Question
Larva migrans
Answer
Larva migrans refers to a group of clinical syndromes caused by the migration of nematode larvae through human tissues, in which the human is an accidental, aberrant host — the larvae are unable to complete their normal life cycle/mature into adult worms in humans, and instead wander through tissue for a variable period before eventually dying, producing disease purely through this aimless migration rather than through establishment of a mature infection.
Two main clinical forms:
1. Cutaneous Larva Migrans (CLM) — caused most commonly by animal hookworm larvae (Ancylostoma braziliense, the dog/cat hookworm). Infective filariform larvae in soil/sand (contaminated by dog/cat faeces) penetrate exposed human skin; unable to penetrate the dermis and enter the bloodstream (as in their natural host), the larvae remain confined to the epidermis, migrating slowly (millimetres to centimetres per day), producing a characteristic serpiginous, intensely pruritic, raised, erythematous track that advances visibly over days — typically on the feet or other skin exposed to contaminated soil/sand. Self-limiting over weeks to months as larvae eventually die; treated with oral albendazole or ivermectin for symptomatic relief and to shorten the course.
2. Visceral Larva Migrans (VLM) — caused most commonly by animal roundworm larvae (Toxocara canis, the dog roundworm; also Toxocara cati). Humans (typically young children, via geophagia/pica or contact with contaminated soil/dog faeces) ingest embryonated eggs; larvae hatch in the intestine and, again unable to complete their normal migratory life cycle to maturity in this aberrant host, disseminate via the bloodstream to various organs — liver (hepatomegaly), lungs (cough, wheeze, eosinophilic pneumonitis), and, importantly, the eye (ocular larva migrans), where larval migration/death can provoke a granulomatous inflammatory reaction mimicking retinoblastoma, a serious diagnostic pitfall in children. Marked peripheral eosinophilia and hypergammaglobulinaemia are characteristic laboratory findings. Diagnosis is largely clinical/serological (ELISA for Toxocara antibody), since larvae are rarely recovered directly; biopsy of an affected organ occasionally demonstrates the larva histologically. Treatment (albendazole/mebendazole) combined with corticosteroids for significant inflammatory/ocular involvement.
Common underlying principle: both syndromes arise because the offending larvae are adapted to a different (animal) definitive host and, when they instead infect an aberrant human host, cannot mature and complete their normal life cycle — the resulting prolonged, aimless tissue migration (rather than established adult-worm infection) is itself the direct cause of the clinical disease, and the self-limiting nature of both conditions (as larvae eventually die without maturing) reflects this fundamental host-parasite mismatch.
Prevention: avoiding contact with soil/sand potentially contaminated by dog/cat faeces (protective footwear, hand hygiene, avoiding pica), and regular deworming of pet animals to reduce environmental egg/larva contamination.