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Comparative in-vitro activity of new quinolones against clinical isolates and resistant mutants

Rohner, P. ; Peebo, M. ; Lew, D. P. ; Auckenthaler, R. ; Pechère, J.-C

In: Journal of Antimicrobial Chemotherapy, 1992, vol. 29, no. 1, p. 41-48

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    Titre
    • Comparative in-vitro activity of new quinolones against clinical isolates and resistant mutants
    Auteur
    • Rohner, P.. University Hospital Geneva, Department of Infectious Diseases, 24, Rue Micheli-du-Crest, CH-1211 Geneva 4, Switzerland
    • Peebo, M.. University Hospital Geneva, Department of Infectious Diseases, 24, Rue Micheli-du-Crest, CH-1211 Geneva 4, Switzerland
    • Lew, D. P.. University Hospital Geneva, Department of Infectious Diseases, 24, Rue Micheli-du-Crest, CH-1211 Geneva 4, Switzerland
    • Auckenthaler, R.. University Hospital Geneva, Department of Infectious Diseases, 24, Rue Micheli-du-Crest, CH-1211 Geneva 4, Switzerland
    • Pechère, J.-C. University Hospital Geneva, Department of Infectious Diseases, 24, Rue Micheli-du-Crest, CH-1211 Geneva 4, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Journal of Antimicrobial Chemotherapy, 1992, vol. 29, no. 1, p. 41-48. Oxford University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:303556
    Summary
    The in-vitro activity of five new fluoroquinolones, WIN 57273, sparfloxacin, flerox-acin, temafloxacin and tiprofloxacin was determined against 543 recent clinical isolates and eight quinolone resistant strains derived by mutation and their five parent strains. WIN 57273 was the most active compound against Gram-positive bacteria, sparfloxacin had a broad spectrum which was similar to that of cipro-floxacin. Ciprofloxacin showed the greatest activity against Gram-negative bacteria. Temafloxacin showing some activity against Gram-positive organisms and Acinetobacter spp. Fleroxacin was the least active compound studied. Compared to wild type parent strains, the mutated strains produced the following results. In Enterobacter cloacae OmpF deficiency increased the MICs of all quinolones by 8-32-fold. In Pseudomonas aeruginosa OmpF deficiency had a limited effect, Omp D2 deficiency combined with an increased lipopolysaccharide content produced greater resistance, i.e. 4-16-fold; mutations in gyrase were associated with variously increased MICs, depending on the strain and compound tested