Development of Multi-Drug Resistant Mutants of Clinical Isolates of <I>Pseudomonas aeruginosa</I> after Exposure to Fluoroquinolone

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  • HASEGAWA Miyuki
    Chemotherapy Divison, Mitsubishi Kagaku Bio Clinical Laboratories, Inc.
  • KOBAYASHI Intetsu
    Chemotherapy Divison, Mitsubishi Kagaku Bio Clinical Laboratories, Inc.
  • SAIKA Takeshi
    Chemotherapy Divison, Mitsubishi Kagaku Bio Clinical Laboratories, Inc.
  • SHIMAZU Mitsunobu
    Department of Genetics, Mitsubishi Kagaku Bio Clinical Laboratories, Inc.
  • NISHIDA Minoru
    Chemotherapy Divison, Mitsubishi Kagaku Bio Clinical Laboratories, Inc. College of Health Profession, Toho University

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Other Title
  • Fluoroquinolone系抗菌薬の存在下における<I>Pseudomonas aeruginosa</I>臨床分離株の耐性化変異について
  • Fluoroquinolone系抗菌薬の存在下におけるPseudomonas aeruginosa臨床分離株の耐性化変異について
  • Fluoroquinoloneケイ コウキンヤク ノ ソンザイカ ニ オケル
  • Development of Multi-Drug Resistant Mutants of Clinical Isolates of Pseudomonas aeruginosa after Exposure to Fluoroquinolone

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Abstract

Eight multi-drug resistant mutants (4.94%) were found in 162 clinical isolates of P. aeruginosa after exposure to norfloxacin at different concentrations (1/4, 1/2, 1, 2 and 4 MICs) and were investigated for the mechanisms of drug resistance.<BR>All the mutants were eight-times more resistant to norfloxacin than the respective parents, and showed the cross-resistance to the other fluoroquinolones. However, these mutants differed in the drug-resistant patterns; the 94-74 mutant was resistant to carbenicillin, ceftazidime and chloramphenicol, TA-15 mutant was resistant to imipenem, and the 93-183 was resistant to carbenicillin, ceftazidime and gentamicin.<BR>TA-16 mutant only showed a marked decrease in the bacterial uptake of norfloxacin. Profiles of the outer membrane proteins of the mutants were analyzed by SDS-PAGE method. The six mutants, except for TA-52 and 93-183 mutants, increased the intensity of bands in the 46 KD region. Three mutants (TA-15, TA-16 and 93-183) decreased the intensity of 44 KD (OMPE) and also the former two decreased the intensity of 22 KD (OMP G). The gryA mutations associated with fluoroquinolone-resistance were investigated for the eight mutants, and the 93-183 mutant showed to have the gyrA mutation caused by the alteration in the amino acid sequence of gyrA; Thr-83 (ACC) to Ile (ATC).<BR>The result of the present study indicate that multi-drug resistance of clinical isolates of P. aeruginosa develops through different types of mechanisms, and is not easily explained fully by the present results, and suggest that many factors attributed to the development of the resistances in those mutants remains to be clarified.

Journal

  • Kansenshogaku Zasshi

    Kansenshogaku Zasshi 70 (2), 123-131, 1996

    The Japanese Association for Infectious Diseases

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