Cases reported "Toxoplasmosis, Ocular"

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1/22. toxoplasma gondii retinochoroiditis after cardiac transplantation.

    PURPOSE: To report 4 cases of toxoplasma gondii retinochoroiditis in patients having recently undergone cardiac transplantation. methods: review of medical records for 4 patients presenting retinochoroiditis and evidence of T. gondii infection. RESULTS: Patient ranged in age from 25 to 53 years. Ocular symptoms began between 3 and 6 months after transplantation. All patients were under immunosuppressive therapy. Foci of retinochoroiditis were observed unilaterally in three patients and bilaterally in one. Intraocular inflammation was minimal in all cases. Serologic responses were highly suggestive of T. gondii as the etiology in all cases; other causes (CMV retinitis and syphilis) were actively sought and were not found. All patients underwent classic therapy. The three unilateral cases evolved favorably, but the bilateral case, seen late, showed extensive macular scarring. CONCLUSION: Infectious retinochoroiditis is a potentially blinding complication seen after cardiac transplantation, justifying close clinical and serological surveillance or, in certain cases such as mismatched donors, anti-parasitic prophylaxis.
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2/22. Ocular toxoplasmosis presenting as neuroretinitis: report of two cases.

    BACKGROUND: Neuroretinitis is a clinical entity usually seen in young healthy adults, that is characterized by rapid profound unilateral loss of vision and includes optic nerve head edema, splinter hemorrhages, macular exudate in a stellate pattern, and variable vitreous inflammation. There are numerous entities that can cause a picture of neuroretinitis ranging from vascular to infectious to autoimmune. PATIENT AND methods: We report two patients with neuroretinitis, who presented with unilateral blurred vision and had serologic evidence of toxoplasma gondii infection. RESULTS: Both patients responded well to treatment with systemic antibiotics and corticosteroids. visual acuity returned to 20/60 in one patient and 20/20 in the other. CONCLUSION: Although the etiology is usually idiopathic, infectious causes of neuroretinitis, including toxoplasmosis, should be kept in mind in order to maintain visual acuity by early diagnosis and appropriate therapy.
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3/22. Frosted branch angiitis and late peripheral retinochoroidal scar in a patient with acquired toxoplasmosis.

    PURPOSE: To report a case of acute frosted branch angiitis associated with acquired toxoplasmosis in which a late peripheral chorioretinal scar developed. RESULTS: A 32-year-old man without systemic symptoms presented with sudden visual loss in his left eye. Examination demonstrated frosted branch angiitis without necrotizing chorioretinitis. serologic tests showed elevated toxoplasma gondii-specific immunoglobulin m antibody titers. Antitoxoplasmic therapy and oral steroids healed the ocular inflammation. In a follow-up visit one year later, a peripheral chorioretinal scar was noted. CONCLUSIONS: Acute frosted branch angiitis without focal necrotizing chorioretinitis can be a manifestation of acquired toxoplasmosis. This could be an important, and sometimes forgotten, sign of the disease.
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4/22. Aggressive toxoplasma retinitis.

    toxoplasma infection is a common cause of infectious uveitis. It usually produces a characteristic fundal appearance, with evidence of previous inflammation. However, it may occur in an atypical and aggressive form. steroids administered to salvage vision may then worsen the clinical course. Retinal biopsy may be diagnostic in cases where doubt exists. We illustrate these points with two cases.
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5/22. Rapid progression of diabetic retinopathy in eyes with posterior uveitis.

    PURPOSE: To report on two patients who developed rapid progression of asymmetric diabetic retinopathy (DRP) in eyes affected by posterior uveitis in contrast to their fellow eyes not affected by uveitis. DESIGN: Observational case report. methods: Two patients with diabetes mellitus (DM) and unilateral uveitis underwent repeated ophthalmologic examinations and fluorescein angiography. RESULTS: Two patients with DM and unilateral posterior uveitis developed proliferative DRP in eyes with previous uveitis within 3 months after the uveitis subsided. In contrast, the retinal findings of nonuveitic eyes remained unchanged on follow-up of several years. CONCLUSIONS: Since the pathogenesis of intraocular inflammation and diabetic retinopathy acts through similar biochemical mediators and pathways, it is feasible that posterior uveitis accelerates the progression of diabetic retinopathy. Our results support this hypothesis and point out a risk for rapid retinopathy development in eyes affected with posterior uveitis.
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6/22. Ocular toxoplasmosis in patients with the acquired immunodeficiency syndrome.

