Prospects for vaccination against equine grass sickness

Neurodegenerative Disorders

“…84 The botulism hypothesis was initially offered in 1919 after presumptive C. botulinum was isolated postmortem from the intestine or spleens of EGS horses. 66,68 Some similarities were noted between the clinical signs of EGS and botulism. Vaccine trials conducted in 1922 and 1923 with an antitoxin-neutralized toxin vaccine produced promising results and led to a commercial antiserum product for the treatment/ prevention of EGS; 66 however, the botulism theory proved controversial and was subsequently abandoned in favor of a short-lived streptococcal theory.…”

“…67 It has been suggested that the initial cases followed the importation of Peruvian guano (bird droppings) for application to fields as fertilizer. 68 Equine dysautonomia has long been recognized in the Patagonia region of South America where it is known as "mal seco." 69 In the years after its first recognition in Scotland, the geographic range of the disease expanded rapidly until 10-20% of the working horses in Scotland were affected.…”

“…67 EGS remains endemic in Scotland, England, and Wales and has also been reported from continental Europe, the Falkland islands, and Colombia with isolated cases in Australia and the United States. 68 International attention was focused on the disease after the death of the prominent Thoroughbred stallion Dubai Millenium 68 from EGS.…”

“…77 Toxins C2 and C3 also may contribute to the neurotoxicity of C. botulinum type C. It has been hypothesized that toxin production and absorption occur in the ileum due to overgrowth from normal intestinal flora and/or spore germination in association with a nutritional trigger. 68 Factors such as changes in feed, pasture, and weather conditions and parasite status are proposed to contribute to changes in flora favoring clostridial growth. According to this hypothesis, the effects of neurotoxin production would then be dependent on factors such as age, previous exposure, presence of neutralizing antibody, and antioxidant status and may lead to neurotoxicosis and the signs of EGS.…”

“…Definitive antemortem diagnosis requires examination of an ileal biopsy although rectal biopsy results may provide strong supportive evidence. 68 Demonstration of characteristic histologic changes in enteric plexuses and ganglia provides definitive diagnosis postmortem.…”