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JAC Advance Access published online on April 3, 2006
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkl110
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Leading article

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

Matthew J. Ellington 1 * and Neil Woodford 1

1 Antibiotic Resistance Monitoring and Reference Laboratory, Centre for Infections, Health Protection Agency, 61 Colindale Avenue, London NW9 5EQ, UK

* To whom correspondence should be addressed.
Matthew J. Ellington, E-mail: matthew.ellington{at}hpa.org.uk


  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 {beta}-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.

Keywords: post-segregational killing; toxin-antitoxin systems; toxin resistance; Qnr; DNA gyrase.
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