Involvement of Mutation in ampD I, mrcA, and at Least One Additional Gene in β-Lactamase Hyperproduction in Stenotrophomonas maltophilia

Asmaa Talfan, Oliver J Mounsey, Matthew Charman, Eleanor Townsend, Matthew B Avison

Research output: Contribution to journalArticle (Academic Journal)peer-review

14 Citations (Scopus)

Abstract

It has been reported that targeted disruption of ampD I or mrcA causes β-lactamase hyperproduction in Stenotrophomonas maltophilia. We show here that β-lactamase-hyperproducing laboratory selected mutants and clinical isolates can have wild-type ampD I and mrcA genes, implicating mutation of at least one additional gene in this phenotype. The involvement of mutations at multiple loci in the activation of β-lactamase production in S. maltophilia reveals that there are significant deviations from the enterobacterial paradigm of AmpR-mediated control of β-lactamase induction. We do show, however, that S. maltophilia ampD I can complement a mutation in Escherichia coli ampD. This suggests that an anhydromuropeptide degradation product of peptidoglycan is used to activate AmpR in S. maltophilia, as is also the case in enteric bacteria.
Original languageEnglish
Pages (from-to)5486-5491
Number of pages6
JournalAntimicrobial Agents and Chemotherapy
Volume57
Issue number11
DOIs
Publication statusPublished - Nov 2013

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