Larva migrans (LM) simply refers to the migration and persistence of helminth larvae in tissues of animals and humans and
is separated clinically and pathologically into visceral (VLM), ocular (OLM) neural, and cutaneous larva migrans (CLM).
There are many helminth parasites that can cause LM; however, Toxocara and Baylisascaris account for the majority of human cases as well as those in other animals. Baylisascaris procyonis, in particular, is well recognized as a cause of clinical LM, affecting a wide variety of wild and domestic species. Best
known as a cause of fatal or severe NLM, having been recognized in >130 species of mammals and birds in North America, the
parasite can also produce ocular or visceral damage as well. Although human NLM infections are not common, they are usually
fatal; thus, B. procyonis has important public health implications.
The life cycle of B. procyonis is direct, although can be indirect with paratenic host involvement. Raccoons are the definitive host, harboring adults
in the small intestine. Females produce eggs which are passed in the feces. Naturally infected raccoons can shed an average
of 20,000-26,000 B. procyonis eggs per gram; thus, raccoons can shed millions of eggs per day. The eggs reach infectivitiy in as little as 11-14 days
under optimal conditions (22-25 C; 100% humidity). Under natural conditions, eggs will reach infectivity more slowly, taking
several weeks to months. Eggs can remain infective in the environment for years. Young raccoons probably becom infected
by ingesting the infective eggs from their mother's contaminated teats or fur, the contaminated den or raccoon latrines near
the den. The larvae hatch from the eggs, enter the mucosa of the small intestine where they develop for several weeks prior
to re-emerging into the lumen where they mature. The prepatent period is 50-76 days. In contrast, older raccoons become
(re)infected through ingestion of the larvae in paratenic hosts. The larvae develop to adults quickly in the intestinal lumen,
reaching patency in 32-38 days. More extensive somatic migration does not appear to occur in raccoons. However, the aggressive
somatic larval migration in other animals contributes to the remarkable ability of B. procyonis to produce disease. Most larvae become encapsulated in various internal organs, but, it is the small percentage that migrate
to the brain that result in fatal NLM. In these hosts, larvae hatch out of the eggs quickly and penetrate the small intestine.
They migrate through the liver to the lungs where they enter the pulmonary veins and are distributed throughout the body.
Larvae in visceral and somatic tissue become encapsulated in eosinophilic granulomas where they survive until ingested by
a raccoon. Larvae entering the brain produce traumatic damage and inflammation, in part as a result of their massive increase
in size – going form ~300 μm when hatching from the egg to 1750 μm at 31 days post-infection. The onset and severity of the
resulting CNS disease depends on the number of larvae present and varies with animal species and prior exposure.
Sources of infection include any area contaminated with raccoon feces. Raccoons tend to defecate in localized sites (latrines);
thus, these areas are highly contaminated with eggs and are important long-term sources of infection for future generations
of animals. Granivorous rodents, birds and other animals can become infected when foraging for undigested seeds present in
the raccoon feces. Infection of other animals during investingation of latrine sites or through grooming after becoming contaminated
at such a site can also occur. Infection has also been linked to the use of bedding (e.g., straw), feed and enclosures contaminated
by wild raccoons or cages and enclosures previously used to house raccoons.