Trichinellosis and OtherTissue Nematode Infections¶

Chapter 238 | Part 5: Infectious Diseases · Part 5 – Infectious Diseases: Parasitic · Chapter 238

Key Clinical Points¶

Trichinellosis severity is linked to larval load: >50 larvae/gram muscle can be life-threatening; <10 larvae/gram are typically asymptomatic.
Blood eosinophilia occurs in >90% of symptomatic trichinellosis cases, often peaking 2–4 weeks post-infection (can exceed 50%).
Presumptive diagnosis of trichinellosis: periorbital edema, myalgias, fever, and eosinophilia following ingestion of suspect pork or wild game.
Confirmatory diagnosis of trichinellosis requires a muscle biopsy showing encysted larvae within a hyalinized capsule.
Trichinellosis treatment is tiered by severity: Supportive (Mild), Anthelmintics (Moderate), or Anthelmintics + Glucocorticoids (Severe).
Visceral larva migrans is often self-limited; however, severe myocardial, CNS, or pulmonary involvement may require glucocorticoids.
Cutaneous larva migrans typically resolves spontaneously but can be treated with Ivermectin (200 μg/kg) or Albendazole (200 mg bid × 3 days).
Angiostrongyliasis (eosinophilic meningitis) requires steroids BEFORE chemotherapy to prevent exacerbation of inflammatory brain lesions.
Gnathostomiasis involves eosinophilic meningoencephalitis and may require steroids for neurologic/ocular involvement.
Prevention of trichinellosis: Cook pork until no longer pink OR freeze at -15°C for 3 weeks (Note: T. nativa is resistant to freezing).

1. DEFINITION & OVERVIEW¶

Nematodes are elongated, symmetric roundworms with a nervous system, muscular system (including muscle cells under cuticle), and developed intestinal tract (oral cavity, elongated gut ending in anal pore). Human acquisition of nematode infections occurs via:

• Ingestion of eggs passed in human feces (e.g., Ascaris lumbricoides) • Larvae penetrating skin exposed to fecally contaminated soil (e.g., Strongyloides stercoralis, hookworms) • Larvae traversing skin after bite of infected insect vectors (filariae) • Ingestion of specific animal-derived foods (trichinellosis from raw/undercooked pork or wild carnivorous mammals)

Only two nematodes (S. stercoralis and C. philippinensis) can internally reinfect humans; all other infections require repeated exposure to increase worm burden.

Tissue nematodes covered in this chapter include: • Trichinellosis • Visceral and ocular larva migrans • Cutaneous larva migrans • Cerebral angiostrongyliasis • Gnathostomiasis

All zoonotic infections result from incidental exposure to infectious nematodes. Clinical symptoms largely stem from invasive larval stages that (except in Trichinella) do not reach maturity in humans.

1.1 Nematode Classification¶

This chapter covers tissue nematodes including:

• Trichinellosis • Visceral and ocular larva migrans • Cutaneous larva migrans • Cerebral angiostrongyliasis • Gnathostomiasis

1.2 Trichinella Species Distribution¶

At least nine Trichinella species and 13 genotypes are recognized as causes of human infection.

Worldwide Distribution: • T. spiralis: Found in various carnivorous and omnivorous animals. • T. pseudospiralis: Found in mammals and birds.

Regional Distributions: • T. nativa: Arctic/subarctic regions (bears, foxes, walruses). • T. nelsoni: Equatorial eastern Africa (felids, hyenas, bush pigs). • T. britovi: Europe, western Africa, western Asia. • T. murrelli: North America and Japan. • T. papuae: Papua New Guinea, Thailand, Taiwan, Cambodia. • T. zimbabwensis: Tanzania. • T. patagoniensis: South America.

Note: T. papuae, T. zimbabwensis, and T. pseudospiralis do not encyst in muscle.

2. EPIDEMIOLOGY¶

Trichinellosis cases in the US have declined from 400–500/year in the 1940s to 10–20 annually, reflecting successful control programs (education, processing, and freezing). Most mild cases remain undiagnosed. Cases are increasingly linked to wild game (bear, walrus) and other animals like dogs (Asia, Africa), horses (Italy, France), and contaminated fodder.

Toxocariasis: • T. canis (canine ascarid): Most common form. • T. cati (feline ascarid) and Ascaris suum (pig ascarid): Less common. • Baylisascaris procyonis (raccoon ascarid): Rare cause of eosinophilic meningoencephalitis.

Cutaneous Larva Migrans: Prevalent among children/travelers in warm, humid climates. Caused by burrowing larvae of animal hookworms (usually Ancylostoma braziliense) from soil contaminated with dog/cat feces.

