TOXOCARIASIS

Etiology

Epidemiology

• Global distribution, with 5% seroprevalence in the US population ≥6 years old.
• Visceral larva migrans (VLM) occurs most commonly in children <5 years; ocular larva migrans (OLM) typically affects older children aged 5–10 years and adolescents.
• Risk is higher in dog/cat owners, people living in poverty, and in hot/humid regions where eggs remain viable in soil.
• Transmission: Ingestion of embryonated eggs from soil contaminated with dog or cat feces (sandboxes, playgrounds). Direct contact with animals is not required — eggs are not infectious immediately when shed, becoming infective after 2–4 weeks in the environment.
• Eggs may persist long-term in soil. — Red Book 2021, p. 1179

Pathogenesis

Signs and Symptoms

Diagnosis

• Clinical context: Compatible presentation + history of dog/cat exposure.
• Serology (ELISA ± immunoblot): Detection of antibodies to Toxocara larval-stage antigens — preferred method. Available through the CDC in the US. Does not distinguish active from past infection; less sensitive for OLM.
• Imaging: Liver ultrasound, CT, or MRI may reveal diffuse nodular lesions <2 cm in VLM. CT and fluorescein angiography help assess OLM and distinguish from retinoblastoma.
• Vitreous fluid: Elevated anti-Toxocara antibody levels relative to serum — suggestive of OLM.
• Liver biopsy: Diagnostic if larvae are identified microscopically, but low sensitivity — rarely indicated.
• PCR: Not currently available. — Goldman-Cecil Medicine, p. 1208; Red Book 2021, p. 1180

Differential Diagnosis

Treatment

• Mebendazole is an alternative to albendazole.
• Albendazole is FDA-approved (though not specifically for this indication) and has been used safely in children as young as 1 year. — Goldman-Cecil Medicine, p. 1215; Red Book 2021, p. 1180

Prevention

• Periodic anthelmintic deworming of dogs and cats (especially puppies and kittens) — reduces environmental egg burden.
• Proper disposal of pet feces.
• Cover sandboxes when not in use.
• Handwashing after contact with dogs/cats or soil.
• Keep children from playing in areas contaminated with animal feces.
• No post-exposure prophylaxis is recommended for asymptomatic contacts. — Goldman-Cecil Medicine, p. 1247; Red Book 2021, p. 1181

FASCIOLIASIS

Etiology

Epidemiology

• Cosmopolitan distribution — affects >70 countries. WHO estimates 2.4–2.6 million people infected globally, with the highest prevalence (>60%) in Peru and Bolivia; also prevalent in South America, Africa, and Asia.
• F. hepatica is found in the Americas, Europe, and Oceania; F. gigantica is additionally found in Africa and Asia.
• Women have higher incidence with more severe disease than men.
• Transmission: Ingestion of aquatic vegetation (watercress, water lettuce, alfalfa, mint, parsley, khat) containing encysted metacercariae, or drinking contaminated fresh water. — Goldman-Cecil Medicine, pp. 569, 591; Tietz Textbook of Laboratory Medicine, p. 3598

Pathogenesis (Life Cycle)

1. Eggs in stool are deposited in water → miracidia hatch in 9–14 days → infect freshwater snails (Lymnaea spp., first intermediate host) → develop through sporocysts, rediae, cercariae (4–7 weeks in snail).
2. Free-swimming cercariae are released → attach to aquatic vegetation as metacercariae (the infective stage for humans).
3. After ingestion, metacercariae excyst in the duodenum → penetrate intestinal wall → cross peritoneal cavity → reach the liver in ~4 weeks → penetrate Glisson's capsule → migrate through liver parenchyma (causing inflammation, hemorrhage, granulomas, track-like lesions) → reach bile ducts at 3–5 months.
4. Adults mature and reside in hepatic/common bile ducts and gallbladder for up to 13 years, producing eggs that exit via the sphincter of Oddi → stool.

