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Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease, the exact etiology of which is unknown. It is characterized by the production of pathological autoantibodies which adhere to cellular surfaces or form immune complexes which deposit in tissue, leading to end-organ damage via inflammatory mechanisms including complement activation. SLE may manifest itself in any organ system. In the eye, keratoconjunctivitis sicca is the most common finding. Other ophthalmic sites of involvement include the cornea, conjunctiva, episclera, sclera, uveal tract, retina, vasculature, optic nerve, and orbit. Therapy varies based on the disease manifestation and severity.

Objective To evaluate whether an intact respiratory burst exists within the orbit of diabetics with rhinocerebral mucormycosis. Methods Immunohistochemical detection of nitrotyrosine in the orbital tissue of diabetics requiring exenteration due to rhinocerebral mucormycosis. Nitrotyrosine is the stable product of the nitration of tyrosine residues by peroxynitrite. Peroxynitrite is a potent oxidant produced by the combination of superoxide and nitric oxide during the respiratory burst. Results Four specimens were analyzed. All showed focal areas of specific staining against nitrotyrosine of the walls and internal structures of fungal organisms. Conclusions An intact respiratory burst is present in the orbit of diabetics during infection with rhinocerebral mucormycosis. Possible mechanisms of peroxynitrite's microbicidal effects and reasons for a deficiency in diabetics are discussed.

Previous studies of cytomegalovirus (CMV) retinitis have failed to definitively explain the exact mechanism by which CMV gains access to and initiates infection in the retina. Proposed theories have included leakage of the virus through vessels with altered permeability, with subsequent infection of surrounding glial cells. In an attempt to shed further light on this subject, a histopathologic examination of 30 autopsy eyes from patients with known systemic CMV disease was carried out using light microscopy, immunohistochemical and immunofluorescent techniques, and in-situ hybridization. Dual-staining methods were used to identify the exact cell type showing the presence of CMV antigens, namely vascular endothelial cells, glial cells, neuronal cells, and/or leukocytes. In those eyes with CMV retinitis, the sites of full-thickness retinal necrosis revealed viral presence mostly within Müller cells and perivascular glial cells, with focal areas of positive staining within retinal pigment epithelial cells (RPE) and neuronal cells. The retinal capillaries were devoid of endothelial cells in these areas. Adjacent to regions of full-thickness necrosis, some vessels showed the presence of a viral antigen within the endothelial cells. These findings suggest that retinal vascular endothelial cells can be infected with CMV. It can further be hypothesized that infection of vascular endothelial cells leads to infection of the surrounding glial and neuronal cells, with eventual spread to the RPE. Endothelial cells might not be present in areas of full-thickness necrosis due to mechanical forces from adjacent blood flow resulting in the sloughing of these cells.

The diagnosis of Vogt-Koyanagi-Harada syndrome is hampered by its variable manifestations and the lack of unique ancillary and laboratory findings. In this study, the diagnostic criteria established in 1978 by the American Uveitis Society (AUS) are retrospectively analyzed via their application to a population of 71 consecutive patients, using only those features present at the initial evaluation. All patients were previously diagnosed with Vogt-Koyanagi-Harada syndrome based on the clinical features and course of the disease combined with fluorescein angiography with or without ultrasonography in selected cases. Mean age of all patients was 36.7 years +/- 15.1 years. Fifty (70%) were female and 45 (65%) were Hispanic. Patients presenting acutely, subacutely, and in the chronic stages met the AUS criteria for Vogt-Koyanagi-Harada syndrome in 56%, 48%, and 58% of cases, respectively. Allowance for variation in features, incomplete cases, and modification of the disease by treatment might increase the sensitivity of the criteria. While diagnostic criteria in general are useful for establishing the likelihood that a patient has a disease, the current AUS criteria for the diagnosis of Vogt-Koyanagi-Harada syndrome do not seem adequate.