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Digestive System
Hepatic Disease in Small Animals
Hepatobiliary Fluke Infection in Small Animals
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  • Hepatocutaneous Syndrome in Small Animals
  • Nodular Hyperplasia in Small Animals
  • Hepatic Neoplasia in Small Animals
  • Miscellaneous Liver Diseases in Small Animals
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  • Cholecystitis in Small Animals
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  • Cholelithiasis in Small Animals
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Hepatobiliary Fluke Infection in Small Animals

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Infection with liver flukes in endemic regions can cause acute and chronic cholangitis in cats and less frequently in dogs. The most common is Platynosomum concinnum infection in cats in Florida, Hawaii, and other tropical areas. Infestation is acquired by ingesting an infected intermediate host, usually a lizard or frog; ~15–85% of cats with access to intermediate hosts are infected in endemic areas. After infection, young flukes emerge in the intestines and migrate into the common bile duct, gallbladder, or hepatic ducts, where they mature within 8–12 wk. Embryonated eggs pass from bile into the alimentary canal, where they may be detected in feces as early as 12 wk after infection.

Clinical signs depend on severity of infection (parasite burden); however, most infested cats are asymptomatic. Symptomatic cats demonstrate progressive illness; these cats may become jaundiced and emaciated secondary to anorexia, vomiting, and mucoid diarrhea. Cats may be lethargic and febrile and have hepatomegaly and abdominal distention. Chronic fluke infestation can be fatal in severely affected cats. First clinical signs of illness develop between 7 and 16 wk of infection. In some cases, clinical signs resolve by 24 wk after infection without treatment. A circulating eosinophilia may develop 3–14 wk after infection and may be persistent. In heavily infected cats, ALT and AST activities may increase, while AP activity may remain normal or only increase mildly. Hyperbilirubinemia may develop within 7–16 wk after infection.

Hepatic histologic changes develop after 3 wk and are progressive in persistent infections. Inflammation and distention of large bile ducts is associated with mixed neutrophilic and eosinophilic inflammation. By 4 mo, severe adenomatous biliary hyperplasia and peribiliary inflammation are established. By 6 mo, progressive fibrosis is obvious and evolves to biliary cirrhosis. Regional lymphadenopathy may be notable. Bile duct distention increases with growth of adult flukes and when flukes become sexually mature, bile ducts become fibrotic. During this time, serum transaminase activities normalize. Abdominal ultrasonography may reveal biliary obstruction involving the gallbladder, common bile duct, and/or intrahepatic ducts. Gallbladder debris associated with flukes may appear as oval hypoechoic structures having echoic centers. A thickened gallbladder wall associated with a double-rim sign may reflect cholecystitis. Hypoechoic hepatic parenchyma with prominent hyperechoic portal regions (ducts) reflects cholangitis and cholangiohepatitis.

Because infected cats may be asymptomatic, diagnosis of fluke infestation can be difficult. Eggs may not be detected on fecal examination because they are only sporadically passed and demonstrate variable morphology (immature and embryonated forms), eggs are small, and routinely used fecal methods are relatively insensitive for fluke egg detection. Furthermore, development of bile duct obstruction and fibrosis may impede passage of fluke eggs into bile and feces.

If fluke infection is suspected, treatment with praziquantel (20 mg/kg/day, SC, for 3–5 days) is recommended. Eggs may continue to be passed in feces for up to 2 mo after successful treatment. Prednisolone is used to reduce the associated eosinophilic inflammation (2 mg/kg/day for 2–4 wk, tapered in 50% decrements every 2 wk). Ursodeoxycholic acid is given (15–20 mg/kg, PO, divided bid and given with food) to initiate hydrocholeresis. Broad-spectrum antibiotic coverage is recommended to protect against retrograde infection into the biliary tree with bacteria introduced by migrating flukes. Infection also may be associated with dying flukes. Vitamin E (10 IU/kg/day, PO) and SAMe (20–40 mg/kg/day, PO) are given until liver enzymes normalize. If necessary, an antiemetic can be administered, eg, metoclopramide (0.2–0.5 mg/kg, PO or SC, every 6–8 hr) or maropitant (1 mg/kg/day for no more than 5 consecutive days).

Treatment results are variable, but prognosis is favorable for mild forms of the disease. Other rare parasites of the biliary tract include Amphimerus pseudofelineus, Metorchis conjunctus, and Eurytrema procyonis. (Also see Gastrointestinal Parasites of Small Animals: Hepatic Flukes.)

Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM

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