Unilateral Pigmentary Retinopathy Associated with Ocular Toxoplasmosis

Silveira, Cássio; Belfort, Rubens; Nussenblatt, Robert B.; Farah, Michel Eid; Takahashi, Walter Yukihiko; Imamura, P M; Burnier, M.

doi:10.1016/0002-9394(89)90274-2

Cited by 22 publications

(14 citation statements)

References 2 publications

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“…Many other atypical presentations of ocular toxoplasmosis have been described 11 including: pseudo‐multiple retinochoroiditis; 8 Coats‐like retinopathy; 24 pigmentary retinopathy; 25 retinal vascular occlusion; 26,27 Roth spots; 28 serous retinal detachment; 29 optic disc granuloma; 14 scleritis; 30 and anterior, intermediate, anterior/intermediate, posterior and pan‐uveitis in the absence of overt retinitis 8,31,32 . Holland et al 31 .…”

Section: Clinical Manifestations Of Ocular Toxoplasmosismentioning

confidence: 99%

Ocular toxoplasmosis II: clinical features, pathology and management

Butler

Furtado²,

Winthrop

et al. 2012

Clinical Exper Ophthalmology

175

121

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The term, ocular toxoplasmosis, refers to eye disease related to infection with the parasite, Toxoplasma gondii. Recurrent posterior uveitis is the typical form of this disease, characterized by unilateral, necrotizing retinitis with secondary choroiditis, occurring adjacent to a pigmented retinochoroidal scar and associated with retinal vasculitis and vitritis. Multiple atypical presentations are also described, and severe inflammation is observed in immunocompromised patients. Histopathological correlations demonstrate focal coagulative retinal necrosis, and early in the course of the disease, this inflammation is based in the inner retina. For typical ocular toxoplasmosis, a diagnosis is easily made on clinical examination. In atypical cases, ocular fluid testing to detect parasite DNA by polymerase chain reaction or to determine intraocular production of specific antibody may be extremely helpful for establishing aetiology. Given the high seroprevalence of toxoplasmosis in most communities, serological testing for T. gondii antibodies is generally not useful. Despite a lack of published evidence for effectiveness of current therapies, most ophthalmologists elect to treat patients with ocular toxoplasmosis that reduces or threatens to impact vision. Classic therapy consists of oral pyrimethamine and sulfadiazine, plus systemic corticosteroid. Substantial toxicity of this drug combination has spurred interest in alternative antimicrobials, as well as local forms of drug delivery. At this time, however, no therapeutic approach is curative of ocular toxoplasmosis.

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Section: Clinical Manifestations Of Ocular Toxoplasmosismentioning

confidence: 99%

Ocular toxoplasmosis II: clinical features, pathology and management

Butler

Furtado²,

Winthrop

et al. 2012

Clinical Exper Ophthalmology

175

121

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“…These lesions when healed show typical toxoplasmic scars [291][292][293] Friedman and Knox [291] were the first to describe these. Silveira et al [294] later described a unilateral pseudoretinitis pigmentosa as a manifestation of T. gondii infection.…”

Section: Clinical Picturementioning

confidence: 99%

Immunopathogenesis of toxoplasmosis

Hegab

Al-Mutawa²

2003

Clinical and Experimental Medicine

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Toxoplasmosis is a ubiquitous infection affecting 500 million persons around the world, with a range of incidence 12%-90%, increasing with age, education, crowding and sanitary habits. Cats are the definitive host. Infection is primarily congenital but acquired ocular infection has been documented. The review focuses on the immunopathogenesis of toxoplasmosis with emphasis on the eye problem due to its morbidity. The response to infection correlates with both parasitic and retinal antigens. The clinical picture and histopathology is a reflection of the immune response which constitutes early humeral response which presents both systemically and locally primary infection and is elevated with reactivation. This is followed by the cellular response, varying from low grade monocular infilterate a total tissue destruction with response of live parasites especially in immuno-compromised patients. Penetration of the parasite and its enclosure within the parasitophorous vacuole and its eneyst all make its eradicatier impossible. This reflects the variability of antiparasitic therapy that include folate antagonists, macrolides, hydroxy naphthoquindones and fluoroquinolones. Use of corticosteroid should be limited to severe reactions and should be associated with specific therapy.

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“…Simultaneously, numerous clinical studies were developed during these years, such as the first description, in Brazil, of ocular toxoplasmosis in AIDS patients (Melamed et al 1989), pigmentary retinopathy accompanying the disease (Silveira et al 1989, Degrazia et al 2007) and toxoplasmosis provoking hypertensive uveitis in a great number of cases (Melamed et al 2006). Complications of the disease, such as macular hole (Melamed & Borges Filho 1985), secondary detachment of the retina reaching very high percentages and the involvement genital lesions (Perkins 1973).…”

mentioning

confidence: 99%

Contributions to the history of ocular toxoplasmosis in Southern Brazil

Melamed

2009

Mem. Inst. Oswaldo Cruz

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Unilateral Pigmentary Retinopathy Associated with Ocular Toxoplasmosis

Cited by 22 publications

References 2 publications

Ocular toxoplasmosis II: clinical features, pathology and management

Ocular toxoplasmosis II: clinical features, pathology and management

Immunopathogenesis of toxoplasmosis

Contributions to the history of ocular toxoplasmosis in Southern Brazil

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