ROLES OF AUTOLYSIN AND PNEUMOLYSIN IN MIDDLE-EAR INFLAMMATION CAUSED BY A TYPE-3 STREPTOCOCCUS-PNEUMONIAE STRAIN IN THE CHINCHILLA OTITIS-MEDIA MODEL

Streptococcus pneumoniae cell wall and pneumolysin are important contr ibutors to pneumococcal pathogenicity in some animal models, To furthe r explore these factors in middle ear inflammation caused by pneumococ ci, penicillin-induced inflammatory acceleration was studied by using three closely related pneumococcal strains: a wild-type 3 strain (WT3) , its pneumolysin-negative derivative (P-1), and its autolysin-negativ e derivative (A-1), Both middle ears of chinchillas were inoculated wi th one of the three pneumococcal strains, During the first 12 h, all t hree strains grew in vivo at the same rate, and all three strains indu ced similar inflammatory cell responses in middle ear fluid (MEF). Pro caine penicillin G was given at 12 h to one-half of the animals in eac h group, and all treated chinchillas had sterile MEF at 24 h, Penicill in significantly accelerated MEF inflammatory cell influx into WT3- an d P-1-infected ears at 18 and 24 h in comparison with the rate for pen icillin-treated A-1-infected ears. inflammatory cell influx was slight ly, but not significantly, greater after treatment of WT3 infection th an after treatment of P-1 infection, Interleukin (IL)-1 beta and IL-6, but not IL-8, concentrations in MEF at 24 h reflected the penicillin effect on MEF inflammatory cells; however, differences between treatme nt groups were not significant. Results suggest that pneumococcal otit is media pathogenesis is triggered principally by the inflammatory eff ects of intact and lytic cell wall products in the middle ear, with at most a modest additional pneumolysin effect. Investigation strategies that limit the release of these products or neutralize them warrant f urther investigation.