Trichinellosis and Other Tissue Nematode Infections¶
Chapter 238 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Trichinellosis is caused by ingestion of Trichinella spp. cysts in undercooked meat, leading to larval migration and muscle encystment.
- Visceral larva migrans (Toxocara canis) and ocular larva migrans are zoonotic infections with eosinophilic inflammation as a hallmark.
- Angiostrongyliasis and gnathostomiasis are caused by migrating larvae in the CNS and viscera, respectively, with distinct epidemiologic patterns.
- Albendazole and mebendazole are first-line treatments for most tissue nematode infections, with corticosteroids for severe inflammation.
- Prevention focuses on meat safety (cooking/freezing) and environmental control of animal feces.
1. DEFINITION & OVERVIEW¶
Tissue nematodes are parasitic roundworms that cause invasive infections in humans. Trichinellosis (Trichinella spp.) and other tissue nematodes (e.g., Angiostrongylus, Gnathostoma) cause larval migration through tissues, leading to eosinophilic inflammation. These infections are zoonotic, acquired via contaminated food or environmental exposure.
Table 238-1: Therapy for Tissue Nematode Infections¶
| Infection | Severity | Treatment |
|---|---|---|
| Trichinellosis | Mild | Supportive care |
| Trichinellosis | Moderate | Albendazole (400 mg bid × 10–14 days) or Mebendazole (200–400 mg tid × 3 days, then 500 mg tid × 10 days) |
| Trichinellosis | Severe | Add glucocorticoids (e.g., prednisone 1 mg/kg qd × 5 days) |
| Visceral larva migrans | Mild to moderate | Supportive care |
| Visceral larva migrans | Severe | Glucocorticoids (as above) |
| Ocular larva migrans | Not fully defined | Albendazole (800 mg bid for adults, 400 mg bid for children) with glucocorticoids × 5–20 days |
| Cutaneous larva migrans | Mild to moderate | Ivermectin (200 mg/kg single dose) or Albendazole (200 mg bid × 3 days) |
| Angiostrongyliasis | Mild to moderate | Albendazole (15 mg/kg/day × 14 days) with glucocorticoids |
| Infection | Severity | Treatment |
|---|---|---|
| Gnathostomiasis | Mild to moderate | Ivermectin (200 mg/kg/day × 2 days) or Albendazole (400 mg bid × 21 days) |
1.1 Nematode Classification¶
Medical nematodes are classified as either intestinal (e.g., Ascaris) or tissue-dwelling (e.g., Trichinella). Tissue nematodes include: Trichinella spp. (muscle/organ encystment), Angiostrongylus cantonensis (CNS migration), Gnathostoma spinigerum (visceral migration), and Toxocara spp. (visceral/ocular migration).
1.2 Life Cycle Overview¶
Infections involve larval migration through tissues, with adult worms typically residing in intestines or other organs. Larvae encyst in muscle or migrate to CNS/viscera, causing inflammation. Eggs or larvae are excreted in feces or expelled via coughing.
2. EPIDEMIOLOGY¶
Trichinella infections are global but endemic in regions with pork consumption (e.g., North America, Europe). T. nativa is Arctic-associated, while T. spiralis is widespread. Angiostrongyliasis is common in Southeast Asia, the Pacific, and the Caribbean. Gnathostomiasis is endemic in Southeast Asia, China, and Japan. Risk factors include eating raw/undercooked meat, contaminated vegetables, or raw snails.
2.1 Demographics¶
Trichinellosis: Common in rural areas with pig farming. Angiostrongyliasis: Urban/rural areas with snail/ slug exposure. Gnathostomiasis: Travelers to endemic regions. Toxocara: Children and immunocompromised individuals.
2.2 Transmission¶
Trichinella: Contaminated pork, wild game. Angiostrongyliasis: Raw snails, vegetables, freshwater crabs. Gnathostomiasis: Raw fish, undercooked meat. Toxocara: Ingestion of infective eggs from dog/cat feces.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Trichinella spp. larvae encyst in skeletal muscle, causing myositis and eosinophilia. Angiostrongylus larvae migrate to CNS, inducing eosinophilic meningitis. Gnathostoma larvae cause visceral inflammation. Toxocara larvae migrate to organs, leading to granulomatous reactions. Pathogenesis involves larval migration, tissue damage, and immune-mediated inflammation.
