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Uniformly severe corneal infections were produced in guinea pigs by intracorneal injection of about 10 viable Pseudomonas aeruginosa. After a brief lag period, multiplication of bacteria was rapid, reaching geometric means of 280,000 after 24 hr and of 5 million after 48 hr. Within 8 hr after inoculation, polymorphonuclear leukocytes (PMNs) began to infiltrate the anterior two thirds of the stroma. Stromal cells adjacent to the injection site became necrotic and appeared to be engulfed by PMNs. By 14 to 16 hr, an abscess containing a dense aggregate of PMNs and multiplying bacteria developed in the central stroma. By 16 to 24 hr, collagen breakdown was apparent within and around the abscess. Ultrastructural evidence of collagen breakdown included loss of intact collagen fibrils, tactoid formation, and accumulation of amorphous electron-dense material. The area of liquefactive necrosis gradually enlarged, and many corneas perforated after 3 to 4 days. Because the course of infection is highly reproducible, this model should prove useful for many studies of experimental Pseudomonas keratitis.

Uniformly severe corneal infections were produced in rabbits by intracorneal injection of a few viable Pseudomonas aeruginosa. The bacteria multiplied rapidly, and within 24 hr, about 10 million organisms were present. The numbers remained stable thereafter. Polymorphonuclear leukocytes (PMNs) began to infiltrate peripheral stroma 24 hr after inoculation. By 32 hr, ring-shaped dense accumulations of PMNs were apparent in the anterior stroma with moderate stromal edema. By 48 hr, the anterior one third of central stroma was severely involved with abscess formation and loss of epithelium, and PMNs had invaded full corneal thickness. The area of liquefactive necrosis eventually involved the entire cornea from limbus to limbus, and collagen staining was lost. Transmission electron microscopy revealed the accumulation of small electron-dense particles in association with collagen fibrils and degranulating PMNs.

Vitamin A-deficient rabbits were used to evaluate the role of secondary bacterial infection in the development of keratomalacia and to describe the resultant clinical and morphologic alterations. The conjunctival sacs of vitamin A-deficient rabbits at different stages of corneal involvement were inoculated with Pseudomonas aeruginosa topically. Approximately two weeks after inoculation, corneal ulceration with stromal melting developed in one of three eyes with severe punctate keratitis and in four of seven eyes with xerosis. Ulceration did not develop in any of the eight eyes with early epithelial graying or mild punctate keratitis. Inflammatory cells (primarily polymorphonuclear leukocytes) infiltrated the anterior corneal stroma of infected corneas. Liquefaction of collagen was observed in association with bacteria alone, as well as in association with polymorphonuclear leukocytes. No signs of infection were observed after conjunctival inoculation of Pseudomonas in the eyes of nine control rabbits.