CONTRIBUTION OF PNEUMOLYSIN AND AUTOLYSIN TO THE PATHOGENESIS OF EXPERIMENTAL PNEUMOCOCCAL ENDOPHTHALMITIS

Abstract

PURPOSE: To determine the contribution of pneumolysin and autolysin, two putative pneumococcal virulence proteins, to the pathogenesis of Streptococcus pneumoniae endophthalmitis. METHODS: Endophthalmitis was established in Lewis rats by intravitreal injection of pneumococcal strains at an inoculum of 10 organisms. The virulence of three closely related type 2 S. pneumoniae strains were compared: a pneumolysin-deficient derivative (PLN-A), an autolysin-deficient derivative (AL-6), and their isogenic wild-type parent (D 39). Clinical and histologic inflammation scores were compared 24 hours and 48 hours after inoculation. RESULTS: Eyes infected with PLN-A and AL-6 strains showed less anterior segment inflammation clinically at 24 hours than did eyes infected with the wild-type strain. Histologic examination at 24 hours showed significantly less corneal infiltration and vitritis and more relative preservation of retinal tissue in eyes infected with PLN-A and AL-6 strains than in eyes infected with the wild-type strain. At 48 hours, no observable differences between PLN-A and wild-type strains were present clinically or histologically. Histologically, however, the AL-6 strain caused less retinal damage than did the wild-type strain. CONCLUSIONS: Intraocular infection with pneumolysin-deficient S. pneumoniae results in less severe tissue damage in the first 24 hours of disease compared with infection with pneumolysin-producing S. pneumoniae. Autolysin-deficient S. pneumoniae shows a similar degree of attenuated virulence. Pneumolysin and autolysin may contribute to the early pathogenesis of pneumococcal endophthalmitis.