Abstract
Fluoroquinolones are broad-spectrum antimicrobials highly effective for treatment of a variety of clinical and veterinary infections. Their antibacterial activity is due to inhibition of DNA replication. Usually resistance arises spontaneously due to point mutations that result in amino acid substitutions within the topoisomerase subunits GyrA, GyrB, ParC or ParE, decreased expression of outer membrane porins, or overexpression of multidrug efflux pumps. In addition, the recent discovery of plasmid-mediated quinolone resistance could result in horizontal transfer of fluoroquinolone resistance between strains. Acquisition of high-level resistance appears to be a multifactorial process. Care needs to taken to avoid overuse of this important class of antimicrobial in both human and veterinary medicine to prevent an increase in the occurrence of resistant zoonotic and non-zoonotic bacterial pathogens that could subsequently cause human or animal infections.
| Original language | English |
|---|---|
| Pages (from-to) | 358-373 |
| Number of pages | 16 |
| Journal | International Journal of Antimicrobial Agents |
| Volume | 25 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 2005 |
Bibliographical note
Funding Information:This work was funded by the UK Department for Environment, Food and Rural Affairs, project number VM02136. The authors thank their scientific colleagues for helpful comments on the manuscript.
Keywords
- DNA gyrase
- Escherichia coli
- Fluoroquinolones
- Salmonella
- mar
- qnr
