A fatal dysautonomia of unknown etiology, equine grass sickness causes marked reduction of GI motility due to widespread degeneration within the autonomic nervous system. It is seen throughout northern Europe, and a few cases have been diagnosed in the USA in the same geographic area (Midwest) that has a high prevalence of canine dysautonomia.
Grass sickness is seen at any age after weaning and at any time of year, but incidence is highest in spring and in horses 2–7 yr old. Although associated with recently acquired horses kept solely at grass, the condition has very rarely been seen in housed stock. All equidae appear susceptible. Acute, subacute, and chronic forms are recognized, categorized by whether death occurs within 24 hr, 7 days, and 1 wk, respectively. However, chronic cases can survive for weeks or months, and a few cases have recovered. The exact etiology is unknown, but the causal agent is thought to be associated with grazing. A Clostridium botulinum toxin may be involved.
Horses are afebrile and show tachycardia, ileus, and colic. Patchy sweating and fine muscular fasciculations are often seen over the shoulders and flanks, and penile prolapse may develop. Horses adopt a "tucked up" stance, similar to that seen in equine motor neuron disease (see Equine Motor Neuron Disease). In contrast to feline dysautonomia, pupillary light reflexes and tear production are normal. Ptosis, with “droopy” eyelashes, tends to be prominent because of smooth muscle paresis. Rhinitis sicca (dry nose) commonly develops in chronic cases and is considered to indicate a poor prognosis. Affected horses often have dysphagia and esophageal dysfunction, which cause drooling, difficulty passing a stomach tube, nasal reflux of gastric contents, and pooling of barium contrast in the thoracic esophagus. On rectal palpation, the mucosa is dry and tacky, and feces are scant and hard. Distended loops of small intestine and an impacted large colon are seen in the more acute cases. Secondary ileal dilation/impaction and displacement of the large colon can be confusing features. Cachexia can be profound in chronic cases.
In acute cases, the stomach and small intestine are markedly distended with fluid (which can result in gastric rupture), and the large intestine is impacted. In chronic cases, the GI tract is usually empty. All forms may show linear ulceration of the esophagus and hard, tarry fecal balls. Neuronal degeneration of pre- and postganglionic sympathetic and parasympathetic neurons is characteristic. A specific distribution of chromatolytic autonomic and somatic lower motor neurons is found in the brain stem and spinal cord.
No reliable in vivo diagnostic test is available, but dysphagia, tachycardia despite few signs of pain, decreased GI tract motility, a tucked-up stance (chronic cases), and ptosis are useful features. Administration of dilute (0.5%) phenylephrine to one eye should, within 20 min, result in marked decrease in ptosis (most easily seen as a decrease in the angle of the eyelashes to the head when viewed from the front). Biopsies of ileal and rectal tissue (1-cm long, formalin-fixed biopsies preferred) can confirm the diagnosis when examined by a pathologist experienced with grass sickness lesions. Postmortem confirmation of diagnosis depends on histopathologic examination of autonomic ganglia. The cranial cervical ganglia are the most accessible ganglia on postmortem examination and can be found in a fold of mucosal tissue in the caudal wall of the medial compartment of the guttural pouch.
A proportion of mildly affected (chronic) cases can survive with dedicated nursing care; a wide variety of feeds should be offered to encourage feed intake. Acute and subacute cases have not survived and should be euthanized on humane grounds. Stabling at-risk stock for part of the day has been recommended.
Last full review/revision March 2014 by Caroline N. Hahn, DVM, MSc, PhD, DECEIM, DECVN, MRCVS