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Isolation and Identification of Waterborne Antibiotic-Resistant Bacteria and Molecular Characterization of their Antibiotic Resistance Genes
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AmpC beta-lactamases.

George A Jacoby1

  • 1Lahey Clinic, Burlington, Massachusetts 01805, USA. george.a.jacoby@lahey.org

Clinical Microbiology Reviews
|January 13, 2009
PubMed
Summary
This summary is machine-generated.

AmpC beta-lactamases are crucial enzymes causing resistance to cephalosporins in bacteria. Overexpression and plasmid acquisition of AmpC genes pose significant challenges in treating infections, requiring careful monitoring and alternative therapies.

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Antibiotic Dereplication Using the Antibiotic Resistance Platform

Published on: October 17, 2019

Area of Science:

  • Microbiology
  • Molecular Biology
  • Clinical Medicine

Background:

  • AmpC beta-lactamases are cephalosporinases found in Enterobacteriaceae, conferring resistance to various beta-lactam antibiotics.
  • These enzymes can be chromosomally encoded and inducible, or acquired via transmissible plasmids, spreading resistance to susceptible bacteria.
  • Overexpression of AmpC enzymes leads to resistance against broad-spectrum cephalosporins, complicating treatment, especially in hospital-acquired infections.

Purpose of the Study:

  • To review the clinical significance and mechanisms of AmpC beta-lactamase-mediated resistance.
  • To highlight the challenges in detecting and managing AmpC-producing bacteria.
  • To discuss evolving resistance patterns and therapeutic implications.

Main Methods:

  • Literature review of studies on AmpC beta-lactamases.
  • Analysis of resistance mechanisms, including chromosomal and plasmid-mediated genes.
  • Evaluation of diagnostic techniques and treatment strategies.

Main Results:

  • AmpC enzymes mediate resistance to cephalothin, cefazolin, cefoxitin, penicillins, and inhibitor combinations.
  • Mutations can lead to high-level AmpC expression, conferring resistance to cefotaxime, ceftazidime, and ceftriaxone.
  • Plasmid-mediated AmpC genes are emerging in bacteria like E. coli and K. pneumoniae, presenting detection and treatment challenges.
  • AmpC enzymes are evolving to hydrolyze broad-spectrum cephalosporins more efficiently.
  • Current diagnostic methods for AmpC producers are not fully optimized for clinical laboratories.

Conclusions:

  • AmpC beta-lactamases are a significant and evolving threat in bacterial infections, often underestimated in clinical settings.
  • Effective management requires improved detection methods and strategic use of antibiotics like carbapenems.
  • Emergence of carbapenem resistance through porin loss or efflux pump activation necessitates ongoing surveillance and research.