Angiostrongyliasis: Primary locations include Southeast Asia, Pacific Basin, Caribbean, Central/South America, and the southern United States. Transmission occurs via ingestion of raw infected mollusks, contaminated vegetables, or crustaceans that have consumed infected mollusks.

Gnathostomiasis: Endemic in Southeast Asia and parts of China/Japan. Infection results from eating raw/undercooked fish, frogs, eels, snakes, chickens, or ducks containing infective larvae developed in Cyclops (water fleas).

2.1 Trichinellosis Epidemiology¶

• US Cases: 10–20 annually (Historical: 400–500/year). • Risk Factors: ◦ Consumption of undercooked pork ◦ Consumption of wild game (bear, walrus) ◦ Consumption of dog meat (Asia, Africa) ◦ Consumption of horse meat (Italy, France) ◦ Ingestion of contaminated fodder

2.2 Toxocariasis Epidemiology¶

• T. canis: Most common; worldwide distribution. • T. cati / Ascaris suum: Less common. • Baylisascaris procyonis: Rare cause of eosinophilic meningoencephalitis.

2.3 Cutaneous Larva Migrans Epidemiology¶

Common in warm, humid climates; caused by Ancylostoma braziliense.

2.4 Angiostrongyliasis Epidemiology¶

Found in Southeast Asia, Pacific Basin, Caribbean, Central/South America, and Southern US.

Endemic in Southeast Asia, China, and Japan.

3. ETIOLOGY & PATHOPHYSIOLOGY¶

Trichinellosis Pathogenesis: • Ingestion of meat → Larvae liberated by digestive acid/proteases → invade small-bowel mucosa → mature into adults → female worms release newborn larvae → migrate via circulation to striated muscle.

Encystment occurs in all species except T. pseudospiralis, T. papuae, and T. zimbabwensis. Encysted larvae reside in "nurse-cells" within the muscle.

3.1 Trichinella Life Cycle¶

Pathogenesis Sequence: Ingestion of trichinous meat → Larvae liberated by digestive acid/proteases → Invasion of small-bowel mucosa → Maturation into adult worms → Release of newborn larvae → Migration via circulation to striated muscle → Encystment (except in T. pseudospiralis, T. papuae, and T. zimbabwensis).

Clinical Progression: Symptoms peak ~3 weeks after infection and subside during convalescence.

3.2 Visceral Larva Migrans Pathogenesis¶

Larvae do not mature into adults in humans but migrate through tissues, causing eosinophilic inflammation. Common forms include toxocariasis (T. canis), T. cati, and Ascaris suum. Baylisascaris procyonis may cause eosinophilic meningoencephalitis. Larvae invade liver, lungs, or CNS, provoking granulomatous responses.

3.3 Cutaneous Larva Migrans Pathogenesis¶

Larvae penetrate skin → form erythematous lesions along dermal-epidermal junction → advance several cm/day. These are intensely pruritic and resolve spontaneously as the larvae die after weeks/months.

3.4 Angiostrongyliasis Pathogenesis¶

Parasites die in CNS, initiating inflammatory responses. Heavy infections cause permanent neurologic sequelae or death. Migrating larvae induce eosinophilic inflammation, hemorrhage, necrosis, and granuloma formation.

Specific Organ Involvement: A. costaricensis inhabits mesenteric arteries, causing abdominal inflammatory masses.

3.5 Gnathostomiasis Pathogenesis¶

Infection with Gnathostoma spinigerum larvae causes: • Eosinophilic meningoencephalitis • Migratory cutaneous swellings • Invasive masses in eye/visceral organs.

4. CLINICAL FEATURES¶

Trichinellosis clinical features: • Initial enteric phase (first weeks): diarrhea, abdominal pain, constipation, nausea. • Larval migration/muscle invasion (second week): fever, eosinophilia, periorbital/facial edema, splinter hemorrhages, rash, headache, cough, dyspnea, dysphagia. • Myocarditis: Tachyarrhythmias or heart failure (common cause of death). • Larval encystment in muscle (2–3 weeks): myositis, myalgias, muscle edema, weakness. Most commonly involved muscles: extraocular, biceps, jaw, neck, lower back, diaphragm.

Uncommon infections with T. pseudospiralis may present as prolonged polymyositis-like illness.

4.1 Trichinellosis Clinical Features¶

See above.

4.2 Visceral Larva Migrans Clinical Features¶

Fever, malaise, anorexia/weight loss, cough, wheezing, rashes, hepatosplenomegaly, peripheral eosinophilia (up to 90%), rare seizures/behavioral disorders.