Signs and Symptoms

Acute (Invasive/Migratory) Phase — first 3–5 months

• Prolonged fever, hepatomegaly, right upper quadrant/epigastric pain
• Marked peripheral eosinophilia (hallmark)
• Anorexia, weight loss, nausea, vomiting, diarrhea (2–5 days before liver invasion)
• Urticaria, cough, lymphadenopathy, arthralgias
• Occasional subcapsular liver hematoma (intense hemorrhage)
• CT: Multiple migrating hypodense lesions (resembling metastases) — change position over time
• Hyperbilirubinemia notably absent in this phase
• Ectopic larvae may reach subcutaneous tissue, pancreas, eye, brain, lung, stomach wall

Chronic (Obstructive/Biliary) Phase — after adult worm establishment

• Biliary obstruction: Colicky right upper quadrant pain, cholangitis, cholelithiasis
• Elevated alkaline phosphatase; eosinophilia absent in ~50% of cases
• Bacterial superinfection → cholangitis, liver abscess
• Hemobilia, liver fibrosis
• ERCP may reveal adult worms in the bile duct

Diagnosis

Acute Phase

• Cathepsin L1-based antibody ELISA (sensitivity 92%, specificity 84%) — first-line serologic test; antibodies detectable within 2–4 weeks of infection.
• If serology unavailable: CT (track-like hepatic lesions) ± liver biopsy (to exclude metastases).
• Stool examination is negative in the acute phase (eggs not yet present).
• A trial of triclabendazole with clinical/eosinophilia resolution can serve as a diagnostic criterion when serology and CT are unavailable.

Chronic Phase

• Stool examination (≥3 samples): Lumbreras rapid sedimentation technique or Kato-Katz technique — identifies large, unembryonated, yellow-brown, operculate eggs (130–150 × 63–90 μm); eggs appear in stool 5–7 weeks after infection.
  • ⚠️ Spurious passage: Eggs in stool may result from ingesting infected cattle/sheep liver (not true infection) — confirm by history and repeat stool after meat-free diet.
• Serology helpful if stool negative; sensitivity >95% with ES-antigen EIA.
• ERCP: Can visualize and retrieve adult worms; useful for biliary obstruction.
• Liver biopsy: May show flukes migrating through parenchyma (with eosinophilic granulomas/fibrosis); differentiated from Clonorchis/Opisthorchis by larger size, cuticular spines, multiple intestinal branches in cross-section.
• In the US, serologic testing available at the CDC.

Differential Diagnosis

Treatment

Prevention

• Avoid eating raw aquatic plants (especially watercress) in endemic areas; cook or wash vegetation thoroughly.
• Do not drink untreated fresh water from streams or ponds in endemic regions.
• Veterinary control: Regular treatment of livestock (sheep, cattle, goats) with anthelmintics to reduce environmental contamination.
• Snail control: Molluscicidal treatment of pastures and water bodies to interrupt the Lymnaea snail intermediate host cycle.
• Public health education in endemic communities, particularly in the Andean regions of South America.
• Improvement of sanitation to prevent fecal contamination of water sources.

Key Comparative Summary

• The most critical differential for ocular larva migrans is retinoblastoma — misdiagnosis can lead to unnecessary enucleation. CT and fluorescein angiography are essential.
• Eosinophilia is the most consistent laboratory clue; serology through the CDC is the preferred diagnostic tool.
• Albendazole is the drug of choice; add corticosteroids for severe or neurologic/cardiac disease.

• Resistance to praziquantel is a unique feature — always use triclabendazole.
• The acute phase mimics hepatic metastases on CT, but lesions change in location and morphology over serial scans because the fluke is still migrating — a key distinguishing feature.
• Stool examination is useless in the acute phase (eggs not yet produced); serology is essential early. Stool becomes the primary test only in chronic infection.
• Women tend to have more severe disease than men.