Difference between revisions of "Grass Sickness"
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| − | '''Equine grass sickness | + | | Also known as: |
| + | | '''Equine Dysautonomia<br> | ||
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| + | ==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== | ==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, | + | 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 | + | 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. |
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==Diagnosis== | ==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 | + | 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 strongly suggestives grass sickness, definitive diagnosis is made on ileal biopsy or at post mortem exam. |
===Clinical signs=== | ===Clinical signs=== | ||
====Acute==== | ====Acute==== | ||
*Depression | *Depression | ||
| − | *Abdominal pain, episodes of | + | *Abdominal pain, episodes of colic |
*Abdominal distension | *Abdominal distension | ||
*Dysphagia | *Dysphagia | ||
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*Patchy sweating | *Patchy sweating | ||
*Tachycardia | *Tachycardia | ||
| − | * | + | *sudden death |
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| − | + | 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. | |
====Chronic==== | ====Chronic==== | ||
| − | *Progressive | + | *Progressive eaciation |
*Dehydration | *Dehydration | ||
*Depression | *Depression | ||
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*Intermittent colic | *Intermittent colic | ||
| − | Other signs such as tachycardia, sweating, | + | Other signs such as tachycardia, sweating, dyspagia 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=== | ===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. | + | A definitive diagnosis is obtained by taking an ileal biopsy at laparotomy and inspecting the intrinsic myenteric plexus. 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=== | ===Pathology=== | ||
| − | + | ** [[Forestomach - Anatomy & Physiology|Stomach]] and [[Small Intestine - Anatomy & Physiology|small intestine]] contain large amounts of yellow fluid. | |
| − | There is an abrupt change in the [[Large Intestine - Anatomy & Physiology|large intestine]], where no fluid is present | + | *** 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. | ||
| + | |||
==Treatment== | ==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 | + | 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. |
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==Prognosis== | ==Prognosis== | ||
| − | The condition is | + | The condition is fatal. |
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==References== | ==References== | ||
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| − | [[Category:Intestine_-_Functional_Obstruction]] | + | [[Category:Intestine_-_Functional_Obstruction]][[Category:Horse]] |
| − | [[Category: | + | [[Category:Medical_Colic_in_the_Horse]][[Category:To_Do_-_lizzyk]] |
| − | [[Category: | ||
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Revision as of 16:49, 23 July 2010
 |
This article is still under construction. |
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-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 strongly suggestives grass sickness, definitive diagnosis is made on ileal biopsy or at post mortem exam.
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.
Chronic
- Progressive eaciation
- Dehydration
- Depression
- Anorexia
- Intermittent colic
Other signs such as tachycardia, sweating, dyspagia 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 and inspecting the intrinsic myenteric plexus. 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
- Stomach and small intestine contain large amounts of yellow fluid.
- There is an abrupt change in the large intestine, where no fluid is present.
- large intestine has very dry mucoid contents.
- There is an abrupt change in the large intestine, where no fluid is present.
- Stomach and small intestine contain large amounts of yellow fluid.
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 |