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PubMed1984

[Acquired ocular toxoplasmosis and immunosuppression of tumoral thymic origin].

A rare case of acute bilateral unifocal chorioretinitis in a 24 years old man is described. The patient had been followed for more than 3 years for a benign thymoma, detected by systematic radiography, that was initially operated on with success. Later, after recurrence of clinical signs a second operation was performed that revealed local invasion of the tumor which was histologically identified as a benign, lymphoid thymoma. Serological data permitted us to attribute the lesions to a sub-acute ganglionary toxoplasmosis, contracted five months before any ocular localization. A treatment including local corticotherapy and oral pyrimethamine and sulfonamide was undertaken. Healing of the retinal lesions occurred slowly. A complete study of the patient's immunity revealed an important deficiency of cell-mediated functions. The problem of diagnosis of opportunistic chorioretinitis is discussed. In patients with impairment of cellular-type immunity, the following are commonly observed: herpes group viral diseases (including cytomegalic inclusion disease), fungus diseases (candida, aspergillus, mucormycosis, cryptococcus), and, rarely, toxoplasmosis. The presence of specific serum antibodies is the most important element in making a diagnosis, considering that the ophthalmoscopic appearance and clinical course may vary.

Adult↗
PubMed2006

Genetic divergence of Toxoplasma gondii strains associated with ocular toxoplasmosis, Brazil.

Previous studies have shown a high prevalence of toxoplasmosis and the frequent occurrence of ocular disease in Brazil. To identify the genotypes of parasite strains associated with ocular disease, we compared 25 clinical and animal isolates of Toxoplasma gondii from Brazil to previously characterized clonal lineages from North America and Europe. Multilocus nested polymerase chain reaction analysis was combined with direct sequencing of a polymorphic intron to classify strains by phylogenetic methods. The genotypes of T. gondii strains isolated from Brazil were highly divergent when compared to the previously described clonal lineages. Several new predominant genotypes were identified from different regions of Brazil, including 2 small outbreaks attributable to foodborne or waterborne infection. These findings show that the genetic makeup of T. gondii is more complex than previously recognized and suggest that unique or divergent genotypes may contribute to different clinical outcomes of toxoplasmosis in different localities.

Animals↗
PubMed1990

Ocular toxoplasmosis in AIDS patients.

We describe 16 cases of ocular and, in some patients, associated CNS toxoplasmosis in AIDS patients. T gondii is commonly associated with infection in the immunocompromised host. The lesions are most often seen in the CNS and eyes; involvement in the brain, heart, lung, liver, spleen, and lymph nodes may be observed. CNS involvement by toxoplasmosis may be an initial manifestation of AIDS and may be associated with discrete or diffuse lesions. CT scan and MR imaging may demonstrate a multitude of lesions often displaying the characteristic ring-shaped enhancement after contrast injection. Ocular involvement by toxoplasmosis, though less common than CNS involvement, is characterized by several features. These may be manifested as single or multifocal retinal lesions in one or both eyes or massive areas of retinal necrosis. Invariably these lesions are unassociated with a pre-existing retinochoroidal scar suggesting that the lesions are a manifestation of acquired rather than congenital disease. Presence of IgM antibodies may support this observation although antibody levels in AIDS patients may not reflect the magnitude of disease. Vitreous reaction is often minimal. Anterior uveitis has been reported in one case. Treatment of the ocular infection with pyrimethamine, clindamycin and sulfadiazine is effective in over 75% of patients. Once resolution of the ocular infection is observed, maintenance therapy is continued as relapses occur in the absence of treatment. Corticosteroid treatment is unnecessary and its use has been associated with the development of CMV retinitis. Other retinal infections in AIDS patients which should be considered in the differential diagnosis include CMV, herpetic-associated ARN and syphilis. Concomitant CMV and toxoplasmosis in the same eye have been seen.

Acquired Immunodeficiency Syndrome↗
PubMed1980

[Diagnostic values of quantitative serological tests of the aqueous humor in ocular toxoplasmosis. A report on 180 cases (author's transl)].

A simultaneous study of 180 recent samples of serum and aqueous humor, taken to study serological factors in cases of toxoplasmosis, demonstrated the production of intra-ocular antibodies in about 1 out of 2 cases (70 cases out of 145) of posterior uveitis. This confirms the value of calculating Witmer-Desmonts "C" coefficient for the diagnosis of the affection, as well as the careful evaluation of its different parameters; serum dye-test, and globulin levels in the aqueous humor nore particularly.