    In seven of eight cases of presumed ocular toxoplasmosis in patients with AIDS, the diagnosis was supported by a reduction or resolution of intraocular inflammation and healing of necrotic retinal lesions after initiation of antiparasitic drug therapy including one or more of the following medications: pyrimethamine, sulfadiazine, clindamycin, tetracycline, or spiramycin. In two cases the diagnosis was confirmed histologically. The cases differed clinically and histopathologically from those in immunocompetent patients. There was no evidence that disease originated in preexisting retinochoroidal scars. Lesions frequently were bilateral and multifocal. Vitreous inflammatory reaction was a common clinical finding, but histopathologic examination demonstrated scant retinal inflammation in areas of necrosis. Ocular toxoplasmosis in these patients with AIDS probably resulted from newly acquired infection or dissemination of organisms from nonocular sites of disease. Infections became clinically inactive with drug therapy in all treated patients, but reactivation and progression of disease occurred when therapy was stopped in two of three patients. Severe retinal necrosis led to retinal tears or detachment in three cases. Ocular lesions were the first manifestation of toxoplasma gondii infection in four of five patients with evidence of multisystem infection.
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7/22. Toxoplasmic scleritis.

    Although toxoplasmosis is the most common infectious cause of posterior intraocular inflammation, it is rarely described in association with scleritis. The authors present five cases of toxoplasmosis with scleritis. Two of the five cases were diagnosed clinically and serologically as having toxoplasmosis. Their retinochoroiditis and scleritis responded well to medical therapy. Retinochroiditis and scleritis that was refractory to treatment developed in the other three patients, two of whom had been receiving immunosuppressive therapy for systemic diseases. Their therapeutic regimens did not include treatment for toxoplasmosis. All three eyes became blind and were enucleated. Results of pathologic examination of all three enucleated eyes showed toxoplasma gondii in the retina. There was severe inflammation of the retina, choroid, and sclera. toxoplasmosis should be considered in the clinical differential diagnosis of scleritis associated with retinochoroiditis, particularly in immunosuppressed patients.
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8/22. Bone-marrow transplantation and toxoplasmic retinochoroiditis.

    A 33-year-old woman underwent bone-marrow transplantation following radiation and chemotherapy for chronic myelocytic leukemia (CML); immunosuppressive therapy was continued for graft-versus-host disease. Five months after successful transplantation, she developed necrotizing retinitis in both eyes with rapid progression over the following weeks. Due to her immunosuppressed state the patient developed pneumonia and died. Postmortem evaluation of the retinal lesions in both eyes disclosed infection by toxoplasma gondii, which was also found in the brain and myocardium. Multiple viable toxoplasmic cysts were observed at the transition zone from a necrotic to a normal retina. Additionally, cysts of toxoplasma gondii a normal retina. Additionally, cysts of toxoplasma gondii were seen in the adjacent intact retina and in areas of necrosis with almost complete absence of retinal or choroidal inflammation. toxoplasmosis should therefore be considered along with fungi and viruses in the differential diagnosis of necrotizing retinochoroiditis in immunocompromised patients.
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9/22. Unusual presentation of acute ocular toxoplasmosis.

    Two unusual cases of ocular toxoplasmosis are presented. A 24 year old woman developed retinal and optic nerve neovascularization in conjunction with acute ocular toxoplasmosis. The neovascularization regressed with resolution of the inflammation. The possibility of retinal ischemia or inflammation alone as an etiology are discussed. A 19 year old woman developed optic nerve edema and a marked decrease in vision associated with a nasal toxoplasma lesion and a macular star. With resolution of the process, optic atrophy developed but visual acuity returned to normal. optic nerve edema and atrophy were felt to result from diffuse inflammation, but not from focal involvement in the nerve itself with the organism.
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10/22. choroidal neovascularization as a late complication of ocular toxoplasmosis.

    Macular detachment caused by choroidal neovascularization in eyes with previous toxoplasmic infections is one possible explanation of sudden loss of visual acuity. Three patients with quiescent chorioretinal scars, presumed to be toxoplasmic in origin, developed choroidal neovascular membranes that caused sudden loss of visual acuity. In none of the three cases was there any ophthalmoscopic evidence of intraocular inflammation. In two patients, the choroidal neovascularization was subfoveal and, therefore, not suitable for photocoagulation. However, visual acuity in each of the affected eyes was only partially impaired (6/15 [20/50] in one patient and 6/30 [20/100] in the other). In the third patient, the choroidal neovascular membrane was treated with argon-laser photocoagulation. Two months after treatment, visual acuity in that eye was 6/9 (20/30), and there was angiographic evidence that the neovascular membrane had closed.
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