Grass sickness is a disease of horses unique to Northern Europe and especially Scotland.
The disease was first recorded at a military camp near Dundee in 1911. It has gradually spread in incidence and is currently found in all parts of the United Kingdom. A similar syndrome has been reported in wild Hares, and in the 1980’s in domestic cats (feline dysautonomia). The disease in cats has virtually disappeared and may have been related to feed manufacturing processes, although no causal link was ever found.
Grass sickness is caused by widespread severe damage to the neurons (nerves) in the autonomic nervous system; this is the part of the nervous system that helps control the intestines.
The disease is arbitrarily divided into three types, however each group overlaps with the others, and they effectively only reflect the severity of the disease in an individual animal.
The acute form is the most serious. It is of rapid onset, the horse is severely distressed, has an elevated heart rate and patchy sweating and may be dull and depressed. Moderate quantities of green fluid may be produced from the nostrils (this should always be considered a serious sign in a horse). There is stasis of gut movements, and usually no faeces will be produced. There are often muscle fasciculations (twitches). Horses with acute grass sickness are often confused with colic, but rarely roll or go down. Choke is another disease that is not infrequently confused with grass sickness. Veterinary attention is required urgently. Often when a stomach tube is passed a vast quantity of grass fluid will flow back. If your vet is sure the horse has acute grass sickness then destruction on humane grounds is the only option, and the horse should not be allowed to continue to suffer.
Subacute grass sickness. This is a milder form of grass sickness. Affected animals rarely have gastric reflux (green discharge) but will show most of the other signs displayed by the acute cases. Patchy sweating is common in all forms of grass sickness. An inability to swallow (dysphagia) is a prominent sign along with drooping of the upper eyelid (ptosis). Subacute cases are always fatal; the course of the disease is 2 – 7 days.
Chronic grass sickness. These cases are less severely affected than subacute cases, and may survive for considerable periods of time. Some of these animals will respond to treatment, and some centres report up to 50 % success rate. Signs include depression, rapid and dramatic weight loss, some degree of dysphagia but the horse will usually eat small quantities, drooping of upper eye lid, patchy sweating, persistently elevated heart rate (60/min. is common), muscle fasciculations and dry, crusty nasal discharge (rhinitis).
Good nursing care and the use of drugs to increase the activity of the intestines (prokinetic agents) such as cisapride have been successful in treating some of these animals. However many are left permanently damaged, and unfortunately euthanasia is the commonest outcome.
The cause of grass sickness has remained a mystery for the last ninety years. Research workers have recently made some interesting advances, but there is still much left to find out about grass sickness.
Risk factors include:
Recent introduction to new pasture.
Previous history of grass sickness on pasture.
No hay or other conserved feed being fed.
Aged 2 to 7 years.
Highest incidence April – July (but occurs all year around).
It must be stated however that all horses can be affected by grass sickness. Infected horses DO NOT appear to be infectious to other horses; indeed horses grazed with grass sickness victims have a DECREASED chance of getting the disease themselves.
The cause of grass sickness has proved elusive. Many causative agents have been suggested including fungal, plant and chemical toxins. Research by Hunter, Miller and Poxon (1999) has revived an old concept that the disease is a toxin-infection associated with Clostridium botulinum type C. The absence of classical signs of botulism in affected horses is explained by the suggestion that the toxin is produced in the intestines after the horse has eaten the infected contaminated grass, rather than by ingestion of preformed toxin. The nerves supplying the intestines are thus exposed to a high dose of locally produced toxin, causing severe neuronal damage and causing the gastro intestinal dysfunction associated with the disease. It is suggested that insufficient neurotoxin reaches the peripheral nerves to cause the signs observed in classic botulism.
It is not possible to protect your horse 100% from grass sickness but the following advice may help:
Always feed some conserved forage (hay/haylage) even when horses are turned out 24 hours a day.
Don’t put horses in the at risk age group (2-7 years) out onto pasture where there have been previous cases.
Make sure your horse is healthy with regular worming or faecal egg count monitoring.