To the Editors: Infection of humans with the larvae of Toxocara canis leads to toxocariasis, one of the most common ascariases. The prevalence in humans ranges between 1 and 4% of the adult population in Western Europe and 60% of children in developing countries.1 Playground sandboxes and domestic canines represent major sources of infection. Geophagia is an important risk factor in children, documented to be etiologic in 10–30% of cases. Visceral larva migrans is the clinical term for Toxocara infection associated with major organs. Generally, it is considered a self-limited disease. Previous reports have demonstrated varied presentations, including chronic hypereosinophilia, pyogenic liver abscesses, hepatic granulomas, abdominal lymph node enlargement, pulmonary involvement, myocarditis, and thrombocytosis. Central nervous system involvement in toxocariasis is extremely rare2,3 and takes several distinct forms, including encephalopathy, meningoencephalitis, meningitis, seizures, motor dysfunction, and neuropsychiatric disturbances.3–5 Magnetic resonance imaging alterations have been described in a few patients with central nervous system toxocariasis that include vasculitic areas identified by angiography, focal lesions, and nonspecific T2-weighted areas of increased signals.2,3,6,7 The case of a male child diagnosed with congenital asplenia at 5 years of age in the context of pneumococcal septic shock is presented. Relevant facts in the patient's history include exposure to various domestic canines (the patient's father was a hunter), psychomotor development impairment with onset at 1 year of age, autistic-like behavior, and ataxia. The medical evaluation has been inconclusive. At 6 years of age, the patient was admitted to this hospital with fever and an associated leukemoid reaction. Laboratory studies showed a WBC count of 65,200/μL (65% eosinophils); normal renal and hepatic studies, and a negative C-reactive protein. Bone marrow morphology was not compatible with eosinophilic leukemia. Additional studies demonstrated a marked hypergammaglobulinemia (26.4 g/L) with markedly increased IgG (2800 mg/dL), IgE (8415 U/mL), and titers of isohemagglutinins (anti-A1, 1/8192; anti-A2, 1/4096; and anti-B, 1/256), the presence of Ascaris lumbricoides eggs in fecal samples, and a positive serologic test for Toxocara canis (passive hemagglutination test: 1/160 and ELISA: 0.662), confirmed by Western blot analysis. Ophthalmologic examination, chest radiograph, an echocardiogram, and an EEG were normal. An abdominal CT scan revealed hepatomegaly with nodules dispersed throughout the liver parenchyma; a biopsy confirmed the presence of a granulomatous hepatitis with intense eosinophilia and fibrosis consistent with parasitic infestation. Cerebral magnetic resonance imaging revealed a moderate bilateral peritrigonal hypersignal. Treatment began with mebendazole, but because of persistent eosinophilia it was changed to albendazole and prednisolone, that resulted in hematologic, radiographic and behavior/neurologic improvement. Serum values of eosinophils, immunoglobulins, and isohemagglutinins returned to normal, hepatic nodules disappeared and Toxocara antibody titers were reduced. Despite implementation of measures aimed at preventing reinfection, the patient died at 9 years of age from pneumococcal meningitis. No association has been reported between toxocariasis and asplenia. It has been suggested that bacterial or viral meningitis may be enhanced by helminthic larvae that migrate to the central nervous system.8 Additionally, it has been speculated that splenectomizated patients may be predisposed to a more rapid or severe infection by free-living parasites, as noted for Trypanosoma brucei rhodesiense.9 The diagnosis of toxocariasis requires a high level of suspicion and delayed treatment may result in pulmonary, hepatic, and neurologic lesions and sequelae. Ana Rita Araújo, JD Idalina Maciel, MD Department of Pediatrics Centro Hospitalar do Alto Minho Viana do Castelo, Portugal Licínia Lima, MD Isabel Chacim, MD Department of Pediatrics Barcelos Hospital, Portugal José Barbot, MD Department of Hematology Children's Hospital Maria Pia Porto, Portugal