Contribution of overproduced chromosomal beta-lactamase and defective outer membrane porins to resistance to extended-spectrum beta-lactam antibiotics in Serratia marcescens.
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.
Weindorf
H
H
Institut für Mikrobiologie, Technische Hochschule Darmstadt, Germany.
Schmidt
H
H
Martin
H H
HH
D001426:Bacterial Proteins / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D002876:Chromosomes, Bacterial; D009238:N-Acetylmuramoyl-L-alanine Amidase / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D018272:Porins / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D012706:Serratia marcescens / Q000187:drug effects* / Q000378:metabolism*; D018440:beta-Lactam Resistance; D001618:beta-Lactamases / Q000378:metabolism*; D047090:beta-Lactams / Q000494:pharmacology
D001426:Bacterial Proteins; C109237:OmpF protein; D018272:Porins; D047090:beta-Lactams; C062460:AmpD protein, Bacteria; D009238:N-Acetylmuramoyl-L-alanine Amidase; D001618:beta-Lactamases