An ocular strain of Pseudomonas aeruginosa is inflammatory but not virulent in the scarified mouse model

Pseudomonas aeruginosa is the most common pathogen among contact lens-associated infections. This study; investigated the response of the murine cornea to infection with an ocular strain of P. aeruginosa isolated from a subject with an inflammatory adverse response to contact lens wear termed GLARE. Although this bacterium was isolated in confluency (greater than 2000 cfu lens(-1)) from the lens at the time of the inflammatory episode, no infection of the cornea subsequently developed. Male C57BL/6J mice (20 per strain) had their corneas scratched with a 26 gauge needle (3 parallel 1.0 mm wounds in the left eye only). The incisions were centered over the pupillary axis and penetrated the epithelial cell basal lamina and into the superficial stroma. The GLARE strain was found to persist (viable bacteria could be cultured from corneal homogenates) up to 8 hr, as did the virulent control strain ATCC 19660. At 24 hr, only ATCC 19660 could be cultured, indicating an inability of the strain isolated from GLARE, Paerl, to persist in the eye consistent with the human inflammatory episode. Histological examination of the mouse tissue showed further differences between infection by the two strains. Infection with ATCC 19660 resulted in tissue necrosis and a large population of polymorphonuclear leukocytes (PMNs) recruited to the wound site. In contrast, during infection with the GLARE strain, PMN recruitment was reduced and temporally delayed. The GLARE strain grew as well as ATCC 19660 in vitro but produced less protease activity, in particular less elastase. The decreased PMN response and decreased protease production by the GLARE strain may have been responsible for the lack of ocular damage and apparent healing of the wound. P. aeruginosa strains are considered to be invasive or cytotoxic to corneal tissue, however this strain may represent a third inflammatory type consistent with its differing pathology. (C) 1998 Academic Press.