Toxocariasis. Fascioliasis. Etiology, epidemiology, pathogenesis, sign and symptoms, diagnosis, differential diagnosis, treatment, prevention
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fascioliasis triclabendazole treatment
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Toxocara canis visceral larva migrans eosinophilic granuloma liver
TOXOCARIASIS
Etiology
Toxocariasis is caused by Toxocara canis (dog roundworm) and, less commonly, Toxocara cati (cat roundworm) — nematode parasites whose natural definitive hosts are dogs and cats, especially puppies and kittens. Most human cases result from T. canis. Humans are accidental (dead-end) hosts; the larvae cannot develop into adult worms in the human body.
— Goldman-Cecil Medicine, p. 3470
Epidemiology
- Infection is ubiquitous worldwide. In the US, approximately 5% of the population ≥6 years has serologic evidence of infection.
- Visceral larva migrans (VLM) typically affects children 2–7 years old; ocular larva migrans (OLM) typically manifests in older children and adolescents (5–10 years).
- Higher risk in dog owners, people living in poverty, and in hot/humid regions where eggs survive longer in soil.
- OLM is more common in southern US states.
- Transmission occurs through ingestion of embryonated eggs from contaminated soil (sandboxes, playgrounds where dogs/cats defecate). Direct animal contact is not required — eggs are not infectious immediately when shed; they require 2–4 weeks in soil to become infective but may persist long-term.
— Red Book 2021, p. 1179; Goldman-Cecil Medicine, p. 3470
Pathogenesis
After ingestion by a human, embryonated eggs hatch in the intestine, releasing larvae that penetrate the intestinal wall and enter the vasculature. Unlike in the animal host, larvae in humans cannot complete their life cycle — they migrate through the body (lungs, liver, CNS, eyes) but do not mature into adult worms. When larvae eventually die, they trigger significant immediate-type and delayed-type hypersensitivity reactions, forming eosinophilic granulomas. VLM and OLM appear to be mutually exclusive syndromes.
Key point: The inflammatory response to larval migration — not direct larval toxicity — is responsible for most tissue damage.
— Goldman-Cecil Medicine, p. 3470
Signs and Symptoms
Most infections are asymptomatic. Clinical disease depends on the affected organ and degree of host inflammatory response.
1. Covert Toxocariasis
- Simple persistent eosinophilia with minimal or no symptoms
- May persist for years during ongoing migratory phase
2. Visceral Larva Migrans (VLM)
- Low-grade fever, cough, wheezing (pulmonary infiltrates)
- Hepatosplenomegaly, right upper quadrant pain
- Malaise, urticaria, lymphadenopathy
- Less common: myocarditis, nephritis, rash
- Lab: leukocytosis, marked eosinophilia, hypergammaglobulinemia, elevated isohemagglutinins to A/B blood group antigens
- Symptoms appear gradually, resolve over 4–8 weeks
3. Neurotoxocariasis
- Eosinophilic meningoencephalitis, space-occupying lesions, myelitis, cerebral vasculitis
- Seizures, encephalopathy, neuropsychiatric symptoms
4. Ocular Larva Migrans (OLM)
- Typically unilateral vision loss in older children
- Uveitis, endophthalmitis, retinal granulomas, strabismus
- Usually without systemic signs of infection
— Red Book 2021, p. 1179; Goldman-Cecil Medicine, p. 3470
Diagnosis
| Test | Notes |
|---|---|
| CBC | Leukocytosis with marked eosinophilia; anemia |
| Serology (ELISA) | ELISA for anti-Toxocara antibodies (serum or vitreous fluid); available via CDC. Does not distinguish past from active infection; less sensitive for OLM |
| Immunoblot | Used to confirm ELISA; improves specificity |
| Recombinant larval antigen ELISA | Improved sensitivity/specificity; not yet widely available |
| Imaging (US/CT/MRI liver) | Diffuse nodular lesions <2 cm; multiple hypodense nodules; helpful in VLM |
| CT/Fluorescein angiography | For OLM — differentiate from retinoblastoma |