3.1 Life Cycle¶
Trichinella: Eggs → larvae → encyst in muscle. Angiostrongyliasis: Snail → larvae → CNS. Gnathostomiasis: Cyclops → larvae → human viscera. Toxocara: Eggs → larvae → visceral/ocular migration.
3.2 Immune Response¶
Eosinophilia is central to pathogenesis. Larvae induce granulomatous inflammation, with immune responses varying by infection site (e.g., CNS vs. muscle).
4. CLINICAL FEATURES¶
Trichinellosis: Early GI symptoms (abdominal pain, diarrhea), followed by myalgia, fever, and eosinophilia. Angiostrongyliasis: Headache, meningismus, CNS inflammation. Toxocara: Visceral granulomas (hepatomegaly) or ocular lesions (retinal granuloma). Gnathostomiasis: Migratory skin swellings, eosinophilic meningoencephalitis.
4.1 Trichinellosis¶
Early phase: GI symptoms (1–2 weeks). Late phase: Myositis, periorbital edema, myocarditis, and eosinophilia. Severe cases may present with encephalitis or pneumonia.
4.2 Angiostrongyliasis¶
CNS symptoms (headache, neck stiffness) develop 2–35 days post-infection. Eosinophilic meningitis with CSF pleocytosis and elevated protein.
4.3 Toxocara¶
Visceral larva migrans: Fever, hepatosplenomegaly, eosinophilia. Ocular larva migrans: Retinal granuloma, visual disturbances, potential enucleation risk.
5. DIFFERENTIAL DIAGNOSIS¶
Trichinellosis: Foodborne illness, bacterial gastroenteritis, viral myositis. Angiostrongyliasis: Meningitis, encephalitis, neurocysticercosis. Toxocara: Tuberculosis, sarcoidosis, granulomatous diseases. Gnathostomiasis: Neurocysticercosis, paragonimiasis, schistosomiasis.
5.1 Key Differentiators¶
Eosinophilia, travel history, dietary exposure, and imaging (e.g., MRI for CNS lesions) help distinguish these infections from other granulomatous or inflammatory conditions.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis relies on clinical history (meat consumption, travel), eosinophilia, and imaging. CSF analysis for angiostrongyliasis, muscle biopsy for trichinellosis, and serology for Toxocara. PCR for Trichinella DNA in CSF or tissue.
6.1 Laboratory Tests¶
Blood eosinophilia (>50% in severe cases), muscle enzymes (CK), CSF analysis (pleocytosis, elevated protein), and serology (Toxocara antibodies).
6.2 Imaging¶
MRI for CNS lesions in angiostrongyliasis, ultrasound for muscle encystment, and CT for visceral involvement.
7. MANAGEMENT & TREATMENT¶
Supportive care for mild cases. Albendazole/mebendazole for larval stages. Corticosteroids for severe inflammation. Prevention via meat safety (cooking/freezing) and environmental control.
7.1 Pharmacologic Therapy¶
Albendazole (15 mg/kg/day × 14 days) for most infections. Ivermectin for cutaneous larva migrans. Corticosteroids for severe myositis or CNS involvement.
7.2 Surgical Intervention¶
Muscle biopsy for diagnosis. Surgical excision for ocular lesions or persistent CNS granulomas.
8. PROGNOSIS & COMPLICATIONS¶
Most mild cases resolve spontaneously. Severe infections may lead to myocarditis, encephalitis, or death. Chronic complications include muscle fibrosis, vision loss, or CNS sequelae. Early treatment reduces morbidity.
8.1 Complications¶
Myocardial damage, CNS inflammation, ocular blindness, and chronic muscle pain. Severe cases may require ICU support.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: Avoid corticosteroids in early gestation. Pediatrics: Monitor for severe eosinophilia. Immunocompromised: Risk of disseminated infection. Travelers: Avoid raw meat/snails in endemic regions.
9.1 Prevention¶
Cook meat to 71°C, freeze pork at − 15°C for 3 weeks, and avoid raw snails/vegetables in endemic areas.
10. KEY POINTS & CLINICAL PEARLS¶
- Trichinellosis is a foodborne zoonosis with muscle encystment.
- Angiostrongyliasis presents with eosinophilic meningitis.
- Toxocara infections require environmental control.
- Albendazole is first-line; corticosteroids for severe inflammation.
- Prevention focuses on meat safety and hygiene.