|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.
Source: Hunter LC, Miller JK, Poxton IR. (1999):
The association of Clostridium botulinum type C with equine grass sickness: a toxicoinfection? In: Equine Vet J. 1999 Nov;31(6):492-9.
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