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==Introduction==

 

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 (TAT). In some cases, the affected horse may not have received the antitoxin but may have been in contact with another horse that received TAT. Other biologic products that have been implicated include encephalitis vaccines and equine serum. Other aetiologies such as alkaloid toxicity and mycotoxins have been reported. Several cases have been reported occurring in groups of horses in which no biologic product had been administered, indicating that there may be an infectious or viral component to the disease.  A [[Type III Hypersensitivity|Type III (immune-complex mediated) hypersensitivity]] reaction has also been proposed.  

 

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 (TAT). In some cases, the affected horse may not have received the antitoxin but may have been in contact with another horse that received TAT. Other biologic products that have been implicated include encephalitis vaccines and equine serum. Other aetiologies such as alkaloid toxicity and mycotoxins have been reported. Several cases have been reported occurring in groups of horses in which no biologic product had been administered, indicating that there may be an infectious or viral component to the disease.  A Type III (immune-complex mediated) hypersensitivity reaction has also 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 ESH.

==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 - Horse|hepatic encephalopathy]] may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as [[Photosensitisation|photosensitisation]] or pruritus may also be seen. The course of the disease is usually around five days, with death usually occurring 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.  

==Diagnosis==

==Diagnosis==

Diagnosis of ESH and evaluation of hepatic function may be achieved using three types of diagnostic test. Serum biochemistry may indicate the following abnormalities:

Diagnosis of ESH and evaluation of hepatic function may be achieved using a combination of clinical history, abrupt onset of clinical signs and diagnostic tests indicative of hepatic insufficiency.  

* Increased conjugated and unconjugated bilirubin

* Increased conjugated and unconjugated bilirubin

* Increased liver enzymes- SDH, AST, GGT and ALP

* Increased liver enzymes- SDH, AST, GGT and ALP

* Hypoglycaemia

* Hypoglycaemia

* Reduced urea

* Increased urea

Bilirubinuria may also be present.  

'''Ultrasound''' may reveal a smaller than normal liver with a loss of parenchymal structure and enlarged bile ducts. In several studies, biopsy is considered as the ‘gold standard’ technique for definitive diagnosis of hepatic disease. Biopsy is usually performed on the right hand side between the twelth and fourteenth intercostal spaces. A coagulation profile is often performed prior to performing the procedure due to the possibility of a clotting defect.  

Ultrasound may reveal a smaller than normal liver with a loss of parenchymal structure and enlarged bile ducts.  

''Post mortem'' examination often shows generalised [[Icterus|icterus]] and ascites, with an enlarged and pale liver. Histologically there may be 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.  

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.  

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 [[Nasogastric intubation in the horse|naso-gastric tube]] can be passed and high energy foods given directly into the stomach.

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.  

|Vetstream = [https://www.vetstream.com/equis/Content/Disease/dis00061.asps Acute hepatitis in equine]

|literature search = [http://www.cabdirect.org/search.html?q=%28%28title%3A%28%22serum+hepatitis%22%29+AND+od%3A%28horses%29%29%29+OR+%28%28title%3A%28%22Theiler%27s+disease%22%29%29%29 Equine Serum Hepatitis publications]

==References==

==References==

[[Category:Liver_-_Inflammatory_Pathology]][[Category:Horse]]

 

 

[[Category:Liver_-_Inflammatory_Pathology]]

 

 

[[Category:To_Do_-_SophieIgnarski]]

[[Category:Expert_Review]]

[[Category:Liver Diseases - Horse]]