Streptococcus pneumoniae cell wall and
pneumolysin are important contributors to pneumococcal pathogenicity in some animal models. To further explore these factors in
middle ear inflammation caused by pneumococci,
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 into
autolysin-negative derivative (A-1). Both middle ears of chinchillas were inoculated with one of the three pneumococcal strains. During the first 12 h, all three strains grew in vivo at the same rate, and all three strains induced similar inflammatory cell responses in middle ear fluid (MEF).
Procaine penicillin G was given as 12 h to one-half of the animals in each group, and all treated chinchillas had sterile MEF at 24 h.
Penicillin significantly accelerated MEF inflammatory cell influx into WT3-and P-1-infected ears at 18 and 24 h in comparison with the rate for
penicillin-treated A-1-infected ears. Inflammatory cell influx was slightly, but not significantly, greater
after treatment of
WT3 infection than
after treatment of P-1
infection.
Interleukin (IL)-1beta and
IL-6, but not
IL-8, concentrations in MEF at 24 h reflected the
penicillin effect on MEF inflammatory cells; however, differences between treatment groups were not significant. Results suggest that pneumococcal
otitis media pathogenesis is triggered principally by the inflammatory effects of intact and lytic cell wall products in the middle ear, with at most a modes additional
pneumolysin effect. Investigation strategies that limit the release of these products or neutralize them warrant further investigation.