PURPOSE:To describe viral infection of the corneal endothelium in a patient with recurrent herpes simplex virus keratitis in the corneal graft.METHODS:Case report. A healthy 28-year-old man presented with necrotizing stromal keratitis and corneal perforation in the corneal graft. A second penetrating keratoplasty was performed. The corneal button was processed for histopathologic, immunohistochemical, and electron microscopic studies.RESULTS:Histopathologically, the corneal endothelium showed viral inclusion bodies. Herpes simplex virus antigens and viral particles were identified in stromal keratocytes and corneal endothelial cells.CONCLUSION:Productive herpes simplex virus infection of the corneal endothelial cells may contribute to corneal graft failure in recurrent herpes simplex virus infections.

Patient A 51-year-old male presented with multiple subcutaneous nodules in both upper eyelids. An excisional biopsy and blepharo-plasty were performed. Histopathologically, centrally located acel-lular necrotic areas of collagen fibers were surrounded by fibroblasts, epitheloid cells and giant cells. Special stains including Gram, Warthin-Starry, Gomorimethenamine silver and Ziehl-Neelsen revealed no evidence of infectious microorganisms. The eyes were otherwise unremarkable. The patient was in good health. He did not show any evidence of rheumatoid arthritis, rheumatic fever or other systemic disease. Results of laboratory studies for rheumatoid factor, antinuclear antibodies, angiotensin converting enzyme, VDRL, FTA-ABS. antistreptolysin-O, erythrocyte sedimentation rate and Immunoelectrophoresis were within normal limits. Based on the negative evaluation for systemic disease and the histopathologic appearance of the lesions, we made the diagnosis of pseudorheumatoid nodules (granuloma anulare, nodular type).

We investigated the histopathologic condition of four lenses with contusion rosette cataract by light and electron microscopy; periods between blunt trauma and cataract extraction varied from 4 months to 40 years. The initial morphologic changes appear to be the formation of intercellular vacuoles within the lens epithelium and the swelling of superficial cortical lens fibers. Signs of beginning fiber degeneration within the edematous zone include fragmentation of fiber cytoplasm into droplets and globules, formation of abnormal membrane arrangements, and enlargement of intercellular spaces. Late rosette opacities manifest as sharply demarcated layers of vacuolic degeneration in the deeper cortex. We suggest that in contusion cataract, a traumatically induced dysfunction of the lens epithelium leads to an edema of superficial cortical lens fibers that subsequently undergo degeneration and produce a localized and permanent lamellar zone of vacuolation. With time and with the formation of new clear lens cells, this layer becomes gradually compressed and displaced deeper into the cortex.

Purpose: To investigate the histopathologic causes for the most prominent clinical observations of the iris of patients with pseudoexfoliation syndrome (PXS), particularly poor mydriasis but also atrophy of the iris pigment epithelium with anterior chamber melanin dispersion, stromal atrophy, and vascular changes,Methods: Thirty-three iris specimens from patients with PXS with and without glaucoma were investigated by transmission electron microscopy with special regard to sphincter and dilator muscle tissues.Results: Pseudoexfoliation fibers were observed consistently in association with fibroblasts and melanocytes in the iris stroma, endothelial cells and pericytes of vessels, both anterior and posterior pigment epithelial cells, and muscle cells of sphincter and dilator muscles. The various cell types showed uniformly surface cell membrane excavations with PXS fibers, indicating local PXS production, Focal disintegration of the pigment epithelial layers was associated with unusual PXS material aggregations along the apical aspects of epithelial cells. Compared with age-matched control specimens, the muscle cells showed, in addition to PXS production, remarkable degenerative and atrophic changes in PXS eyes.Conclusion: The authors suggest that abnormal extracellular matrix production and/or vascular abnormalities leading to tissue hypoxia cause degenerative tissue changes and that atrophy of muscle cells might potentiate the reduction of dilating properties of the iris.