Mechanisms of quinolone action and resistance: where do we stand?

Michel Hébraud, José Luis Capelo, Gilberto Igrejas, Susana Correia, Patricia Poeta

Research output: Contribution to journalReview articlepeer-review

181 Citations (Scopus)


Quinolone antibiotics represent one of the most important classes of anti-infective agents and, although still clinically valuable, their use has been compromised by the increasing emergence of resistant strains, which has become a prevalent clinical problem. Quinolones act by inhibiting the activity of DNA gyrase and topoisomerase IV – two essential bacterial enzymes that modulate the chromosomal supercoiling required for critical nucleic acid processes. The acquisition of quinolone resistance is recognized to be multifactorial and complex. The main resistance mechanism consists of one or a combination of target-site gene mutations that alter the drug-binding affinity of target enzymes. However, other mechanisms such as mutations that lead to reduced intracellular drug concentrations, by either decreased uptake or increased efflux, and plasmid-encoded resistance genes producing either target protection proteins, drug-modifying enzymes or multidrug efflux pumps are known to contribute additively to quinolone resistance. The understanding of these different resistance mechanisms has improved significantly in recent years; however, many details remain to be clarified and the contribution of less-studied mechanisms still needs to be better elucidated in order to fully understand this phenotype.

Original languageEnglish
Article number000475
Pages (from-to)551-559
Number of pages9
JournalJournal of Medical Microbiology
Issue number5
Publication statusPublished - May 2017


  • Antimicrobial resistance
  • Genomics
  • Mutations
  • Quinolone resistance


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