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JAC Advance Access published online on November 22, 2007
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkm447
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© The Author 2007. 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

Variation in the mutation frequency determining quinolone resistance in Chlamydia trachomatis serovars L2 and D

Jan Rupp, Werner Solbach and Jens Gieffers*

Institute of Medical Microbiology and Hygiene, University of Luebeck, Ratzeburger Allee 160, 23538 Luebeck, Germany

Received 20 June 2007; returned 15 August 2007; revised 7 September 2007; accepted 22 October 2007

* Corresponding author. Tel: +49-451-5004409; Fax: +49-451-5002808; E-mail: jens.gieffers{at}gmx.de

Objectives: Quinolone resistance of chlamydiae is supposed to be extremely rare. To assess the risk for the emergence of chlamydial quinolone resistance, we analysed the occurrence of resistant mutants in a quantitative perspective.

Methods: Infectious elementary bodies of Chlamydia trachomatis serovar L2 (ATCC VR-902B) and D (ATTC VR-885) clones were purified on density gradients, and mutants resistant to moxifloxacin and rifampicin were selected by a plaque assay. Plaque assays were conducted with 2 x 109 inclusion forming units (IFUs) of each serovar for rifampicin and 2.66 x 109 IFUs for moxifloxacin. Resistant clones were analysed for mutations in the gyrA, gyrB, parC and parE genes, and respective MICs were determined by titration experiments.

Results: Mutation frequencies for rifampicin (MIC ≥ 0.2 mg/L) did not differ significantly between serovars L2 and D (5.7 x 10–7 versus 6.3 x 10–7). In contrast, the occurrence of moxifloxacin-resistant mutants (MIC ≥ 0.6 mg/L) was determined to be 2.0–2.2 x 10–8 for the serovar L2 isolate and less than 2.66 x 10–9 for the serovar D isolate. Moxifloxacin resistance of all serovar L2 clones depended on single-nucleotide point mutations in the quinolone resistance-determining region of the gyrA, whereas no additional mutations were found in the gyrB, parC or parE genes.

Conclusions: C. trachomatis isolates have the potential to present with clinically relevant antibiotic resistance in future. Serovar-specific differences in the occurrence of spontaneous mutations should be taken into account to predict quinolone resistance in different chlamydial diseases.

Key Words: plaque assay , intracellular pathogens , C. trachomatis


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