Abstract

A clinical isolate of Salmonella typhimurium serovar copenhagen (80190) with high-level fluoroquinolone resistance (MIC ciprofloxacin 32 mg/L) was examined for the occurrence of alterations of gyrA and gyrB by a dominance test with the introduction of plasmids carrying either the gyrA or the gyrB gene of Escherichia coli K-12. Either plasmid resulted in enhanced susceptibilities of each of the resulting heterodiploid strains. Introduction of a plasmid carrying both gyrA and gyrB genes into S. typhimurium 80190 restored the wildtype sensitivity. These observations provide evidence that alterations of both gyrA and gyrB are responsible for the high-level fluoroquinolone resistance of this isolate of S. typhimurium

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