Flock and Herd logo

CASE NOTES


Advances in control, prevention and eradication of footrot in small ruminants

Om Dhungyel and Richard Whittington, Sydney School of Veterinary Science, The University of Sydney

Posted Flock & Herd September 2018

Introduction

Footrot is a contagious disease caused by the interaction of the essential causative agent Dichelobacter nodosus and sympatric bacteria, in the complex environment of the epidermal tissues of the hoof and the host immune system. D. nodosus is not capable of invading healthy feet on its own (Beveridge, 1941). Infection by D. nodosus is preceded and accompanied by maceration and colonisation of the interdigital skin by Fusobacterium necrophorum (Egerton et al., 1969).  Strains of D. nodosus differ in virulence and their ability to cause disease. The interactions between the host, environment and the pathogen determines the severity of the disease which is expressed as a spectrum of clinical entities ranging from benign, in which lesions are self limiting interdigital dermatitis, to highly virulent in which severe underrunning of the hoof occurs. Three clinical forms of footrot have been accepted for descriptive purposes and they are: virulent, intermediate and benign. These terms are also used to describe the strains of D. nodosus based on their potential to cause the respective clinical forms in exposed, susceptible animals. D. nodosus is an obligate parasite, lives only in the diseased feet of the animals, and survives for only 7 to 14 days in faeces, soil or pastures. Transmission of footrot occurs only in warm and wet environments (Graham and Egerton, 1968). Virulent footrot can remain endemic in infected farms for months or years and is an economically significant disease of sheep in most sheep farming countries. 

D. nodosus have fine filamentous non-flagellar appendages on cell surface known as pili or fimbriae. Based on the fimbrial antigenicity there are 10 major serogroups (A, B, C, D, E, F, G, H, I and M) of D. nodosus in the Australian environment (Claxton, 1986; Dhungyel et al., 2013) and within these serogroups additional heterogeneity was observed in the form of serotypes. 

Treatment and control

Control and management of footrot ideally should principally be aimed at a flock/farm or regional level. Foot paring of overgrown hooves, exposure of under-run lesions and footbathing in antiseptic solutions like formalin, zinc sulphate or zinc sulphate with anionic detergents are the commonly used methods for treatment and control (Egerton, 1986; Stewart, 1989). Broad-spectrum antibiotics can also be used effectively in treatment and control of footrot cases but the limitations are the costs for repeated treatments at a flock level. For control and eradication of the disease selective treatment and disposal of affected animals can be effectively used during the non-transmission period. Eradication programmes are most likely to succeed if the prevalence of infection at the start is 5% or less. Eradication depends on accurate diagnosis, reduction of prevalence if initially high, eliminating infection (through a combination of treatment and control strategies) and then surveillance to evaluate the success of the strategies in place.

In addition to the control and eradication methods mentioned above sheep and goats can be immunised against and also treated for footrot using vaccine containing either whole cell antigens or fimbrial antigen, either native or recombinant . Immunity is serogroup-specific and multiple serogroups have been reported from individual flocks from different parts of the world (Claxton, 1986). Up to seven serogroups have been identified from a single flock in Australia (Dhungyel et al., 2013). Vaccination is not dependent on environmental conditions and can be applied irrespective of the season and disease status of the animals. In contrast foot bathing is most effective in non transmission periods and systemic antibiotic treatment needs to be accompanied by placement of sheep on dry substrate for 24 hrs. Both measures offer only temporary relief.

Vaccination for treatment, control and eradication

Ideally vaccines would contain antigens representing all the serogroups but commercial multivalent vaccines containing nine serogroups (A-I), protect sheep only for up to 10 weeks (Hunt et al., 1994; Raadsma et al., 1994; Schwartzkoff et al., 1993). In contrast, at least 16 weeks or longer protection against homologous challenge was provided by specific monovalent or bivalent vaccines. Reduced antibody production against individual components of a multivalent vaccine is believed to be due to the phenomenon of antigenic competition (Hunt et al., 1994; Raadsma et al., 1994; Schwartzkoff et al., 1993). However, multivalent footrot vaccine available commercially is being used in some countries as a control measure. In contrast vaccination with specific mono or bivalent fimbrial vaccines combined with ancillary treatments have been tested to treat, control and eradicate footrot in Nepal, Bhutan and Australia and shown to be highly successful (Dhungyel et al., 2013; Dhungyel et al., 2008; Egerton et al., 2002; Gurung et al., 2006). 

