Grass Sickness

Description

Equine grass sickness causes a paralysis of the gastro-intestinal tract, by disruption of the autonomic nervous system. The condition may occur acutely, or progress chronically over several weeks, but is invariably fatal. The aeitology is unknown but an ingested neurotoxin appears to be involved. The neurotoxic is absorbed from the intestinal tract and selectively binds to the autonomic nerve terminals resulting in degeneration and loss of neurons.

Signalment

Cases of Grass sickness are restricted to Northwestern Europe and South America with the highest incidence in the UK, in some parts of Eastern Scotland 1% of horses die annualy from the disease. Young animals, 2-7 years old are predisposed. The disease occurs in warm wet weather with peak incidences in spring and autumn. Affected horses usually live at pasture, those that have moved pasture within the preceding two months are also at greater risk. In many cases the disease appears to be related to specific pastures or fields with a history of grass sickness affected horses, however it has been reported in animals with none of the usual risk factors.

Diagnosis

Ante-mortem diagnosis of the disease is difficult because changes are confined to the gastro-intestinal tract. However the combination of a supportive history and clinical signs is strongly suggestive of grass sickness, definitive diagnosis is made on ileal biopsy or at post mortem examination.

Clinical signs

Acute

• Depression
• Abdominal pain, episodes of colic
• Abdominal distension
• Dysphagia
• Inappetence
• Muscular tremors
• Reduced faecal output
• Hypersalivation
• Patchy sweating
• Tachycardia
• Sudden death

Rectal examination reveals dry faecal balls, large colon impaction and distented loops of small intestine. Gut sounds are reduced or absent due to gastrointenstinal atony. Passage of a stomach tube often results in gastric reflux of up to 20L.

Subtle signs of ptosis and dry rhinitis should be noted.

Chronic

• Progressive emaciation
• Dehydration
• Depression
• Anorexia
• Intermittent colic

Other signs such as tachycardia, sweating, dysphagia and muscle tremors are present but usually less severe than in acute grass sickness. The nasal passages are frequently blocked with dried mucopurulent discharge.

Biopsy

A definitive diagnosis is obtained by taking an ileal biopsy at laparotomy. A 1-2cm eliptical biopsy should be taken from the anti-mesenteric border of the ileum at the level where the ileocaecal ligament ends. Degenerative lesions and necrosis are seen in the autonomic nerve ganglia and enteric nervous system.

Pathology

On post mortem examination the stomach and small intestine may be distented and contain large amounts of yellow fluid. There is an abrupt change in the large intestine, where no fluid is present and the contents are very dry and mucoid.

Treatment

There is no effective treatment, prompt euthanasia is indicated in acute cases, some chronic cases can be managed with intensive nursing care for a limited time period. In chronic cases where the neuronal degeneration is very mild and supportive management is successful 40% of horses have been reported to return to excercise. Recovery is slow, 6-8 weeks of supportive therapy is needed during which clinical signs persist but it may take up to a year for horses to return to work and they will be predisposed to future problems of oesophageal choke and dysphagia.

Supportive treatment in appropriate cases consists of IV fluid therapy and feeding by stomach tube and liquid parafin in the early stages of the disease, however horses with a chance of making a recovery do not usually require these treatments. A diet high in energy and protein that is easy to swallow should be given in small quantities at frequent intervals. Short walks in hand with increasing lengths at pasture will aid gut motility and prevent boredom. Other measures to improve the comfort of the horse include regular grooming, cleaning around the eyes and removal of nasal crusting. Episodes of mild colic should be managed appropriately with non-steriodal anti-inflammatory drugs such as phenylbutazone or flunixin meglumine. Progress should be monitored regularly by reassessing clinical signs, body weight and quality of life.

Prognosis

The condition is usually fatal. Horses likely to survive have mild clinical signs with little difficultly swallowing.

References

• Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students University of Liverpool
• Rose, R. J. and Hodgson, D. R. (2000) Manual of Equine Practice (Second Edition) Sauders.

Also known as:

Equine Dysautonomia