|
Pony with chronic grass sickness (McGorum et al) |
An international team of researchers has identified what they believe to be the probable cause of equine grass
sickness (EGS). Their findings suggest that a neurotoxin, similar in action to snake venom toxins but produced by pasture microbes, is the likely culprit. The work is set to be published in the Equine Veterinary Journal (EVJ) and is currently freely available online. A special editorial in the January 2025 issue of EVJ, authored by Bruce McGorum and colleagues, highlights the study’s findings and their implications. This breakthrough has the potential to pave the way for novel treatments and improved diagnostics for this devastating disease.
Equine grass sickness (EGS), also known as equine dysautonomia, is a major cause of mortality in horses and ponies in Great Britain, with more than 80% of cases proving fatal. First recognised in Scotland over 100 years ago, EGS remains most prevalent in Great Britain but has been reported in several northern European countries, South America, and very infrequently in North America.
EGS damages the autonomic nervous system, which controls involuntary bodily functions, with particularly severe effects on the gastrointestinal tract. Clinical signs range from depression, difficulty eating and swallowing, and weight loss to gastric reflux, abdominal pain, and death. The disease causes rapid degeneration of nerves, leading to paralysis of the gastrointestinal tract and other systemic effects such as muscle weakness, drooping eyelids, excessive salivation, sweating, and muscle tremors.
As there is currently no effective treatment for the most severe (acute and sub-acute) forms of the disease, horses are euthanised on humane grounds, typically within 24-48 hours of showing abnormal signs. In contrast, up to 50% of horses with the mild (chronic) form of grass sickness may survive with intensive nursing and supportive care.
Researchers from the Dick Vet Equine Hospital (RDSVS University of Edinburgh), Newcastle University, Istituto Zooprofilattico Sperimentale delle Venezie, and the University of Padova have made significant strides in identifying the neurotoxin responsible for EGS. Using electron microscopy, they examined post-mortem samples from horses with EGS and compared them to control samples. Their findings revealed that 72.2% of neuromuscular junctions (NMJs) in EGS-affected horses displayed abnormal morphology, compared to just 6.9% in controls.
These abnormalities are believed to represent a toxin-specific signature for a neurotoxic enzyme known as phospholipase A2. This enzyme disrupts the microscopic sites of communication between nerves and muscles (NMJs), which are crucial for normal muscle function.
Ongoing work aims to definitively identify the source of this toxin. Researchers suspect it is produced by a microbe, such as a bacterium or fungus, that thrives on pasture during the cold and dry weather conditions that typically precede outbreaks of EGS.
Interestingly, neurotoxic phospholipase A2 enzymes are also found in the venom of many poisonous snakes. While venomous snakes are not implicated in EGS, researchers hope that drugs being developed to treat nerve damage in snakebite victims could help promote nerve regeneration and recovery in horses with grass sickness.
Professor Bruce McGorum, R(D)SVS said: “Identifying a probable cause of Equine Grass Sickness represents a significant breakthrough. We hope that this discovery will lead to novel treatments and improved diagnostics for this devastating condition. We are very grateful for the generous support we have received from horse owners, veterinary surgeons, scientists, charities and funding bodies.”
“Further work is underway to determine the source of this neurotoxin; it is likely to be produced by a microbe such as a bacterium or fungus which grows on the horse’s pasture during the cold and dry weather which precedes the disease.”
This discovery represents a significant step forward in understanding equine grass sickness. By pinpointing the probable cause, researchers can now focus on developing effective treatments and preventive strategies. Advances in identifying the toxin’s source and exploring therapeutic interventions for nerve regeneration offer hope for reducing the impact of this devastating disease.
For more details, see:
McGorum, B., Pirie, R.S., Bano, L., Davey, T., Harris, J. and Montecucco, C. (2025),
Neurotoxic phospholipase A2: A proposed cause of equine grass sickness and other animal dysautonomias (multiple system neuropathies).
Equine Vet J, 57: 11-18.
https://doi.org/10.1111/evj.14442
McGorum BC, Davey T, Dosi MCM, Keen JA, Morrison LR, Pirie RS, Shaw DJ, Harris JB.
Equine grass sickness is associated with major abnormalities in the ultrastructure of skeletal neuromuscular junctions.
Equine Vet J. 2025; 57(1): 193–202.
https://doi.org/10.1111/evj.14063