Footrot vaccines have been developed and evaluated over 4 decades but fimbrial antigen, which is also the determinant of serogroup variation, remains as the main and the most effective antigen for immunological treatment and prevention of footrot in sheep and goats. Vaccine composition has evolved from whole cell bacterins in alum via multivalent recombinant fimbrial, to outbreak-specific mono or bivalent recombinant fimbrial vaccines in oil adjuvants. Unless universal antigens to cover all serogroups are found, outbreak-specific mono or bivalent fimbrial vaccines are likely to remain the best option for those aiming to control and eradicate footrot in sheep. It is critical to be able to determine the degree and duration of immunity and herd immunity that is afforded by the range of vaccine types and protocols that are developed, as this determines the potential for vaccines to assist in eradication. This has previously been highlighted as a research priority. That virulent footrot can be eradicated through vaccination as a primary strategy confirms that stringent criteria for herd immunity can be met. Future research in footrot vaccines is being focused on developing vaccine/s based on universal antigens to cover all the serogroups.

References

  1. Beveridge, WIB 1941. Foot-rot in Sheep: a Transmissible Disease due to Infection with Fusiformis nodosus (n.sp.). Studies on its Cause, Epidemiology and Control. Bulletin No. 40. Council for Scientific and Industrial Research, Melbourne, 64 p
  2. Claxton, PD 1986. Serogrouping of Bacteroides nododus isolates, In:  Stewart, D.J., Peterson, JE, McKern, NM, Emery, DL (Eds.) Footrot in Ruminants. Proceedings of a Workshop, Melbourne 1985. CSIRO Division of Animal Health and Australian Wool Corporation, Melbourne, 131-134
  3. Dhungyel, O, Schiller, N, Eppleston, J, Lehmann, D, Nilon, P, Ewers, A, Whittington, R, 2013. Outbreak-specific monovalent/bivalent vaccination to control and eradicate virulent ovine footrot. Vaccine 31, 1701-1706
  4. Dhungyel, OP, Lehmann, DR, Whittington, RJ, 2008. Pilot trials in Australia on eradication of footrot by flock specific vaccination. Vet Microbiol 132, 364-371
  5. Egerton, JR 1986. Control and eradication of ovine footrot. In:  Footrot in ruminants, Melbourne
  6. Egerton, JR, Ghimire, SC, Dhungyel, OP, Shrestha, HK, Joshi, HD, Joshi, BR, Abbott, KA, Kristo, C 2002. Eradication of virulent footrot from sheep and goats in an endemic area of Nepal and an evaluation of specific vaccination. The Veterinary Record 151, 290-295
  7. Egerton, JR, Roberts, DS, Parsonson, IM 1969. The aetiology and pathogenesis of ovine footrot. I. A histological study of the bacterial invasion. Journal of Comparative Pathology 79, 207-216
  8. Graham, NPH, Egerton, JR 1968. Pathogenesis of ovine foot-rot: the role of some environmental factors. Australian Veterinary Journal 44, 235-240
  9. Gurung, RB, Dhungyel, OP, Tshering, P, Egerton, JR 2006. The use of an autogenous Dichelobacter nodosus vaccine to eliminate clinical signs of virulent footrot in a sheep flock in Bhutan. Vet J 172, 356-363
  10. Hunt, JD, Jackson, DC, Brown, LE, Wood, PR, Stewart, DJ 1994. Antigenic competition in a multivalent foot rot vaccine. Vaccine 12, 457-464
  11. Raadsma, HW, O'Meara, TJ, Egerton, JR, Lehrbach, PR, Schwartzkoff, CL 1994. Protective antibody titres and antigenic competition in multivalent Dichelobacter nodosus fimbrial vaccines using characterised rDNA antigens. Veterinary Immunology and Immunopathology 40, 253-274
  12. Schwartzkoff, CL, Egerton, JR, Stewart, DJ, Lehrbach, PR, Elleman, TC, Hoyne, PA 1993. The effects of antigenic competition on the efficacy of multivalent footrot vaccines. Australian Veterinary Journal 70, 123-126
  13. Stewart, DJ 1989. Footrot of sheep, In:  Egerton, J.R., Yong, W.K., Riffkin, G.G. (Eds.) Footrot and Foot Abscess of Ruminants. CRC Press, Boca Raton, 5-45

 


All site contents and design Copyright 2006-18©