Line 6: |
Line 6: |
| |} | | |} |
| | | |
− |
| |
− |
| |
− |
| |
− |
| |
− |
| |
− |
| |
− |
| |
− | *reported in horses given serum of equine origin
| |
− | **tetanus
| |
− | **pregnant mare serum
| |
− | *uknown aetiology
| |
− | **suggested it may be of infectious cause, perhaps a virus
| |
− | *disease manifests itself between one to two months post injection
| |
− | ===Clinical===
| |
− | *jaundice
| |
− | *neurological signs
| |
− | *death follows quickly
| |
− | ===Gross===
| |
− | *jaundice
| |
− | *ascites
| |
− | *haemorrhages on and in many organs
| |
− | *[[Liver - Anatomy & Physiology|liver]] is greeenish with reddish and pale blotches
| |
− | *fibrin strands on the [[Liver - Anatomy & Physiology|liver]] surface
| |
− | ===Microscopically===
| |
− | *[[Liver - Anatomy & Physiology|liver]] cells very fatty (large single vacuoles), some degenerated and a few leukocytes
| |
− | *moderate portal fibrosis
| |
− | *heavily bile stained
| |
| | | |
| ==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 others such as encephalitis vaccines and equine serum have been implicated. | + | 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 others such as encephalitis vaccines and equine serum have been implicated. Other causes including alkaloid toxicity and mycotoxins have been hypothesised. |
| | | |
| | | |
| ==Signalment== | | ==Signalment== |
| | | |
− | ESH occurs predominantly in older horses. Cases (both individual cases and outbreaks) occur relatively frequently during the autumn months in north western USA. | + | 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. |
| | | |
| | | |
− | ==History==
| |
| | | |
| + | ==Clinical Signs== |
| | | |
| + | The history may include administration of an equine-derived biologic product. Clinical signs 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. |
| | | |
− | ==Clinical Signs==
| + | Signs may include the following: |
− | | |
− | The history may include administration of an equine-derived biologic product. Clinical signs may range from mild lethargy or inappetance to signs of hepatic failure. These may include the following:
| |
| | | |
| * Depression | | * Depression |
Line 56: |
Line 28: |
| * Icterus | | * Icterus |
| * Neurological signs such as head pressing (hepatic encephalopathy) | | * 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. |
− | | |
− | | |
− | Clinical signs 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.
| |
− | | |
| | | |
| ==Diagnosis== | | ==Diagnosis== |