2009 Southern Regional Meeting Abstracts

Case Report: Purpose of Study: To describe a cohort of complicated cases of pediatric toxocariasis.
Methods Used: Retrospective chart review of three patients with Toxocara canis infection.
Summary of Results: Patient 1 was diagnosed with visceral larvae migrans (VLM) at age 11 months following a clinical course complicated by febrile seizures, rash, vomiting, diarrhea, cough, respiratory failure and eosinophilia (peak absolute eosinophil count (AEC) >55,000 mm3). Two yearts after initial diagnosis, he continues to have eosinophilia, despite treatment with mebendazole and daily oral corticosteroids (0.15mg/kg/d). Primary hypereosinophilic syndrome has been ruled out in this patient with fluorescence in-situ hybridization (FISH) being negative for deletions at the CHIC2 locus (chromosome 4q12) as well as no observed abnormalities of the platelet-derived growth factor receptor α (PDGFRA) or Fip1-like 1 (FIP1L1). Patient 2 presented with left exotropia at age 3 years, and was subsequently diagnosed with ocular larvae migrans (OLM). Clinical course has been complicated by urticaria, chronic rhinitis, mild eosinophilia (AEC 1415) and cataract formation, requiring surgical intervention, despite intraocular steroids. Patient 3 was diagnosed with toxcariasis at age 3 years after presenting with fatigue, lymphadenapathy, and eosinophilia (peak AEC 9568 mm3). One year after diagnosis and treatment with mebendazole, she has persistent uncontrolled asthma and eosinophilia despite daily oral corticosteroids (2mg/kg/d) and anti-parasitic treatment. She has also been evaluated for primary hypereosinophilic syndrome and FISH for deletion at the CHIC2 locus was not detected.
Conclusions: Clinical complications of Toxocara canis infection can be variable, and clinical presentations often parallel atopic diseases. A high index of suspicion is required for early diagnosis to prevent tissue pathology due to release of toxic eosinophil mediators. Further studies are vital to determine the factors that predispose to chronic disease complications, persistent eosinophilia, and steroid resistance, including evaluation of genetic susceptibility of the host to infection or atopy, timing/duration of infection, and treatment modalities utilized.