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

L Pumbwe, M J Everett, R E Hancock, L J Piddock

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)25-8
Number of pages4
JournalFEMS Microbiology Letters
Volume143
Issue number1
Publication statusPublished - 15 Sep 1996

Keywords

  • Anti-Infective Agents
  • Base Sequence
  • DNA Gyrase
  • DNA Topoisomerases, Type II
  • DNA, Bacterial
  • Drug Resistance, Multiple
  • Fluoroquinolones
  • Genes, Bacterial
  • Humans
  • Mutation
  • Phenotype
  • Plasmids
  • Porins
  • Pseudomonas Infections
  • Pseudomonas aeruginosa
  • Transformation, Genetic

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