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The clinician must differentiate toxocariasis from other causes of uveitis, particularly retinoblastoma, 6 reduce ocular inflammation, and prevent loss of vision and amblyopia.

A degenerated structure compatible in size with a larva was found ( Figure 5). The subretinal fibrocellular tissue had a granulomatous infiltrate composed of plasma cells, lymphocytes, epithelioid cells, eosinophils, multinucleated giant cells, and hyperplastic retinal pigment epithelium. Surrounding this was a zone of epithelioid histiocytes and multinucleated giant cells and an outer zone of plasma cells, lymphocytes, and eosinophils. Eosinophilic material encapsulating the structure may represent antigen-antibody precipitate (Splendore-Hoeppli phenomenon) ( Figure 4). An encapsulated eosinophilic cystic structure measuring 22.5 µm with an amorphous core of 10.5 µm within a central area of necrosis was consistent with a degenerated Toxocara canislarva. The epiretinal component of the dumbbell-shaped lesion was fibrocellular tissue with a granuloma ( Figure 3). Histopathologic examination findings for the fibrocellular membrane revealed plasma cells, lymphocytes, and eosinophils.

Adjacent fluffy infiltrate in papillomacular bundle. Intraretinal macular lesion with epiretinal membrane (black arrow) and subretinal granuloma (white arrow). During membrane stripping the nasal white nodules peeled off the retinal surface. A pars plana vitrectomy, membrane stripping, retinotomy, and removal of the epiretinal, retinal, and subretinal granuloma were done.Īt vitrectomy, the macular lesion was dumbbell shaped: an intraretinal core connected a round epiretinal component and subretinal component ( Figure 2). He improved until macular traction developed in July 1996. The clinical presentation was now consistent with toxocariasis. A partial posterior vitreous detachment was noted over the nasal retina with vitreous inflammation. The macular lesion enlarged into a solid, elevated mass with subretinal hyperpigmentation. A chalky appearing intraretinal lesion appeared preretinal and temporal to the fovea. The nasal retinal lesion was now raised and its surface was contiguous with a band of vitreous inflammatory membranes. One month later, the visual acuity OS dropped to 20/80. Nasal intraretinal infiltrate with adjacent satellite lesions.