传背景特征。
Characterization of the Genetic Background of KPC-2-Producing with Insertion Elements Disrupting the Porin Gene.
机构信息
The Institute of Medical Science and Department of Microbiology, China Medical University Hospital, Taichung, Taiwan.
Infection Control Office, Tungs' Taichung MetroHarbor Hospital, Taichung, Taiwan.
出版信息
Microb Drug Resist. 2020 Sep;26(9):1050-1057. doi: 10.1089/mdr.2019.0410. Epub 2020 Apr 13.
Carbapenemase-producing combined porin loss is one of the primary mechanisms for carbapenem resistance. Although mutations in and genes have often been identified in carbapenem-resistant , reports on the porin protein gene disruption by insertion sequence (IS) elements are varied. The porin protein gene disruption by IS elements and OmpK36 production loss in six -carrying isolates were detected in this study. IS, IS and IS insertions were noted in the 3, 2, and 1 isolates, respectively. The six isolates showed five different pulsed-field gel electrophoresis patterns and belonged to four multilocus sequence typing types, ST4, ST11, ST15, and ST39. This study increases our understanding of the genetic background of KPC-2 carbapenemases in porin-defective clinical isolates and the contribution of OmpK36 production loss to carbapenem resistance.
产碳青霉烯酶的孔蛋白缺失是碳青霉烯类耐药的主要机制之一。虽然在碳青霉烯类耐药菌中经常发现 和 基因突变，但关于插入序列（IS）元件引起孔蛋白基因中断的报道却各不相同。本研究检测到 6 株携带 基因的菌株中存在 IS 元件引起的 孔蛋白基因中断和 OmpK36 产生缺失。在 3、2 和 1 株菌中分别观察到 IS、IS 和 IS 的插入。这 6 株分离株表现出 5 种不同的脉冲场凝胶电泳图谱，属于 4 种多位点序列分型类型，即 ST4、ST11、ST15 和 ST39。本研究加深了我们对产 KPC-2 碳青霉烯酶的孔蛋白缺陷临床分离株的遗传背景以及 OmpK36 产生缺失对碳青霉烯类耐药性的贡献的理解。
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