Involvement of mutation in ampD I, mrcA, and at least one additional gene in β-lactamase hyperproduction in Stenotrophomonas maltophilia.

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.