Toxocariasis & Fascioliasis — Comprehensive Review

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PART I: TOXOCARIASIS

Etiology

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Epidemiology

• Toxocara infections in animals are ubiquitous worldwide.
• A nationally representative US survey found 5% of the population ≥6 years had serologic evidence of infection.
• Visceral larva migrans (VLM) typically affects children 2–7 years of age; ocular larva migrans (OLM) manifests in older children and adolescents (ages 5–10).
• Higher risk among dog owners, people living in poverty, and those in hot, humid regions.
• Transmission: ingestion of soil contaminated with embryonated Toxocara eggs. Eggs are shed in feces of infected dogs/cats and become infective after 2–4 weeks in the environment. They can persist in soil for years. Common locations: sandboxes, playgrounds.
• Direct contact with pets is NOT required, as fresh feces are not yet infectious.

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Pathogenesis

1. Larvae hatch in the small intestine and penetrate the bowel wall.
2. They enter the portal circulation and migrate throughout the body — liver, lungs, CNS, and eyes are most commonly affected.
3. They cannot develop into adult worms and continue migrating for months to years.
4. When larvae eventually die, they provoke immediate-type and delayed-type hypersensitivity reactions, producing eosinophilic granulomas in affected tissues.
5. VLM and OLM appear to be mutually exclusive presentations — different larvae reach different tissues.

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Clinical Manifestations

• VLM: symptoms appear gradually and resolve over 4–8 weeks; leukocytosis, marked eosinophilia, hypergammaglobulinemia.
• OLM: often mimics retinoblastoma or intraocular tuberculosis.
• CNS disease: seizures, encephalopathy, or space-occupying lesions.

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Diagnosis

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Differential Diagnosis

• VLM: Ascariasis, trichinosis, eosinophilic pneumonia, hypereosinophilic syndrome, Löffler syndrome, hepatic metastases
• OLM: Retinoblastoma (most important), intraocular tuberculosis, toxoplasmosis, endophthalmitis of other etiology, other causes of posterior intraocular lesions
• Neurotoxocariasis: Bacterial/viral/fungal meningitis, CNS tumors, eosinophilic meningitis from Angiostrongylus cantonensis

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Treatment

• Albendazole safe in children as young as 1 year.
• No person-to-person transmission; standard precautions in hospital.

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Prevention

• Proper disposal of dog and cat feces.
• Regular veterinary deworming of pets, especially puppies and kittens, to reduce environmental egg contamination.
• Cover sandboxes when not in use.
• Hand hygiene after playing in soil or sand; discourage geophagy (pica) in children.
• No post-exposure prophylaxis recommended.

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PART II: FASCIOLIASIS

Etiology

• Fasciola hepatica — adult measures 30 × 13 mm; found in the Americas, Europe, Oceania, Africa, and Asia. The main causative species.
• Fasciola gigantica — adult measures up to 75 × 20 mm; found in Africa and Asia only.

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Epidemiology

• The WHO estimates ≥2.4–2.6 million people infected worldwide, in over 70 countries.
• Highest prevalence (>60%) in Peru and Bolivia; also highly endemic in Egypt, Iran, Bolivia, and parts of Africa and Asia.
• Estimated ~10,635 new cases in 2010, with 90,041 DALYs.
• In non-endemic areas (e.g., USA), cases are primarily imported in immigrants and returning travelers; rare autochthonous cases reported.
• Women have higher incidence, with more severe infections than men.
• Transmission occurs via ingestion of metacercariae on freshwater aquatic plants — watercress, water lettuce, alfalfa, mint, parsley, khat — or contaminated water.

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Life Cycle & Pathogenesis

1. Adult flukes lay eggs in the bile ducts → eggs pass into bile → shed in stool.
2. Eggs deposited in water hatch into miracidia in 9–14 days.
3. Miracidia infect freshwater snails (Lymnaea spp.) — first intermediate host → develop into sporocysts, rediae, cercariae over 4–7 weeks.
4. Free-swimming cercariae encyst as metacercariae on aquatic vegetation.
5. Humans ingest metacercariae on raw plants or water.
6. After ingestion, metacercariae excyst in the duodenum, penetrate the bowel wall, enter the peritoneal cavity, and migrate to the liver (~4 weeks to reach the liver).
7. Flukes penetrate the Glisson capsule, migrate through liver parenchyma (causing track-like tissue damage), and ultimately colonize the hepatic biliary ducts where they mature into adults.

• Larvae migrating through peritoneum and liver parenchyma cause intense inflammation.
• Pathology: hepatocyte necrosis, eosinophilic infiltrates, granuloma formation, hemorrhagic tracks through the liver.
• CT shows track-like hypodense lesions that migrate and change position over time (distinguishing from fixed metastases).
• Rare: subcapsular hematoma from intense hemorrhage.
• Occasionally, larvae reach ectopic sites — subcutaneous tissue, lungs, brain, eye, pancreas, stomach wall.

• Adult flukes reside in bile ducts for years, causing:
  • Biliary inflammation, duct thickening, hyperplasia, periductal fibrosis.
  • Dilated, thick-walled, calcareous bile ducts.
  • Bile stasis → biliary obstruction, cholelithiasis, hemobilia.
  • Bacterial superinfection → cholangitis, liver abscess.
• Serum alkaline phosphatase commonly elevated.
• Eosinophilia may be absent in up to 50% of chronic cases.

