Difference between revisions of "Grass Sickness"

Revision as of 16:03, 23 July 2010

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 fatal in all cases. 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 preceeding two months are also at greater risk. In many cases the disease appears to be related to specific pstures 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-mortm diagnosis of the disease is difficult because changes are confined to the gastro-intestinal tract.

Clinical signs

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

Biopsy

A definitive diagnosis is obtained by taking an ileal biopsy and inspecting the intrinsic myenteric plexus. Degenerative lesions and necrosis are seen in the autonomic nerve ganglia and enteric nervous system.

Pathology

- Stomach and small intestine large amounts of contain watery yellow fluid.
  - There is an abrupt change in the large intestine, where no fluid is present.
    - large intestine has very dry mucoid contents.

Treatment

There is no effective treatment, prompt euthanasia is indicated in acute and per acute cases, some chronic cases can be managed with intensive nursing care for a limited time period.

Prognosis

The condition is fatal.

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

@@ Line 15: / Line 15: @@
 ==Diagnosis==
+Ante-mortm diagnosis of the disease is difficult because changes are confined to the gastro-intestinal tract.
 ===Clinical signs===
 *Depression
@@ Line 28: / Line 29: @@
 ===Biopsy===
-A definitive diagnosis is obtained by taking an ileal biopsy, and inspecting the intrinsic myenteric plexus. Degenerative lesions are seen in the autonomic nerve ganglia,
+A definitive diagnosis is obtained by taking an ileal biopsy and inspecting the intrinsic myenteric plexus. Degenerative lesions and necrosis are seen in the autonomic nerve ganglia and enteric nervous system.
@@ Line 35: / Line 36: @@
 *** There is an abrupt change in the [[Large Intestine - Anatomy & Physiology|large intestine]], where no fluid is present.
 **** [[Large Intestine - Anatomy & Physiology|large intestine]] has very dry mucoid contents.
-===Pathogenesis===
-** Due to functional obstruction at ileocaecal valve and a degree of paralytic ileus of the [[Small Intestine - Anatomy & Physiology|small intestine]].
-** The exact cause is unknown, but a type of bacterial or fungal toxin which may damage autonomic nervous system ganglia may be involved.
-*** ''[[Clostridium botulinum]]'' is thought to be involved.
-* A similar condition seen in hares
-** At post mortem look for degenerative changes in coeliaco-mesenteric ganglia -  need to examine histologically.
-*** Ganglia are peanut sized and found in perirenal fat between adrenal gland and the aorta.