ABSTRACT
This chapter illustrates the role of fimbriae in disease with two model systems: K88-positive Escherichia coli which cause neonatal diarrhea in piglets and P-fimbriated E. coli which cause urinary tract infections (UTI). The protective potential of adhesion inhibition was first realized by Freter. The antibodies elicited by V. cholera vaccination protected by intenupting the adhesion. This focused the interest on the anti-adhesive effects of mucosal antibodies. P-fimbriated E. coli cause symptomatic infections by mechanisms other than P fimbriae-negative strains. The secretor state influences the derivatization of epithelial glycoconjugates with the A, B, and H blood group determinants. The prevalence theory suggested that the quantitatively dominating strain in the large intestine has an increased chance of causing UTI. These two theories may be reconciled if the bacterial properties that promote large intestinal colonization also increase the ability of E. coli to reach and persist in the urinary tract.
