Difference between revisions of "Ragwort Toxicity"

From WikiVet English
Jump to navigation Jump to search
Line 10: Line 10:
 
It is poisonous to livestock with Horses and cattle being more susceptible than sheep. When ingested over long periods of time it causes hepatotoxicity which in the severe form is invariably fatal. Exposure to the toxin is usually via ingestion of contaminated hay or silage as the animal will avoid it in the fresh form.  
 
It is poisonous to livestock with Horses and cattle being more susceptible than sheep. When ingested over long periods of time it causes hepatotoxicity which in the severe form is invariably fatal. Exposure to the toxin is usually via ingestion of contaminated hay or silage as the animal will avoid it in the fresh form.  
  
The toxin is a pyrrolizidine alkaloid.
+
The toxin is a pyrrolizidine alkaloid which is converted in the body to the toxic intermediate '''pyrroles''' and their esters which cause intitial and continued damage to hepatocytes. They have an anti-mitotic effect whilst allowing continued synthesis within the cell and its nucleus resulting in a marked increase in the size of the hepatocytes. The attempted repair by fibrosis aids the shunting from the portal triads to the central vein, thereby bypassing the hepatocytes and resulting in the clinical signs associated with liver failure.
  
 
==Signalment==
 
==Signalment==
  
 
==Diagnosis==
 
==Diagnosis==
 
 
 
===Clinical signs===
 
===Clinical signs===
 
*Weight loss
 
*Weight loss
Line 27: Line 26:
 
===Biopsy===
 
===Biopsy===
 
A liver biopsy will reveal hepatomegalocytosis and bilary hyperplasia.
 
A liver biopsy will reveal hepatomegalocytosis and bilary hyperplasia.
 +
 +
===Post Mortem===
 +
On gross post mortem examination the liver is small, dense and fibrotic with prominent biliary tracts.
  
 
==Treatment==
 
==Treatment==
Line 36: Line 38:
 
* Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''' ''University of Liverpool''
 
* 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.
 
*Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) Sauders.
 
 
==Hepatotoxicity==
 
*'''pyrrolizidine alkaloids'''
 
**toxic principle converted in the body to the toxic intermediate '''pyrroles''' and their esters
 
**cause intitial and continued damage to hepatocytes
 
**have an anti-mitotic effect whilst allowing continued synthesis within the cell and its nucleus
 
***causes a marked increase in the size of parenchymal cells, a phenomenon termed ''''megalocytosis''''
 
***these very enlarged hepatocytes can be up to 20 times bigger
 
***the enlarged cells are closely apposed so that the sinusoids may not be evident
 
*it is likely that the vascular component of the attempted repair of the chronic damage by fibrosis (really a type of granulation tissue) aids the shunting from the portal triads to the central vein and thereby bypassing the hepatocytes
 
*other plant and fungal toxins perform in the same way
 
 
  
 
[[Category:Hepatotoxicity, Chronic]][[Category:Horse]][[Category:Sheep]]
 
[[Category:Hepatotoxicity, Chronic]][[Category:Horse]][[Category:Sheep]]
 
[[Category:To_Do_- lizzyk]]
 
[[Category:To_Do_- lizzyk]]

Revision as of 16:49, 25 July 2010



Description

Ragwort (Senecio jacobea) is part of the daisy family, a flowering plant with completely yellow flowerheads. It commonly grows on wasteland and grazing pastures. It is poisonous to livestock with Horses and cattle being more susceptible than sheep. When ingested over long periods of time it causes hepatotoxicity which in the severe form is invariably fatal. Exposure to the toxin is usually via ingestion of contaminated hay or silage as the animal will avoid it in the fresh form.

The toxin is a pyrrolizidine alkaloid which is converted in the body to the toxic intermediate pyrroles and their esters which cause intitial and continued damage to hepatocytes. They have an anti-mitotic effect whilst allowing continued synthesis within the cell and its nucleus resulting in a marked increase in the size of the hepatocytes. The attempted repair by fibrosis aids the shunting from the portal triads to the central vein, thereby bypassing the hepatocytes and resulting in the clinical signs associated with liver failure.

Signalment

Diagnosis

Clinical signs

  • Weight loss
  • Annorexia
  • Hepatic insufficiency
  • Hepatic encephalopathy

Biochemistry

Rasised liver enzymes (AST, GGT, AP and LDH) and elevated bilirubin and bile acids indicate liver disease, however in very severe, chronic cases where active damage is no longer occurring, liver enzymes may be normal.

Biopsy

A liver biopsy will reveal hepatomegalocytosis and bilary hyperplasia.

Post Mortem

On gross post mortem examination the liver is small, dense and fibrotic with prominent biliary tracts.

Treatment

Prognosis

Horses with chronic liver failure due to ragwort poisoning have a poor prognosis for survival as the damage to the liver is severe by the time clinical signs are obvious.

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: Senecio jacobea