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Testing the Role of Multicopy Plasmids in the Evolution of Antibiotic Resistance
09:00

Testing the Role of Multicopy Plasmids in the Evolution of Antibiotic Resistance

Published on: May 2, 2018

Quinolone resistance from a transferable plasmid

L Martínez-Martínez1, A Pascual, G A Jacoby

  • 1Department of Clinical Microbiology, School of Medicine, University of Seville, Spain.

Lancet (London, England)
|March 31, 1998
PubMed
Abstract

Insights

A multiresistance plasmid from Klebsiella pneumoniae can transfer quinolone resistance between bacteria. This plasmid accelerates the development and spread of resistance to important antimicrobial agents.

Area of Science:

  • Microbiology
  • Genetics
  • Antimicrobial Resistance

Background:

  • Bacteria develop quinolone resistance through target alteration or reduced drug accumulation.
  • Plasmid-mediated quinolone resistance in clinical isolates remains unconfirmed.
  • This study investigates the transferability of quinolone resistance via a multiresistance plasmid.

Purpose of the Study:

  • To determine if a multiresistance plasmid can transfer quinolone resistance between bacterial strains.
  • To assess the impact of plasmid transfer on quinolone resistance levels.
  • To investigate the role of spontaneous mutation in enhancing plasmid-mediated quinolone resistance.

Main Methods:

  • Conjugation was used to transfer the resistance plasmid (pMG252) between bacterial strains.
  • Agarose-gel electrophoresis visualized the plasmid in various hosts.
  • Frequencies of spontaneous mutations conferring resistance to ciprofloxacin and nalidixic acid were determined in Escherichia coli strains with and without the plasmid.

Main Results:

  • The pMG252 plasmid increased quinolone resistance in Klebsiella pneumoniae strains lacking outer-membrane porins (ciprofloxacin MIC up to 32 µg/mL).
  • Lower resistance levels were observed in strains with normal porins, but the plasmid showed a broad host range, including E. coli, other enterobacteriaceae, and Pseudomonas aeruginosa.
  • Quinolone-resistant mutants arose over 100 times more frequently in plasmid-containing E. coli, reaching higher minimum inhibitory concentrations (MICs).

Conclusions:

  • Transferable quinolone and nalidixic acid resistance was confirmed in a clinical Klebsiella pneumoniae isolate on a broad-host-range plasmid.
  • While plasmid-mediated resistance was low in wild-type strains, spontaneous mutations readily increased resistance levels.
  • Such plasmids can significantly accelerate the emergence and dissemination of resistance to critical antimicrobial drugs.

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