Multiple Mechanisms of Antimicrobial Resistance in Pseudomonas Aeruginosa: Our Worst Nightmare?

Clin Infect Dis. 2002 Mar 1;34(5):634-40. doi: 10.1086/338782. Epub 2002 Jan 25.

Abstract

Pseudomonas aeruginosa carries multiresistance plasmids less often than does Klebsiella pneumoniae, develops mutational resistance to cephalosporins less readily than Enterobacter species, and has less inherent resistance than Stenotrophomonas maltophilia. What nevertheless makes P. aeruginosa uniquely problematic is a combination of the following: the species' inherent resistance to many drug classes; its ability to acquire resistance, via mutations, to all relevant treatments; its high and increasing rates of resistance locally; and its frequent role in serious infections. A few isolates of P. aeruginosa are resistant to all reliable antibiotics, and this problem seems likely to grow with the emergence of integrins that carry gene cassettes encoding both carbapenemases and amikacin acetyltransferases.

MeSH terms

  • Anti-Bacterial Agents / pharmacology
  • Cell Membrane Permeability / genetics
  • Drug Resistance, Bacterial / genetics*
  • Drug Resistance, Multiple / genetics
  • Gene Frequency
  • Humans
  • Integrins / genetics
  • Microbial Sensitivity Tests
  • Multigene Family
  • Mutation
  • Pseudomonas aeruginosa / drug effects
  • Pseudomonas aeruginosa / genetics*
  • Pseudomonas aeruginosa / physiology

Substances

  • Anti-Bacterial Agents
  • Integrins