The diagnosis of infection with Baylisascaris is
based primarily on clinical findings, history, and serology. Clinical
findings vary from mild illness to severe central nervous system (CNS)
disease depending on the level and frequency of infection and the
degree of CNS involvement. Signs of visceral larva migrans, including
hepatomegaly, eosinophilia, and elevated isohemagglutinin titers,
may be present and are similar to those of toxocariasis. Because B
procyonis demonstrates neurotropism, larvae tend to concentrate
in the head, neck, and thoracic regions. If enough Baylisascaris eggs
are ingested, severe central nervous system disease can develop within
2 to 4 weeks. Clinical signs in such cases include sudden lethargy,
loss of muscle coordination, decreased head control, torticollis,
hemiparesis, ocular muscle paralysis, cortical blindness, and nystagmus,
which may quickly progress to coma and death.5 An important
diagnostic finding in baylisascariasis is eosinophilic pleocytosis
of the cerebrospinal fluid, especially in a patient with concurrent
peripheral eosinophilia and progressive central nervous system disease. However,
other parasitic pathogens, notably Angiostrongylus cantonensis, may
also produce eosinophilic meningitis. Computed tomography and magnetic
resonance imaging findings may include marked periventricular contrast
enhancement of the brain and diffuse cerebral and cerebellar atrophy.
Brain biopsies have shown mixed eosinophilic inflammation and occasionally
larvae.