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 mu rine cornea to infection with an ocular strain of P. aeruginosa isolat ed from a subject with an inflammatory adverse response to contact len s wear termed GLARE. Although this bacterium was isolated in confluenc y (greater than 2000 cfu lens(-1)) from the lens at the time of the in flammatory 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 epi thelial cell basal lamina and into the superficial stroma. The GLARE s train was found to persist (viable bacteria could be cultured from cor neal homogenates) up to 8 hr, as did the virulent control strain ATCC 19660. At 24 hr, only ATCC 19660 could be cultured, indicating an inab ility of the strain isolated from GLARE, Paerl, to persist in the eye consistent with the human inflammatory episode. Histological examinati on of the mouse tissue showed further differences between infection by the two strains. Infection with ATCC 19660 resulted in tissue necrosi s and a large population of polymorphonuclear leukocytes (PMNs) recrui ted to the wound site. In contrast, during infection with the GLARE st rain, PMN recruitment was reduced and temporally delayed. The GLARE st rain grew as well as ATCC 19660 in vitro but produced less protease ac tivity, in particular less elastase. The decreased PMN response and de creased protease production by the GLARE strain may have been responsi ble for the lack of ocular damage and apparent healing of the wound. P . aeruginosa strains are considered to be invasive or cytotoxic to cor neal tissue, however this strain may represent a third inflammatory ty pe consistent with its differing pathology. (C) 1998 Academic Press.