Saksenaea vasiformis Infection, French Guiana

qnrS1, in nontyphoidal salmonellae in the United Kingdom. These data are in contrast to those of recent studies in the United States and France, which show low incidences of qnrS genes in larger strain collections (9,10). The qnr phenotype is in contrast to resistance mediated by mutations in the topoisomerase genes whereby 1 mutation confers low-level resistance to fl uoroquinolones and full resistance to nalidixic acid. Our previous study demonstrated that qnrS1 was suffi cient to cause decreased susceptibility to ciprofl oxacin in the absence of mutations in gyrA (1). In this study, a qnr gene was suffi cient to increase the ciprofl oxacin MIC to 0.38–0.75 μg/mL. In addition, a qnr gene contributed to high-level ciprofl oxacin resistance in 10 isolates, thereby potentially jeopardizing fi rst-line treatment of vulnerable patient groups with ciprofl oxacin.