Pathogenesis of meningitis caused by Streptococcus suis type 2.

The neuraxes of 26 pigs inoculated intravenously with a pathogenic isolate of Streptococcus suis type 2 and killed 17-47 h later were examined using histologic and scanning microscopic techniques. The only pathologic lesions detected in all pigs were associated with the choroid plexus: disruption of the plexus brush border, a decrease in the number of Kolmer cells, and exudation of fibrin and inflammatory cells into the ventricles. Lesions affecting the cerebral and choroid plexus endothelium, such as vasculitis, were not detected. Intracellular bacteria were demonstrated in the parenchyma of the choroid plexus, in the ventricular exudate, and within peripheral blood monocytes. Separate studies found that circulating monocytes containing phagocytosed bacteria-sized particles migrated into the cerebrospinal fluid compartment with the choroid plexus acting as a major site of cellular ingress. These observations support the concept that in the pathogenesis of meningitis, bacteria may gain access to the cerebrospinal fluid compartment in association with monocytes migrating along normal pathways.