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Four siblings in an East Indian family showed typical ophthalmoscopic findings of toxoplasmic retinochoroiditis. Serologic data confirmed exposure to Toxoplasma gondiiand the results of other tests excluded other etiologic agents. Three siblings had documented episodes of ocular inflammation consistent with recurrent toxoplasmic retinochoroiditis. The fourth sibling developed a de novo lesion following an illness consistent with systemic toxoplasmosis.

Anterior radial keratotomy was performed on nine Green monkey eyes. Four of these eyes received subconjunctival corticosteroid injections immediately after surgery and three times thereafter at three-week intervals. Two eyes received subconjunctival physiologic salt solution injections on the same schedule. Three eyes received no injections after surgery. Although endothelial cell loss in the first week after surgery was reduced in the drug-treated eyes, there were no statistically significant differences in cell densities at nine months after surgery. Corticosteroid therapy after anterior radial keratotomy appeared to confer no long-range benefits in terms of the numbers of corneal endothelial cells in these primate eyes.

The extent of visual function loss from nuclear cataractous change can be estimated by observing the extinction of blue light compared to white light as a function of saggital lens depth in standard slit lamps. Apparent extinction (loss of transmissivity) of 50% or more of the depth of the lens in blue light of maximal intensity compared to white light at minimal intensity is associated with marked visual loss. However, this transmissivity ratio of 0.5 or less also applies if light intensity remains constant and the blue filter is simply moved in and out of the light beam. Therefore, if 50% or more of the lens appears dark to blue-filtered light, nuclear changes have significantly decreased effective visual acuity. Relative blue-light extinction associated with nuclear change that may be amenable to surgical correction can thus be distinguished from the extinction effect caused by age alone.

Seventeen patients (ten women and seven men, 23 to 72 years old) with stromal herpetic disease were treated with topical and oral acyclovir for 14 days. Of the 12 patients with disciform edema, five showed minimal improvement, four showed no change, and three showed worsening of their disease. Of the five patients with necrotizing stromal keratitis, one improved, one showed no change, and three became worse. The patients who had been treated with corticosteroids previously had a statistically significantly worse outcome than those who had not been so treated. One patient with necrotizing stromal keratitis showed virus particles in tissue specimens obtained by superficial lamellar keratectomy. Thus, acyclovir was not effective in the treatment of disciform edema or necrotizing stromal keratitis. Further studies are needed to ascertain whether the drug is therapeutically ineffective or whether acyclovir did not reach the stroma in amounts sufficient to affect the course of stromal disease in the human eye.