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PubMed2004

A multihousehold study reveals a positive correlation between age, severity of ocular toxoplasmosis, and levels of glycoinositolphospholipid-specific immunoglobulin A.

A cross-sectional household study involving 499 individuals was undertaken in an area of Minas Gerais state, Brazil, where infection with Toxoplasma gondii is endemic. Nearly 50% (n=247) of the sample had T. gondii-specific antibodies, even individuals in the 5-9-year-old age group. Approximately 12.5% (n=28) of a random subsample of participants who were positive for T. gondii antibodies had ocular lesions associated with T. gondii infection. The frequency of ocular toxoplasmosis increased significantly with age, with approximately 50% of individuals >60 years of age having lesions. The size of the ocular lesion correlated positively (r=0.85; P=.01) with the serum level of immunoglobulin A specific for tachyzoite-derived glycoinositolphospholipids. We found that sharing the same residence accounted for 30% of the variation in infectivity among residents in the sample, whereas age was the main risk factor for development of ocular toxoplasmosis in patients who were positive for T. gondii antibodies.

Adolescent↗

PubMed2004

CD4+ T cells in the pathogenesis of murine ocular toxoplasmosis.

The role of CD4(+) T cells in the pathogenesis of ocular toxoplasmosis was investigated in murine models utilizing inbred C57BL/6 mice deficient either in CD4(+), CD8(+), or B cells (microMT). Severe necrosis and inflammation with replicating parasites were observed in the eyes of control mice after primary ocular infection, and near-normal histology with few tachyzoites was observed in the eyes of mice immunized intraperitoneally with the avirulent ts-4 strain followed by intraocular challenge with the RH strain of Toxoplasma gondii. In contrast, mild inflammation without evidence of necrosis associated with increased parasite burdens were observed in the eyes of CD4 knockout (KO) mice after both primary ocular infection and challenge with RH tachyzoites. CD8 KO mice, as well as microMT mice, demonstrated increased ocular necrosis in response to either primary ocular infection or challenge. The parasite burden was increased in the eyes of both CD8 KO and microMT mice in which the parasite load was even higher. As expected, there were no increases in the levels of immunoglobulin G in serum or aqueous humor in microMT mice, and there was no increase in the levels of gamma interferon and tumor necrosis factor alpha in the sera of CD4 KO mice after both infection and challenge. These results suggest that the ocular inflammatory response to the parasite is mediated primarily by the CD4(+)-T-cell response. CD8(+) T cells and B cells may play an important role in limiting tachyzoite proliferation in the eyes. Mice deficient in CD8(+) CD4(+) T cells or B cells exhibit diminished vaccine-induced resistance and increased ocular parasite burden after challenge.

Animals↗

PubMed1976

Ocular toxoplasmosis in an adult receiving long-term corticosteroid therapy.

Sudden death of a 58-year-old woman who developed ocular toxoplasmosis while receiving long-term systemic corticosteroid therapy permitted correlation of early histopathologic lesions with their clinical counterpart recorded on fundus photographs. A wide-spread, paravascular, whitish, retinal opacification dominated the initial clinical picture. These lesions were represented histologically by focal zones of inner retinal necrosis located adjacent to arteries and veins. No associated inflammatory cell infiltrate was present, and numerous viable free Toxoplasma organisms were consistently present at the interface between necrotic and healthy retina. Electron microscopy of formaldehyde-fixed tissue provided a useful technique for confirming the identity of the infecting organism in the absence of serologic or culture data.

Adrenal Cortex Hormones↗

PubMed1996

Recurrent ocular toxoplasmosis in patients treated with systemic corticosteroids.

PURPOSE: The authors discuss a possible relationship between systematic corticosteroid use and reactivation of ocular toxoplasmosis. METHODS: Patients were identified who developed foci of recurrent toxoplasmic retinochoroiditis while being treated with systemic corticosteroids. Case histories were reviewed retrospectively. RESULTS: During a 10-year interval, three patients were identified at the University of California, Los Angeles, who had been receiving systemic corticosteroid therapy (dose range, 0.27-1.23 mg/kg/day) when they developed recurrent toxoplasmic retinochoroiditis. Disease occurred at intervals of 20 days to approximately 1 year after start of corticosteroid therapy. Lesions were typical in appearance, course, and manner in which they responded to antimicrobial therapy. CONCLUSION: Recurrent toxoplasmosis in patients receiving corticosteroid therapy probably is uncommon. These cases do not confirm a causal relationship between corticosteroid use and initiation of disease recurrence.

