Based on dissemination of larvae, a number of patients suffering from Baylisascaris NLM also have had DUSN due to concomitant invasion of the eye (2, 36, 38, 40, 44). Toxic substances can also be generated by the inflammatory response, including various eosinophil products from degranulation of these cells in lesions and areas affected by larvae (98). 8). CNS invasion takes place as part of somatic migration, and in the case of B. procyonis, a low proportion (usually 5% to 7%) of invading larvae actually enter the CNS (1, 2, 19, 29). Typically, the brain is affected the worst, although involvement of the cervical and thoracic spinal cord in a 14-month-old boy has also been described (48, 49). Children who survive may be profoundly neurologically impaired, suffering from blindness, seizures, incontinence, and partial paralysis (2, 6, 55). Molecular tests have also been developed for environmental investigations and for the diagnostic identification of Baylisascaris DNA in definitive host fecal samples and tissue samples from biopsies and autopsies performed in clinical cases of NLM (128 Baylisascaris? While Baylisascaris can infect different types of animals, Baylisascaris procyonis, carried by raccoons, is thought to pose the greatest risk to humans because raccoons often live in close proximity to humans. It is well known that there is a lag time in the development of CNS disease in experimentally infected animals following infection with B. procyonis; the earliest that CNS signs have been seen in mice is about 8 to 10 days p.i. A differential diagnosis of eosinophilic meningoencephalitis has been reviewed elsewhere (106). They have involved severe ocular disease and were identified based on the lesions of DUSN and by visualizing the characteristically large larvae in the retina or vitreous. – The latter case is unique in that the patient did not present with typical DUSN lesions but instead presented with advanced granulomatous OLM with retinal detachment similar to that seen in toxocariasis. Baylisascaris, baylisascariasis, can lead to severe illness. It is interesting that transient respiratory signs have been observed at between 2 and 5 days after the experimental inoculation of rodents and primates with B. procyonis (1, 90); in the primates, respiratory signs were still present but were less severe 8 days postinfection (p.i.) Both ELISA and immunoblotting methods are quite sensitive, since patients with clinical CNS disease usually have strongly positive immunological results from both serum and CSF samples (119, 120, 121) (Table 2). They may be hard to detect, and it might take repeated examinations before they are seen. They can then be ingested by, and infest, a variety of other animals (including humans) that serve as paratenic hosts. Two to 4 weeks after infection, the larvae grow in their third stage of development to achieve lengths of 1,300 to 1,900 μm, while actively migrating (20, 21, 22). (19). In numerous clinical cases of B. procyonis NLM in animals and in a child treated with ivermectin, the subjects failed to improve and continued to deteriorate, and living larvae were later recovered from the brain (1). Weinstein SB, Lake CM, Chastain HM, et al. However, raccoons also defecate in garages and barn lofts and on woodpiles, decks, roofs, and other peridomestic sites (1, 9, 62, 63). The classic example of this is Toxocara canis, whose larvae migrate extensively and last for years walled off in the tissues of humans and other hosts (10, 11, 54, 91). 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