Grass sickness: current thinking on aetiology and pathogenesis

Equine grass sickness (EGS, equine dysautonomia) is a polyneuronopathy affecting both the central and peripheral nervous systems of horses. As the name implies, EGS almost exclusively affects grazing horses resulting in the development of a characteristic array of clinical signs, most of which can be attributed to neuronal degeneration in the autonomic (ANS) and enteric (ENS) nervous systems.
Since it was first reported in 1909 in Eastern Scotland, a vast array of aetiological hypotheses have been proposed and addressed experimentally; yet to date, the definitive cause remains elusive. Historical routes of investigation have included the contributing role of alsike clover (Trifolium hybridum) ingestion, C. perfringens enterotoxicity, insect vectors, fungi and C. botulinum toxicoinfection. The development of these hypotheses has largely been informed by clinical observations and the data derived from both epidemiological and pathological studies.
It is currently accepted that the epidemiology of the disease supports the role of an ingested soil-borne agent capable, under certain conditions, of producing or liberating a putative neurotoxin. Pathological studies have mapped the neuroanatomic distribution of typical chromatolytic neuronal changes, which, despite some conflicting results, may partly reflect a response to axonal damage at the level of the ENS. However, the widespread nature of the neuropathology in EGS is also consistent with more extensive distribution of the toxin, for example via haematogenous dissemination. Furthermore, the pivotal study by Gilmour and Mould in 1977 [1] clearly demonstrated the presence of a toxic component within the serum of acute EGS cases which, when injected intra-peritoneally into recipient ponies, induced the classic neuropathology. Unfortunately, the identity […]