Abstract
Fatal Type I pneumococcal meningitis may be produced in rabbits by intracisternal injection of pneumococci; when of high virulence, the rabbit does not tend to localize them in the meninges, but an early septicemia results in death. Active or passive immunization previous to intracisternal infection inhibits septicemia partially and permits development of reactional processes in the meninges; it also retards the meningeal disease, but the retardation is not correlated with presence of agglutinins in spinal fluid at time of infection. Rapidity of production of meningitis is influenced by phase of growth and growth activity of the culture used. In the partially immune rabbit the meningeal spaces constitute a relatively non-immune reservior, constantly feeding the blood stream and breaking down systemic resistance. Intrathecal serum treatment causes rapid agglutination and phagocytosis of pneumococci, and has very rarely, possibly, resulted in cure. Phagocyted pneumococci stained supravitally take up the neutral red stain and are therefore probably injured. The treatment employed subsequent to infection only slightly prolonged life in the majority of cases but retarded septicemia; it improved the cellular reactional processes in the meninges. The location of pneumococci in the rabbit precludes complete contact with serum introduced intrathecally, and these locations provide isolated foci from which organisms may reinfect the meningeal spaces. In recovered rabbits, postmeningeal symptoms, weakness, ataxia, nystagmus, and paralyses arise. There appears to be some objective evidence of benefit from serum therapy; rabbits are too susceptible, however, and conditions too artificial to admit of definite conclusions. Rough Type I pneumococci introduced in large quantity cisternally may kill and may be recovered from spinal fluids 24 hrs. after infection. In a series of 11 passages, no reversion to smooth type occurred. In. all animals injected with rough forms, transient bacteremia resulted.

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