Diseases of the gallbladder are rare in ruminants. Obstruction may be associated with liver fluke infestation, foreign bodies, abscesses, neoplasia, suppurative cholecystitis, or abdominal fat necrosis. Rupture of the gallbladder has been reported in a cow. Cholangitis (inflammation of the biliary system) has been reported in horses with chronic active liver disease. Mild behavior changes, weight loss, variable colic, icterus, and alterations in hepatic enzyme activity may be seen in affected horses. Treatment consists of longterm antimicrobial and supportive therapy as indicated.
Hepatic failure in neonatal foals may follow septicemia (especially Actinobacillus equuli), endotoxemia, perinatal asphyxia, Leptospira Pomona infection, equine herpesvirus 1, hepatic duct obstruction secondary to gastroduodenal obstruction, biliary atresia, and iron toxicity. Gastric ulcers and duodenitis in foals can cause strictures of the duodenum and subsequent cholangiohepatitis due to bile stasis. Neonatal isoerythrolysis and hemolysis may cause hypoxic and cholestatic hepatic disease. Administration of total parenteral nutrition may cause cholestasis and concurrent hepatic disease.
Biliary atresia (extrahepatic) has been reported in foals and in a neonatal lamb. Affected foals presented for anorexia, depression, lethargy, poor growth, colic, polydipsia, polyuria, pyrexia, and icterus at 1 mo of age. Markedly increased serum γ-glutamyl transpeptidase or transferase (GGT) and bilirubin with mildly increased sorbitol dehydrogenase (SDH) supported a diagnosis of biliary obstruction. Diagnosis of biliary atresia was confirmed at necropsy.
Hemochromatosis is an iron storage disease in which hemosiderin is deposited in the parenchymal cells, causing damage and dysfunction of the liver and other tissues. The disease is either primary (idiopathic) or secondary. It is reported in people, Mynah birds, Salers cattle, and horses.
In Salers cattle, the condition appears to be a homozygous recessive condition with inappropriate intestinal absorption of iron, excessive hepatic storage, and eventual loss of hepatic function. In horses, there is no evidence of a familial tendency or of excessive iron being consumed in the diet. Rather, it appears there is cirrhosis of the liver with secondary iron overload. In horses and cattle, increased iron is deposited in the liver.
In horses, primary clinical signs are weight loss, lethargy, and intermittent anorexia. In cattle, signs include decreased weight gain, poor body condition, dull hair coat, and diarrhea. In both species, serum liver enzyme concentrations, including GGT, alkaline phosphatase, AST, and SDH, are increased. Serum total bile acid concentrations are increased in horses, and serum iron, total iron binding capacity (TIBC), and percent saturation of the TIBC are usually normal. In some cases, serum iron and ferritin may be increased, but TIBC is not saturated. In cattle, total serum iron, TIBC, and saturation of transferrin are increased. Iron content of the liver tissue is greatly increased in horses (normal 100–300 ppm) and cattle (normal 84–100 ppm). Hepatomegaly and hemosiderin accumulation in the liver, lymph nodes, pancreas, spleen, thyroid, kidney, brain, and glandular tissue are typically present.
Diagnosis is based on history, clinical signs, and laboratory findings. Finding abundant hemosiderin in the hepatocytes on histopathologic examination of a liver biopsy supports the diagnosis. High liver iron concentrations in animals with no history of excess iron intake help confirm the diagnosis. Differential diagnoses include iron toxicosis from exogenous sources and diseases causing chronic weight loss and hepatic dysfunction or disease.
Phlebotomies to remove blood and reduce the iron stores have been used in treatment of people with hemochromatosis. Similar treatment in horses and cattle has been unsuccessful. Deferoxamine is also used in people to induce a negative ion balance and reduce the rate at which iron accumulates. The effect in cattle and horses has not been evaluated.
The right lobe of the liver is the largest lobe in young horses but frequently atrophies in older animals and becomes fibrous. Right hepatic lobe atrophy was previously considered an incidental postmortem finding, but some consider it to be a pathologic condition.
Right hepatic lobe atrophy has been proposed to result from chronic compression of this portion of the liver by the right dorsal colon and base of the cecum. Feeding horses high-concentrate, low-fiber diets may contribute to atony of the right dorsal colon with resultant distention; this compresses the right hepatic lobe against the visceral surface of the diaphragm. Although there is no morphologic evidence of direct vascular impairment to the right hepatic lobe, vascular compromise may result secondary to compression. With chronicity, the portal circulation to the right lobe is impaired, resulting in hepatic anoxia, deprivation of nutrients, and gradual atrophy of the right lobe of the liver. No evidence of biliary tract disease has been noted. Colic may be seen. Some horses may have signs not related to the GI tract.
Amyloidosis refers to disease characterized by the extracellular deposition of amyloid, a proteinaceous fibril substance, in the tissue. Deposition of amyloid within an organ distorts normal tissue architecture and possibly function. In horses, the liver and spleen are the most common organs affected by systemic amyloidosis. Reactive or secondary systemic amyloidosis with deposition of amyloid A (AA) fibrils in the liver has been associated with severe parasitism and chronic infection or inflammation in horses. (Also see Amyloidosis.)
In a retrospective study of the records from the University of Berne, Institute of Animal Pathology, 30 Swiss Freiberger foals with pathologic lesions compatible with congenital hepatic fibrosis were identified. Affected foals were 1–12 mo old (average 3.7 mo). Most showed signs and had clinicopathologic changes reflecting severe liver damage. Pedigree analysis traced the disease back to one stallion. Results suggest that congenital hepatic fibrosis in Swiss Freiberger horses is a recessively inherited autosomal genetic defect. A similar condition has been reported in a calf.
In this syndrome of hyperammonemia, blindness and severe neurologic signs are seen in adult horses. The etiology is unknown, but a primary intestinal problem with overgrowth of urease-producing bacteria within the intestine is suspected.
The syndrome is nearly always associated with enteric disease, diarrhea, or colic. Diarrhea and, in some cases, protein-losing enteropathy may persist for several days. In most cases, diarrhea or colic precedes the neurologic signs by 24–48 hr. Laboratory abnormalities include increased blood ammonia concentrations (200–400 μm/L), severe metabolic acidosis, low plasma bicarbonate (≤12 mEq/L) concentration, and profound hyperglycemia (250–400 mg/dL). Serum concentrations of liver enzymes, total bile acids, and bilirubin are normal.
In most horses, neurologic signs resolve within 2–3 days with supportive treatment (IV fluids, potassium chloride, glucose, sodium bicarbonate) and administration of drugs to reduce ammonia absorption (lactulose, neomycin).
Portosystemic shunts are seen in foals and calves. Hyperammonemia and neurologic signs result from liver dysfunction with little laboratory or microscopic evidence of liver disease.
Clinical signs are first seen when affected foals are ~2 mo old and start to ingest larger amounts of grain and forage. Neurologic signs include staggering, wandering, blindness, circling, and seizures. Poor growth and intermittent neurologic signs (ataxia, weakness, depression, bruxism, tenesmus) have been reported in affected 2- to 3-mo-old calves. Serum concentrations of hepatic enzymes are often normal. Blood ammonia and total bile acid concentration are increased, and BSP® clearance is prolonged.
The liver is often small, with a smooth surface, and normal in color and texture. Microscopically, the hepatocytes are small. Portal veins in the triads may be small or absent. Hepatic arteries are often prominent and multiple.
A portosystemic shunt should be suspected in foals or calves exhibiting repeated episodes of cerebral signs without obvious reasons. Signs may be most pronounced and associated with feedings. Catheterizing the mesenteric vein and performing a portogram or nuclear scintigraphy can confirm and locate the shunt. In some cases, the shunt may be seen on ultrasonographic examination of the liver.
Surgical repair may be attempted in animals in which the site of the shunt can be identified, but the prognosis is guarded. Clinical signs in some foals may be controlled by restricting protein intake and by careful dietary management. Neomycin or lactulose are given orally to decrease ammonia production within the bowel. Supportive care with polyionic fluids, potassium, and dextrose may be needed to help decrease neurologic signs.
A syndrome of depression, ill thrift, and hyperammonemia with a variable degree of hepatic involvement is seen in Morgan foals. Affected foals have been related, but the cause of the syndrome is undetermined. Clinical signs are usually first seen around weaning time. Encephalopathy may temporarily improve with aggressive supportive therapy but recurs after withdrawal of treatment. Liver enzymes and blood ammonia concentrations are increased. Bilirubin concentration is often normal. Pathologic hepatic lesions include portal and bridging fibrosis, bile duct hyperplasia, karyomegaly, and cytomegaly. The disease is fatal.