The association of Clostridium botulinum type C with equine grass sickness: a toxicoinfection?
Abstract: The cause of grass sickness, an equine dysautonomia, is unknown. The disease usually results in death. Gastrointestinal (GI) dysfunction is a common clinical manifestation in all forms of the disease. It is generally thought that equine grass sickness (EGS) is caused by an ingested or enterically produced neurotoxin which is absorbed through the GI tract. Clostridium botulinum was first implicated as a causative agent when it was isolated from the GI tract of a horse with EGS in 1919. The aim of the present study was to investigate the hypothesis that EGS results from toxicoinfection with C. botulinum type C: growth of the bacterium in the GI tract with production of toxin (BoNT/C). Ileum contents and faeces from horses with EGS were investigated for BoNT/C, and indirectly for the presence of C. botulinum type C, and compared with control samples from horses without EGS. BoNT/C was detected directly by ELISA in the ileum of 45% (13/29) of horses with EGS compared to 4% (1/28) of controls, and in the faeces of 44% (20/45) of horses with EGS compared to 4% (3/77) of controls. Levels of up to 10 Mlg toxin/g wet weight of gut contents were observed. The one control horse with detectable toxin in the ileum had been clinically diagnosed as having acute EGS, but this was not confirmed by histopathology. The organism was detected indirectly by assaying for BoNT/C by ELISA after enrichment in culture medium. C. botulinum type C was shown to be present in 48% (14/29) of ileum samples and 44% (20/45) of faecal samples from horses with EGS, compared with 7% (2/27) of ileum samples and 8% (6/72) of faecal samples from controls. These results support the hypothesis that EGS results from a C. botulinum type C toxicoinfection.
Publication Date: 1999-12-22 PubMed ID: 10596931DOI: 10.1111/j.2042-3306.1999.tb03857.xGoogle Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This study explores the possibility that equine grass sickness, a serious disease affecting horses’ nervous system, is caused by a toxin-producing bacteria (Clostridium botulinum type C) present in the gut. The findings reveal significant presence of the botulinum toxin and the bacterium in the intestine and feces of affected horses compared to healthy ones, suggesting that the disease may indeed result from a bacterial toxicoinfection.
Background
- Equine Grass Sickness (EGS) is a fatal disease among horses with gastrointestinal dysfunction as a common symptom. The cause of this disease remains unidentified, though suspicion has been cast on the presence of a neurotoxin that horses might ingest or produce in their gut.
- The bacterium Clostridium botulinum was first associated with EGS in 1919 when it was found in the gastrointestinal tract of an afflicted horse. This bacterium is known to produce Botulinum Neurotoxin type C (BoNT/C), which led to the hypothesis of a ‘toxicoinfection’: the bacterium grows in the horses’ gut and produces the toxin.
Objective and Methodology
- With the intention of examining this toxicoinfection theory, the study evaluated samples of small intestine content and feces from horses diagnosed with EGS, searching for the presence of BoNT/C and C. botulinum type C.
- The contents were compared to those from healthy horses. The detection of the toxin was done directly using an enzyme-linked immunosorbent assay (ELISA), while the existence of the bacteria was inferred through an indirect method by testing for the toxin after nurturing the samples in a culture medium.
Results
- Results revealed the presence of BoNT/C in 45% of the intestine samples and 44% of the feces samples from afflicted horses. In comparison, the toxin was detected in only 4% of both sample types from healthy horses.
- Samples from horses with EGS also showed the indirect presence of C. botulinum type C in 48% and 44% of intestine and feces samples, respectively, compared to 7% and 8% in control horses’ samples.
Conclusion
- The findings from this research provide significant support to the hypothesis that EGS may result from a toxicoinfection by C. botulinum type C, with the toxin produced by this bacterium significantly present in the gastrointestinal tract of affected horses.
Cite This Article
APA
Hunter LC, Miller JK, Poxton IR.
(1999).
The association of Clostridium botulinum type C with equine grass sickness: a toxicoinfection?
Equine Vet J, 31(6), 492-499.
https://doi.org/10.1111/j.2042-3306.1999.tb03857.x Publication
Researcher Affiliations
- Department of Medical Microbiology, University of Edinburgh Medical School, Scotland.
MeSH Terms
- Animals
- Autonomic Nervous System Diseases / microbiology
- Autonomic Nervous System Diseases / veterinary
- Botulinum Toxins / analysis
- Botulism / complications
- Botulism / veterinary
- Clostridium botulinum
- Digestive System / microbiology
- Digestive System / physiopathology
- Enzyme-Linked Immunosorbent Assay / veterinary
- Feces / chemistry
- Horse Diseases / microbiology
- Horses
- Ileum / chemistry
- Longitudinal Studies
Citations
This article has been cited 11 times.- Černá P, Botts MM, Watson A, Carr SV. Dysautonomia in two littermate kittens.. JFMS Open Rep 2023 Jan-Jun;9(1):20551169231164579.
- 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.
- Laus F, Corsalini J, Mandara MT, Bazzano M, Bertoletti A, Gialletti R. Equine grass sickness in italy: a case series study.. BMC Vet Res 2021 Aug 6;17(1):264.
- Milne EM, Pirie RS, Hahn CN, Del-Pozo J, Drummond D, Moss S, McGorum BC. A study of residual lesions in horses that recovered from clinical signs of chronic equine dysautonomia.. J Vet Intern Med 2019 Sep;33(5):2302-2311.
- Randleff-Rasmussen PK, Leblond A, Cappelle J, Bontemps J, Belluco S, Popoff MR, Marcillaud-Pitel C, Tapprest J, Tritz P, Desjardins I. Development of a clinical prediction score for detection of suspected cases of equine grass sickness (dysautonomia) in France.. Vet Res Commun 2018 Mar;42(1):19-27.
- 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.
- McGorum BC, Pirie RS, Eaton SL, Keen JA, Cumyn EM, Arnott DM, Chen W, Lamont DJ, Graham LC, Llavero Hurtado M, Pemberton A, Wishart TM. Proteomic Profiling of Cranial (Superior) Cervical Ganglia Reveals Beta-Amyloid and Ubiquitin Proteasome System Perturbations in an Equine Multiple System Neuropathy.. Mol Cell Proteomics 2015 Nov;14(11):3072-86.
- Malekinejad H, Alizadeh-Tabrizi N, Ostadi A, Fink-Gremmels J. The role of sera from equine grass sickness on apoptosis induction in PC12 Tet-off p53 cell line.. Vet Res Forum 2015 Winter;6(1):9-15.
- Zhang Y, Lou J, Jenko KL, Marks JD, Varnum SM. Simultaneous and sensitive detection of six serotypes of botulinum neurotoxin using enzyme-linked immunosorbent assay-based protein antibody microarrays.. Anal Biochem 2012 Nov 15;430(2):185-92.
- Edwards SE, Martz KE, Rogge A, Heinrich M. Edaphic and Phytochemical Factors as Predictors of Equine Grass Sickness Cases in the UK.. Front Pharmacol 2010;1:122.
- Böhnel H, Gessler F. Botulinum toxins--cause of botulism and systemic diseases?. Vet Res Commun 2005 May;29(4):313-45.
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