| Aqueous/vitreous anti-Toxocara antibodies | Elevated relative to serum in OLM |
| Liver biopsy | Rarely indicated; microscopically diagnostic but low sensitivity |
| PCR | Not currently available |
— Red Book 2021, p. 1180; Goldman-Cecil Medicine, p. 3470
CT abdomen: Acute VLM showing multiple small hypodense nodules scattered in liver parenchyma (left), with resolution to residual calcific granulomas on follow-up (right)
Differential Diagnosis
- Asthma / allergic bronchitis — persistent eosinophilic pulmonary disease
- Löffler syndrome (other helminth migration)
- Hepatic metastases — CT lesions can mimic metastatic disease
- Retinoblastoma — OLM with intraocular mass
- Tuberculosis — focal intraretinal lesions
- Other helminth infections: ascariasis, hookworm, strongyloidiasis, baylisascariasis (Baylisascaris procyonis — raccoon roundworm, causes more severe neurologic disease)
- Hypereosinophilic syndrome
- Eosinophilic leukemia
Treatment
| Condition | Drug | Regimen |
|---|---|---|
| Visceral toxocariasis | Albendazole (preferred) | 400 mg twice daily × 5 days |
| Visceral toxocariasis (alternative) | Mebendazole | Per dosing guidelines |
| Severe (CNS, myocarditis) | Albendazole + corticosteroids | Prednisone 60 mg/day × 5 days concurrently |
| Ocular toxocariasis | Albendazole + corticosteroids (oral/topical) | Anti-inflammatory control; surgical therapy for complications |
- Albendazole is FDA-approved (though not specifically for this indication); safe in children ≥1 year.
- No person-to-person transmission — standard precautions only.
— Red Book 2021, p. 1180; Goldman-Cecil Medicine, p. 3470
Prevention
- Proper disposal of dog and cat feces
- Regular veterinary deworming of dogs, cats, especially puppies and kittens
- Cover sandboxes when not in use to prevent animal defecation
- Wash hands after contact with soil; wash vegetables thoroughly
- No post-exposure prophylaxis is recommended
— Red Book 2021, p. 1181
FASCIOLIASIS
Etiology
Fascioliasis is a zoonosis caused by the liver fluke:
- Fasciola hepatica (adult: 30 × 13 mm) — cosmopolitan distribution
- Fasciola gigantica (adult: up to 75 × 20 mm) — Africa and Asia only
Natural definitive hosts: cattle, sheep, and goats. Humans are incidental hosts.
— Goldman-Cecil Medicine, p. 3470
Epidemiology
- WHO estimates 2.4–17 million people infected in >70 countries
- Both species found in Africa and Asia; only F. hepatica in the Americas, Europe, and Oceania
- Highest prevalence rates (>60%) reported in Peru and Bolivia
- In non-endemic countries (e.g., USA), cases are primarily imported in immigrants and returning travelers; rare autochthonous cases exist
- Women have higher incidence and more severe infections than men
- Estimated ~90,000 DALYs lost annually
— Goldman-Cecil Medicine, p. 3470; Tietz Textbook of Laboratory Medicine, p. 3598
Life Cycle & Pathogenesis
Complete life cycle:
- Eggs passed in feces → deposited in water
- Miracidia hatch (9–14 days) → invade freshwater snail (Lymnaea spp.) — first intermediate host
- In snail: develop through sporocysts → rediae → cercariae (4–7 weeks)
- Free-swimming cercariae leave snail → encyst as metacercariae on aquatic plants (watercress, water lettuce, alfalfa, mint, parsley, khat)
- Human infection: ingestion of metacercariae-contaminated plants or water
- Metacercariae excyst in the duodenum → penetrate bowel wall → migrate through peritoneal cavity → penetrate liver capsule (4 weeks)
- Larvae migrate through liver parenchyma → reach hepatic biliary ducts (3–5 months) → mature into adult flukes
- Adults lay eggs → passed via bile into intestine → excreted in feces
Pathologic response: Larval migration causes a track of eosinophilic inflammation and necrosis. Larvae may die and leave cavities filled with necrotic debris → replaced by scar/calcification. In the bile ducts, adults cause chronic inflammation, hyperplasia, fibrosis, and biliary obstruction.
