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JAC Advance Access originally published online on October 20, 2006
Journal of Antimicrobial Chemotherapy 2006 58(6):1279-1282; doi:10.1093/jac/dkl427
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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

In vitro activity of sitafloxacin against clinical strains of Streptococcus pneumoniae with defined amino acid substitutions in QRDRs of gyrase A and topoisomerase IV

Masato Touyama1,2, Futoshi Higa1,*, Chikara Nakasone1, Takashi Shinzato3, Morikazu Akamine1, Shusaku Haranaga1, Masao Tateyama1, Isamu Nakasone4, Nobuhisa Yamane4 and Jiro Fujita1

1 Department of Medicine and Therapeutics, Control and Prevention of Infectious Diseases, Graduate School of Medicine, University of the Ryukyus 207 Uehara, Nishihara-cho, Okinawa 903-0215, Japan 2 Yonabaru Central Hospital Okinawa, Japan 3 Nakagami General Hospital Okinawa, Japan 4 Department of Laboratory Medicine, Graduate School of Medicine, University of the Ryukyus Okinawa, Japan

Received 10 June 2006; returned 17 August 2006; revised 22 September 2006; accepted 28 September 2006

*Corresponding author. Tel: +81-98-895-1144; Fax: +81-98-895-141; E-mail: fhiga{at}med.u-ryukyu.ac.jp

Objectives: Fluoroquinolone-resistant Streptococcus pneumoniae are increasing worldwide rapidly. In vitro activities of sitafloxacin were evaluated against clinical isolates of S. pneumoniae resistant to levofloxacin (MIC of levofloxacin ≥4 mg/L), which were characterized genetically.

Methods: The quinolone resistance determining regions (QRDRs) of gyrA, gyrB, parC and parE of these strains were analysed by PCR-based sequencing. MICs of sitafloxacin and other quinolones were determined by a microdilution broth method.

Results: All 18 strains had at least one amino acid substitution in the QRDRs of GyrA and ParC, which included Ser-81->Tyr/Phe and Glu-85->Lys in GyrA and Ser-79->Phe/Ile/Tyr, Asp-83->Tyr, Asn-91->Asp, Ser-107->Phe, Lys-137->Asn and Ala-142->Ser in ParC. Most isolates had Asp-435->Asn/Ile-460->Val/Ala-596->Thr substitutions in ParE, while no amino acid substitution in GyrB was noted in all isolates. Ten isolates for which levofloxacin MICs were 16 or 32 mg/L had multiple mutations in both GyrA and ParC. The MIC80 value of sitafloxacin for levofloxacin-resistant isolates was 0.25 mg/L. The range of MICs of sitafloxacin for isolates resistant to levofloxacin (MIC 4–32 mg/L) was 0.016–0.5 mg/L.

Conclusions: These findings warrant further studies to evaluate the usefulness of sitafloxacin in the treatment of levofloxacin-resistant S. pneumoniae infection.

Keywords: levofloxacin-resistant S. pneumoniae , drug resistance , sitafloxacin , target alteration , efflux pump


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