Equine Grass Sickness
Learn what the condition is, how it may be detected early, how it is treated or managed, and which breeds or species are linked to it.
Learn what the condition is, how it may be detected early, how it is treated or managed, and which breeds or species are linked to it.
A concise guide to the condition’s pattern, detection, management and urgency.
This snapshot is a general guide, not a diagnosis or treatment plan. New, severe or worsening signs require veterinary assessment.
Equine grass sickness, or equine dysautonomia, is a frequently fatal disease caused by degeneration of autonomic nerve cells in the gastrointestinal tract, peripheral ganglia and parts of the brain. Its precise cause remains uncertain. Disease is strongly associated with grazing and particular premises, with most cases reported in the United Kingdom and parts of northern Europe, although it occurs elsewhere. Young adult horses and the spring season are commonly represented.
Loss of autonomic control severely reduces gut motility and also affects the eyes, nose, sweating and other involuntary functions. Acute and subacute cases develop colic, gastric fluid accumulation, difficulty swallowing, drooling, reduced or absent intestinal sounds, constipation, muscle tremors, sweating and a tucked-up abdomen. Drooping upper eyelids and a dry, crusted nose may be noticeable. Acute gastric distension can become dangerous because horses cannot vomit.
Chronic disease progresses over weeks with profound weight loss, patchy sweating, difficulty eating and a characteristic narrow abdomen, while appetite may remain surprisingly interested. Some chronic horses survive; acute and subacute forms are effectively fatal. The condition is not the same as botulism, obstruction or routine impaction, although early signs can overlap.
Cases may cluster on a property, but direct horse-to-horse contagion has not been established as the usual pattern. Risk factors reported in affected regions include recent introduction to a pasture, soil disturbance and certain weather or grazing conditions, but no prevention method is completely reliable. The severity of neuronal loss determines whether useful gastrointestinal function can return and therefore dominates prognosis.
Three clinical patterns are recognised. Acute and subacute cases develop severe intestinal paralysis, reflux, colic and rapid deterioration; chronic cases show profound weight loss, a tucked-up abdomen and patchy sweating but may retain some appetite. The disorder clusters geographically and seasonally on particular pastures, yet it is not transmitted directly from an affected horse to companions.
Grass sickness should be considered in a grazing horse from an affected region that develops gastrointestinal stasis together with dysphagia, drooping eyelids, dry nasal mucosa, sweating or rapid weight loss. The veterinarian examines gut sounds, stomach reflux, swallowing, pupil and eyelid function, heart rate and evidence of obstruction. Local disease occurrence and pasture history materially affect suspicion.
A dilute phenylephrine eye-drop test may temporarily reverse characteristic eyelid drooping and support the diagnosis, but it is not definitive alone. Routine blood results are nonspecific and largely assess dehydration and complications. Rectal biopsy can demonstrate characteristic nerve-cell degeneration when an adequate sample is obtained and interpreted by an experienced pathologist. Full-thickness ileal biopsy collected during surgery or post-mortem examination provides stronger confirmation.
Acute cases with substantial reflux require immediate gastric decompression while competing surgical colics are assessed. Chronic cases must be evaluated for ability to swallow safely, maintain hydration and consume enough energy. Because definitive testing can be invasive and prognosis differs sharply by clinical form, diagnosis often combines characteristic signs, regional context, exclusion of obstruction and specialist pathological confirmation.
There is no treatment that reverses the autonomic neuronal degeneration. Acute and subacute grass sickness causes profound gastrointestinal failure and has an extremely poor prognosis; humane euthanasia is generally indicated once the diagnosis and clinical form are established. Gastric decompression and supportive measures may be required while the horse is assessed, but they do not restore intestinal nerve function.
Selected chronic cases can recover with prolonged, intensive nursing. The horse must retain enough swallowing and gastrointestinal function to eat safely. Highly palatable, energy-dense feeds are offered in small frequent amounts, with texture adjusted to swallowing ability. Fluids, analgesia, skin care, warmth, companionship and treatment of secondary problems may be required. Body weight and intake should be measured objectively because apparent interest in food can exceed the amount actually swallowed.
Recovery may take months and demands realistic welfare review. Horses that continue losing weight, aspirate feed or cannot maintain hydration despite support should not undergo indefinite treatment. On affected premises, pasture changes and region-specific risk-reduction advice may be discussed, but no measure guarantees prevention. New suspect cases should be reported promptly to the attending veterinarian and relevant surveillance scheme. Surviving chronic horses can regain useful quality of life, although return of condition and strength is slow.
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