Intravitreal infection of guinea pigs with second-stage larvae of Toxocara canis and second- and fourth-stage larvae of Ascaris suum induced intraocular IgE antibodies and a dense eosinophil infiltration in the anterior chamber and throughout the uveal tract. The eosinophil infiltrate began within 1 day after infection and persisted for as long as 51 days. By day 12 after intravitreal infection, the injected ascarid larvae were surrounded by granulomas which consisted almost entirely of eosinophils. Firm adherence of eosinophils to the parasite cuticle, morphologic alterations and degranulation of eosinophils with the deposition of free eosinophil granules on the parasitic surfaces, and ingestion of eosinophils and eosinophil granules by the parasite larvae also were observed. Intravitreal injection of a soluble antigen derived from third-stage A. suum molting to the fourth-stage in defined media in vitro also induced intraocular IgE antibody and a diffuse ocular eosinophil infiltrate. Dense eosinophil infiltration of the choroid, not immediately adjacent to a parasite larva, was accompanied by destruction of the overlying outer retina, with cystic changes in the retina and between the retina and the choroid. Few eosinophils were observed within the retina, and the retinal destruction may be the result of direct toxic action of constituents of the choroidal eosinophils. Evidence which indicates that the eosinophil is the principal effector cell in immunity to helminth infections and is cytotoxic for the parasites, possible mechanisms for the induction of the ocular eosinophil infiltrates, and evidence for autotoxicity by eosinophils are briefly reviewed, and the potential roles of the eosinophil in the ocular response to helminth parasites are discussed.
|Original language||English (US)|
|Number of pages||13|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Dec 1 1979|