Adolescent↗

PubMed2004

Aqueous humor and serum immunoblotting for immunoglobulin types G, A, M, and E in cases of human ocular toxoplasmosis.

The purpose of this study was to compare the local and systemic Toxoplasma-specific humoral immune responses in individuals with ocular toxoplasmosis (OT). To this end, paired aqueous humor and serum samples from 46 individuals with active OT and from 30 individuals without inflammatory eye disease (controls) were analyzed by immunoblotting for anti-Toxoplasma immunoglobulin G (IgG), IgA, IgM, and IgE directed against 20- to 120-kDa antigens. The presence in the aqueous humor of a unique band, or of at least three bands that were at least three times more intense in aqueous humor than in serum, was taken as evidence of local antibody production. IgG bands were detected in 98% of the aqueous humor samples, while IgA bands were detected in 76%, IgM bands were detected in 8%, and IgE bands were not detected in any. Evidence of local production of specific antibodies was found in 32 cases (70%) (IgG in 23 [50%]; IgA in 16 [35%]). In 10 instances (22%), routine laboratory tests were not indicative of OT. In 14 cases (30%), no local antibody production was detected by immunoblotting; 3 of these cases yielded evidence of local antibody production according to the Goldmann-Witmer coefficient. Local antibody production was revealed for 7 of the 30 controls (23%). Hence, the sensitivity of immunoblotting for IgG and IgA is 70%, and the specificity is 77%. We conclude that immunoblotting for local specific IgG and IgA supports the clinical diagnosis of OT in 70% of cases. In 22% of these, the diagnosis is not confirmed by other laboratory tests. Hence, immunoblotting increases the sensitivity of routine laboratory tests and should be considered for samples that register negative by such tests.

Animals↗

PubMed1983

Detection of toxoplasmal antigen and antibody in ocular fluids in experimental ocular toxoplasmosis.

Enzyme-linked immunosorbent assays were used to detect intraocular toxoplasmal antigen and antitoxoplasmal IgG antibodies in a rabbit model of experimental ocular toxoplasmosis. Toxoplasmal antigen could be detected in the vitreous humor of the infected eye at the height of clinical activity of the lesion. Antitoxoplasmal IgG antibodies were detected in the aqueous and vitreous humors of the infected eyes five weeks following the onset of toxoplasmic retinochoroiditis.

Animals↗

PubMed1999

[Fuchs' uveitic syndrome in a patient with ocular toxoplasmosis].

We report a case of Fuchs' uveitic syndrome associated with toxoplasmic chorioretinis scars, and a positive Desmonts' coefficient. This allows us to emphasize ocular toxoplasmosis as a main association to be searched for clinically. In the cases in which this association is found, it would be warranted, if a high level of specific antitoxoplasmic antibodies is demonstrated in aqueous humor, to consider toxoplasmosis as one of the potential etiopathogenic factors of the Fuchs' uveitic syndrome.

Adult↗

PubMed1989

Ocular toxoplasmosis in the immunocompromised host.

Disseminated toxoplasmosis is a well-known complication of immunodeficiency states, including those induced by malignancies, steroid and cytotoxic drug therapy, and AIDS. In immunodeficient patients, toxoplasmic infections of the eye are less common than toxoplasmic infections of other organs for unknown reasons. When ocular toxoplasmosis does occur in the immunodeficient host, or if immunosuppressive therapy is administered to patients with active disease, widespread tissue destruction by proliferating organisms may result. Immunodeficiency alone may not be sufficient, however, to cause reactivation of encysted organisms in retinochoroidal scars. Ocular toxoplasmosis in the immunocompromised host presents difficult problems in diagnosis and management. There may be a variety of clinical lesions, including single foci of retinochoroiditis in one or both eyes, multifocal lesions, or diffuse areas of retinal necrosis. The majority of lesions do not arise from the borders of preexisting scars, which suggests that they result from acquired infection or dissemination of organisms from nonocular sites of disease. Toxoplasma gondii may infect iris, choroid, and vitreous-tissues that are not usually infected in the immunocompetent host. Ocular lesions appear to respond to standard antiparasitic drug therapies, but continued treatment is probably necessary to prevent reactivation of disease in the most immunocompromised patients. The best treatment regimens have yet to be determined. Histopathologic studies show little retinal inflammation; therefore anti-inflammatory drugs, such as oral steroids, probably have no role in the management of infection.

