Influence of fluoroquinolones on expression and function of P fimbriae in uropathogenic Escherichia coli

P fimbriae are the major adhesins mediating attachment of pyelonephritogenic Escherichia coli to urinary tract tissues, and they therefore constitute a recognized virulence factor. In this work, the effect of fluoroquinolones on P fimbria expression and function in E. coli SS142 and C1212 was assessed. Ciprofloxacin, fleroxacin, and norfloxacin were compared with their precursor nalidixic acid and with trimethoprim in sublethal concentrations ranging from 1/32 to 1/4 of the MIC. Fimbria function was assessed in a standard hemagglutination assay and in a parallel hemagglutination inhibition assay in which the tier of antifimbrial antiserum necessary to inhibit hemagglutination by SS142 was determined. Adhesion of antibiotic-exposed bacteria to human uroma T24 cells in suspension was also measured. Fimbria production was quantitated in an inhibition enzyme-linked immunosorbent assay. Trimethoprim produced a dose-dependent decrease of three to four hemagglutination titers for both strains and a decline in the antiserum titer from 1:16 (control) to 1:128 (1/4 MIC) for E. coli SS142. Adherence exhibited similar decrements from 130 +/- 28 (control) to 16 +/- 3 (1/4 MIC) and from 83 +/- 19 (control) to 30 +/- 11 (1/4 MIC) E. coli cells per uroepithelial cell (mean +/- standard error) for SS142 and C1212, respectively (P less than 0.015). By enzyme-linked immunosorbent assay, the inhibition following exposure decreased in a dose-dependent manner from 31% (control) to 8% (1/4 MIC). By contrast, none of the quinolones produced significant changes in the parameters assessed above. At sublethal concentrations, trimethoprim decreased fimbria production. Following exposure to fluoroquinolones, however, E. coli expressed morphologically and functionally intact P fimbriae.