— Goldman-Cecil Medicine, p. 3470; Tietz Textbook, p. 3599
Intestinal and hepatic trematodes. (C) Adult F. hepatica with cone-shaped anterior end, oral sucker (arrow), ventral sucker (arrowhead); up to 3 cm long. (D) F. hepatica migrating through liver parenchyma showing intestinal branches (arrowheads) in cross-section, ventral sucker (arrow) (H&E 100×), with cuticular spines inset (1000×). — Tietz Textbook of Laboratory Medicine
Signs and Symptoms
Disease is biphasic:
Acute (Invasive/Migratory) Phase
Begins when larvae penetrate the bowel wall and migrate through the liver (weeks to months after infection):
- Prolonged fever, malaise
- Hepatomegaly, right upper quadrant / epigastric pain
- Marked peripheral eosinophilia (hallmark)
- Anorexia, weight loss, nausea, vomiting
- Cough, urticaria, lymphadenopathy, arthralgias
- Acute diarrhea (2–5 days, before liver invasion)
- Rare: subcapsular liver hematoma (intense hemorrhage)
- Ectopic fascioliasis: larvae reach subcutaneous tissue, pancreas, eye, brain, stomach wall
- Note: Hyperbilirubinemia is notably absent in the acute phase
Chronic (Biliary) Phase
After adult flukes establish in bile ducts:
- Colicky right upper quadrant and epigastric pain (biliary obstruction)
- Eosinophilia may be absent in ~50% of chronic cases
- Elevated serum alkaline phosphatase
- Bacterial superinfection → cholangitis
- Complications: hemobilia, liver abscess, liver fibrosis, cholelithiasis
- Adults survive in bile ducts for up to 13 years
— Goldman-Cecil Medicine, p. 3470
Diagnosis
Acute Phase
| Test | Notes |
|---|---|
| Serology (Fas2 ELISA / cathepsin L1 ELISA) | Sensitivity 92%, specificity 84%; antibodies detectable within 2–4 weeks of infection. First-line test in acute phase |
| Immunoblot | Confirms positive/equivocal ELISA; cross-reactivity with schistosomiasis may occur |
| CT / MRI / Ultrasound | Track-like hypodense lesions, hepatomegaly, subcapsular hematoma, serpiginous tunneling lesions 2–10 mm; lesions shift in position over time (distinguishing feature from metastases); enhancement of Glisson capsule |
| Liver biopsy | May show flukes migrating through parenchyma; used when serology/CT unavailable |
| Stool exam | Negative during acute phase (adults not yet in ducts) |
Chronic Phase
| Test | Notes |
|---|---|
| Stool microscopy | Eggs detected by Lumbreras rapid sedimentation or Kato-Katz technique; ≥3 stool examinations preferred |
| Egg morphology | Oval, yellow-brown, thin-shelled, 130–150 μm × 63–90 μm; small often indistinct operculum; among the largest eggs in human parasitology |
| ERCP | Can visualize adult flukes in bile duct; allows retrieval and removal |
| Serology | May remain positive >1 year after treatment |
Important caveats:
- Spurious egg passage can occur after eating infected sheep/cattle liver — correlate with clinical presentation
- F. hepatica and F. buski eggs are essentially indistinguishable microscopically
- In the USA, serology available only at the CDC
— Goldman-Cecil Medicine, p. 3470; Tietz Textbook, p. 3599–3600
Differential Diagnosis
Acute phase:
- Acute cholecystitis — similar RUQ pain and fever, but eosinophilia distinguishes fascioliasis
- Hepatic metastases — CT lesions appear similar; in fascioliasis lesions change in position, attenuation, and shape over time
- Hepatic abscess (amoebic or bacterial)
- Schistosomiasis (Katayama fever)
- Other causes of eosinophilic hepatitis: drug reactions, other helminthiases
Chronic phase:
- Cholelithiasis / cholangitis from other causes
- Cholangiocarcinoma (unlike Clonorchis / Opisthorchis, fascioliasis does not cause cholangiocarcinoma)
- Primary sclerosing cholangitis
- Other liver flukes: Clonorchis sinensis, Opisthorchis spp.
