SUMMARY We report for the first time to our knowledge the histopathological findings in the eye of a patient with type II mesangiocapillary glomerulonephritis (dense deposit disease) in which a deposit of material morphologically very similar to that which is pathognomonic for the disease in the kidney was demonstrated in Bruch's membrane. The nature of the deposit in the renal lesion is unknown but is considered to represent a structural alteration secondary to a reaction with anticomplement antibody. Clinically the fundus appearance resembled that seen in drusen.

To determine how subcomponents of ERMs change with time we have undertaken an immunohistochemical study of (1) various subpopulations of cells (including glia and RPE) and extracellular matrix constituents (collagen types I to IV and the glycoproteins fibronectin and laminin) in surgically excised specimens, and (2) a correlation between the cellular and extracellular components of the membranes. We restricted this investigation to PVR membranes (to minimise the effects of aetiological factors on membrane content). Relationships between the cellular and extracellular components of the specimens were recorded from comparisons of immunostained sequential ERM sections. Both intra-and extracellular collagens and glycoproteins may show immunoreactivity,39 but we did not attempt to quantitate immunolabelling at either of these sites. Materials and methods

Unilateral corneal epithelial inclusion cysts are recorded in a series of 16 dogs. The cysts were not congenital, there was no breed incidence, and in 11 patients there was history of corneal trauma or ulceration before cyst formation. There was some variability in clinical presentation, and sight was affected in six dogs. Fifteen patients were treated successfully by superficial keratectomy without cyst recurrence.

SUMMARY Examination of the retinal tissues obtained at necropsy from a 14-year-old boy with Kearns-Sayre syndrome showed marked photoreceptor and pigment epithelial cell loss in the retinal periphery and around the optic nerve head. Electron microscopy of surviving retinal pigment epithelial (RPE) cells indicated a loss of apical microvilli and basal infoldings. The RPE was unusually devoid of melanosomes and showed no evidence of phagocytosis of photoreceptor debris. The cytoplasm of the RPE contained numerous, often enlarged, mitochondria. These structural changes suggested that a breakdown in the energy dependent interrelationships between the RPE and the photoreceptor layer was responsible for the outer retinal degeneration. The finding of numerous macrophages in the subretinal space suggests a secondary inflammatory component in the retinal degeneration.

SummaryOnchocerciasis (river blindness) is a major blinding disease in Africa, Central America, and South America. Loss of vision can be due to corneal change, optic atrophy, or chorioretinal disease. It has been suggested that autoimmunological reactions resulting from crossreactivity between parasite antigens and components of eye tissues contribute to development of ocular pathology. Using sera collected from onchocerciasis patients as a screening reagent, a cDNA clone (Ov39) has been isolated from a Xgt11 expression library of Onchocerca volvulus . This antigen exhibits immunological crossreactivity with a component of retinal pigment epithelium cells (RPE).Antiserum raised against this recombinant peptide immunoprecipitates a 22,000 M, antigen of adult O volvulus and recognizes a 44,000 M component of bovine RPE by Western blotting. A 44,000 Mr antigen of cultured human RPE metabolically labeled with 35S-methionine can be immunoprecipitated with the same antiserum . An antigen of the same size is recognized by a rabbit antiserum raised against whole Q volvulus extract . Immunocytochemical studies on cryostat sections of the bovine eye using the antirecombinant sera localizes this antigen to the RPE. 0 nchocerca volvulus is a filarial nematode and the causative agent of onchocerciasis (river blindness) . The clinical manifestations ofeye disease in onchocerciasis have been well described (1-4) and include punctate keratitis, sclerosing keratitis, iridocyclitis, optic neuritis, optic nerve atrophy, and chorioretinitis. Inflammatory responses directed against dead microfilariae may explain development ofpathological changes in the anterior segment (5, 6), however, the aetiology of lesions in the posterior segment is unclear. In the'case of degenerative chorioretinitis, migrating microfilariae (7, 8) and direct interaction ofcells of the immune system with microfilariae, accompanied by infiltrate oflymphocytes and plasma cells, have been implicated in pathogenesis (discussed by Donnelly et al. [9]). In addition, lymphocyte-derived chemotactic factors and direct chemotactic effects of microfilarial excretions/secretions may also have a role in pathogenesis (10). More recently, Vingtain et al. (11) have provided evidence to support the idea that autoantibodies may play a significant role in retinal damage. These investigators demonstrated the presence of antibodies with specificity for bovine retinal S antigen and human retinal extract in onchocerciasis patients presenting with chorioretinitis. Van der Lelij et al. (12) extended these observations through experiments using purified human S antigen and interphotoreceptor retinoid binding protein (IRBP) .t High levels of specific antibody were found in onchocerciasis patients, but these studies failed to reveal an association with chorioretinitis. In addition, Chan et al. (13) demonstrated the presence of autoantibodies in infection sera that could not be absorbed with either S antigen or IRBP; rather, these antibodies were directed against the inner retina, inc...