Changes

==Clinical Signs==

==Clinical Signs==

The affected animal's history may include administration of an equine-derived biologic product, often four to six weeks prior to the onset of clinical signs. They are generally sudden in onset and rapidly progressive.  

The affected animal's history often includes administration of an equine-derived biologic product approximately four to six weeks prior to the onset of clinical signs. Clinical signs are generally sudden in onset and rapidly progressive.  

Signs may range from mild lethargy or inappetance to signs of acute or chronic hepatic failure. They may be non-specific such as depression, anorexia or weight loss. Affected horses are often severely icteric and may pass dark urine due to the presence of bilirubin. Signs relating to hepatic encephalopathy may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as photosensitisation or pruritus may also be seen. The course of the disease is usually around five days, with death ususally occuring within ten days.  

Signs may range from mild non-specific signs of lethargy, weight loss or inappetance to signs of acute or chronic hepatic failure. Affected horses are often severely icteric and pass dark urine due to the presence of bilirubin. Signs relating to hepatic encephalopathy may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as photosensitisation or pruritus may also be seen. The course of the disease is usually around five days, with death ususally occuring within ten days.  

Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations.  

Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations.