Diseases of the gallbladder are rare in ruminants. Obstruction may be associated with liver fluke infestation Fasciola hepatica in Ruminants Fasciola hepatica is one of the most important flukes of domestic ruminants worldwide, causing liver fluke disease (liver rot, fascioliasis). Chronic liver fluke disease is more common... read more , foreign bodies, abscesses, neoplasia, suppurative cholecystitis, or abdominal fat necrosis. Rupture of the gallbladder has been reported in a cow. Cholangitis (inflammation of the bile ducts) may occur in horses as an acute disease or as an acute exacerbation of chronic progressive hepatitis Chronic Progressive Hepatitis in Large Animals Chronic progressive hepatitis, or "chronic active hepatitis," is any progressive fibrosing process within the liver, secondary to multiple etiologies. It is a histopathologic diagnosis in which... read more . Fever, depression, anorexia, weight loss, variable colic, icterus, and alterations in hepatic enzyme activity may be evident in affected horses. Treatment consists of longterm antimicrobial and supportive care as indicated.
Hepatic Failure in Foals
Hepatic failure in neonatal foals may follow septicemia (especially septicemia due to Actinobacillus equuli), endotoxemia, perinatal asphyxia, Leptospira pomona infection, equine herpesvirus 1 infection, hepatic duct obstruction secondary to gastroduodenal obstruction, biliary atresia Biliary Atresia 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... read more , and iron toxicosis Iron Toxicosis Hepatotoxins manifest their effects by one or more mechanisms: centrilobular necrosis, midzonal necrosis, periportal necrosis, cholestasis, biliary hyperplasia, fatty or hydropic change near... read more . Gastric ulcers and duodenitis in foals can cause strictures of the duodenum and subsequent cholangiohepatitis Cholangiohepatitis Tyzzer disease is caused by Clostridium piliforme (previously Bacillus piliformis) and results in acute necrotizing hepatitis, myocarditis, and colitis in foals 8–42 days old.... read more due to bile stasis. Neonatal isoerythrolysis Alloimmune Hemolysis Hemolytic anemia results from loss of RBCs. Immune-mediated destruction is the most common cause in dogs, although infections, tumors, and other causes also occur. Immune-mediated hemolytic... read more and hemolysis may cause hypoxic and cholestatic hepatic disease.
Biliary atresia (extrahepatic) is a rare congenital defect; it has been described in individual case reports of foals and in a neonatal lamb. Affected foals presented for anorexia, depression, lethargy, poor growth, colic, polydipsia, polyuria, pyrexia, and icterus at 1 month of age. Markedly increased plasma gamma-glutamyl transferase (GGT) and bilirubin with mildly increased sorbitol dehydrogenase (SDH) supported a diagnosis of biliary obstruction. A 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 humans, Mynah birds, Salers cattle, and horses.
In Salers cattle, hemochromatosis appears to be a homozygous recessive condition with inappropriate intestinal absorption of iron, excessive hepatic storage, and eventual loss of hepatic function. In horses and cattle, increased iron is deposited in the liver.
In cattle, clinical signs include decreased weight gain, poor body condition, dull hair coat, and diarrhea. In both horses and cattle, plasma GGT, alkaline phosphatase (AP), AST, SDH and total bile acids are increased. Serum iron, total iron binding capacity (TIBC), and percentage saturation of the TIBC are usually normal. Iron content of the liver tissue is greatly increased in horses (normal 100–300 ppm) and cattle (normal 84–100 ppm).
Diagnosis of hemochromatosis is based on history, clinical signs, and laboratory findings. Differential diagnoses include iron toxicosis Iron Toxicosis Hepatotoxins manifest their effects by one or more mechanisms: centrilobular necrosis, midzonal necrosis, periportal necrosis, cholestasis, biliary hyperplasia, fatty or hydropic change near... read more from exogenous sources, and diseases causing chronic weight loss and hepatic dysfunction or disease.
