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JAC Advance Access published online on May 31, 2005
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dki182
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org
Received January 24, 2005
Revised April 28, 2005
Accepted April 29, 2005

Brief report

Preservation of topoisomerase genetic sequences during in vivo and in vitro development of high-level resistance to ciprofloxacin in isogenic Stenotrophomonas maltophilia strains

Sylvia Valdezate 1, Ana Vindel 1, Juan Antonio Saéz-Nieto 1, Fernando Baquero 2, and Rafael Cantón 2*

1 Departamento de Bacteriología, Centro Nacional de Microbiología, Instituto Carlos III, Majadahonda, Madrid-28220, Spain
2 Servicio de Microbiología, Hospital Ramón y Cajal, Crta. Colmenar, Km 9, Madrid-28034, Spain

* To whom correspondence should be addressed.
Rafael Cantón, E-mail: rcanton.hrc{at}salud.madrid.org


  Abstract

Objectives: To ascertain the participation of topoisomerase mutations in the development of ciprofloxacin resistance in isogenic Stenotrophomonas maltophilia mutants.

Methods: gyrAB and parCE sequences in three paired in vivo isogenic ciprofloxacin-susceptible (MIC range 0.5-4 mg/L) and resistant (16-128 mg/L) S. maltophilia strains (PFGE-characterized) sequentially isolated from three patients, and their corresponding in vitro mutants (ciprofloxacin MIC range 2->128 mg/L), were studied. Efflux phenotype was also investigated.

Results: Despite different quinolone susceptibilities, each paired clinical strain displayed identical gyrAB and parCE sequences as well as their corresponding in vitro mutants. Up to 50% (18/36) of in vitro mutants displayed a positive efflux phenotype when nalidixic acid was combined with MC-207,110, while 6% (2/36) showed the phenotype when exposed to nalidixic acid and reserpine. Carbonyl cyanide m-chlorophenylhydrazone or arsenite failed to alter quinolone MICs.

Conclusions: The increase of ciprofloxacin MICs in in vivo and in vitro isogenic S. maltophilia mutant strains was not related to quinolone resistance determining region mutations. Highly effective efflux mechanisms might preserve topoisomerase targets from a ciprofloxacin challenge in S. maltophilia.

Keywords: QRDR; fluoroquinolone resistance; efflux pump inhibitors.
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