Immunopathology of acute experimental histoplasmic choroiditis in the primate.
(41/59)
The immunopathologic features of experimental acute histoplasmic choroiditis were studied in the nonhuman primate. Using an indirect immunoperoxidase technique, a panel of hybridoma-derived anti-human monoclonal antibodies, recognizing distinct lymphoid cell and macrophage surface antigens, have been adapted for use in the primate system. Twenty-two individual foci of histoplasmic choroiditis from five eyes were studied at time periods from 20 to 60 days post intracarotid injection of yeast phase Histoplasma capsulatum. A mononuclear and granulocytic cell infiltration was seen in all lesions. The predominant cell type was the CAPPEL+ T lymphocyte (suppressor/cytotoxic subset). Other cell types found in smaller numbers were OKT4+ T cells (helper/inducer subset), OK7+ (peripheral B lymphocytes), IgD+ (mantle B cells) and OKM1+ cells (macrophages and polymorphonuclear leukocytes). Herein, we present immunopathologic data on the acute phase of experimental ocular histoplasmosis. (+info)
Ocular toxoplasmosis in immunosuppressed nonhuman primates.
(42/59)
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. (+info)
Retinal pigment epitheliopathy and neuroretinal degeneration in ascarid-infected eyes.
(43/59)
The generalized choroidal and retinal response to a focal nonreplicating infection of the eye with ascarid larvae was examined in an animal model. Intravitreal injection of Ascaris suum larvae in guinea pigs induced a diffuse eosinophilic choroiditis, retinal pigment epitheliopathy and neuroretinal degeneration, distant from focal reactions about larvae. As the choroiditis progressed, inflammatory cells separated the choriocapillaris from Bruch's membrane, and the endothelial cells lost their fenestrations. Focal disruption of the elastic and outer collagenous layers of Bruch's membrane occurred, but inflammatory cells rarely invaded the retina. Progressive generalized degenerative and proliferative RPE changes produced a multilayered RPE with loss of cell polarity, RPE basal infoldings and apical microvilli, formation of multiple giant cystic spaces, and proliferation of subretinal fibroblasts. Early loss of photoreceptor outer segments progressed to a generalized disruption of the outer neural retina and cystoid retinal degeneration. Eosinophil mediators and alterations of the choriocapillaris may contribute to the generalized progressive retinal degeneration distant from a parasite larva in ascarid-infected eyes. (+info)
Relapse infection after chemotherapy in goats experimentally infected with Trypanosoma brucei: pathological changes in central nervous system.
(44/59)
Fourteen goats were experimentally infected with Trypanosoma brucei with the following results: Four animals became terminally ill 24 to 47 days after inoculation of trypanosomes and were killed for necropsy. A second group of four goats became sick, had signs of systemic trypanosomiasis, were treated with diminazine aceturate (Berenil) and recovered showing no signs of disease over observation periods of 151 to 163 days. A third group of six goats, were treated with Berenil and temporarily recovered and in 60 to 79 days after therapy; four of these goats underwent relapse infection characterized by severe central nervous system (CNS) disease. Two of these goats were necropsied 45 days after chemotherapy, before clinical signs were evident, to show early neurological lesions. In group 3 (the relapse group), the microscopic changes became more severe as relapse infection progressed. Microscopically, the central nervous system lesions were edema, hyperemia, and infiltration of plasma cells, small lymphocytes, and some macrophages in the leptomeninges, choroid plexus, and brain parenchyma. Relapse infection is discussed from the standpoint of an occult phase of the disease where parasites are protected from the effects of trypanocidal drugs by the blood-brain barrier. (+info)
Schistosomotic choroiditis. I. Funduscopic changes and differential diagnosis.
(45/59)
This paper presents the results of biomicroscopy and funduscopy on five patients with hepatosplenic schistosomiasis mansoni. Fluorescein angioretinography was performed on two patients. All cases showed yellowish white multiple billateral nodules of various sizes, located in the choroidal plane. The nature and differential diagnosis of these nodules is discussed, and the suggestion is made that they represent cases of schistosomotic nodular choroiditis. (+info)
Schistosomotic choroiditis. II. Report of first case.
(46/59)
The first case of granulomatous choroiditis produced by Schistosoma mansoni with histological confirmation is reported. The patient had the hepatosplenic and cardiopulmonary forms of the disease and presented with cerebral schistosomiasis. The funduscopic aspects of the lesion and the possible pathways taken by the parasite to reach the choroid are discussed. (+info)
Oculokinetic perimetry: a simple visual field test for use in the community.
(47/59)
A method of visual field examination is described which enables an unsupervised person to carry out self-assessment using only a paper test chart, a record sheet, and a pencil. It is entitled 'oculokinetic perimetry' because it is the subject's eye that moves and not the test target. By providing non-ophthalmic health care workers with a simple means of performing perimetry in the community, and by allowing susceptible people to carry out self-assessment of the visual fields at home, this test should facilitate the detection and management of glaucoma, especially in underdeveloped countries. (+info)
Juxtapapillary choroiditis in association with rising antichlamydial antibody.
(48/59)
We present the case of a 21-year-old girl with a uniocular juxtapapillary choroiditis. During the course of her illness the titre of antichlamydial IgG increased from 1/32 to 1/4096 against Chlamydia trachomatis TRIC serotypes J and C, and antichlamydial IgM appeared in her blood. Toxoplasma dye test was positive at a level of 1/128 but no increase in the titre of antibody was detected during the course of her infection. The relevance of these findings to her ocular lesion is discussed. (+info)