About Equine GRASS SICKNESS
WHAT IS EGS?
Equine grass sickness (EGS) is a frequently fatal disease with a mortality rate in excess of 85%, which can affect all members of the equine family. The disease results in severe and extensive damage in neurons (nerves) in both the central and the peripheral nervous systems. 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. Much of the characteristic never degeneration is found in the nervous system that controls involuntary functions, the so-called ‘autonomic nervous system’ and hence an alternative name for the disease ‘equine dysautonomia’.
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.
HISTORY OF EGS
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. The disease spread rapidly throughout eastern Scotland, and had been reported in many regions in northern England and Wales by the 1920s. Ever since then 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 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 Britain and Ireland, EGS remains uncommon in Ireland. EGS is not contagious so it will not be spread directly from horse to horse.
WHAT CAUSES EGS?
Almost all cases of EGS occur in horses with access to grazing, and we think they are exposed to some form of noxious agent present in the soil and ingested as a contaminant of grass. 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. It is probable that multiple factors are involved and that pasture-associated or dietary risk factors play a role in causing the disease.
There is growing scientific evidence to suggest that EGS may be caused by the bacterium Clostridium botulinum (C. botulinum) type C, which is found commonly within soil and is capable of producing a range of toxins, including potent neurotoxins (toxins that damage the nervous system), to which horses are particularly sensitive.
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 similarities observed between EGS and botulism in both horses and humans. 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 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.
If EGS is caused by a toxico-infection with C. botulinum, 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’). The on-going EGS vaccine trial has been designed to determine whether vaccination against C. botulinum type C reduces the risk of EGS – click here for more information about the trial.