Acquired Immunodeficiency Syndrome↗

PubMed1999

Use of the polymerase chain reaction for diagnosis of ocular toxoplasmosis.

OBJECTIVE: To report a cohort of patients in whom polymerase chain reaction (PCR) was performed on vitreous samples and to place in perspective the current role of PCR in the diagnosis of ocular toxoplasmosis. DESIGN: Noncomparative case series. PARTICIPANTS: Fifteen patients in whom toxoplasmic retinochoroiditis was considered in the differential diagnosis and in whom the clinical presentation was not diagnostic and/or response to treatment was inadequate. INTERVENTION: Examination of vitreous fluid by PCR and of serum for the presence of Toxoplasma-specific antibodies. MAIN OUTCOME MEASURES: Presence of Toxoplasma gondii DNA, serologic test results, clinical findings, treatment, and outcome. RESULTS: In 7 of 15 patients, vitreous fluid examination results by PCR were positive for the presence of T. gondii DNA. Five of these seven patients had serologic test results consistent with Toxoplasma infection acquired in the distant past; the other two patients had serologic test results consistent with retinochoroiditis in the setting of acute toxoplasmosis. The PCR results influenced the management of these patients in six of the seven positive cases. In the eight patients in whom vitreous examination results were negative by PCR, either Toxoplasma serology was negative (6), the retinal lesions were caused by cytomegalovirus (1), or, on further consideration, the eye signs were not consistent with those of toxoplasmic retinochoroiditis (1). CONCLUSION: In patients in whom toxoplasmosis is considered in the differential diagnosis but in whom the presentation is atypical, PCR was frequently a useful diagnostic aid.

Adult↗

PubMed1982

Minocycline in experimental ocular toxoplasmosis in the rabbit.

We studied the effects of minocycline, a semisynthetic tetracycline, on experimentally induced toxoplasmic retinochoroiditis in the rabbit. In two experiments we found that this drug effectively ameliorated the clinical disease and sterilized the ocular tissues from Toxoplasma organisms. Minocycline prevented death from toxoplasmic encephalitis in 75% of the animals, whereas all the control animals died of toxoplasmic encephalitis. Minocycline appears to be a promising agent for ocular toxoplasmosis.

Animals↗

PubMed1991

The epidemiologic association of Fuchs' heterochromic iridocyclitis and ocular toxoplasmosis.

Between January 1983 and July 1987, I examined 25 patients at the Department of Ophthalmology, West Virginia University, who had the anterior segment characteristics of Fuchs' heterochromic iridocyclitis. Of these patients, 16 had fundus lesions suggestive of ocular toxoplasmosis. Of these 16 patients, 13 had a positive serologic test for toxoplasmosis, two patients were not tested, and one patient had a negative test at 1:16. The remaining nine patients with Fuchs' heterochromic iridocyclitis had no fundus lesions suggestive of toxoplasmosis. A chart review of 792 consecutive patients at the Retinal Unit, West Virginia University, during a six-month period disclosed that 24 of 590 patients (4%) had chorioretinal scars suggestive of toxoplasmosis. I concluded from these data that in at least one subgroup of patients with Fuchs' heterochromic iridocyclitis there is a significant association with the chorioretinal scars of toxoplasmosis (P less than .01), and this is suggestive of a causal relationship.

Adult↗

PubMed2006

Outbreak of ocular toxoplasmosis in Coimbatore, India.

Toxoplasma gondii is a protozoan parasite that infects up to a third of the world's population. Infection is mainly acquired by ingestion of food that is contaminated with oocysts. We report an outbreak of ocular toxoplasmosis, which is an acute acquired type rather than reactivation of congenital toxoplasmosis. Our preliminary investigation points to municipal water contamination. This outbreak only proves the need of an effective public health system and health education in curtailing any outbreak.

Adolescent↗

PubMedDate not supplied

Ocular toxoplasmosis.

1. Women with no immunity to Toxoplasma organisms acquire toxoplasmosis during pregnancy; the infection spreads to the fetus by transplacental transmission. 2. Blurred vision, floaters, photopsia, pain, and redness are common complaints of the active retinochoroiditis. 3. The diagnosis of ocular toxoplasmosis can be confirmed by blood tests, the most common being the indirect fluorescent antibody (IFA) and the enzyme-linked immunosorbent assay (ELISA).

