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JAC Advance Access published online on October 20, 2006
Journal of Antimicrobial Chemotherapy, 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
Received June 10, 2006
Revised September 22, 2006
Accepted September 28, 2006

Brief report

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 Touyama 1, Futoshi Higa 2 *, Chikara Nakasone 2, Takashi Shinzato 3, Morikazu Akamine 2, Shusaku Haranaga 2, Masao Tateyama 2, Isamu Nakasone 4, Nobuhisa Yamane 4, and Jiro Fujita 2

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; Yonabaru Central Hospital, Okinawa, Japan
2 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
3 Nakagami General Hospital, Okinawa, Japan
4 Department of Laboratory Medicine, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan

* To whom correspondence should be addressed.
Futoshi Higa, E-mail: fhiga{at}med.u-ryukyu.ac.jp


  Abstract

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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