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The dual role of small rodents and domestic cats in the natural course of toxoplasma infection has been known for some 25 years,1 but the nature of the interplay between the protozoan and its human host remains elusive. Nowhere is this more evident than in ocular toxoplasmosis.
Active peripheral toxoplasmic retinochoroiditis may impair vision in the short term because of deposition of inflammatory debris in the vitreous humor. Involvement of the macula or optic nerve may result in permanent visual loss in one eye, or occasionally both eyes. Ocular infection with toxoplasma is one of the commonest causes of postnatal posterior granulomatous uveitis in immunocompetent people, accounting for between a third and a half of cases in the West. Despite this frequency and considerable research, strategies for accurate diagnosis and effective treatment have yet to be devised.
Although toxoplasma was first observed in
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