Hepatitis in horses is inflammation of the liver, which can arise from multiple causes: ingestion of hepatotoxic plants such as ragwort (Senecio spp.) or pyrrolizidine alkaloid-containing forage, infection by viruses or bacteria, mycotoxins in moldy feed, drug toxicity, or chronic copper accumulation. The liver has a large functional reserve, meaning a horse can lose a substantial portion of hepatic tissue before signs of liver failure become apparent — this latency makes early-stage hepatitis difficult to detect without blood testing.
Clinical signs of hepatic disease in horses range from subtle to severe. Early signs may include abdominal pain that mimics colic, weight loss, reduced appetite, and behavioral change. As liver function deteriorates, photosensitization (sunburn-like skin lesions in unpigmented areas), jaundice (icterus) visible in the sclera and mucous membranes, head pressing, circling, apparent blindness, and hepatic encephalopathy may develop. These neurological signs indicate advanced compromise. Serum liver enzyme elevations — notably gamma-glutamyltransferase (GGT), sorbitol dehydrogenase (SDH), and bilirubin — are the primary diagnostic indicators and should be part of the routine veterinary workup in horses with access to pasture containing unknown plants.
Prognosis depends on the cause, extent of liver damage, and whether the toxic source has been removed. Pyrrolizidine alkaloid toxicity causes progressive and irreversible fibrosis; affected horses may survive months before decompensation. Serum heme breakdown products tracked in prognosis degradation markers and liver biopsy can guide prognosis. Management focuses on removing the toxic source, providing a low-protein diet to reduce hepatic load, and supporting the horse through the underlying condition if treatable. Pasture safety — identifying and removing hepatotoxic plants — is the primary prevention strategy.