[Toxoplasmosis. III. Ocular diseases and therapy].
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Tuberculosis and syphilis are often missed by ophthalmologists. The remedy is to perform complete PPD and FTA-ABS testing in all cases of uveitis in which the diagnosis is not apparent. Ocular toxoplasmosis should never be treated with corticosteroids alone but should be covered by at least one antitoxoplasmic agent. From none to four systemic medications may be used depending on the position and severity of the retino-choroiditis. There are currently two schools of thought in the diagnosis of ocular toxoplasmosis. It is suggested that each school should combine their minimal diagnostic criteria as a start in developing common diagnostic measures.
Toxoplasmic retinochoroiditis is an important opportunistic retinal infection in human immunodeficiency virus (HIV)-infected patients. It may present as diffuse necrotizing retinochoroiditis instead of a focal lesion and may be the initial manifestation of HIV infection. A 50-year-old heterosexual man presented with blurred vision in his left eye of 3 months' duration. Fundus examination revealed diffuse necrotizing retinochoroiditis, mainly at the posterior pole, with marked vitritis in the left eye. Serologic studies and aqueous fluid antibody titers indicated recent toxoplasmic infection. Positive enzyme immunoassays (EIA) and Western blot tests proved HIV infection. The retinochoroiditis and vitritis improved after an antitoxoplasmic regimen with trimethoprim-sulfamethoxazole (TMP-SMX). Nonetheless, toxoplasmic encephalitis developed 6 months after the onset of ocular toxoplasmosis and responded well to TMP-SMX. This is the first case of toxoplasmic retinochoroiditis as the initial manifestation of AIDS reported in Taiwan. We suggest that Toxoplasma infection should be included in the differential diagnosis of diffuse necrotizing retinochoroiditis and vitritis. We also recommend that adults with newly diagnosed ocular toxoplasmosis be screened for HIV infection.
BACKGROUND: Ocular toxoplasmosis can cause a variety of retinal vascular changes including branch retinal arterial occlusion, which is a rare complication of the disease. PATIENT AND METHODS: We report a case of toxoplasmic chorioretinitis in a pregnant woman, who developed branch retinal arterial obstruction adjacent to the active chorioretinitis lesion. RESULTS: The patient received an appropriate steroid and antibiotic treatment and the retinitis lesion resolved over a six-week period. At two months after diagnosis, visual acuity in her right eye was 20/30 and there was a hyperpigmented scar at the site where active retinitis had been observed. CONCLUSION: Especially in young patients with branch retinal vascular occlusion associated with posterior uveitis, the diagnosis of ocular toxoplasmosis should be kept in mind and serologic test results should be obtained.
By using a modified enzyme immunoassay we have conducted a detailed study on the intraocular synthesis of toxoplasma antibodies during ocular toxoplasmosis. In control patients operated on for cataracts, the ratio of immunoglobulin G (IgG) toxoplasma antibodies in serum to those in aqueous humor was more than 100. In eight of the nine patients with clinically diagnosed toxoplasmic chorioretinitis, the ratio ranged between 6 and 56. In five patients with some other type of uveitis, the ratio was comparable with that in controls. Parallel determinations of mumps IgG antibody ratios were carried out to prove that the increased intraocular toxoplasma antibody levels were not a result of increased diffusion or polyclonal antibody stimulation. In all patients, mumps antibody ratios were within normal range. We also tested the samples of aqueous humor for IgM and IgA antibodies, but the antibodies in the aqueous humor were found to be exclusively IgG. Our results indicate that IgG-class anti-toxoplasma antibodies are produced locally within the eye in cases of toxoplasmic chorioretinitis. The determination of these antibodies can offer a valuable aid to make a specific etiological diagnosis of ocular toxoplasmosis.
