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Carbapenem resistance in clinical isolates of Pseudomonas aeruginosa

F Walsh1, S G B Amyes

  • 1University of Edinburgh, United Kingdom.

Journal of Chemotherapy (Florence, Italy)
|September 15, 2007
PubMed

Insights

Clinical Pseudomonas aeruginosa isolates show carbapenem resistance through OprD loss and efflux pump activity. Novel mexR mutations were found, but in vitro resistance mechanisms don't fully explain clinical resistance.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Pseudomonas aeruginosa is an opportunistic pathogen.
  • Carbapenem resistance in P. aeruginosa is a growing clinical concern.
  • Understanding resistance mechanisms is crucial for effective treatment.

Purpose of the Study:

  • To identify carbapenem resistance mechanisms in clinical Pseudomonas aeruginosa isolates.
  • To compare in vitro and in vivo resistance mechanisms.
  • To investigate the role of OprD porin and efflux pumps.

Main Methods:

  • Phenotypic characterization of carbapenem resistance.
  • Analysis of OprD protein expression.
  • Minimum inhibitory concentration (MIC) testing with and without efflux pump inhibitors.
  • Genetic analysis of mexR and mexT genes.

Main Results:

  • Imipenem-resistant strains showed OprD protein loss.
  • Resistance to imipenem and meropenem involved OprD loss and reduced MICs with efflux pump inhibitors.
  • A novel mexR gene mutation (Gln106 to stop codon) was identified in one isolate.
  • No significant mexT gene changes were observed.
  • Mutations associated with in vitro carbapenem resistance were not found in clinical isolates.

Conclusions:

  • Carbapenem resistance in clinical P. aeruginosa involves OprD loss and efflux pump activity.
  • A previously unidentified mexR mutation contributes to resistance.
  • In vitro-derived resistance mechanisms are insufficient to explain clinical carbapenem resistance in P. aeruginosa.

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