Equine grass sickness (EGS), or equine dysautonomia, is a rare and fatal disease in horses. It almost exclusively affects grazing horses kept on pasture.

EGS is characterized by the development of severe lesions on the neurons of the peripheral and central nervous systems. [2][7] Symptoms vary in severity depending on the neuronal degeneration in the horse.

EGS results in loss of normal function of the gastrointestinal tract, affecting the horse’s ability to swallow and digest food. [10][11] This disease results in a decrease in gut motility, increasing the risk of colic and causing severe weight loss.

Although the exact cause of EGS is unknown, it is believed to result from a combination of environmental factors and bacterial infection.

While there is currently no cure for this condition, preventative management practices may help protect your horse from this dangerous disease.

Equine Grass Sickness

Horses with Equine Grass Sickness are believed to develop enteric neuropathy from ingesting a neurotoxin while grazing on pasture (mycotoxicosis). [11]

The condition causes gut dysfunction, impairing the horse’s ability to digest and absorb nutrients from feed.

EGS can present in an individual horse, or in multiple horses at once as part of an outbreak.

Currently, researchers suspect that equine grass sickness may be caused by a toxin-producing bacterium called Clostridium botulinum type C. [5] This bacteria lives in soil and is linked to botulism – a neuroparalytic disease.

Types of Equine Grass Sickness

EGS occurs in three forms – acute, subacute and chronic – reflecting the severity of nerve damage. [10]

While these categories are helpful when making a diagnosis to determine the horse’s prognosis, a horse’s symptoms can worsen and change over time. [4]

Acute EGS

Acute (“severe”) cases of EGS can be identified by the sudden onset of symptoms. Horses typically present with mild or moderate abdominal pain and nasogastric reflux, in which fluid in the intestine returns to the stomach. [8] This can lead to fluid distention.

Unfortunately, acute EGS is always fatal, and horses usually die or require euthanasia within 48 hours of symptom onset.

Subacute EGS

The symptoms of subacute (“moderate”) equine grass sickness are similar to acute symptoms, but occur gradually and are less severe.

Gastric reflux or gut distention are rare in subacute cases. The horse may be able to consume small amounts of feed, but this does not mean that the horse’s health will improve.

Horses with subacute EGS often die or require euthanasia within two to seven days, but this varies depending on the severity of symptoms.

Chronic EGS

Chronic EGS (“mild”) has a gradual onset and is not always fatal. The most common symptom of chronic EGS is weight loss or cachexia (wasting away).

Affected horses can be found standing in a tucked up posture indicative of gut discomfort. Unlike acute cases, horses with chronic EGS usually have an empty intestinal tract with no fluid distention or build-up. [1].

Horses may develop rhinitis sicca, otherwise known as a dry and crusty nose, due to alterations in the nasal mucosa caused by autonomic dysregulation. [9] This symptom often indicates a poor prognosis for chronic cases.

Signs & Symptoms

The symptoms of equine grass sickness vary depending on whether the horse has the chronic, subacute or acute form of the disease.

Clinical signs typically reflect the degree of neuronal loss in the autonomic nervous system, which regulates the function of muscles and internal organs.

Common signs of EGS include: [4]

  • Decreased gut motility
  • Dull demeanor
  • Patchy sweating
  • Dehydration
  • Hypersalivation and difficulty swallowing
  • Droopy eyelids (ptosis)
  • Reduced feed intake
  • Weight loss
  • Rapid muscle twitching
  • High heart rate (tachycardia)
  • High rectal temperature
  • “Tucked up” and base narrow stance
  • Gut paralysis (absence of intestinal sounds) and colic

Risk Factors

The exact cause of EGS is unknown, although the condition strongly correlates with grazing.

Several risk factors and toxic agents are associated with the development of the disease.

Geographical Distribution

Most cases of equine grass sickness occur in the northeast region of Scotland. However, affected horses have been identified throughout Northern Europe, the United Kingdom, the Falkland Islands and Australia.

Cases of EGS rarely develop in North America. [4]


Young horses (between the ages of 2-7) with access to grass on pasture have a higher risk of contracting the disease. Most affected horses are between 3 and 4 years of age.

EGS can occur anytime after weaning, as foals are rarely affected. [6]

It is rare for older horses to develop EGS. This may be explained by a developed tolerance to the causative agent and immunity to certain diseases.