Acute ocular toxoplasmosis is characterized by a focal retinochoroidal infiltrate, often appearing in the immediate vicinity of an old retinochoroidal scar (satellite lesion). There are atypical forms of ocular toxoplasmosis, including retinal granulomas, intraretinal and subretinal neovascularization, preretinal gliosis and retinal detachment. In rare instances, associated immunological phenomena, i.e. concomitant vasculitis and perivasculitis, have been described. We report on a 28-year-old male patient presenting with signs of congenital toxoplasmosis with intracerebral calcifications and internal hydrocephalus (Whytt's disease). Ocular manifestations included an acute retinochoroidal infiltrate adjacent to a retinochoroidal scar and segmental retinal periarteritis. All arterioles were involved, but there was no inflammation of the venules. Fluorescein angiography revealed filling irregularities of the vessel segments involved. Like a tubercular patient with segmental periarteritis reported on as long ago as 1939, our patient had undergone treatment for active tuberculosis of the lung 6 years earlier. Considering the fact that segmental periarteritis without concomitant periphlebitis is very rarely seen, the coincidence of acute toxoplasmosis and previous tuberculosis suggests a complex immunological etiology of retinal vasculitis. This assumption may be supported by the fact that a combined systemic treatment with pyrimethamine, trimethoprim, sulfamethoxazole and prednisolone reduced the retinochoroidal inflammation and periarterial infiltrates.
Toxoplasmosis is a major and preventable cause of severe visual loss and blindness in young people. Ocular toxoplasmosis is the leading cause of posterior uveitis and in most cases it represents a late manifestation of a congenital infection. The clinical picture and anti-Toxoplasma therapy of seven patients referred to the Department of Infectious Diseases, Hvidovre Hospital is described. All patients had clinical ocular toxoplasmosis at initial examination with unilateral focal necrotizing retinitis associated with typical old, pigmented scars. All patients had anti-toxoplasmosis IgG antibodies. After anti-Toxoplasma therapy with sulfadiazine, pyrimethamine and corticosteroid the ocular lesions were healed to atrophic scars and the inflammatory activity disappeared. We conclude that when the clinical picture is compatible with toxoplasmosis, antibodies to Toxoplasma gondii are demonstrated and there is no other diagnosis, anti-Toxoplasma treatment should be considered. It is important to inform pregnant women about prophylactic measures, and to perform a serological screening of newborns, since treatment of congenital toxoplasmosis from birth improves the prognosis.
AIMS: To determine the incidence and severity of symptomatic toxoplasma infection presenting during childhood due to congenital or postnatally acquired infection. METHODS: Between 2002 and 2004, newly diagnosed children (<16 years) with signs or symptoms of congenital or ocular toxoplasmosis were reported by clinicians to the British Paediatric and Ophthalmic Surveillance Units or by toxoplasma referral laboratories. Confirmed cases were estimated to have a greater than 50% probability of congenital and/or ocular toxoplasmosis, based on clinical and serological findings. RESULTS: Thirty eight children had confirmed toxoplasma infection. Twenty two (58%) were classified with congenital infection (cumulative incidence for England and Wales 1.62[corrected]/100,000 live births; 95% CI 0.85[corrected] to 2.83[corrected]), of whom 2 (9%) were stillborn, 7 (32%) live births had intracranial abnormalities and/or developmental delay (5 of whom had retinochoroiditis), and 10 (45%) had retinochoroiditis with no other abnormalities reported. A further 16 (42%) children were classified as infected after birth; all had retinochoroiditis. CONCLUSIONS: The low burden of symptomatic congenital toxoplasmosis combined with the lack of evidence of an effective treatment support current policy not to offer prenatal or neonatal screening for toxoplasma infection. Primary prevention strategies need to address acquisition of infection in childhood which accounts for half the ocular disease due to toxoplasma infection in children in the UK and Ireland.
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In this report we describe the lesions produced by the protozoal organism, Toxoplasma gondii, in the eyes and brain of the common yellow canary (Serinus canaria). Nine of 15 birds in a flock were affected with blindness, which developed over a 3-mo span, and two birds developed torticollis. Microscopic alterations within the eye consisted of a nonsuppurative chorioretinitis with large numbers of macrophages that contained the tachyzoite form of T. gondii in the subretinal space, and aggregates of tachyzoites were found in the nerve fiber layer of the retina with and without necrosis. Tissue cysts with bradyzoites were scattered throughout the meninges and neuropil of the cerebrum and cerebellum. Both forms were confirmed by transmission electron microscopy in the eye and brain. Frozen brain samples reacted with T. gondii-specific cat sera in indirect fluorescent antibody tests. The source of infection was hypothesized to be from a stray cat the owner kept that had access to some of the bird feed. Treatment (trimethoprim 0.08 g/ml H2O and sulfadiazine 0.04 g/ml in water for 2 wk) was instituted by the referring veterinarian on the remaining birds. A second treatment regime was given for 3 wk. The owner of the canaries did not return for further treatment.
