Role of gyrA mutation and loss of OprF in the multiple antibiotic resistance phenotype of Pseudomonas aeruginosa G49

FEMS Microbiol Lett. 1996 Sep 15;143(1):25-8. doi: 10.1111/j.1574-6968.1996.tb08456.x.

Abstract

A clinical isolate of Pseudomonas aeruginosa G48, became resistant during fluoroquinolone treatment giving rise to the post-therapy isolate, G49. To determine whether mutation in gyrA gave rise to fluoroquinolone resistance, G49 was transformed with a plasmid encoding gyrA (pNJR3-2); this reduced the MIC of fluoroquinolones for G49 two-fold. DNA sequencing of gyrA of G49 demonstrated a mutation at Thr-83, substituting with isoleucine. The outer membrane of G49 was shown to lack OprF, suggesting that loss of this protein may be involved in the multiple antibiotic resistance phenotype; however, when G49 was transformed with a plasmid encoding oprF (pRW5), expression of oprF was shown to have no effect upon the phenotype.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Infective Agents / pharmacology
  • Base Sequence
  • DNA Gyrase
  • DNA Topoisomerases, Type II / genetics*
  • DNA, Bacterial / genetics
  • Drug Resistance, Multiple / genetics*
  • Fluoroquinolones
  • Genes, Bacterial*
  • Humans
  • Mutation*
  • Phenotype
  • Plasmids / genetics
  • Porins / genetics*
  • Pseudomonas Infections / drug therapy
  • Pseudomonas Infections / microbiology
  • Pseudomonas aeruginosa / drug effects*
  • Pseudomonas aeruginosa / genetics*
  • Pseudomonas aeruginosa / isolation & purification
  • Transformation, Genetic

Substances

  • Anti-Infective Agents
  • DNA, Bacterial
  • Fluoroquinolones
  • Porins
  • DNA Gyrase
  • DNA Topoisomerases, Type II