Fluoroquinolone resistance and plasmid addiction systems: Self-imposed selection pressure?

Matthew Ellington*, Neil Woodford

*Corresponding author for this work

Research output: Contribution to journalEditorial

31 Citations (Scopus)

Abstract

Multi-antibiotic-resistant Gram-negative pathogens are becoming more prevalent and an association exists between chromosomally conferred fluoroquinolone resistance and the presence of plasmid-borne resistances, such as extended spectrum β-lactamases. This link is not wholly explained by strain spread or the presence of fluoroquinolone-modifying enzymes. Plasmid-encoded toxin-antitoxin addiction systems enforce plasmid maintenance in bacteria and, like fluoroquinolones, some toxins target DNA gyrase. Bacteria can develop resistance to these toxins, which would free the cell of the plasmid addiction and allow it to ditch the 'excess baggage'. We hypothesize that these plasmid-encoded gyrase toxins might contribute to, or predispose towards, clinically significant fluoroquinolone resistance, and that the plasmid-encoded quinolone resistance determinant, Qnr, may facilitate this. Establishing the extent and mechanisms of cross-resistance to toxins and fluoroquinolones will aid the management of resistance and may contribute to the development of novel antimicrobials.

Original languageEnglish
Pages (from-to)1026-1029
Number of pages4
JournalJournal of Antimicrobial Chemotherapy
Volume57
Issue number6
DOIs
Publication statusPublished - Jun 2006

Keywords

  • DNA gyrase
  • Post-segregational killing
  • Qnr
  • Toxin resistance
  • Toxin-antitoxin systems

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