Baylisascaris procyonis raccoon roundworm is a well-recognized zoonotic infection and the most common cause of clinical larva migrans among wild and domestic animals. Over 130 species of animals can become infected with Baylisascaris procyonis larva. Several dozen fatal or severe cases of human baylisascariasis have made this parasite an important public health problem. Neural larva migrans (NLM) with meningoencephalitis caused by raccoon roundworm infection has been reported in rural and suburban areas of North America and Europe. Most cases of raccoon roundworm neural larva migrans have occurred in infants less than two years of age exposed to areas of raccoon fecal contamination. In adults, infection is usually restricted to people who had close contact with raccoons (pet owners).1,2
Unfortunately, originally this zoonotic infection was downplayed by medical professionals given the fact that most affected people resided in densly urban areas, "making exposure to raccoons highly unlikely." This geographical bias may lead to delayed diagnosis and poor outcomes. As raccoons have migrated from rural to urban settings, more city dwellers will be exposed to Baylisascaris procyonis infection and may suffer grave consequences.
Raccoons defecate at specific areas (latrines) close to their resting and sleeping places, and in case of raccoons adapted to urban areas these can be located in barns, lofts, attics, chimneys and garages. The surroundings of such latrines may become heavily contaminated with B. procyonis eggs, increasing the risk of human infections.2 As much as raccoons have been documented rummaging through garbage cans, their feces may also contaminate sidewalks, front porches, small yards, and local parks in cities. When domestic animals such as rabbits become exposed to raccoon feces, outbreaks occur. Apart from raccoons, this nematode can also develop into the mature stage in dogs (but not cats).2 Dogs can harbor undetected infections and their indiscriminant defecation patterns can result in more widespread environmental contamination with Baylisascaris procyonis eggs.3
Mature female worms produce, on average, over 100,000 eggs per day resulting in an infected raccoon shedding millions of eggs per day. Eggs develop into the infective stage within 11–14 days, and can remain infectious for months or even years in humid soil or water. When small mammals or birds ingest eggs, the larva emerge and enters the central nervous system (CNS) causing damage, clinical disease and death.
Once the central nervous system is infected with Baylisascaris procyonis larva, infected people will have acute eosinophilic meningoencephalitis. Mechanical damage to the CNS caused by larval migration is compounded by the inflammatory response. One of the most serious problems with this condition is the lag time in development of clinical signs. Even in heavy infections, it typically takes two to three weeks before enough CNS damage occurs so that clinical signs are manifested and medical assistance is sought; by then the ensuing damage and complications may be very difficult to deal with. Unfortunately in most cases treatment initiation with albendazole will be delayed due to the lag time in development of clinical signs.1 In clinical cases of Baylisascaris larva migrans, an initial screening with ELISA, followed by Western blot analysis using BPES antigen should prove very useful for specific diagnosis.4