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.
Keywords: beta-lactamases; ceftazidime; regulation.
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