4.3 Ocular Larva Migrans Clinical Features¶

Eosinophilic granulomatous mass in posterior pole of retina (mimics retinoblastoma). Symptoms include endophthalmitis, uveitis, chorioretinitis, unilateral visual disturbances, strabismus, and eye pain.

4.4 Cutaneous Larva Migrans Clinical Features¶

Erythematous lesions along dermal-epidermal junction; intensely pruritic.

4.5 Angiostrongyliasis Clinical Features¶

Eosinophilic meningitis with headache, fever, altered mental status.

CSF Findings: • Elevated opening pressure • 150–2000 WBC/μL (eosinophils >20%) • Elevated protein • Normal glucose

4.6 Gnathostomiasis Clinical Features¶

Eosinophilic meningoencephalitis, migratory cutaneous swellings, invasive masses in eye/visceral organs.

DIAGNOSTIC APPROACH¶

Trichinellosis Clinical Suspicion: a. Identify periorbital edema, myalgias, fever, and eosinophilia following ingestion of raw pork or wild game.
Laboratory Screening: a. Check for blood eosinophilia (present in >90% of symptomatic cases; peaks 2–4 weeks post-infection).
Confirmatory Testing: a. Perform muscle biopsy → identify encysted larvae within a hyalinized capsule.
Angiostrongyliasis Diagnosis: a. Clinical presentation of eosinophilic meningitis (headache, fever) → CSF analysis showing 150–2000 WBC/μL with >20% eosinophils and elevated protein.
Ocular Larva Migrans: a. Identification of eosinophilic granulomatous mass in the posterior pole of the retina.

MANAGEMENT & TREATMENT¶

Trichinellosis Treatment (based on severity): a. Mild → Supportive care. b. Moderate → Anthelmintic therapy: i. Albendazole: 400 mg bid × 10–14 days ii. Mebendazole: 200–400 mg tid × 3 days, then 500 mg tid × 10 days. c. Severe → Add glucocorticoids (e.g., prednisone 1 mg/kg qd × 5 days).
Cutaneous Larva Migrans Treatment: a. Ivermectin: single dose 200 μg/kg b. Albendazole: 200 mg bid × 3 days.
Angiostrongyliasis Treatment: a. Pre-treatment → Steroids are essential before chemotherapy to prevent exacerbation of inflammatory brain lesions.
Gnathostomiasis Treatment: a. Ivermectin: 200 μg/kg per day × 2 days b. Albendazole: 400 mg bid × 21 days c. Additional → Steroids often given for neurologic or ocular involvement.
Summary Table (Treatment Summary): • Trichinellosis (Moderate): Albendazole (400 mg bid × 10–14 days) OR Mebendazole (200–400 mg tid × 3 days, then 500 mg tid × 10 days). • Cutaneous larva migrans: Ivermectin (single dose, 200 μg/kg) or Albendazole (200 mg bid × 3 days). • Gnathostomiasis: Ivermectin (200 μg/kg per day × 2 days) or Albendazole (400 mg bid × 21 days).

KEY PEARLS & HIGH-YIELD POINTS¶

• Trichinella Species: T. spiralis and T. pseudospiralis are the primary global causes; T. nativa is specific to Arctic/subarctic regions. • Encysting vs. Non-encysting: T. papuae, T. zimbabwensis, and T. pseudospiralis do NOT encyst in muscle. • Angiostrongyliasis Warning: Steroids must precede chemotherapy to prevent worsening of inflammatory brain lesions. • Prevention: Cook pork until no longer pink OR freeze at -15°C for 3 weeks (Note: T. nativa is resistant to freezing). • Clinical Hallmark: Periorbital edema and eosinophilia are classic indicators of trichinellosis.

Reference Tables¶

TABLE 238-1 Therapy for Tissue Nematode Infections INFECTION Trichinellosis¶

Harrison's 22e, p.1812

INFECTION	SEVERITY	TREATMENT
Trichinellosis	Mild	Supportive
	Moderate	Albendazole (400 mg bid × 10–14 days) or
		Mebendazole (200–400 mg tid × 3 days, then 500 mg tid × 10 days)
	Severe	Add glucocorticoids (e.g., prednisone, 1 mg/kg qd × 5 days)
	Mild to moderate
	Severe
	Ocular
Cutaneous larva migrans		Ivermectin (single dose, 200 μg/kg) or
		Albendazole (200 mg bid × 3 days)
	Mild to moderate
	Severe
Gnathostomiasis		Ivermectin (200 μg/kg per day × 2 days)a or
		Albendazole (400 mg bid × 21 days)a