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Equine veterinary journal2001; 33(6); 547-553; doi: 10.2746/042516401776563418

Systemic antibodies to Clostridium botulinum type C: do they protect horses from grass sickness (dysautonomia)?

Abstract: The aetiology of equine grass sickness (EGS) is still unknown. There is increasing evidence that toxicoinfection with Clostridium botulinum type C is involved. Epidemiological evidence shows that resistance to EGS can occur in older horses and those that have been on a particular pasture for longer or have been in prior contact with the disease. This resistance may be in the form of an immune response to the aetiological agent. Levels of systemic antibodies to the surface antigens of C. botulinum type C (using the closely related and safe C. novyi type A as a phenotypic marker) and to the botulinum type C neurotoxin (BoNT/C) were investigated in horses with and without EGS. Horses with grass sickness were found to have significantly lower levels of systemic IgG to both surface antigens and BoNT/C. Horses with low levels of systemic immunity to these antigens may be more susceptible to developing EGS. There were no significant differences in antibody levels between the different categories of EGS, suggesting systemic immunity to C. botulinum type C does not play a significant role in influencing the severity of the disease. However, horses that had been in contact with EGS or that were grazing land where it had occurred frequently in the past had significantly higher antibody levels to these antigens. These horses may have been exposed to subclinical doses of C. botulinum type C and BoNT/C, resulting in the production of a protective immune response against the putative aetiological agent. This finding is of potential significance for the prospect of prevention of EGS by vaccination against C. botulinum type C.
Publication Date: 2001-11-27 PubMed ID: 11720025DOI: 10.2746/042516401776563418Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This study explores the potential link between the antibodies produced against the bacterium Clostridium botulinum type C and the susceptibility of horses to Equine Grass Sickness (EGS), a severe disease of horses. The study reveals that horses with lower systemic levels of such antibodies are more prone to EGS, suggesting the role of vaccines as a potential preventive measure.

Background of the Research

  • The research addresses the etiology of Equine Grass Sickness (EGS), a condition that severely affects horses, but its cause is yet to be fully understood.
  • Previous studies have suggested a possible link between the disease and infection with a bacteria known as Clostridium botulinum type C. This research aims to further investigate this connection.
  • The research also explores the correlation between the levels of systemic antibodies that target the antigens of this bacterium and the neurotoxin it produces, and the susceptibility of horses to EGS.

Findings of the Research

  • The study found that horses suffering from EGS had significantly lower systemic levels of the Immunoglobulin G (IgG) antibodies against the C. botulinum type C surface antigens and the botulinum type C neurotoxin.
  • The researchers suggest that horses with lower systemic immunity to these bacterial elements may be more prone to EGS development.
  • Interestingly, the study did not find a significant correlation between the levels of these antibodies and the severity of EGS, suggesting that the systemic immunity to C. botulinum type C might not influence the progression of the disease.
  • However, the study found higher levels of these antibodies in horses that had been exposed to EGS or grazed in areas with frequent EGS occurrences. This suggests exposure to C. botulinum type C and its neurotoxin can lead to the production of systemic antibodies, possibly as a protective response.

Implications of the Study

  • This research provides valuable insights into the possible role of systemic antibodies against C. botulinum type C and its neurotoxin in the susceptibility of horses to EGS.
  • The information can potentially be used to develop preventive strategies against EGS, such as vaccination against C. botulinum type C. This protective immunity could potentially decrease the prevalence and severity of EGS in horse populations.

Cite This Article

APA
Hunter LC, Poxton IR. (2001). Systemic antibodies to Clostridium botulinum type C: do they protect horses from grass sickness (dysautonomia)? Equine Vet J, 33(6), 547-553. https://doi.org/10.2746/042516401776563418

Publication

ISSN: 0425-1644
NlmUniqueID: 0173320
Country: United States
Language: English
Volume: 33
Issue: 6
Pages: 547-553

Researcher Affiliations

Hunter, L C
  • Medical Microbiology, University of Edinburgh Medical School, UK.
Poxton, I R

    MeSH Terms

    • Age Factors
    • Animals
    • Antibodies, Bacterial / blood
    • Antibodies, Bacterial / immunology
    • Antigens, Surface / blood
    • Autonomic Nervous System Diseases / microbiology
    • Autonomic Nervous System Diseases / veterinary
    • Botulinum Toxins / immunology
    • Clostridium botulinum / immunology
    • Clostridium botulinum / pathogenicity
    • Enzyme-Linked Immunosorbent Assay / veterinary
    • Horse Diseases / etiology
    • Horse Diseases / microbiology
    • Horse Diseases / prevention & control
    • Horses
    • Immunoglobulin G / blood
    • Plant Poisoning / prevention & control
    • Plant Poisoning / veterinary
    • Poaceae / poisoning

    Citations

    This article has been cited 2 times.
    1. McGorum BC, Chen Z, Glendinning L, Gweon HS, Hunt L, Ivens A, Keen JA, Pirie RS, Taylor J, Wilkinson T, McLachlan G. Equine grass sickness (a multiple systems neuropathy) is associated with alterations in the gastrointestinal mycobiome.. Anim Microbiome 2021 Oct 9;3(1):70.
      doi: 10.1186/s42523-021-00131-2pubmed: 34627407google scholar: lookup
    2. McGorum BC, Symonds HW, Knottenbelt C, Cave TA, MacDonald SJ, Stratton J, Leon I, Turner JA, Pirie RS. Alterations in amino acid status in cats with feline dysautonomia.. PLoS One 2017;12(3):e0174346.
      doi: 10.1371/journal.pone.0174346pubmed: 28333983google scholar: lookup