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

Antimicrob Agents Chemother. 2018 Jul 27;62(8):e00638-18. doi: 10.1128/AAC.00638-18. Print 2018 Aug.

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 Stenotrophomonas maltophilia and Pseudomonas aeruginosa, important pathogens notorious for their β-lactam-resistant phenotypes.

Keywords: beta-lactamases; ceftazidime; regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Bacterial Agents / pharmacology
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism
  • Carbapenems / pharmacology
  • Ceftazidime / pharmacology
  • Microbial Sensitivity Tests
  • Pseudomonas aeruginosa / drug effects*
  • Pseudomonas aeruginosa / metabolism*
  • Stenotrophomonas maltophilia / drug effects*
  • Stenotrophomonas maltophilia / metabolism*
  • beta-Lactamases / pharmacology*

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • Carbapenems
  • Ceftazidime
  • beta-Lactamases