The Latest Updates On Equine Grass Sickness
Equine Grass Sickness (EGS) is a serious, often fatal disease that has been a major concern for horse owners since it was first recognized in Scotland around 1907. In the early stages, EGS can mimic the signs of mild colic, but as the disease progresses, more distinct symptoms emerge, leading to partial or complete paralysis of the digestive tract. Horses with EGS often experience rapid weight loss, difficulty swallowing, drooling, patchy sweating, muscle tremors, an elevated heart rate, and poor gut motility.
There are three forms of EGS: acute, subacute, and chronic. In acute and subacute cases, the symptoms are usually severe, and the prognosis is poor, with most horses succumbing to the disease. Chronic cases are less severe and develop more gradually. Horses with chronic EGS may show reduced appetite and difficulty swallowing, but survival is possible if they can be persuaded to eat high-energy concentrated feeds. Intravenous fluid therapy is used to prevent dehydration. Cisapride, a human medication that increases gut activity, has been helpful in some cases. Recovery takes time as these horses are likely to lose significant weight.
Risk Factors for Developing EGS
Although this disease occurs throughout much of Northern Europe, it is most common in the United Kingdom. Despite the movement of horses from affected regions, only a handful of cases have been reported in other parts of the world, such as North America and Ireland. This suggests that an environmental factor plays a key role in the development of EGS.
Some horses appear to be more vulnerable to EGS than others. Whilst foals seem to be protected from the disease, horses under the age of 5 are most affected, likely because they have not yet developed sufficient levels of antibodies against the disease. The condition is also more common in horses grazing on certain types of soil, such as acidic loam and sand soils, and in areas where the soil has been disturbed. Other factors that increase the risk of EGS include the presence of domestic poultry, sudden changes in feeding regimes, and stress. Some research suggests that grazing on ruminal pasture may reduce the risk. These insights highlight the complex interplay of environmental, dietary, and possibly microbial factors in the development of EGS.
New Insights into the Cause of EGS
For years, researchers have suspected a connection between EGS and Clostridium botulinum type C, which produces botulinum toxins. Horses with EGS have been found to have lower levels of antibodies to this bacterium than healthy horses. However, the widespread presence of Clostridium botulinum in the environment and the fact that many horses are exposed to it without developing EGS has left researchers searching for other explanations. A recent study by McGorum et al., (2024), identified abnormalities to over 70% of the neuromuscular junctions in the diaphragm and intercostal muscles of horses with EGS. These abnormalities are not consistent with the effects of botulinum neurotoxins, therefore contradicting the hypothesis that EGS is caused by botulinum neurotoxins from Clostridium botulinum C or D.
Recent studies have shifted the focus toward a potential neurotoxin responsible for the disease. Specifically, a neurotoxic enzyme called Phospholipase A2 (PLA2) has been proposed as a likely cause of EGS. PLA2 is an enzyme found in snake venom. In fact, the same study by McGorum et al., (2024) found that the neuromuscular junction structural abnormalities in horses with EGS were similar to those seen in animals exposed to neurotoxins from snake venom.
Clinical signs induced by snake PLA2 envenomation in humans, dogs, and cats are similar to those of EGS. Any minor differences in clinical signs are likely due to differing routes of exposure, toxin dose and action of the specific neurotoxic PLA2s (nPLA2s). For example, the route of intoxication in EGS is via the gastrointestinal tract, potentially explaining the main clinical signs affecting this system (difficulty swallowing, poor gut motility). Alternatively, neurotoxins from snake bites are spread via the blood and lymphatic system, potentially accounting for the more severe skeletal muscle and respiratory tract paralysis.
The epidemiology of EGS is inconsistent with the involvement of snake venoms. It is more likely that PLA2 could be ingested from pasture or produced by microbes in the horse's gastrointestinal tract. Most terrestrial plants, especially under stress, produce secretory PLA2s, which could contribute to the disease if ingested by grazing horses. Microbial PLA2s, either ingested or produced in the gut, could explain the gastrointestinal symptoms seen in EGS, such as bacterial and fungal dysbiosis.
Current Treatments and Future Directions
With the recent identification of PLA2 as a potential cause of EGS, new therapeutic options may be on the horizon. Ongoing research aims to identify the specific type of PLA2 responsible for the disease and determine its source, whether it is from microorganisms in the pasture or produced within the horse’s gastrointestinal system. This could help identify preventive strategies to reduce the risk of EGS. Additionally, scientists are looking for potential biomarkers that could aid in diagnosing the disease before it becomes fatal. Understanding the precise mechanisms behind the disease will also inform the development of targeted treatments, offering hope for future therapeutic breakthroughs.
Equine Grass Sickness remains a challenging and often deadly disease, but recent research has brought us closer to understanding its cause and finding new treatments. While much remains to be learned, the identification of neurotoxic phospholipase A2 as a possible culprit marks a significant step forward in the fight against EGS. By continuing to investigate the environmental and microbial factors that contribute to this devastating condition, researchers hope to find ways to prevent and better manage EGS in horses, improving the outlook for affected animals.
McGorum, B. C., Davey, T., Dosi, M. C., Keen, J. A., Morrison, L. R., Pirie, R. S., ... & Harris, J. B. (2025). Equine grass sickness is associated with major abnormalities in the ultrastructure of skeletal neuromuscular junctions. Equine Veterinary Journal, 57(1), 193-202. Doi: https://doi.org/10.1111/evj.14063
McGorum, B., Pirie, R. S., Bano, L., Davey, T., Harris, J., & Montecucco, C. (2024). Neurotoxic phospholipase A2: A proposed cause of equine grass sickness and other animal dysautonomias (multiple system neuropathies). Equine Veterinary Journal, 57(1), 11-18. Doi: https://doi.org/10.1111/evj.14442
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