Anterior Chamber↗
PubMed1989

Herpes zoster ophthalmicus, contralateral hemiplegia, and recurrent ocular toxoplasmosis in a patient with acquired immune deficiency syndrome-related complex.

A 42-year-old man presented with herpes zoster ophthalmicus on the right side. He was found to have acquired immune deficiency syndrome-related complex. Two weeks later he developed toxoplasmic retinochoroiditis in the left eye. He also presented later with left hemiplegia, which was probably caused by herpes zoster arteritis. Nine months after the retinal lesion resolved he developed another area of toxoplasmic retinochoroiditis adjacent to the first lesion. Herpes zoster may be the first presentation of acquired immune deficiency syndrome-related complex in a young healthy individual. Ophthalmologists are encountering patients with acquired immune deficiency syndrome who may have multiple organisms as the cause for their ocular infections and this might pose a treatment dilemma. The combination of herpes zoster ophthalmicus and ocular toxoplasmosis in this patient makes this case unusual.

Acquired Immunodeficiency Syndrome↗
PubMed1979

Ocular toxoplasmosis in wallabies (Macropus rufogriseus).

We initiated a pathologic investigation of ocular disease in wallabies. Of 21 animals examined, the eyes were investigated histologically in 11; in four of these animals the brains were also available for section and the sera were investigated in three. In ten animals only sera were received. Histologic studies showed bilateral or unilateral cataract in five animals. Eight animals, with or without cataracts, showed various degrees of keratitis, uveitis, choroidoretinitis, or endophthalmitis. In three animals Toxoplasma cysts were found within the retina or brain, or both. Of the 13 cases examined serologically 11 were positive for toxoplasmosis; three reached high titers.

Animals↗
PubMed1996

Protective role of nitric oxide in ocular toxoplasmosis.

AIMS: To evaluate the role of nitric oxide (NO) in ocular involvement during systemic toxoplasmosis. METHODS: C57B1/6 mice were infected with Toxoplasma gondii strain ME49. The synthesis of NO was inhibited by an intraperitoneal injection of aminoguanidine every 8 hours, starting on the day of infection. Control infected mice received phosphate buffered saline vehicle alone. After 14 days, the ocular lesions were evaluated by histopathological examination. The expression of NO synthase induced in the spleen by toxoplasma infection was evaluated by immunostaining. The production of NO by the spleen cells of infected mice was measured by the colorimetric assay of Griess in the supernatant of cultures stimulated with toxoplasma antigen or concanavalin A. RESULTS: The inhibition of NO production in T gondii infected mice resulted in a marked increase in the symptoms of ocular inflammation. We observed a strong induction of NO synthase expression in the spleen of infected animals. In culture, the spleen cells from these mice produced high levels of NO in response to T gondii antigens. This elevation of NO synthesis was suppressed in the presence of aminoguanidine. CONCLUSION: This study indicates that NO plays a crucial role in the protection against T gondii infection as reflected by the severity of the ocular involvement.

Animals↗
PubMed2000

[Acquired ocular toxoplasmosis (panuveitis) after liver transplantation].

We present one case of acquired Toxoplasma gondii retinochoroiditis after livrer transplantation. Three weeks after receiving liver transplant from a seropositive donor for Toxoplasma gondii, the fundus examination showed a vitreal haze and an edematous retinal lesion with retinal hemorrhages. Routine screening tests for uveitis were performed. The serum toxoplasmosis titers revealed a seroconversion for toxoplasmosis (pre-transplantation tests were negative). The PCR assay on aqueous humor resulted in an amplified product identical to toxoplasmosis. This immunocompromised patient likely received an infected hepatic transplant. The patient's ocular inflammation cleared on 1-month pyrimethamine-sulfadiazine medication. Four months later, the patient developed a retinal detachment with massive proliferative vitreoretinopathy.

Adult↗
PubMed1999

Immunoglobulin G avidity in diagnosis of toxoplasmic lymphadenopathy and ocular toxoplasmosis.

