DISEASE AND EPIDEMIOLOGY

Dichelobacter nodosus causes footrot in sheep and is occasionally recovered from interdigital infections in cattle, pigs, and goats. The disease in sheep is a mixed infection, but the essential causative agent is D. nodosus. It is probably noteworthy that footrot, especially in cattle, is rarely an etiologic diagnosis, so dogma is not necessarily congruent with current fact.

Footrot is characterized by rapid onset of severe lameness, manifesting initially as interdigital dermatitis. Affected animals often become recumbent (Figure 36-1), are unable to feed efficiently, and will lose weight and productivity; decreased milking by ewes, reduced fertility, and discontinuity in wool fibers also occur. Affected rams often fail to serve their intended purpose. Disease is most common in sheep with poorly maintained hooves. Cracking of overgrown and underrun hooves allows invasion by D. nodosus. Warm, wet conditions encourage bacterial growth, contributing to both severity of individual cases and spread within the flock. High stocking densities increase incidence. Infected animals are important sources of continued infection in a flock.

FIGURE 36-1 Sheep affected with footrot, unable to stand.

(Courtesy Julian I. Rood.)

Footrot is likely the most economically significant bacterial disease of sheep in most wool- and lamb-producing countries. Surveys suggest that the prevalence of footrot is nearly 30%, ranking it among the top five ovine infectious diseases. Costs are difficult to estimate, but effects on meat and wool quality, as well as the labor-intensive nature of treatment regimes, suggest that economic losses are substantial.

PATHOGENESIS

A well-defined experimental model is in place for ovine footrot. Sheep inoculated with D. nodosus grown on solid medium develop severe footrot within 28 days. Assessment of the extent of disease is based on severity of inflammation and degree of invasiveness.

Unraveling of the mechanisms of pathogenesis has been hampered by lack of genetic methods for manipulation of D. nodosus, but type IV fimbriae, extracellular proteases, and a 27 kb pathogenicity island (the vrl locus) are putative contributors. Polar type IV fimbriae confer twitching motility and are composed of monomeric pilin subunits encoded by fimA, which is essential for virulence in sheep (Figure 36-2). fimA mutants do not exhibit twitching motility, no longer secrete proteases, and are completely avirulent.

FIGURE 36-2 Fimbriae of Dichelobacter nodosus.

(Courtesy J. Glenn Songer.)