EGS Causes

Studies have to date failed to definitively identify a specific cause of EGS.  Previous investigations have examined the role of various agents including: poisonous plants, bacterial toxins, insects and viruses.  In 1923 it was suggested that there was a connection between equine grass sickness and Clostridium botulinum, a soil based bacterium, due to the nature of damage to the nervous system and the similarity of clinical signs with the disease botulism.  The current favoured theory is that EGS is a toxico-infectious form of botulism caused by C botulinum type C, with the disease occurring when the neurotoxin is produced locally in the intestine. This is in contrast to classical botulism in which the preformed neurotoxin is eaten in contaminated feed such as spoiled silage.  While further research is required to definitively prove the causal link between toxico-infection with Clostridium botulinum and EGS, if this is proved, then prevention of this invariably 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’).

This picture shows a horse exhibiting excessive salivation at the mouth – a feature of acute or subacute grass sickness which is not seen in chronic grass sickness cases.  It is not known whether excess salivation occurs due to increased saliva production, paralysis of the mouth, or both.