Traditional serological techniques have some limitations in evaluating the duration of Toxoplasma gondii infection in pregnant women, patients with lymphadenopathy, and older children suspected of having congenital toxoplasmosis. In these three groups of patients, two variants of T. gondii immunoglobulin G (IgG) avidity tests were used: an EIA Kit (Labsystems) and a noncommercial enzyme-linked immunosorbent assay specially elaborated in the laboratory. The avidity of specific IgG in sera from 23 patients with a known recently acquired infection (mainly pregnant women) was low (less than 30%), whereas that in sera from 19 patients with toxoplasmic lymphadenopathy of 3 weeks to 6 months in duration (mean, 8.3 weeks) covered a large range (between 0.2 and 57.8%; mean, 25. 7%); high avidity results were observed for 10 of 19 patients (52. 6%). The large range of IgG avidity in patients with toxoplasmic lymphadenopathy suggests various durations of infection in these patients, with a tendency for a chronic phase of toxoplasmosis. According to the avidity marker, five patients with lymphadenopathy for less than 3 months did not have a recent Toxoplasma infection. In 6 of 19 patients with lymphadenopathy (31.6%), low IgG avidity values persisted until 5 months after the first serological examination. In all four patients with a documented chronic course of Toxoplasma infection (6 months to 8 years after the first positive serology), high IgG avidity values were observed. Among sera from 10 children and young immunocompetent adults suspected of having ocular reactivation of congenital toxoplasmosis, all had high IgG avidity values (over 40%), suggesting congenitally acquired ocular infection rather than noncongenital infection. In conclusion, the avidity of IgG is a valuable marker of recent toxoplasmosis in pregnant women, suggests the duration of invasion in patients with lymphadenopathy, and may be helpful for differentiation between reactivation of congenital infection and recently acquired ocular toxoplasmosis in immunocompetent patients. A low IgG avidity does not always identify a recent case of toxoplasmosis, but a high IgG avidity can exclude primary infections of less than 5 months' duration.

Adult↗
PubMed2002

Ocular toxoplasmosis: more than just what meets the eye.

Toxoplasma gondii is an intracellular parasite whose life cycle may include the man as an intermediate host. Close to a billion people are infected with this parasite worldwide. Ocular lesions may occur in up to 25% of those individuals infected. The infection may occur intra-uterus, through the placenta when the mother is infected during pregnancy. The parasite may also infect adults after the ingestion of contaminated food products, most notably meats or water. We have shown that although congenital and post-natal (acquired) infection results in similar ocular lesions, the immunological mechanisms behind the development of disease are different. On the other hand, contrary to published data obtained in mice, we were unable to find evidence that the T. gondii express superantigen activity for human lymphocytes. Our findings are important because they suggest that superantigen activity is not important as a pathological mechanism in human disease. Our data also suggest that, whereas the ocular lesion caused by infection after birth is the result of an excessive or dysfunctional immune response, the lesions caused by congenital infection may be due to a lack of an appropriate response to the parasite.

Animals↗
PubMed1990

Ocular toxoplasmosis.

Toxoplasmosis is a common infection of man and animals. The disease is widespread in nature and has a worldwide distribution. The infection is caused by the organism Toxoplasma gondii which was first isolated by Nicolle and Manceaux in Tunis from a North African rodent. The disease can be congenital or acquired with a variety of clinical manifestations that may range from a subclinical course to a generalized infection with fatal outcome. The ocular manifestations of the disease include sudden onset of floaters with blurring of vision. Toxoplasmosis causes a localized necrotizing retinitis with inflammation of the subjacent choroid. The retina sustains the primary injury and the major damage.

Animals↗
PubMed1982

Immunology of ocular toxoplasmosis.

Toxoplasma gondii, due to its ability to escape and modify the normal immune response, is able to survive within the retina indefinitely with the production of an occasional acute inflammatory response. The cellular immune system is mainly responsible for limiting infection. Diagnosis is based on clinical features coupled with measurements of antibody response (systemic and ocular) and cell mediated immunity. The treatment of toxoplasma chorioretinitis when indicated should be specific and immunosuppressive agents should only be used in conjunction with antibiotics to avoid dissemination of the organism.

Humans↗
PubMed2004

[Stevens-Johnson's syndrome after treatment for ocular toxoplasmosis].

CLINICAL CASE: We present a case of a 9 year-old male, who was treated with sulfadiacine, pirimetamine and folinic acid following diagnosis of an active toxoplasmic chorioretinitis. After 9 days of treatment he developed serious multiorganic mucocutaneous lesions and was diagnosed with Stevens-Johnson's syndrome. DISCUSSION: Stevens-Johnson's syndrome is a potentially fatal multiorganic disease, where drugs are clearly linked as causal factors. Fifty per cent of cases progress to severe ocular disease. The multiorganic aspect of the disease and its severity demand an early diagnosis and a multidisciplinary treatment.

