Grass Sickness (Equine Dysautonomia)

Grass sickness is a disease of the nervous system of Equids i.e. horses, ponies and donkeys most commonly but cases in captive zebra and Przewalski’s horses have been reported. The autonomic nervous system is primarily affected. This system controls the involuntary functions such as gut motility which is why many of the clinical signs are related to gut function.

Grass sickness has been recognised in this country since the early 1900’s. First documented in Scotland, Great Britain has the highest incidence of the disease in the world. It also occurs in northern Europe especially Sweden, Denmark, Germany but less so in France, Belgium, Italy, Holland, Norway, Finland and Switzerland. There is an identical disease named ‘mal secco’ or dry sickness in Argentina, the Falkland’s, Columbia and Chile. It is rare in Ireland and the USA and there have been no confirmed reports in Africa, Asia and Australia. It has been shown to affect hares and rabbits too.

Almost all cases occur in grazing horses, grazing full time or at least part of the day. Horses between the ages of 4 months and 30 years have been affected but most cases occur in horses between 2 and 7 years with a peak between 3 and 4 years. Horses that have undergone stress are more susceptible as are horses that have moved to an affected premises in the last two months. Interestingly, horses grazing with a previous grass sickness case seem to be at lower risk.

Most cases occur between April and July with a peak in cases in May. Certain premises and even a certain field on certain premises can have a higher incidence of cases. Horses grazing a field in which there has been a horse with grass sickness in the previous 2 years are at a higher risk. Soil disturbance i.e. harrowing or mechanical faeces removal seems to increase the risk of horses grazing the pasture developing grass sickness, probably due to ingesting more soil as they graze. Higher nitrogen levels in the soil have been attributed to higher risk.

Unfortunately, despite all the research, grass sickness remains a disease with a high mortality rate, approximately 85%. Invariably, horses with the acute and subacute form will die or require euthanasia within days of clinical signs starting. Some chronic cases (approx. 50%) have been shown to pull through with intensive care requiring a huge commitment from the owner, veterinary and nursing team. Those that keep eating, even small amounts, have the best prognosis. Happily, many of those that have recovered have returned to full health and their previous occupation.

There are three forms of grass sickness;

  • Acute; the digestive system is paralysed from the throat resulting in difficulty swallowing (dysphagia), depression, excessive salivation, moderate colic, absence of gut sounds (ileus), constipation (any faeces that are passed are hard, dark and covered in a distinctive mucus coating). Patchy sweating (usually flanks, neck, base of ears and below tail) and muscle tremors of the shoulder, flank and hindquarters may also be noted. The heart rate is very high (70-120bpm) and the eyelids may droop (ptosis) giving a sedated appearance. The stomach distends and foul smelling stomach contents can, in severe cases, spontaneously flow out of the nostrils. This occurs more commonly when a nasogastric tube is introduced into the horses’ stomach by a veterinary surgeon (nasogastric reflux). The stomach is a risk of rupturing, resulting in severe pain and prompt euthanasia is recommended, this is usually necessary within 48hours.
  • Sub-acute; as acute but clinical signs are less severe with stomach distention and gastric reflux are not a feature. There is rapid weight loss. Small amounts of food may continue to be eaten but the patient generally lasts less than a week.
  • Chronic; a more gradual onset with variable depression, mild to moderate intermittent colic (often after feeding), varying degrees of difficulty swallowing, reduced appetite to complete anorexia and rapid weight loss resulting in emaciation and a ‘tucked up’ appearance. The gut sounds are reduced and the heart rate is moderately increased to between 50-60bpm. The odd faeces, patchy sweating, muscle tremors and droopy eyelids feature in this form too. Horses can show odd behaviour, ‘playing’ with their water and dunking their feed in their water. They may lean on walls and adopt a base narrow stance like an ‘elephant on a drum’. They may develop Rhinitis sicca or ‘dry nose’ where thick mucus collects and dries in the nostrils making the horses breathing noisy. Gastric distention and salivation are not a feature. Horses that survive longer than a week are termed as chronic sufferers. Recovery is possible.

How do we diagnose grass sickness?

A definitive diagnosis can only be made by examining nervous tissue microscopically. This can only be achieved by taking samples surgically (which is expensive and general anaesthesia is risky in such an unwell animal) or, unfortunately samples taken at post mortem. Trials are going ahead at taking samples in the standing sedated horse via laparoscope. Our diagnosis is generally made by taking a careful history including whether the disease has been on the premises before, clinical signs, and ruling out other reasons for colic via blood, urine and peritoneal fluid sample (although taps are not always possible in a horse with grass sickness). Abdominal ultrasound may identify small intestinal distention seen in grass sickness and aid our diagnosis. Rectal biopsies may help but negative results do not rule the disease out.

As mentioned previously treatment should only be undertaken in chronic cases. Their prognosis increases if their demeanour and appetite improve in the first month. Treatment is very intensive and often involves a period of hospitalisation on intravenous fluids and ongoing medical treatment for colic signs, potential choke, appetite stimulants, laxatives and gastric ulcer treatment. High energy and protein food should be given but focus should be on getting then to eat anything as this increases their chances of survival. Some may need feeding via stomach tube to begin with. They need a deep bed, hand walks when they are able and as they improve, gradually increasing turn out. They need to be groomed to brush away dried sweat and their dry nose cleaned and Vaseline applied. Their body temperature may be low but they will continue to sweat so a warm but breathable rug must be used. Human contact and stimulation is very important too. It will be a very long process, between 6 and 12 months but of those that do recover 80% return to their previous level of work and are highly unlikely to succumb again despite the nerve damage never fully healing microscopically.

So what causes grass sickness?

Studies have been ongoing for 100 years and we still aren’t entirely sure exactly what the causative agent is. Due to the patterns of the disease and the type of damage to the nervous system we know that it not a contagious disease but due to an ingested toxin. Many have been investigated and it is most likely a combination of factors but one that is at the forefront of investigation is Clostridium botulinum type C. The reason that this is seemingly the most likely cause is for a number of reasons.

Clostridium botulinum type C is common in the soil and produces a range of neurotoxins to which the horse is particularly sensitive to.  It seems that a number of risk factors, like those mentioned above, trigger neurotoxin production in the horses’ intestines. This has been supported as neurotoxins have been found in the intestinal contents of grass sickness cases, horses with low antibody levels to C. botulinum are more susceptible and those with high antibody levels are at lower risk.  However, recent advances believe this may not be the case and more research is required. All avenues are being investigated to give us the best chance to find a way of preventing this disease.

Can we protect our horses?

With the comprehensive and ongoing research into risk factors of grass sickness, good pasture management, knowledge of disease risk in the area and stress reduction can help us reduce risk. There is also exciting research into a vaccine based on the research that Clostridium botulinum is the main risk factor in developing grass sickness. Clostridium botulinum is a bacterium in the same family as tetanus for which there is a very effective vaccine. With evidence that horses can develop immunity, the fact it is rare in horses under 2 years suggesting they get some passive immunity from their dam’s colostrum and that horses with higher antibody levels to C. botulinum are at a lower risk it seems a vaccine could be a very real preventative measure.