Low Antibodies

Researchers believe that ingesting neurotoxin-producing bacteria, such as Clostridium botulinum, could be responsible for EGS. [4]

Botulinum toxins are lethal and cause paralysis by blocking nerve function in horses. Research shows that horses with acute EGS have higher levels of C. botulinum bacteria in their gut than unaffected horses. [4]

Horses with low levels of antibodies to C. botulinum may be at higher risk of EGS infection when forages are contaminated by bacteria. This includes younger horses with less acquired immunity. [6]


All breeds of horses can develop EGS, and all species of equids are susceptible, including horses, ponies, donkeys and zebras.

It has been suggested that native Scottish horse breeds, such as the Clydesdale, Shetland Pony or Highland Pony, are more susceptible to EGS. [8] However, further research is needed to determine whether there is a genetic link to EGS.

Premises & Pasture

Recently disturbed pastures are more prone to causing grass sickness in grazing horses. Disturbed pastures may provide a better growth environment for bacteria in the soil or bring toxins to the surface where they can be ingested. [3]

Construction of buildings or septic tanks near pastures may also put horses at higher risk.

Some cases have been linked to high soil nitrogen content, but no connections between EGS and fertilizer application or harrowing have been made. [3]

Season & Weather

In the UK, there is a high incidence of EGD cases during the spring and summer months. Elsewhere, most incidences of EGS occur between April and July with the highest prevalence in May. [6]

Cool, dry weather (between 7 – 11°C) and irregular frosts on pasture are associated with an increase in EGS cases.

Dietary Changes

Dietary changes are reported to be a significant risk factor for EGS in horses. [3] Changing a horse’s feed can impact the gut microbiome and affect hindgut fermentation.

Most grass sickness cases occur in the spring when horses transition to a diet of fast-growing forage. Soil nitrogen content has also been linked to grass sickness, likely by promoting growth of abundant, lush forage.

Researchers speculate that this may provoke the development of EGS in at-risk horses. [3]

Body Condition

Overweight horses and horses with a healthy body condition have a higher risk of developing EGS than underweight horses. [8][10]

Other Risk Factors

Other proposed risk factors for developing equine grass sickness include: [6][4]

  • Overcrowding of horses on pasture
  • Previous EGS cases on premises
  • Changes in feed (type, quantity, etc.)
  • Stress (recent move to new pasture, mixing groups of horses, etc.)
  • Castration
  • Frequent deworming with Ivermectin

Some sources suggest that dewormers are linked to the development of EGS, but this has not been proven. [4] The consequences of not properly deworming horses can be dangerous, so deworming is always recommended under vet supervision.


Not every case of EGS can be prevented, but some management recommendations can help to minimize the risk of your horse contracting this disease.

Stabling horses during high-risk times of the year (early spring and summer) can reduce the incidence of EGS. [6] Horses that have been moved to a pasture or farm with a history of EGS should be kept off pasture and stabled for a period of time.

If a case of EGS occurs in your herd, all horses should be removed from the pasture.

There is currently no vaccine for equine grass sickness.


Contact your veterinarian immediately if your horse shows signs of acute, subacute or chronic EGS.

Several diagnostic methods for equine grass sickness have been developed with variable success rates between individual cases. Diagnosis is usually made based on a small intestine biopsy, an eye drop test, patient history, and exposure to known risk factors for the condition.

Biopsy of Small Intestine

A definitive diagnosis for EGS relies on ante mortem biopsy of intestinal tissue. This examination and diagnosis can also be conducted post mortem.

The ileum experiences significant neuronal loss in horses with grass sickness. [8]

During an exploratory laparotomy, tissues can be removed and sampled to identify lesions in nerve cells. Tissue samples are stained and examined for nerve damage.

While this is the most reliable diagnostic test for EGS, it is invasive, and the results are not immediately available. Histological examination of affected tissues can take 2-3 days to process. [7]

Phenylephrine Eye-drop Test

Fast diagnosis of EGS is essential to prevent outbreaks in co-grazing horses.

Eye-drop tests can indicate paralytic damage to the nerves that control eyelash and eyelid positioning in the horse, which is a sign of EGS. [10]

Phenylephrine eye drops are used to reverse ptosis or eye drooping caused by some EGS cases. In horses with ptosis, the smooth muscle in the eyelid is paralyzed.

Administering 0.5% phenylephrine eye drops in one of the affected eyes can reduce drooping in as little as 30 minutes. This is demonstrated by the eyelashes of the treated eye lifting 15-30 degrees. [5]

Differential Diagnosis

Horses with chronic E