Theiler's disease

Theiler's disease
Classification and external resources
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Theiler's disease, also known as idiopathic acute hepatitis disease (IAHD), serum-associated hepatitis, serum sickness, and postvaccinal hepatitis, is a viral hepatitis that affects horses. It is one of the most common cause of acute hepatitis and liver failure in the horse.

There is a rapid onset of clinical signs over the period of 2–7 days, beginning with anorexia, lethargy, and hyperbilirubinemia (icterus and discolored urine). Signs of hepatic encephalopathy (ataxia, blindness, aggression, and coma) and fever can also occur. Other signs include photodermatitis, hemorrhagic diathesis, dependent edema, and colic. The reason for colic is unknown, but is thought to be due to rapid decrease in the size of the liver, and the increased risk of gastric impaction. Rarely, weight loss can occur.

The most current theory is a result of a recent study that suggests it is caused by a pegivirus, referred to as Theiler's disease-associated virus (TDAV). Eight horses that had received prophylactic botulinum antitoxin and developed subsequent signs of Theiler's disease were subjected to a test for a viral infection based on RNA sequencing techniques. When TDAV was found, the original source of virus (the antitoxin) was injected into 4 additional healthy horses, with one displaying increased liver enzymes and all 4 having increased levels of TDAV, showing that the virus can be spread by inoculation. Measuring levels of virus in the originally infected horses has shown that the disease can become chronic, with some horses displaying low virus levels one year after initial infection. All horses that were initially negative remained so, suggesting that the virus is poorly transmitted horizontally.

However, not all horses that tested positive for this virus showed clinical signs, so additional causative factors such as immune mediated hypersensitivity or co-infections with other agents may be required to produce disease.

At present this can only be made definitively by liver biopsy or post mortem examination. Given the isolation of a causative virus it should soon be possible to diagnose this by serology, polymerase chain reaction or viral culture. On necropsy, the liver will be small, flaccid, and "dish-rag" in appearance. It has a mottled and bile stained surface. On microscopy there is marked centrilobular to midzonal hepatocellular necrosis and a mild to moderate mononuclear infiltrate. Mild to moderate bile duct proliferation may also be present. On radiology, the liver may be shrunken and difficult to visualize on ultrasound. Ascites may be present.

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