Treatment
| Regimen | Details |
|---|---|
| Triclabendazole (drug of choice) | 10 mg/kg orally on 2 consecutive days; cure rate >90% |
| Monitoring cure | Stool examinations negative for ≥3 months |
| Praziquantel | Not effective against Fasciola — a critical distinction from other flukes |
| Treatment failure | Multiple rounds of triclabendazole; some infections are resistant |
| Serology post-treatment | May take >1 year to resolve — not used to confirm cure |
| Biliary obstruction | Dead parasites can cause obstruction requiring surgical or ERCP intervention |
FDA approval: Triclabendazole approved for fascioliasis in patients ≥6 years old.
— Goldman-Cecil Medicine, p. 3470; Tietz Textbook, p. 3599
Prevention
- Avoid eating raw aquatic plants (watercress, water lettuce) from endemic or potentially contaminated areas
- Treat water used for washing vegetables in endemic regions
- Control of intermediate host snails (Lymnaea spp.) in livestock-rearing areas
- Veterinary control of fascioliasis in cattle and sheep (main reservoir hosts)
- Health education in endemic communities (Bolivia, Peru, Africa, Asia)
- Washing vegetables does not reliably destroy metacercariae — avoidance is the safest approach
Side-by-Side Comparison
| Feature | Toxocariasis | Fascioliasis |
|---|---|---|
| Causative organism | Toxocara canis, T. cati (nematode) | Fasciola hepatica, F. gigantica (trematode) |
| Animal reservoir | Dogs, cats | Cattle, sheep, goats |
| Transmission | Ingestion of embryonated eggs in soil | Ingestion of metacercariae on aquatic plants |
| Intermediate host | None (eggs directly infective) | Freshwater snail (Lymnaea spp.) |
| Human role | Accidental dead-end host | Accidental dead-end host |
| Primary organs | Liver, lungs, CNS, eyes | Liver, bile ducts |
| Eosinophilia | Prominent | Prominent (acute); absent in ~50% chronic |
| Imaging | Hepatic nodules <2 cm | Track-like/serpiginous hypodense lesions |
| Key serology | ELISA (CDC) | Fas2 / cathepsin L1 ELISA (CDC) |
| Stool exam | Not useful (no eggs in humans) | Positive in chronic phase; negative acutely |
| Treatment | Albendazole 400 mg BID × 5 days | Triclabendazole 10 mg/kg × 2 days |
| Praziquantel | Not used | Ineffective |
| Corticosteroids | For severe/ocular/CNS disease | Not standard |
Sources: Red Book 2021: Report of the Committee on Infectious Diseases, p. 1179–1181 | Goldman-Cecil Medicine International Edition, p. 3470 | Tietz Textbook of Laboratory Medicine, 7th Edition, p. 3598–3600Both conditions are covered in full detail above. Here is a brief orientation to the two sections:
Toxocariasis is a nematode infection (roundworm larvae of dogs/cats) transmitted by ingesting soil-contaminated embryonated eggs. It produces four distinct syndromes — covert, visceral larva migrans (VLM), ocular larva migrans (OLM), and neurotoxocariasis — all driven by eosinophilic granuloma formation around migrating larvae that cannot mature in humans. Diagnosis rests on serology (ELISA) and imaging; stool exam is useless since adults never develop. Treatment is albendazole ± corticosteroids for severe/ocular disease.
Fascioliasis is a trematode (liver fluke) infection with a two-phase course: an acute invasive/migratory phase (fever, hepatomegaly, intense eosinophilia, shifting CT lesions) and a chronic biliary phase (colicky pain, obstruction, cholangitis, eosinophilia often absent). A key clinical pearl: praziquantel does not work — the only effective drug is triclabendazole. Diagnosis in the acute phase relies on serology (Fas2 ELISA); in the chronic phase, stool microscopy (Kato-Katz) identifies the large operculate eggs.
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