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Escherichia coli mutants defective in the ability to agglutinate guinea pig erythrocytes (HA-) were isolated from a nalidixic acid-resistant derivative, 31-B, of E. coli TN 675 that produces type 1 fimbriae and induces urinary tract infection in mice fed a 5% glucose solution. All nine HA- mutants were defective not only in their ability to agglutinate Candida albicans cells and erythrocytes from various species, but also in their capacity to adhere to mouse bladder epithelial cells. None of the mutants were agglutinated by anti-type 1 fimbriae antiserum. Although most of the mutants were fimbriated when examined by electron microscopy, their fimbriae differed serologically from type 1 fimbriae. All of the mutants showed 100 to 1,000 times lower bacterial recovery from the bladder walls of mice 3 h after inoculation into the bladder and lacked urinary tract infectivity in mice. These results suggest that all of the HA- mutants are defective in type 1 fimbriae production and that type 1 fimbriae facilitate the development of urinary tract infection in mice, probably by mediating bacterial adherence to the bladder epithelial cells.

Role of type 1 fimbriae in the pathogenesis of ascending urinary tract infection induced by escherichia coli in mice