Fluoroquinolones are among the drugs most extensively used for the treatment of
bacterial infections in human and veterinary medicine. Resistance to
quinolones can be chromosome or plasmid mediated. The chromosomal mechanism of resistance is associated with mutations in the
DNA gyrase- and
topoisomerase IV-encoding genes and mutations in regulatory genes affecting different efflux systems, among others. We studied the role of the acquisition of a mutation in the gyrA gene in the virulence and
protein expression of uropathogenic Escherichia coli (UPEC). The HC14366M strain carrying a mutation in the gyrA gene (S83L) was found to lose the capacity to cause
cystitis and
pyelonephritis mainly due to a decrease in the expression of the fimA, papA,
papB, and ompA genes. The levels of expression of the fimA,
papB, and ompA genes were recovered on complementing the strain with a plasmid containing the gyrA wild-type gene. However, only a slight recovery was observed in the colonization of the bladder in the GyrA
complement strain compared to the mutant strain in a murine model of ascending
urinary tract infection. In conclusion, a mutation in the gyrA gene of uropathogenic E. coli reduced the virulence of the bacteria, likely in association with the effect of
DNA supercoiling on the expression of several
virulence factors and
proteins, thereby decreasing their capacity to cause
cystitis and
pyelonephritis.