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Clinical Manifestations

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Diagnosis

• Stool is typically negative for eggs during the migratory phase (eggs not yet produced).
• Cathepsin L1-based antibody ELISA (Fas2 ELISA): sensitivity 92%, specificity 84% — first-line test for acute disease; antibodies detectable within 2–4 weeks of infection.
• CT of the liver: characteristic track-like or serpiginous hypodense lesions, subcapsular hematoma, hepatomegaly; must be distinguished from metastases (liver biopsy may be needed if serology unavailable).
• If serology/CT unavailable: empirical triclabendazole with clinical/eosinophilia resolution serves as a diagnostic criterion.

• Stool microscopy (Lumbreras rapid sedimentation technique or Kato-Katz technique): eggs appear in stool 5–7 weeks after infection; at least 3 stool samples on alternate days preferred.
• Egg morphology: oval, yellow-brown, thin-shelled, 130–150 μm × 63–90 μm (F. hepatica), larger for F. gigantica (up to 200 μm); have a small indistinct operculum. Essentially indistinguishable from Fasciolopsis buski eggs — clinical correlation required.
• ERCP: may visualize adult worms directly in bile duct; useful for biliary obstruction.
• Serology: EIA with excretory-secretory (ES) antigens + immunoblot confirmation; sensitivity >95%; cross-reactivity with schistosomiasis possible; available only at CDC in the US.
• Spurious passage: false-positive stool eggs can result from eating infected liver — must correlate with clinical findings.
• Imaging (US/CT): low sensitivity in chronic phase; CT may show hepatomegaly, serpiginous tunnel-like branching lesions, cystic calcifications.
• Liver biopsy: rarely needed; flukes identified by large size, cuticular spines, multiple intestinal branches on cross-section.

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Differential Diagnosis

• Acute cholecystitis (clinically very similar — but fascioliasis has marked eosinophilia and no jaundice in acute phase)
• Hepatic abscess (pyogenic, amoebic)
• Viral hepatitis
• Hepatic metastases (CT lesions can look identical)
• Other parasitic migrations: toxocariasis, ascariasis, trichinosis
• Lymphoma with liver involvement

• Cholangiocarcinoma
• Primary sclerosing cholangitis
• Other liver flukes (Clonorchis, Opisthorchis)
• Choledocholithiasis
• Hepatic hydatid disease

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Treatment

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Prevention

• Avoid eating raw aquatic vegetation (watercress, water lettuce, mint, parsley, alfalfa) from endemic areas.
• Avoid drinking untreated water from freshwater sources in endemic regions.
• Control of definitive animal hosts (cattle, sheep, goats) with veterinary anthelmintics reduces environmental egg burden.
• Snail control (intermediate host eradication) — impractical on large scale.
• Health education about risks of raw vegetable consumption in endemic countries.
• Travelers to endemic areas (Bolivia, Peru, Egypt, Iran) should receive counseling.
• Mass drug administration (triclabendazole) programs in highly endemic populations.
• Cooking or heating aquatic plants (≥60°C) destroys metacercariae.

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Key Comparison Summary

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What Was Covered

Toxocariasis

• Etiology: Toxocara canis (primary) and T. cati; nematode roundworms of dogs/cats; humans are dead-end hosts
• Epidemiology: 5% US seroprevalence; VLM in children 2–7 yr; OLM in older children/adolescents; soil/sandbox transmission via embryonated eggs
• Pathogenesis: Larvae migrate through liver, lungs, CNS, eye; eosinophilic granuloma formation; VLM and OLM are mutually exclusive
• Clinical syndromes: Covert (asymptomatic eosinophilia), VLM (fever/wheeze/hepatomegaly), Neurotoxocariasis (seizures/meningoencephalitis), OLM (unilateral visual loss/endophthalmitis)
• Diagnosis: ELISA for Toxocara antibodies (CDC); imaging for VLM; CT/fluorescein angiography for OLM; eosinophilia hallmark
• Differential: Retinoblastoma (for OLM), other eosinophilic parasitoses, CNS tumors
• Treatment: Albendazole 400 mg BID × 5 days; add corticosteroids for severe CNS/cardiac disease
• Prevention: Deworm pets, cover sandboxes, hand hygiene

Fascioliasis

• Etiology: Fasciola hepatica and F. gigantica (liver flukes/trematodes); sheep, cattle, goats as natural hosts
• Epidemiology: 2.4–2.6 million infected globally; Peru, Bolivia, Egypt highest burden; transmitted via metacercariae on watercress/aquatic plants
• Pathogenesis: Two phases — acute migratory (peritoneum → liver parenchyma, 3–5 months) and chronic biliary (adult flukes in bile ducts for years)
• Clinical signs: Acute: fever, eosinophilia, hepatomegaly, RUQ pain, urticaria, no jaundice; Chronic: biliary colic, cholangitis, obstruction, eosinophilia absent in 50%
• Diagnosis: Fas2 ELISA (acute, 92% sensitivity); Kato-Katz stool technique (chronic); CT track-like lesions; ERCP in biliary obstruction
• Differential: Acute cholecystitis, hepatic abscess, metastases; chronic: cholangiocarcinoma, other liver flukes
• Treatment: Triclabendazole 10 mg/kg × 2 days — praziquantel is ineffective (critical distinction)
• Prevention: Avoid raw watercress/aquatic plants; treat water; veterinary control of livestock; health education