Type IV fimbriae are essential virulence factors of Dichelobacter nodosus, the principle causative agent of ovine footrot. The fimA fimbrial subunit gene is required for virulence but fimA mutants exhibit several phenotypic changes and it is not certain if the effects on virulence result from the loss of type IV fimbriae-mediated twitching motility, cell adherence, or from reduced protease secretion. We have shown that mutation of either the pilT or pilU genes abrogated the ability to carry out twitching motility. However, the pilT mutants displayed decreased adhesion to epithelial cells and reduced protease secretion, whereas the pilU mutants had wild-type levels of extracellular protease secretion and adherence. These data provided evidence that PilT was required for the type IV-fimbriae dependent protease secretion pathway in D. nodosus. It was postulated that sufficient fimbrial retraction must be occurring in the pilU mutants to allow protease secretion to take place, but not twitching motility. Although no cell movement was detected in a pilU mutant of D. nodosus, aberrant motion was detected in an equivalent mutant of P. aeruginosa. These observations explain how in D. nodosus protease secretion can occur in a pilU mutant but not in a pilT mutant. In addition, virulence studies in sheep showed that both the pilT and pilU mutants were avirulent, providing evidence that mutation of the type IV fimbrial system affects virulence by abrogating twitching motility, not by altering cell adherence or protease secretion.
|Pages (from-to)||3323 - 3335|
|Number of pages||13|
|Journal||Journal of Bacteriology|
|Publication status||Published - 2008|