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The cause (aetiology) and development (pathogenesis) of footrot

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Best practice to control footrot
and scald in sheep

Scald is a disease of the skin between the digits, or claws, of the foot. Normally the skin is pale pink/grey, hairy, slightly waxy and smooth. When a sheep has scald the skin may be inflamed and look deep pink, the hairs are often missing and the skin might look rough or grazed. There is often grey scum over the skin and a pungent smell. It is common for some skin to be normal and some to be affected. Sheep often limp when they have scald and it can be painful to the touch.

Footrot affects both the skin and horn of the foot. As well as the skin changes described above sheep with footrot have separation of the claw horn, typically starting at the inner wall and spreading under the sole. There is often a grey scum and a very pungent smell but little blood.

There is confusion about the cause of scald in GB. Our recent work and established work from Australia (Beveridge, 1941; Egerton et al., 1969; Kennan et al., 2011) indicate that D. nodosus is the typical cause of scald on farms where footrot is known to be present. Several bacteria are involved in causing the damage seen in footrot. The skin of the foot has a healthy population of different species of bacteria living on it (Calvo Bado et al., 2011) and the type and number of species change when scald and footrot occur.

The role of another bacterium, Fusobacterium necrophorum, is still under debate. Some scientists report that colonisation of the interdigital skin by F. necrophorum helps Dichelobacter nodosus (the bacteria that causes footrot) to replicate (Graham and Egerton, 1968), while others speculate that F. necrophorum is a secondary infection. From a practical point of view, the series of events is not important. It is generally accepted that if D. nodosus is not present, then cases of scald heal rapidly with treatment and do not lead to footrot. As D. nodosus is detected more commonly and in greater numbers from sheep with scald than from sheep with footrot (Moore et al., 2005; Witcomb, 2012), scald should be considered as an early stage of footrot on farms where clinical footrot is present. Whether or not scald cases progress to become footrot is likely to depend on several factors, such as the virulence and dose of the D. nodosus involved, the susceptibility of the sheep, and whether or not the sheep is treated before separation of the hoof horn occurs (Wassink et al., 2010). These factors will be discussed in greater detail below.

Sheep that are infected with D. nodosus harbour the bacteria within their feet, and may or may not show signs of lameness. Infected sheep are the main source of infection to other sheep (Moore et al., 2005; Witcomb et al., submitted 2012). Transmission of the bacteria from one sheep to another always occurs via the surface that sheep are standing or walking on, such as the pasture or standing areas at gatherings. In Australia it has been estimated that D. nodosus can survive in soil for a maximum of 7 –10 days. Survival rates on other surfaces, such as bedding when the animals are housed, are not known but the organism survives best in a warm, damp environment (Whittington, 1995). Thus, when sheep are housed, damp bedding is likely to be a good environment for D. nodosus to thrive, contributing to the rapid spread of scald and footrot in housed sheep. Periods of extreme temperatures and dry conditions prevent the bacteria spreading. Survival time in the UK is not yet known but our work suggests it is short; it is only currently possible to detect bacteria in heavily soiled areas where sheep have been gathered or from a footprint where a sheep has recently stood (Witcomb 2012).

When disease has reached the skin-horn junction, D. nodosus has a special affinity for the epidermal cells of the hoof matrix (connective tissue between the horn and the flesh of the hoof) associated with its high levels of heat-stable protease production. It is thought to be the only organism able to initiate bacterial invasion of the hoof matrix, and thereby separation of the hoof horn and damage to the underlying epidermis that produces the characteristic footrot lesions (Beveridge, 1941; Deane and Jensen, 1955; Egerton et al., 1969).

D. nodosus has the capacity for slow persistent growth in the presence of limited nutrients (Roberts and Egerton, 1969). This contributes to its ability to persist in the foot and cause chronic or repeated episodes of lameness. Therefore, sheep that are frequently lame with scald or footrot are probably carriers of D. nodosus and removing these sheep from the flock is one of the best strategies to reduce the occurrence of lameness.

There are 19 serotypes of D. nodosus which are classified into 10 serogroups; A–I and M (Claxton, 1989; Chetwin et al., 1991). The virulence of D. nodosus varies between and within serotypes. Virulence is positively associated with the number of fimbriae on a D. nodosus bacterium (Billington et al., 1996), which is in turn associated with twitching motility and secretion of heat-stable proteases (Kennan et al., 2001). These proteases enable D. nodosus to digest the connective tissue between the horn and the flesh of the hoof (Palmer, 1993).

Another factor which influences occurrence of disease is the heritability of resistance to footrot. A difference in susceptibility to footrot has been reported between sheep breeds (Emery et al., 1984). Breed selection for resistance to footrot has been successful in Broomfield Corriedale sheep in New Zealand, with <10% of the selected line contracting footrot when severely challenged, compared with 80% of a standard Corriedale flock under the same challenge (Skerman and Moorhouse, 1987). This pattern of resistance to footrot may be associated with phenotypes (e.g. small, hard hooves and a light sheep) considered less susceptible to invasive bacteria, and also variation within physiology (e.g. a specific range of MHC II haplotype is required to generate a sufficient immune response against D. nodosus) (Escayg et al., 1997). In GB there is no one breed that is clearly resistant to footrot. Recent work indicates that heritability is about 0.1 (Conington et al., 2007), which would suggest that resistance to footrot is of moderate to low heritability. Therefore, slow improvement in levels of footrot may be possible by breeding from ewes and rams whose parents, and who themselves, have never had footrot. However, the year on year variability in levels of footrot can be influenced by the weather conditions, making this process difficult.


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Claxton, P.D. (1989) Antigenic classification of Bacteroides nodosus. In: Egerton, J.R., Yong, W.K., Riffkin, G.G. (Eds.), Footrot and Foot Abscesses of Ruminants. CRC Press Inc., Boca Raton, FL.

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Kennan, R.M., Dhungyel, O.M.P., Whittington, R.J., Egerton, J.R., Rood, J.I. (2001) The type IV fimbrial subunit gene (fimA) of Dichelobacter nodosus is essential for virulence, protease secretion and natural competence. Journal of Bacteriology 183: 4451–4458.

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Palmer, M.A. (1993) A gelatin test to detect activity and stability of proteases produced by Dichelobacter (Bacteroides) nodosus. Veterinary Microbiology 36: 113–122

Roberts, D.S., Egerton, J.R. (1969) The aetiology and pathogenesis of ovine foot-rot. II. The pathogenic association of Fusiformis nodosus and F. nodosus. Journal of Comparative Pathology 79: 217–227

Skerman, T.M., Moorhouse, S.R. (1987) Broomfield Corriedales: a strain of sheep selectively bred for resistance to footrot. New Zealand Veterinary Journal 35: 101–106.

Whittington, R.J. (1995): Observations on the indirect transmission of virulent ovine footrot in sheep yards and its spread in sheep on unimproved pasture. Australian Veterinary Journal 72: 132–134

Witcomb, L. Quantifying D. nodosus and F. necrophorum and their role in footrot and the environment. PhD thesis, University of Warwick.