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AS the seasons now move from late winter into early spring and the ‘potholes’ on Britain's roads grow ever deeper and wider, the predictable spectre of the seasonal increase in the numbers of cases of equine grass sickness (EGS) looms larger as well. Since it was first recognised in the early 1900s, much EGS research has focused on investigation of risk factors and the identification of an aetiological agent. While the aetiopathogenesis has yet to be completely elucidated, there is growing evidence to suggest that EGS is a toxico-infectious form of botulism, with local neurotoxin production by Clostridium botulinum within the gastrointestinal tract (Hunter and others 1999, Hunter and Poxton 2001, McCarthy and others 2004). The great hope in this theory lies in the premise that, as for other clostridial toxic diseases, prevention by vaccination should be theoretically possible (Hunter and Poxton 2001, Hedderson and Newton 2004).
EGS represents a polyneuronopathy, and many clinical signs of the disease reflect damage to the autonomic nervous system, with the majority of signs attributed to dysfunction of the enteric nervous system. Antemortem diagnosis of EGS is often presumptive, based on epidemiological information and clinical signs, yet some cases represent a diagnostic challenge as no clinical sign is pathognomonic for all forms of the disease (Doxey and others 1991). However, reaching a definitive diagnosis is important, not only to inform likely prognosis and decisions on timing of euthanasia for affected horses or …