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[Baylisascaris procyonis]

Cross-sections of larvae of Baylisascaris columnaris (a skunk parasite) in the brain of a laboratory-infected mouse. The larval morphology and microscopic manifestations would be similar with B. procyonis in human tissue.Image taken at 400x magnification.

Cross-sections of larvae of Baylisascaris columnaris (a skunk parasite) in the brain of a laboratory-infected mouse. The larval morphology and microscopic manifestations would be similar with Baylisascaris procyonis in human tissue. Image taken at 400x magnification.

Unembryonated egg of B. procyonis

Unembryonated egg of B. procyonis.

Causal Agents

Human baylisascariasis is caused by larvae of Baylisascaris procyonis, an intestinal nematode of raccoons.

Life Cycle

Life cycle of baylisascariasis

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 patent and shed eggs). Unembryonated eggs are shed in the environment The Number 1, where they take 2-4 weeks to embryonate and become infective The Number 2. Raccoons can be infected by ingesting embryonated eggs from the environment The Number 3. Additionally, over 100 species of birds and mammals (especially rodents) can act as paratenic hosts The Number 4 for this parasite: eggs ingested by these hosts hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst The Number 5. The life cycle is completed when raccoons eat these hosts The Number 6. The larvae develop into egg-laying adult worms in the small intestine The Number 7 and eggs are eliminated in raccoon feces. Humans become accidentally infected when they ingest infective eggs from the environment; typically this occurs in young children playing in the dirt The Number 8. Migration of the larvae through a wide variety of tissues (liver, heart, lungs, brain, eyes) results in VLM and OLM syndromes, similar to toxocariasis The Number 9. In contrast to Toxocara larvae, Baylisascaris larvae continue to grow during their time in the human host. Tissue damage and the signs and symptoms of baylisascariasis are often severe because of the size of Baylisascaris larvae, their tendency to wander widely, and the fact that they do not readily die. Diagnosis is usually made by serology, or by identifying larvae in biopsy or autopsy specimens.

Geographic Distribution

Raccoons infected with Baylisascaris procyonis appear to be common in the Middle Atlantic, Midwest, and Northeast regions of the United States and are well documented in California and Georgia. Proven human cases have been reported in California, Oregon, New York, Pennsylvania, Illinois, Michigan, and Minnesota, with a suspected case in Missouri.

Clinical Presentation

Human infections can be asymptomatic. However, because these larvae continue to grow and wander in the human host, infections often result in severe disease manifestations. Much like toxocariasis, infection with Baylisascaris can result in visceral larva migrans (VLM) or ocular larva migrans (OLM) syndromes. The larvae of B. procyonis have a tendency to invade the spinal cord, brain, and eye of humans, resulting in permanent neurologic damage, blindness, or death. Human infection with Baylisascaris appears to be rare. To date, 13 well documented Baylisascaris encephalitis cases, and 1 suspected case in a young girl with CNS larva migrans, have been reported. The prevalence of subclinical cases is unknown. Because there is no widely available definitive diagnostic test for humans infected with this parasite, many cases are not diagnosed initially.

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  • Page last reviewed November 29, 2013
  • Page last updated November 29, 2013
  • Content source: Global Health - Division of Parasitic Diseases and Malaria
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