Equine grass sickness

Abstract

Equine grass sickness (EGS; equine dysautonomia) is a polyneuronopathy affecting both the central and the 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 and enteric nervous systems. Varying disease severities occur, largely determined by the extent of neuronal degeneration in the myenteric and submucous plexuses of the enteric nervous system. Extensive neuronal degeneration, as seen in acute and subacute forms of EGS, results in intestinal dysmotility, the severity of which is incompatible with survival. In comparison, a proportion of chronic forms of EGS, characterised by less severe neuronal degeneration, will survive. Despite extensive research efforts since EGS was first reported over 100 years ago, the precise aetiology remains elusive. This article reviews much of the scientific literature on EGS, covering epidemiology, pathology, diagnosis, treatment and aetiological hypotheses.

Equine grass sickness, but not botulism, causes autonomic and enteric neurodegeneration and increases soluble N‐ethylmaleimide‐sensitive factor attachment receptor protein expression within neuronal perikarya

“…This study confirmed anecdotal reports [7,8] that CCG and ileal enteric neurones are not chromatolytic in horses with botulism, in contrast to EGS, suggesting that EGS is unlikely to be caused by the particular BoNTs that caused neuroparalysis in the neuroparalytic botulism horses included here. Since 4 of 5 botulism cases were associated with BoNT/C1 intoxication, these data are inconsistent with the hypothesis that EGS is a toxicoinfection associated with BoNT/C1 producing C. botulinum, unless this toxin has different mechanisms of action when produced in vivo during a toxico-infection rather than following oral toxin exposure.…”

Alterations in amino acid status in cats with feline dysautonomia

“…The predominant clinical features of FD are attributable to paralysis of the entire gastrointestinal tract caused by severe enteric neuropathy [3]. Striking similarities in the clinico-pathological features of FD with multiple system neuropathies reported in horses (equine grass sickness; EGS), dogs (canine dysautonomia), hares (leporine dysautonomia), rabbits, alpacas, llamas and sheep (abomasal emptying defect) suggest these represent a specific disease entity with a common aetiology [4]. The authors are unaware of a human neurodegenerative disorder which shares the exquisitely localised neuroanatomic lesions of these animal diseases.…”

Neurologic Diseases in Horses

“…All factors are considered together; a resilient soil-borne agent that, in certain climate conditions, produces a neurotoxin to which the horse may mount an immune response may be a plausible hypothesis. 25 Clinical disease can be classified as acute (<2 days), subacute (2-7 days), or chronic (>7 days). Clinicopathological findings reflect dysfunction of the autonomic nervous system, especially of the gastrointestinal tract.…”

“…22), of the myenteric and submucosal ganglia, and, to a lesser extent, from the brain and spinal cord. 25,26 Fig. 22.…”