Equine grass sickness, is a poorly understood disease that was first reported in Scotland in 1907. Also known as equine dysautonomia, and in some areas as mal seco (dry sickness) the cause remains unknown. The eastern side of Scotland continues to have the highest incidence but it is not recognized in many northern European countries, Patagonia region of Argentina, and in Chile. It is not believed to occur in Australasia, Africa, North America, or Ireland. Though the etiology remains unknown and mycotoxins have been hypothesized, recent work suggests a form of botulism may be at work. This leaves open the possibility that this may be a preventable problem. This article discusses the symptoms, diagnosis, treatment, and prevention of this difficult to mange disease.

Pasture myodystrophy is often affects grazing horses under frosty, windy and rainy conditions. Dry weather often precedes the occurrence. Such conditions can favor toxin elaboration by some fungi. However in 1999 a survey of grass sickness cases found an unusually high incidence of Clostridium botulinum type C in the digestive tracts when compared with healthy horses. In 2003 the prescense of mixed types (A-E) of botulinum toxin in the grass and victims of grass sickness strengthen this hypothesis. Perhaps it has been hard to prove the problem because several types of toxin at very low levels work together synergistically? Also implicated have been other clostridial organisms including Clostridium sordellii and Clostridium bifermentans.

The botulism hypothesis is not a new one but was rejected in the 1920's because vaccination did not prevent the disease but it has been noted that the vaccine used may not have been specific enough to provide protection against this form of botulism. Definitive proof that C. botulinum causes grass sickness can only come from causing the disease by administration of the bacteria or toxin and/or by showing that grass sickness can be prevented by vaccination against C. botulinum. It is possible that toxin production may simply be a secondary consequence of the disruption of the normal bowel function

The association of Clostridium botulinum type C with equine grass sickness: a toxicoinfection? L. C. HUNTER, J. K. MILLER? and I. R. POXTON* Department of Medical Microbiology, University of Edinburgh Medical School, Teviot Place, Edinburgh EH8 9AG and ?Biotrix, Peebles, Scotland. Keywords: horse; Clostridium botulinum type C; neurotoxin; equine grass sickness; dysautonomia; C2 toxin; C3 exoenzyme 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 ìg 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. Equine vet. J. (1999) 31 (6) 492-499