Overview

• Platynosomum concinnum infection occurs in cats in Florida, Hawaii, and other tropical-semitropical areas. One report of infection in a cat from Ohio and 1from Illinois. Most common trematode infection affecting the liver of companion pets in North America.
• Infestation acquired from ingestion of infected intermediate host (e.g., lizard or frog).
• Estimated 15–85% of cats with intermediate host access are infected in endemic areas.
• Metorchis conjunctus also may infect the liver and biliary structures of cats.
• Flukes reported in dogs: Heterobilharzia americana (North America); raccoon is the natural definitive host and most important reservoir host; Metorchis conjunctus; Clonorchis sinensis (China), Schistosoma japonicum (Philippines), Metorchis bilis and Opisthorchis felineus (Germany) in sled dogs fed a diet including raw fish.

Signalment

Platynosmum concinnum: young (6–24 months) cat with access to local fauna.

Signs

• Depend on severity of infection.
• Most infested cats lack clinical signs.
• With severe infestation: jaundice, emaciation, anorexia, vomiting, mucoid diarrhea, hepatomegaly, abdominal distention, malaise, fever.

Causes & Risk Factors

Differential Diagnosis

• Cholangiohepatitis; hepatic lipidosis; bile duct carcinoma; hepatic lymphoma; choleliths and any disorder causing major bile duct occlusion.
• Identified by finding trematode eggs in feces, rarely observing anechoic ovoid structures with echoic center in biliary tree by ultrasound, cytologic examination of bile or hepatic aspirates; most definitively from histopathology of biopsied liver, biliary structures, or pancreas.

Clinicopathologic Features

Best defined for Platynosmum concinnum in cats.

CBC/Biochemistry/Urinalysis

• CBC-variable; eosinophilia beginning 3 weeks after infection; persists for months; not all infected cats demonstrate eosinophilia.
• Biochemistry-high liver enzyme activities, especially ALT and AST; ALP may be normal or only slightly increased initially.
• Bilirubin-increased; markedly high in advanced severe disease.
• Urinalysis-bilirubinuria.

Other Laboratory Tests

• Fasting/postprandial bile acid-increased.
• Fecal examination-noninvasive definitive diagnostic test: P. concinnum eggs detected in only 25% of infected cats.
• Fecal egg retrieval-sedimentation most successful; formalin-ether or sodium acetate most reliable (demonstrates eight-fold more eggs than direct fecal examination).
• Patients with few parasites (one to five flukes)-may shed only two to ten eggs/g of feces; thus, may not discover eggs by fecal testing.
• Serial fecal examinations-may be necessary.

Imaging

• Abdominal radiography-may show mild hepatomegaly.
• Abdominal ultrasonography-differentiates biliary obstruction from hepatocellular disease; shows one or more of the following: (1) biliary obstruction: dilated gallbladder, common bile duct (>2 mm), and intrahepatic ducts; (2) gallbladder sediment with flukes (oval hypoechoic structures with echoic center), mildly thick gallbladder wall with a double-layered appearance (cholecystitis); (3) hypoechoic hepatic parenchyma with prominent hyperechoic portal areas (ducts) associated with cholangiohepatitis.

Diagnostic Procedures

• Fecal examination for trematode eggs
• Cholecystocentesis-discloses fluke eggs
• Liver biopsy-reveals signs of infection

Pathologic Findings

• Gross-liver may appear large and yellow-green with dilated bile ducts; may see flukes in bile ducts or gallbladder; increased size and tortuosity of bile ducts on cut section.
• Histologic lesions-depend on the number of flukes and duration of infestation; early stage (4–6 weeks): enlarged bile ducts and periductal areas infiltrated with inflammatory cells, especially eosinophils; mid-stage (4 months): severe adenomatous hyperplasia of bile duct epithelium and coincident periductal inflammation; late stage (6 months): extensive peribiliary fibrous connective tissue that may cause bile duct stenosis.

Inpatient

• Balanced polyionic fluids with supplemental potassium chloride-20–40 mEq/L; as appropriate; based on serum electrolytes.
• Nutritional support-avoid development of hepatic lipidosis; feed high-protein calorically dense food and ensure food intake; use feeding tubes if needed to ensure adequate food intake in inappetent cats; rarely, severe clinical signs may require parenteral nutrition; rarely hepatic encephalopathy necessitates protein restriction.
• B vitamin supplementation-important for anorectic and ill cats on fluid therapy; 2 mL B-soluble vitamins/L fluids.

Drug(s)

• Praziquantel 20 mg/kg SC q24h for 3–5 days is treatment of choice for cats; eggs may pass in feces for up to 2 months after treatment. Praziquantel at 30 mg/kg PO once and 50 mg/kg SC once cleared a dog symptomatic for Heterobilharzia americana.
• Prednisolone-initial dose for cats showing eosinophilia, significant inflammation on biopsy or having severe clinical signs: 1–2 mg/kg/day for 2–4 weeks; then tapered in 50% decrements every 2 weeks.
• Ursodeoxycholic acid 10–15 mg/kg q24h PO; tablet form and divided dose administered with feeding achieves best bioavailability; avoid if evidence of extrahepatic bile duct obstruction.
• Broad-spectrum antibiotic coverage to protect against retrograde biliary tree infection with enteric organisms introduced by parasite; infection encouraged by fluke death in tissues.
• Antioxidant therapy-suggested by necroinflammatory tissue injury; vitamin E (10 IU/kg day PO) and S-adenosyl-l-methionine (SAMe; Denosyl-SD4 has proven bioavailability in cats as a GSH donor): 20 mg/kg PO daily, enteric coated tablets, until liver enzymes normalize.
• Antiemetic-metoclopramide (0.2–0.4 mg/kg PO, SC q6–8h or by constant rate infusion 1–2 mg/kg/day); ondansetron (0.5 mg/kg q12h, IV or PO 30 minutes before feeding); maropitant (1.0 mg/kg [5 mg/cat] IV, SC or PO once per day; maximum of 5 days).

Contraindications

Pregnancy-use caution with drug use.

Patient Monitoring

• Monitor clinical signs, appetite, body condition and weight, liver enzymes, bilirubin, and fecal sedimentation.
• Watch for signs of biliary tree occlusion after administration of praziquantel.

Prevention/Avoidance

• Restrict outdoor access if endemic parasite.
• Praziquantel prophylaxis-every 3 months; outdoor cats in endemic, tropical climates.

Possible Complications

• Death from liver failure; untreated symptomatic disease.
• Biliary tree obstruction.
• Pancreatitis.
• Pancreatic exocrine insufficiency-with chronic infection.
• Cholangitis/cholangiohepatitis (suppurative or nonsuppurative).

Expected Course and Prognosis

Uncomplicated recovery with treatment expected in most patients.

Zoonotic Potential

None

See Also

• Bile Duct Obstruction
• Cholangitis/Cholangiohepatitis Syndrome
• Hepatic Lipidosis

Abbreviations

• ALP = alkaline phosphatase
• ALT = alanine aminotransferase
• AST = aspartate aminotransferase
• GSH = glutathione