Twenty-nine eyes, representing an infection rate of 4.9%, developed corneal ulcers following corneal transplant surgery; 26 with available data are presented. All occurred in the graft or at the wound margin. The median postoperative time to ulcer development was 5.5 months. All eyes were on topical steroids when the ulcer developed. Other associated factors were: loose sutures, bandage lenses and eyes grafted for herpes simplex keratitis. Ninety percent of the ulcers had one or more of these factors. Positive cultures for organisms were obtained in 75% and positive gram stain in 68% of the ulcers. Nine genera of bacteria were cultured; S. epidermidis, S. pneumoniae, P. aeruginosa and Corynebacterium were the most common organisms. Ninety-five percent of the bacteria tested were sensitive to gentamicin. Visual reduction occurred in 46% of the cases overall; herpetic corneas had an 88% incidence of visual loss.

The normal human corneal endothelial monolayer maintains stromal water equilibrium and thus, transparency, by means of a pump-leak mechanism. Water leaks into the stroma through non-tight lateral cell junctional complexes and is drawn out by an energy dependent cell membrane ion pump. We investigated the histochemical localization of cytochrome oxidase activity (CO), an important energy-deriving mitochondrial enzyme in dysfunctional corneas with Fuchs' endothelial dystrophy (ED), which is a regionally distributed disease. Keratoconus corneas were used as controls for functional control endothelium. In the central area of the corneal button, decreased CO activity was demonstrated which correlated clinically with central corneal edema. This reflects decreased metabolic activity and/or decreased numbers of mitochondria in the attenuated dysfunctional cells. In the mid-periphery, CO activity was increased in the cellular rosettes surrounding guttata, which may be related to increased synthesis of abnormal Descemet's membrane and guttata. Peripherally, the large polygonal cells resembled functional endothelium in their morphology and CO activity. We have, therefore, demonstrated regional differences in energy metabolism in endothelium from Fuchs' ED patients which may be related to decreased numbers of mitochondria in the dysfunctional cells, and/or to synthesis of abnormal Descemet's membrane material.

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