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==Description==

==Description==

Equins Serum Hepatitis (ESH) leading to acute liver failure is most commonly associated with prior administration of an equine biologic product. This is most commonly tetanus antitoxin, but encephalitis vaccines and equine serum have also been implicated. Other possible hypotheses include alkaloid toxicity and mycotoxins. Several cases have been reported in which no biologic product had been administered, leading to the possibility that an infectious agent may be involved.   

Equine Serum Hepatitis (ESH) is the most common cause of acute hepatitis in horses. It is often associated with prior administration of an equine biologic product, most commonly tetanus antitoxin. Encephalitis vaccines and equine serum have also been implicated as well as alkaloid toxicity and mycotoxins. Several cases have been reported occurring in groups of horses in which no biologic product had been administered, leading to the possibility of an infectious or viral aetiology.  A Type III (immune-complex mediated) hypersensitivity reaction also has been proposed.

 

==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, however some parts of the world have no reported cases. Some reports suggest that lactating broodmares given tetanus antitoxin after parturition are particularly prone to Theiler's disease.

ESH occurs predominantly in older horses. Cases (both individual cases and outbreaks) occur relatively frequently during the autumn months in north western USA, however some parts of the world have no reported cases. Some reports suggest that lactating broodmares given tetanus antitoxin after parturition are particularly prone to Theiler's disease.

==Clinical Signs==

==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.  They are generally sudden in onset and rapidly progressive.  

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.  

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 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.  

==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 signs of acute hepatocellular degeneration. be centrilobular to midzonal necrosis with mononuclear cell accumulation within the portal triads. Contusions, lacerations or fractures may be present if the disease has had a violent clinical course.  

Post mortem examination often shows generalised icterus and ascites, with an enlarged and pale liver. Histologically there may signs of acute hepatocellular degeneration including centrilobular to midzonal necrosis with mononuclear cell accumulation within the portal triads. Contusions, lacerations or fractures may be present if the disease has had a violent clinical course.  

==Treatment==

==Treatment==

Affected horses should be housed in a quiet, darkened stable in order to minimise stimulation. Sedation may be required if signs of hepatic encephalopathy are present. If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. The protein should be high in branched-chain amino acids, and corn and molasses are often used to achieve this.

The aims of treatment are mainly to support liver function until hepatic compromise can occur. Affected horses should be housed in a quiet, darkened stable in order to minimise stimulation. Sedation may be required if signs of hepatic encephalopathy are present. If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. In order to reduce the severity of neurological signs, the protein should be high in branched-chain amino acids; corn and molasses are often used to achieve this. If the horse is anorexic, a naso-gastric tube can be passed and high energy foods given directly into the stomach.

==Prognosis==

==Prognosis==

The prognosis for horses with signs of hepatic encephalopathy is extremely poor with a mortality rate approaching 100%. Horses that survive for a week after the onset of clinical signs may recover. A fall in SDH is associated with a better prognosis.  

The prognosis for horses with signs of hepatic encephalopathy is extremely poor with a mortality rate approaching 88%. Horses that survive for a week after the onset of clinical signs may recover. A fall in SDH is associated with a better prognosis.  

==References==

==References==