Beta-lactam resistance in clinical isolates of Escherichia coli caused by elevated production of the ampC-mediated chromosomal beta-lactamase

Antimicrob Agents Chemother. 1979 Oct;16(4):427-33. doi: 10.1128/AAC.16.4.427.

Abstract

Among cephalothin-resistant isolates from patients with urinary tract infections, six Escherichia coli strains were found to produce elevated amounts of a beta-lactamase indistinguishable from that coded by the ampC gene of E. coli K-12. The resistance levels displayed by these isolates toward a number of beta-lactams were, for five of them, considerably higher as compared with E. coli K-12 with the same amount of beta-lactamase, implying the importance of intrinsic resistance in these isolates. Cefuroxime, and to a lesser extent cefamandole, were stable to hydrolysis by E. coli chromosomal beta-lactamase but acted as inhibitors of the enzyme. Nevertheless, increased beta-lactamase production mediated an increased resistance toward these drugs. No plasmids were found in the isolates, suggesting a chromosomal location for the respective ampC locus.

MeSH terms

  • Anti-Bacterial Agents / pharmacology*
  • Cephalothin / pharmacology
  • Chromosomes, Bacterial / physiology
  • DNA, Bacterial / metabolism
  • Drug Resistance, Microbial
  • Escherichia coli / drug effects*
  • Escherichia coli / enzymology
  • Escherichia coli Infections / microbiology
  • Humans
  • beta-Lactamases / genetics
  • beta-Lactamases / metabolism*
  • beta-Lactams / pharmacology

Substances

  • Anti-Bacterial Agents
  • DNA, Bacterial
  • beta-Lactams
  • beta-Lactamases
  • Cephalothin