We characterize alterations in the QRDR fragment of gyrA and parC in Salmonella spp. following repeated exposure to different quinolones in two in vitro models. Mutations in QRDR of gyrA were found in only 25% of the mutants. The most frequent mutations were Asp87(R)Asn and Asp87(R)Tyr. Strains with the former mutation had a higher ciprofloxacin MIC than those with the latter. We did not find mutations in parC. Our data confirm that mutation in the QRDR fragment of gyrA is the mechanism that produces the greatest decrease in fluoroquinolone susceptibility. There is a greater reduction in the ciprofloxacin susceptibility of strains that were originally nalidixic acid-resistant than in that of strains that were originally susceptible, and this confirms that there is a greater likelihood of therapeutic failures with such strains.
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