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Resume Les CMI de sept quinolones, acide nalidixique, pefloxacine, ofloxacine, d-ofloxacine, ciprofloxacine, sparfloxacine et levofloxacine ont ete determinees par methode de dilutions en milieu gelose comparativement a celles de l'amoxicilline, cefpodoxime, doxycycline et clarithromycine vis-a-vis de 75 souches humaines de Pasteurella multocida, P. dagmatis et P. canis. Des cinetiques de bactericidies ont ete realisees avec trois souches de P. multocida. Les quinolones sont les molecules les plus actives. Une concentration de 0,016 mg/L de sparfloxacine ou de levofloxacine inhibait les 75 souches etudiees. En termes de CMI la levofloxacine et la sparfloxacine ont une activite deux a quatre fois superieure a celle des autres quinolones testees. Les courbes de survie, realisees avec une concentration d'antibiotique double de la CMI, montrent que la bactericidie est obtenue en six heures avec la pefloxacine, l'ofloxacine, la d-ofloxacine, la ciprofloxacine, la sparfloxacine et la levofloxacine. La bactericidie des quinolones est plus rapide que celle de l'amoxicilline et du cefpodoxime. La doxycycline et la clarithromycine n'etaient pas bactericides.

Well-defined community- and nosocomially-acquired isolates of Escherichia coli responsible for urinary tract infections were studied for their resistance to β-lactams, quinolones, and co-trimoxazole, antibiotics widely used for treatment of urinary infections. For each strain, an antibiogram was obtained using the Vitek ® automat, which estimates the minimal inhibitory concentrations of various drugs. Nosocomial strains were significantly more amoxycillin-resistant than community strains ( P =0·01) and were also significantly more resistant to co-trimoxazole ( P =0·025) and first generation quinolones ( P =0·02) than the latter. To determine whether this was due to transmission of strains within the hospital, DNA restriction patterns, established using Xba I enzyme and separation by pulsed-field gel electrophoresis, were compared. Extreme genomic diversity was found among both the community and nosocomial strains. The increased frequency of resistance among nosocomial strains is thus not due to transmission of resistant hospital strains but probably results from the selection of resistant strains from the endogenous flora of patients.