Carbapenemase-producing combined porin loss is one of the primary mechanisms for carbapenem resistance. Although mutations in ompK35 and ompK36 genes have often been identified in carbapenem-resistant Klebsiella pneumoniae, reports on the porin protein gene disruption by insertion sequence (IS) elements are varied. The ompK36 porin protein gene disruption by IS elements and OmpK36 production loss in six bla_KPC-2-carrying K. pneumoniae isolates were detected in this study. IS903, ISEc68, and IS1 insertions were noted in the 3, 2, and 1 isolates, respectively. The six K. pneumoniae 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.

中文翻译：

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带有破坏ompK36 Porin基因插入元件的KPC-2肺炎克雷伯菌的遗传背景的表征。

产生碳青霉烯酶的联合孔蛋白损失是对碳青霉烯耐药的主要机制之一。尽管在耐碳青霉烯的肺炎克雷伯菌中经常鉴定到ompK35和ompK36基因的突变，但有关通过插入序列（IS）元件破坏孔蛋白蛋白质基因的报道却很多。所述ompK36通过孔蛋白基因破坏IS元件和OmpK36生产损失在六个BLA _KPC-2 -carrying肺炎克雷伯菌在本研究中检测到的分离株。在3、2和1个分离物中分别注意到IS 903，IS Ec68和IS 1插入。六个肺炎克雷伯菌分离株显示出五种不同的脉冲场凝胶电泳图谱，并属于四种多位点序列分型，即ST4，ST11，ST15和ST39。这项研究增加了我们对孔蛋白缺陷型临床分离株中KPC-2碳青霉烯酶的遗传背景以及OmpK36产量减少对碳青霉烯耐药性的贡献的了解。