The data presented indicate that in experimental infections of the mouse cornea, toxin A of Pseudomonas aeruginosa contributes to the organism's pathogenicity, whereas active elastase may not be required. After traumatization, corneas were infected with wild-type parental toxin A-producing strains, two toxin A-deficient mutants (Tox-), or an elastase mutant. The infections produced by both Tox- mutants were less severe than infections produced by their parental strains. Furthermore, the Tox- mutants were not able to persist in the eyes as long as their parental strains. Addition of subdamaging doses of exogenous toxin A to eyes infected with the Tox- mutant PA103-29 significantly increased is virulence. The course of infection and the resulting corneal damage produced by the elastase mutant were indistinguishable from those of its parental strain.