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Journal of Antimicrobial Chemotherapy, Vol 41, 189-195, Copyright © 1998 by The British Society for Antimicrobial Chemotherapy

ORIGINAL ARTICLES

Contribution of overproduced chromosomal beta-lactamase and defective outer membrane porins to resistance to extended-spectrum beta-lactam antibiotics in Serratia marcescens

H Weindorf, H Schmidt and HH Martin
Institut fur Mikrobiologie, Technische Hochschule Darmstadt, Germany.

Using clinical strains of Serratia marcescens with low and high resistance to extended-spectrum beta-lactam antibiotics, the relative contribution of chromosomal beta-lactamase and defective outer membrane porins to resistance was determined. Low-level resistance was caused by overproduced beta-lactamase alone. High-level resistance was due to beta-lactamase overproduction and defects of porin OmpF or OmpF and OmpC. Overproduction of beta-lactamase in bacteria with both degrees of resistance was eliminated by transformation with cloned ampD+, the gene (from Escherichia coli) for negative modulation of beta-lactamase induction. In transformants of highly resistant bacteria with normally low and inducible beta-lactamase production, the remaining porin defects alone imparted only minimal resistance to extended-spectrum beta-lactam antibiotics.
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