WHAT IS EGS
Equine grass sickness (EGS) is a frequently fatal disease of horses with a mortality rate in excess of 85%. The condition affects the nervous system that controls involuntary functions, the so-called ‘autonomic nervous system’ and hence an alternative name for the disease ‘equine dysautonomia’. The gastrointestinal tract is particularly affected although some of the signs of the disease are related to nerve damage in other parts of the body.
EGS is classified into 3 broad types, based on the duration and severity of clinical signs:
- Acute Grass Sickness cases survive 1-2 days
- Subacute Grass Sickness cases survive 2-7 days
- Chronic Grass Sickness cases survive more than 7 days
The most severely affected body system is the gastrointestinal tract, resulting in clinical signs of intestinal paralysis of varying degree or colic, although other signs are also often seen.
EGS has been recognised for over 100 years since it was first reported near Broughty Ferry, Scotland in the first decade of the 20th Century. Ever since then Great Britain has had the highest frequency of cases in the world, with disease now occurring in all areas of Scotland, England and Wales. The disease also occurs in several northern European countries and an identical condition called mal seco (literally translated as ‘dry sickness’) has been recognised in Argentina, the Falklands, Colombia and Chile. Interestingly, EGS is rare in the rest of the world including the U.S.A., Africa, Australia and Asia. Notably, despite extensive horse movements between mainland Great Britain and Ireland, EGS remains uncommon in the Emerald Isle.
What might cause Equine Grass Sickness?
At present we do not know definitively what causes EGS. Previous studies have attempted to identify the cause of the disease and numerous infective or toxic agents have been investigated, including toxic plants, fungi, chemicals, mineral and vitamin deficiencies, insects, viruses and bacterial toxins. However, these studies have all failed to demonstrate consistent associations with the disease. EGS is not contagious so it will not be spread directly from horse to horse. It is probable that multiple factors are involved and that pasture-associated or dietary risk factors play a role in causing the disease.
Almost all cases of EGS occur in horses with access to grazing, and we think they are exposed to a noxious agent present in the soil and ingested as a contaminant of grass. It is suggested, though not proven, that the aetiological agent is Clostridium botulinum (C. botulinum), a bacterium which is found commonly within soil. C. botulinum bacteria are capable of producing a range of toxins, including potent neurotoxins (toxins that damage the nervous system), to which horses are particularly sensitive.
This picture illustrates characteristic changes to nerve cells in the intestine of a case of EGS. Microscopic examination of intestinal biopsy samples collected during abdominal surgery (performed with the horse under a general anaesthetic) may be used to confirm the diagnosis of EGS in some cases.
Role of Clostridium botulinum in EGS
In 1923 it was suggested that there was a connection between EGS and C. botulinum, due to the nature of damage to the nervous system and the similarity of clinical signs with the disease botulism. In classical botulism, preformed neurotoxin is eaten in contaminated water or feed such as spoiled silage. In contrast, the current theory is that EGS is a toxico-infectious form of botulism caused by C. botulinum type C, with the disease occurring when a combination of risk factors triggers the production of neurotoxin locally in the horse’s intestinal tract.
Several research studies have provided strong evidence to support this toxico-infection hypothesis. Neurotoxin has been detected in intestinal contents from EGS cases, and was also detected in the faeces from a larger proportion of EGS cases compared to unaffected horses. Horses with EGS have lower antibody levels to C. botulinum type C and neurotoxin, and horses with higher antibody levels have a reduced risk of disease. Additionally, horses that have been in contact with a case of EGS have a lower risk of developing the disease, suggesting they may acquire some degree of immunity.
There is a low incidence of disease in very young animals, with around 6% of cases occurring in horses less than 2 years of age. Antibodies to both the C. botulinum type C and neurotoxin have been detected in the colostrum of mares, suggesting that foals may acquire some immunity from their dam, which may provide some explanation for the lower incidence of disease seen in very young horses.
While further research is required to definitively prove the causal link between toxico-infection with C. botulinum and EGS, if this is proved then prevention of this highly fatal disease by vaccination is theoretically possible in the same way that tetanus (caused by another clostridial toxin) has been very effectively controlled by vaccination with a simple inactivated toxin vaccine (a so-called ‘toxoid’).