[1] 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).
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.
[1][2] 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).
[2] 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.
[2][4] 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.
[1] Given the isolation of a causative virus it should soon be possible to diagnose this by serology, polymerase chain reaction or viral culture.
Moderate to severe acidosis, leukocytosis, polycythaemia, increased creatine kinase and hyperammonemia may be present, and hemolysis can occur at the end stage.
Increasing dietary levels of branched chain amino acids and feeding low protein diets can help signs of hepatic encephalopathy, which is often accomplished by feeding small amounts of grain and/or beet pulp, and removing high-protein feedstuffs such as alfalfa hay.
[3] Grazing on non-legume grass may be acceptable if it is late summer or fall, although the horse should only be permitted to eat in the evening so as to avoid photosensitization.
Cases with rapid progression of clinical signs, uncontrollable encephalopathy, haemorrhage or haemolysis have a poor prognosis.