Difference between revisions of "Equine Serum Hepatitis"
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==Description== | ==Description== | ||
| − | Equins Serum Hepatitis (ESH) leading to acute liver failure is most commonly associated with administration of an equine biologic product. This is usually tetanus antitoxin, but | + | Equins Serum Hepatitis (ESH) leading to acute liver failure is most commonly associated with administration of an equine biologic product. This is usually tetanus antitoxin, but encephalitis vaccines and equine serum have also been implicated. Other possible hypotheses include alkaloid toxicity and mycotoxins. |
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==Clinical Signs== | ==Clinical Signs== | ||
| − | The history may include administration of an equine-derived biologic product. | + | The history may include administration of an equine-derived biologic product, often four to six weeks prior to the onset of clinical signs. These may range from mild lethargy or inappetance to signs of acute or chronic hepatic failure. They are generally sudden in onset and rapidly progressive. The course of the disease is usually around five days, with either death or recovery occuring within ten days. |
Signs may include the following: | Signs may include the following: | ||
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==Pathology== | ==Pathology== | ||
| − | + | Post mortem examination often shows the liver to be enlarged and pale with rounded edges. Generalised icterus is often present. Histologically there may be centrilobular necrosis with mononuclear cell accumulation within the portal triads. | |
Revision as of 10:43, 24 July 2010
| Also known as: | Theiller's disease |
Description
Equins Serum Hepatitis (ESH) leading to acute liver failure is most commonly associated with administration of an equine biologic product. This is usually tetanus antitoxin, but encephalitis vaccines and equine serum have also been implicated. Other possible hypotheses include alkaloid toxicity and mycotoxins.
Signalment
ESH occurs predominantly in older horses. Cases (both individual cases and outbreaks) occur relatively frequently during the autumn months in north western USA. Some parts of the world have no reported cases.
Clinical Signs
The history may include administration of an equine-derived biologic product, often four to six weeks prior to the onset of clinical signs. These may range from mild lethargy or inappetance to signs of acute or chronic hepatic failure. They are generally sudden in onset and rapidly progressive. The course of the disease is usually around five days, with either death or recovery occuring within ten days.
Signs may include the following:
- Depression
- Anorexia
- Icterus
- Neurological signs such as head pressing (hepatic encephalopathy)
Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations.
Diagnosis
Pathology
Post mortem examination often shows the liver to be enlarged and pale with rounded edges. Generalised icterus is often present. Histologically there may be centrilobular necrosis with mononuclear cell accumulation within the portal triads.
Treatment
Prognosis
Prevention
References
- Fox, M and Jacobs, D. (2007) Parasitology Study Guide Part 2: Helminths Royal Veterinary College
- White, N.A., Edwards, G.B. (1999) Handbook of Equine Colic Reed Educational and Professional Publishing Ltd
- Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students University of Liverpool
- Edward Robinson, N and Sprayberry, K. A. (2009) Current Therapy In Equine Medicine Sixth edition Saunders Elsevier
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
- Giles, C.J., Urquhart, K.A. and Longstaffe, J.A. (1985) Larval cyathostomiasis (immature trichonema-induced enteropathy): A report of 15 clinical cases Equine Veterinary Journal 17, 196-201
- Murphy, D., Keane, M.P. and Goulding, R. (1997) Cyathostome associated disease in the horse: investigation and management of four cases Equine Veterinary Journal 9 247-252