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Ocular toxoplasmosis is the major cause of posterior uvetis in European populations. The clinical diagnosis of toxoplasmic chorioretinitis is based upon ophthalmoscopic findings, which are often but not always typical. Laboratory testing is therefore important to confirm the etiology of the disease. In the present 2-year prospective study, the relative diagnostic sensitivities of the three analytical techniques (enzyme-linked immunosorbent assay [ELISA], immunoblotting, and PCR) were compared by using a group of patients (n = 19) with suspected ocular toxoplasmosis. The relative specificities of the three techniques were assessed by including two control groups of patients: one with nontoxoplasmic and noninflammatory ocular disease (n = 48) and the other with nontoxoplasmic and inflammatory ocular disease (n = 20). All 19 of the clinically suspect patients had serological evidence of exposure to Toxoplasma gondii: 17 had been previously infected, and 2 had current infection. The analysis of paired aqueous humor and serum samples by ELISA and immunoblotting revealed the local production of specific antibodies of the immunoglobulin G type in 63% (12 of 19) and 53% (10 of 19) of patients, respectively. PCR analysis of aqueous humor samples confirmed the presence of T. gondii DNA in 28% (5 of 18) of cases. When combined, ELISA, immunoblotting, and PCR findings confirmed the toxoplasmic origin of retinal lesions in 83% (15 of 18) of patients. The relative specificities of the three techniques were 89% for ELISA and immunoblotting and 100% for PCR.
PURPOSE: To understand better the natural history of ocular toxoplasmosis by reexamining a well-characterized population in Southern Brazil. METHODS: Ophthalmological examination and serologic tests for Toxoplasma gondii infection were performed in 1997 on 383 individuals who had undergone the same evaluation in 1990. RESULTS: Of 109 seronegative subjects in 1990, 21 (19.3%) became seropositive by 1997, and 2 (1.5% of previously seronegative patients; 9.5% of those known to have seroconverted) developed ocular toxoplasmosis. Seroconversion occurred more frequently in individuals under 17 years of age (16 of 46 patients, 34.8%) than in those greater than 17 years of age (5 of 63 patients, 7.9%; p = 0.002). Of 131 seropositive individuals who did not have ocular lesions in 1990, 11 (8.3%) had typical toxoplasmic lesions in 1997. Of the 13 individuals with non-specific hyperpigmented small retinal lesions in 1990, 3 (23%) presented with typical lesions in 1997. CONCLUSIONS: Acquired T. gondii infection can result in late development of ocular lesions. Small, non-specific hyperpigmented retinal lesions may represent sites of T. gondii infection in seropositive individuals.
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The authors prospectively evaluated 445 HIV positive patients for the presence of ophthalmological manifestations. PURPOSE--To evaluate patients HIV positive with or without AIDS and correlate the data with the ocular findings mentioned in the literature. METHODS--445 HIV positive patients (66% with AIDS) were evaluated in one year at the Paulista School of Medicine, São Paulo Hospital, Brazil. There was a predominance of males (87%) and homosexuals (58.2%). RESULTS--Of the 445 patients, 52% presented ocular findings secondary to HIV infection at the first examination. The diagnosis included: CMV retinitis (25%), ocular toxoplasmosis (8.5%), herpes retinitis (3.6%), papilledema (2.2%), optic atrophy (1.6%), phthisis bulbi (1.5%), multifocal choroiditis (1.2%), retinal hemorrhages (0.9%), syphilitic uveitis (0.6%) and central vein occlusion (0.2%). CONCLUSION--The incidence of ophthalmic manifestations of AIDS in Brazil is similar to that found in the international literature. We found though a higher incidence of ocular toxoplasmosis than that in other countries. No ocular pneumocystosis was presents in the population evaluated by us.