高产 OXA-663β-内酰胺酶导致 OmpK36 缺陷型肺炎克雷伯菌临床分离株碳青霉烯类耐药。
Carbapenem Resistance Caused by High-Level Expression of OXA-663 β-Lactamase in an OmpK36-Deficient Klebsiella pneumoniae Clinical Isolate.
机构信息
The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.
Department of Molecular Biology, Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, Massachusetts, USA.
出版信息
Antimicrob Agents Chemother. 2018 Oct 24;62(11). doi: 10.1128/AAC.01281-18. Print 2018 Nov.
Abstract
Carbapenem resistance is mainly mediated by carbapenemases or extended-spectrum β-lactamases (ESBL) plus a loss of porins. However, we have identified a clinical isolate that contains neither carbapenemases nor ESBLs. Instead, we found that high-level expression of a novel -derived β-lactamase gene, , in conjunction with OmpK36 deficiency results in high-level carbapenem resistance. This finding demonstrates the combinatorial complexity of factors, including β-lactamase activity, its expression levels, and porin activity, that yield carbapenem resistance.
摘要
碳青霉烯类耐药性主要由碳青霉烯酶或超广谱β-内酰胺酶 (ESBL) 加上孔蛋白缺失介导。然而，我们已经鉴定出一种临床分离株既不含有碳青霉烯酶也不含有 ESBL。相反，我们发现一种新型的β-内酰胺酶基因， ，高水平表达，同时 OmpK36 缺失导致高水平的碳青霉烯类耐药性。这一发现表明了导致碳青霉烯类耐药性的因素的组合复杂性，包括β-内酰胺酶活性、其表达水平和孔蛋白活性。
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