Anti-Infective Agents↗
PubMed2005

The genotype of Toxoplasma gondii strains causing ocular toxoplasmosis in humans in Brazil.

PURPOSE: To determine Toxoplasma gondii genotype in scars of retinochoroiditis in humans. DESIGN: Immunopathology analysis. METHODS: DNA was isolated from retinochoroidal specimens taken from the borders of the scars from eye bank eyes as well as enucleated eyes from uveitis patients with retinochoroidal toxoplasmic scars. The SAG2 region was amplified by polymerase chain reaction and analyzed by restriction fragment length polymorphism. RESULTS: Of the 92 eyes studied, 9 had toxoplasmic scars. All of them, as well as the 2 enucleated eyes, disclosed the presence of type I parasites by the gel electrophoresis analysis of the restriction fragment length polymorphism from SAG2. CONCLUSION: These results suggest that type I strain seems to be responsible for the ocular infections in the population studied.

Animals↗
PubMed1996

The evolution of ocular toxoplasmosis in anti-interferon gamma treated mice.

PURPOSE: A clinico-histopathological cross correlation was made to study the mechanism of tissue damage in toxoplasmic retino-choroiditis during an experimental reactivation of chronic toxoplasmosis and to compare the influence of treatment by sulfadiazine on the retinal lesions. METHODS: Chronically infected Swiss-Webster mice were treated, six weeks after infection, with an avirulent strain of Toxoplasma gondii (Beverley strain) with polyclonal rabbit antibody directed against murine interferon gamma. RESULTS: Mice treated by anti-interferon gamma developed clinical lesions between day 5 and day 30 (lesions including single foci of retinochoroiditis, multifocal lesions or diffuse areas of retinal necrosis). These lesions did not arise from borders of pre-existing scars. The retina was photographed with an operating microscope fitted with a 90 diopter lens. Biological study showed a significant rise of parasitic loads in the eye and brain. Histological examination is in favour of free organism dissemination via retinal vessels; the lesions are restricted to the inner retina and ciliary body, the parasites migrated from extra-ocular cysts via the vasculature. No cysts were seen at the beginning of the study; they were found at the scar phase and appeared in mice treated with sulfadiazine. The clinical lesions were not caused by cysts but by coagulated necrosis in the retinal tissue. Parasite migration may have played a trigger role. CONCLUSIONS: The retinal damage was constituted either as a result of a toxic effect of the organisms or as a hypertensive reaction to the toxoplasma organism. The results of this study showed that the treatment with anti interferon gamma was sufficient to reactivate chronic infection.

Adrenal Cortex Hormones↗
PubMed1988

Ocular toxoplasmosis in immunosuppressed nonhuman primates.

To investigate the role of cellular immunodeficiency in recurrent toxoplasmic retinochoroiditis, six Cynomolgus monkeys (Macaca fascicularis) with healed toxoplasmic lesions of the retina were immunosuppressed by total lymphoid irradiation. Three months prior to irradiation 30,000 Toxoplasma gondii organisms of the Beverley strain had been inoculated onto the macula of eye in each monkey via a pars plana approach. Toxoplasmic retinochoroiditis developed in each animal, and lesions were allowed to heal without treatment. During total lymphoid irradiation animals received 2000 centigrays (cGy) over a 7-week period. Irradiation resulted in an immediate drop in total lymphocyte counts and decreased ability to stimulate lymphocytes by phytohemagglutinin. Weekly ophthalmoscopic examinations following irradiation failed to show evidence of recurrent ocular disease despite persistent immunodeficiency. Four months after irradiation live organisms were reinoculated onto the nasal retina of the same eye in each animal. Retinochoroidal lesions identical to those seen in primary disease developed in five of six animals. Toxoplasma organisms therefore were able to proliferate in ocular tissue following the administration of immunosuppressive therapy. This study fails to support the hypothesis that cellular immunodeficiency alone will initiate recurrent toxoplasmic retinochoroiditis. Results suggest that reactivation of disease from encysted organisms involves factors other than suppression of Toxoplasma proliferation. If reactivation occurs by other mechanisms, however, cellular immunodeficiency then may allow development of extensive disease.

Animals↗