contrast, neither of the mutant strains deficient in protease
production (PA103-AP1 and PA103-AP2) was able to in-duce pathological changes beyond minimal corneal opacity
and neovascularization, with average corneal damage in
these groups of mice ranging from 0 to 1.5 early in infection
and resolving rapidly (Fig. 1). Infection with either of these
mutant strains resulted in essentially no permanent damage.