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激活β-内酰胺酶在嗜麦芽窄食单胞菌和铜绿假单胞菌临床分离株中的产生。

Disruption of Activates β-Lactamase Production in Stenotrophomonas maltophilia and Pseudomonas aeruginosa Clinical Isolates.

机构信息

School of Cellular & Molecular Medicine, University of Bristol, Bristol, United Kingdom.

School of Cellular & Molecular Medicine, University of Bristol, Bristol, United Kingdom

出版信息

Antimicrob Agents Chemother. 2018 Jul 27;62(8). doi: 10.1128/AAC.00638-18. Print 2018 Aug.

DOI:10.1128/AAC.00638-18
PMID:29844045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6105801/
Abstract

The hyperproduction of chromosomally encoded β-lactamases is a key method of acquired resistance to ceftazidime, aztreonam, and, when seen in backgrounds having reduced envelope permeability, carbapenems. Here, we show that the loss of Mpl, a UDP-muramic acid/peptide ligase, is a common and previously overlooked cause of chromosomally encoded β-lactamase hyperproduction in clinical isolates of and , important pathogens notorious for their β-lactam-resistant phenotypes.

摘要

染色体编码β-内酰胺酶的过度产生是对头孢他啶、氨曲南和当在渗透性降低的包膜背景下产生的碳青霉烯类抗生素产生获得性耐药的关键方法。在这里，我们表明 Mpl 的缺失，一种 UDP-胞壁酸/肽连接酶，是 和 临床分离株中染色体编码β-内酰胺酶过度产生的常见且以前被忽视的原因，这些重要病原体以其β-内酰胺耐药表型而臭名昭著。

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