Baylisascaris procyonis, the raccoon roundworm, is a rare but serious cause of neurologic and ocular disease in humans. Only larval stages are involved in zoonotic infections. It is not known whether other Baylisascaris species, such as B. columnaris of skunks, can cause baylisascariasis in humans.
Baylisascaris procyonis completes its life cycle in raccoons, with humans acquiring the infection as accidental hosts (dogs serve as alternate definitive hosts, as they can harbor adult worms and shed eggs). Unembryonated eggs are shed in the environment , where they take 2–4 weeks to embryonate and become infective . Raccoons can be infected by ingesting embryonated eggs from the environment . Many mammals and birds can act as paratenic hosts for this parasite: eggs ingested by these hosts hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst . The life cycle is completed when raccoons eat these hosts . The larvae develop into adult worms in the raccoon’s small intestine and eggs are passed in raccoon feces. Humans become accidentally infected when they ingest infective eggs from the environment . Migration of the larvae through a wide variety of tissues (liver, heart, lungs, brain, eyes) results in visceral (VLM) and ocular larva migrans (OLM) syndromes, but severe neurologic disease with eosinophilic meningoencephalitis may occur following neural larva migrans (NLM) . B. procyonis larvae continue to increase in size up to about 1.8 mm in human hosts, but they are not capable of migrating to the intestine and developing to adulthood. Tissue damage and the signs and symptoms of baylisascariasis are often severe because of the larger size of B. procyonis larvae and their more invasive course of migration.
Life cycle and information courtesy of DPDx.