Phlebotomy to remove blood and decrease the iron stores has been used in the treatment of humans with hemochromatosis, but it is not effective in large animals.
Right Hepatic Lobe Atrophy
Right hepatic lobe atrophy in older horses has been proposed to result from chronic compression of this portion of the liver by the right dorsal colon and base of the cecum. 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 occur. Some horses may have clinical signs not related to the GI tract.
Hepatic Lobe Torsion
Hepatic lobe torsion can be a rare cause of colic in horses. Liver enzymes and fibrinogen are increased; abdominal fluid analysis varies. Bacteria, including Clostridium spp, may be found in the necrotic portion of the liver. Exploratory celiotomy is required for a definitive diagnosis.
Hepatic amyloidosis Amyloidosis is characterized by the extracellular deposition of amyloid, a proteinaceous fibrillar 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.
Congenital Hepatic Fibrosis
Congenital hepatic fibrosis is a rare condition that has been identified as a recessively inherited autosomal genetic defect in Swiss Freiberger horses.(1 References 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... read more ) A similar condition has been reported in a calf.
Primary Hyperammonemia in Adult Horses
In primary hyperammonemia of adult horses, blindness and severe neurologic signs are observed. The etiology of this syndrome is unknown, but a primary intestinal problem with overgrowth of urease-producing bacteria within the intestine is suspected. Excessive ammonia production is believed to ensue, overwhelming the liver's ability to metabolize it through the urea cycle.
Primary hyperammonemia 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 hours. Laboratory abnormalities include increased blood ammonia concentrations (200–400 mcmol/L), severe metabolic acidosis, and profound hyperglycemia (250–400 mg/dL). Plasma concentrations of liver enzymes, total bile acids, and bilirubin are normal.
In most horses, neurologic signs resolve within 2–3 days with supportive care (intravenous fluids, potassium chloride, glucose, sodium bicarbonate) and administration of drugs (eg, lactulose, neomycin) to decrease ammonia absorption.
Portosystemic shunts occur rarely in foals and calves. Hyperammonemia and neurologic signs result from liver dysfunction with little laboratory or microscopic evidence of liver disease.
Clinical Findings and Lesions of Portosystemic Shunts in Foals and Calves
Clinical signs of portosystemic shunts in affected foals are first observed when they are ~2 months old and are starting to ingest a more adult diet consisting of increased 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-month-old calves. Plasma activities of hepatic enzymes are often normal. Blood ammonia and total bile acid concentrations are increased.
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.
Diagnosis of Portosystemic Shunts in Foals and Calves
History of intermittent neurologic signs, possibly associated with periods of hyperammonemia
Imaging, which is difficult but definitive
A portosystemic shunt should be suspected in foals or calves exhibiting repeated episodes of cerebral clinical signs without obvious reasons. Signs may be most pronounced after feeding. Catheterizing the mesenteric vein and performing a portogram or nuclear scintigraphy can confirm and locate the shunt. In some cases, the shunt may be evident on ultrasonographic examination of the liver.
Treatment of Portosystemic Shunts in Foals and Calves
Surgical repair—possible, but difficult in large animals
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 restriction of protein intake and by careful dietary management. Neomycin or lactulose given orally may decrease ammonia production within the bowel. Supportive care with polyionic fluids, potassium, and dextrose may be needed to help decrease neurologic signs.
Hyperammonemia in Morgan Foals
A syndrome of depression, ill thrift, and hyperammonemia with a variable extent of hepatic involvement occurs in Morgan foals. Affected foals are often related, but a genetic cause has not been determined. Clinical signs are usually first observed around weaning time. Encephalopathy may temporarily improve with aggressive supportive care, but it 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.
Drögemüller M, Jagannathan V, Welle MM, et al. Congenital hepatic fibrosis in the Franches-Montagnes horse is associated with the polycystic kidney and hepatic disease 1 (PKHD1) gene. PLoS One. 2014;9(10):e110125. doi: 10.1371/journal.pone.0110125. PMID: 25295861; PMCID: PMC4190318.