Disruption of mpl Activates β-Lactamase Production in Stenotrophomonas maltophilia and Pseudomonas aeruginosa Clinical Isolates
Author(s) -
Karina Calvopiña,
Matthew B. Avison
Publication year - 2018
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.00638-18
Subject(s) - stenotrophomonas maltophilia , microbiology and biotechnology , pseudomonas aeruginosa , biology , aztreonam , ceftazidime , pseudomonadaceae , stenotrophomonas , bacteria , pseudomonas , genetics
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 Stenotrophomonas maltophilia and Pseudomonas aeruginosa , important pathogens notorious for their β-lactam-resistant phenotypes.
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