Overview of Hepatic Disease in Large Animals

INTRODUCTION Hepatic disease is usual in large animals. Increases in serum hepatic enzymes and total bile acid concentration may indicate hepatic dysfunction, insult, disease, or failure. While liver disease is particularly usual in foals, progression to liver failure is not. Diseases that frequently result in hepatic failure in horses include Theiler's disease, Tyzzer's disease, pyrrolizidine alkaloid toxicosis, hepatic lipidosis, suppurative cholangitis or cholangiohepatitis, cholelithiasis, and chronic active hepatitis. Obstructive disorders, aflatoxicosis, leukoencephalomalacia, pancreatic disease, kleingrass or alsike clover poisoning, portal caval shunts, hepatic abscess, and perinatal herpesvirus 1 infections sporadically result in hepatic failure. Less frequently, hepatic failure is related by endotoxemia, steroid administration, inhalant anesthesia, systemic granulomatous disease, and drug-induced amyloidosis, hyperammonemia in Morgan foals, parasite damage, iron toxicity, or following neonatal isoerythrolysis[33]. In ruminant animals, hepatobiliary disease is relatedby hepatic lipidosis, hepatic abscesses, endotoxemia, pyrrolizidine alkaloid and other plant toxicoses, certain clostridial diseases, liver flukes, mycotoxicosis, and mineral toxicosis or deficiency. Vitamin E or selenium deficiency, aflatoxicosis, ascaridmigration, bacterial hepatitis, and ingestion of toxic substances are related by hepatic damage in swine.Thus, the exact incidence of hepatic disease in camelids is unknown; it appears to be usual in North America. Hepatic lipidosis is reportedly the most usual liver disease in llamas and alpacas, occurring in crias and adults. Bacterial cholangiohepatitis, adenoviral hepatitis and pneumonia, fungal hepatitis, toxic hepatopathy, halothane-induced hepatic necrosis, hepatic neoplasia, and liver fluke infestation have also been indicating in camelids. The liver can respond to insult in only a limited many of ways. Fat droplets in the liver may be early and usual reversible divers. Biliary hyperplasia is also reversible if the insult is removed early. Necrosis of hepatocytes indicates more recent damage. The dead cells are removed with an inflammatory process and replaced by new hepatocytes or fibrosis. Unless the dysfunction is severe and hepatocellular regeneration is evident, prognosis for animals by liver failure is commonly unfavorable. Early hepatic fibrosis may be reversible by prompt recognition and intervention. Chronic disease by extensive loss of hepatic parenchyma and fibrosis, particularlyby portal bridging, warrants a poor prognosis [11, 24].