Female↗

PubMed1994

Toxoplasma gondii: acquired ocular toxoplasmosis in the murine model, protective role of TNF-alpha and IFN-gamma.

DNA and mRNA amplification by the polymerase chain reaction (PCR), immunohistochemical, and histopathology were performed in the eyes and brains from C57BL/6 mice infected with an avirulent strain of Toxoplasma gondii (ME49). Focal ocular inflammation and retinal pigment epithelial involvement were commonly observed after 15 days of infection. Four weeks after infection a stable number of cysts was observed in the brain but rarely in the eye, and they did not elicit an inflammatory response. In most of the ocular lesions the presence of the parasite could not be demonstrated even with the PCR technique. B1 DNA fragments of T. gondii were detected in only 4 of 11 eyes tested by PCR and Southern blot hybridization. Treatment of mice with mAbs against T cells (CD4 plus CD8) or cytokines (IFN-gamma or TNF-alpha) resulted in a marked increase of ocular lesions, more often associated with the presence of the parasite and the severity of inflammatory response. This model and the techniques utilized here can improve our understanding of the respective roles of parasite proliferation and immune mechanisms involved in the pathogenesis of acquired ocular toxoplasmosis.

Animals↗

PubMed1978

Congenital ocular toxoplasmosis. Possible occurrence in siblings.

In two siblings, we saw bilateral macular lesions that were consistent with the diagnosis of congenital toxoplasmosis. Although the congenital nature of this type of infection cannot be proven conclusively, there is considerable evidence that the lesions in our young patients were scars from congenital toxoplasmic retinochoroiditis. To our knowledge, congenital ocular toxoplasmosis in siblings has not previously been reported.

Adolescent↗

PubMed1997

Uveitis: is ocular toxoplasmosis only a clinical diagnosis?

Between 1981 and 1994, the detection of specific antibodies against Toxoplasma gondii was performed simultaneously in serum and aqueous humor from 90 patients, and the Witmer-Desmonts coefficient measuring the relative concentration of antibodies produced locally was calculated to confirm the clinical diagnosis of ocular toxoplasmosis. Thirty-seven results were positive (41.1%), 12 uncertain (13.3%) and 41 negative (45.6%). These results are compared with the data obtained by the polymerase chain reaction for the genomic detection of an infectious agent in the aqueous humor that have recently been published.

Animals↗

PubMed2002

Ocular toxoplasmosis: a 50th anniversary tribute to the contributions of Helenor Campbell Wilder Foerster.

In 1952, Helenor Campbell Wilder (later Helenor Campbell Wilder Foerster) confirmed the growing suspicion that Toxoplasma gondii was a cause of uveitis in otherwise healthy adults by identifying the presence of parasites in eyes enucleated because of severe intraocular inflammation. Ocular toxoplasmosis was previously known to occur only in newborns with congenital T gondii infection. Her report ushered in a new era in the field of uveitis in which toxoplasmosis, rather than tuberculosis, was confirmed to be the most common cause of retinochoroiditis. Fifty years later, issues raised in her landmark publication are still being investigated.

Anniversaries and Special Events↗

PubMed1995

Presumed acquired ocular toxoplasmosis.

OBJECTIVE: To describe the clinical characteristics and laboratory findings of eight patients with focal chorioretinitis presumably caused by acquired toxoplasmosis. DESIGN: Case series. SETTING: Referral hospitals in the Netherlands. PATIENTS: Eight patients, aged 42 to 75 years, with unilateral focal chorioretinitis and laboratory evidence of a recently acquired infection with Toxoplasma gondii. MAIN OUTCOME MEASURES: Findings from ocular examination and analysis of both serum and aqueous humor samples for Toxoplasma and viral antibodies. RESULTS: All patients had unilateral focal chorioretinitis without associated old scars in the posterior pole. Patients treated with systemic or periocular corticosteroids not accompanied by antiparasitic medication showed a rapid increase of inflammation. All eight patients had Toxoplasma IgM antibodies in their serum samples, seven of whom had high Toxoplasma IgG titers. Five of eight patients had increased intraocular production of IgG antibodies against T gondii. CONCLUSION: Unilateral focal chorioretinitis in patients of any age should alert the clinician to consider acquired ocular toxoplasmosis in the differential diagnosis.

Adult↗