Emergence of ertapenem resistance in an Escherichia coli clinical isolate producing extended-spectrum beta-lactamase AmpC

Antimicrob Agents Chemother. 2011 Sep;55(9):4443-6. doi: 10.1128/AAC.01513-10. Epub 2011 Jul 11.

Abstract

Escherichia coli isolate MEV, responsible for a bloodstream infection, was resistant to penicillins, cephalosporins, and ertapenem. Molecular and biochemical characterization revealed the production of a novel, chromosome-borne, extended-spectrum AmpC (ESAC) β-lactamase with a Ser-282 duplication and increased carbapenemase activity. This study demonstrates for the first time that chromosome-borne ESAC β-lactamases can contribute to the emergence of ertapenem resistance in E. coli clinical isolates.

MeSH terms

  • Amino Acid Sequence
  • Anti-Bacterial Agents / pharmacology*
  • Bacterial Proteins / metabolism*
  • Ertapenem
  • Escherichia coli / drug effects*
  • Escherichia coli / enzymology*
  • Microbial Sensitivity Tests
  • Molecular Sequence Data
  • Sequence Homology, Amino Acid
  • beta-Lactam Resistance / genetics
  • beta-Lactamases / metabolism*
  • beta-Lactams / pharmacology*

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • beta-Lactams
  • AmpC beta-lactamases
  • beta-Lactamases
  • Ertapenem

Associated data

  • GENBANK/HQ419012