Difference between revisions of "Grass Sickness"

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Also known as: '''''Equine Dysautonomia
  
{| cellpadding="10" cellspacing="0" border="1"
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==Introduction==
| Also known as:
+
'''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 neurotoxin is absorbed from the intestinal tract and selectively binds to the autonomic nerve terminals resulting in degeneration and loss of neurons.
| '''Equine Dysautonomia<br>
 
|-}
 
 
 
==Description==
 
Equine grass sickness, or equine dysautonomia causes a paralysis of the gastro-intestinal tract, by disruption of the autonomic nervous system. This leads to a pooling of ingesta throughout all parts of the gastro-intestinal tract.  The condition may occur acutely, or progress chronically over several weeks, but all cases will eventually die. A definitive diagnosis is obtained by taking an ileal biopsy, and inspecting the intrinsic myenteric plexus. There is no effective treatment, although in the short to medium term, horses can be successfully managed by informed and attentive owners.
 
  
 
==Signalment==  
 
==Signalment==  
Grass sickness has been reported in 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.  
+
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 usually occurs in spring or summer in horses at pasture, those that have moved pasture recently are also at greater risk.  
+
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.
Young animals 2-7 years old are predisposed.
 
  
 
==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 is strongly suggestive of grass sickness, definitive diagnosis is made on '''ileal biopsy''' or at post mortem examination.
 +
 
 
===Clinical signs===
 
===Clinical signs===
 +
====Acute====
 
*Depression
 
*Depression
*Abdominal pain, episodes of colic
+
*Abdominal pain, episodes of [[:Category:Colic in Horses|colic]]
 
*Abdominal distension
 
*Abdominal distension
 
*Dysphagia
 
*Dysphagia
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*Reduced faecal output
 
*Reduced faecal output
 
*Hypersalivation
 
*Hypersalivation
*
+
*Patchy sweating
 +
*Tachycardia
 +
*Sudden death
  
 +
[[Rectal Examination of the Horse|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. [[Nasogastric intubation in the horse|Passage of a stomach tube]] often results in gastric reflux of up to 20L.
  
** Degenerative lesions are seen in the autonomic nerve ganglia, including enteric plexuses
+
Subtle signs of ptosis and dry rhinitis should be noted.
** May either:
 
*** Progress rapidly to death
 
*** Take a slower clinical course.
 
**** Eat a bit, but food drops out of mouth
 
**** Go on to die slowly.
 
** Some horses recover
 
*** This is very unlikely, and the condition is usually fatal. 
 
** Clinically difficult to diagnose - signs are confined to the gut.
 
*** Easy to diagnose on post mortem
 
  
===Pathology===
+
====Chronic====
** [[Forestomach - Anatomy & Physiology|Stomach]] and [[Small Intestine - Anatomy & Physiology|small intestine]] large amounts of contain watery yellow fluid.
+
*Progressive emaciation
*** There is an abrupt change in the [[Large Intestine - Anatomy & Physiology|large intestine]], where no fluid is present.
+
*Dehydration
**** [[Large Intestine - Anatomy & Physiology|large intestine]] has very dry mucoid contents.
+
*Depression
===Pathogenesis===
+
*Anorexia
** Due to functional obstruction at ileocaecal valve and a degree of paralytic ileus of the [[Small Intestine - Anatomy & Physiology|small intestine]].
+
*Intermittent colic
** 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. 
+
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.
* A similar condition seen in hares
 
** Certain yeares almost seem to have outbreaks.
 
* Certain pastures at certain times of year produce grass sickness quite often.
 
** A definitive diagnosis must be made -  if the condition is due to the grazing we need to know.
 
*** E.g. if on livery or stud grazing, may put people off going there.
 
* 'Diagnosis''' 
 
** 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.
 
  
 +
===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 [[Monogastric Stomach - Anatomy & Physiology|stomach]] and [[Small Intestine Overview - Anatomy & Physiology|small intestine]] may be distented and contain large amounts of yellow fluid.
 +
There is an abrupt change in the [[Large Intestine - Anatomy & Physiology|large intestine]], where no fluid is present and the contents are very dry and mucoid.
  
 
==Treatment==
 
==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.  
+
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==
 
==Prognosis==
The condition is fatal.
+
The condition is usually fatal.
 +
Horses likely to survive have mild clinical signs with little difficultly swallowing. 
 +
 
 +
{{Learning
 +
|literature search = [http://www.cabdirect.org/search.html?q=%28%28title%3A%28%22Equine+Dysautonomia%22%29%29%29+OR+%28%28title%3A%28%22Grass+Sickness%22%29%29%29 Grass sickness publications]
 +
}}
  
 
==References==
 
==References==
 +
* Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''' ''University of Liverpool''
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*Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) Sauders.
 +
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{{review}}
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 +
{{OpenPages}}
  
[[Category:Intestine_-_Functional_Obstruction]][[Category:Horse]]
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[[Category:Intestine_-_Functional_Obstruction]]
[[Category:Medical_Colic_in_the_Horse]][[Category:To_Do_-_lizzyk]]
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[[Category:Medical_Colic_in_the_Horse]]
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[[Category:Expert_Review]]
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[[Category:Alimentary Diseases - Horse]]
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[[Category:Neurological Diseases - Horse]]

Latest revision as of 16:12, 6 July 2012


Also known as: Equine Dysautonomia

Introduction

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 neurotoxin 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.


Grass Sickness Learning Resources
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Literature Search
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Grass sickness publications


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.




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