Late-onset Moraxella catarrhalis endophthalmitis after filtering surgery.

We describe a young man in whom endophthalmitis caused by Moraxella catarrhalis developed 5 years after glaucoma filtering surgery. The infection responded to treatment with broad-spectrum antibiotics, and 2 months after presentation the visual acuity had returned to 20/50. To our knowledge this is the first report of late-onset endophthalmitis due to M. catarrhalis complicating glaucoma filtering surgery.

Suppression of corneal neovascularization with cyclosporine.

We sought to determine if cyclosporine, which has been shown to suppress corneal allograft rejection, could also suppress corneal neovascularization induced by interleukin 2. Thirty A/J mice were treated with daily intramuscular injections of cyclosporine (25 mg/kg in olive oil) for 3 days before and 2 weeks following the intrastromal injection of 0.5 microL (5 IU) of recombinant mouse interleukin 2. Controls received intramuscular injections of olive oil. The mean area of corneal neovascularization 4, 8, and 12 weeks after injection was 9.2, 9.1, and 9.2 mm2, respectively, in controls, and 5.0, 5.2, and 5.2 mm2 in cyclosporine-treated mice (P less than .02; Student's t test). Cyclosporine causes a significant reduction in interleukin 2-induced corneal neovascularization that may, in part, account for its ability to prolong corneal allograft survival in high-risk cases.

Keratoconus and Fuchs' corneal endothelial dystrophy in a patient and her family.

A 44-year-old patient with bilateral keratoconus and bilateral Fuchs' dystrophy underwent penetrating keratoplasty. Examination of the patient's family revealed keratoconus in the patient's son and central guttata and abnormal endothelial cells in the patient's mother and daughter. Histopathologic evaluation of the corneal button demonstrated a thinned central epithelium and folds and keratocytes in Bowman's layer consistent with keratoconus. Central guttata, subepithelial bullae, and a decreased number of endothelial cells, consistent with Fuchs' endothelial dystrophy, were also seen. This case demonstrates that two distinct familial corneal diseases can occur in the same patient. Although one cannot conclude inheritance patterns based on this limited evaluation, the findings in this family support previous observations that keratoconus can be familial, and that Fuchs' corneal dystrophy has a female predilection with an autosomal-dominant inheritance pattern.

Cataracts induced by microwave and ionizing radiation.

Microwaves most commonly cause anterior and/or posterior subcapsular lenticular opacities in experimental animals and, as shown in epidemiologic studies and case reports, in human subjects. The formation of cataracts seems to be related directly to the power of the microwave and the duration of exposure. The mechanism of cataractogenesis includes deformation of heat-labile enzymes, such as glutathione peroxide, that ordinarily protect lens cell proteins and membrane lipids from oxidative damage. Oxidation of protein sulfhydryl groups and the formation of high-molecular-weight aggregates cause local variations in the orderly structure of the lens cells. An alternative mechanism is thermoelastic expansion through which pressure waves in the aqueous humor cause direct physical damage to the lens cells. Cataracts induced by ionizing radiation (e.g., X-rays and gamma rays) usually are observed in the posterior region of the lens, often in the form of a posterior subcapsular cataract. Increasing the dose of ionizing radiation causes increasing opacification of the lens, which appears after a decreasing latency period. Like cataract formation by microwaves, cataractogenesis induced by ionizing radiation is associated with damage to the lens cell membrane. Another possible mechanism is damage to lens cell DNA, with decreases in the production of protective enzymes and in sulfur-sulfur bond formation, and with altered protein concentrations. Until further definitive conclusions about the mechanisms of microwaves and ionizing radiation induced cataracts are reached, and alternative protective measures are found, one can only recommend mechanical shielding from these radiations to minimize the possibility of development of radiation-induced cataracts.