Penetration of the bloodbrain barrier

Once in the bloodstream, the invading organism may either be neutralized by the combined action of circulating antibacterial factors, including antibodies, complement proteins, and phagocytic cells, or, for reasons which are not yet fully understood, may survive and proliferate in the bloodstream to initiate the bacteremic stage of the illness.

Most episodes of meningitis arise by hematogenous spread of the causative organism, with a primary bacteremia and secondary focal infection of the meninges by seeding. The mechanisms by which circulating organisms penetrate the blood-brain barrier and seed the cerebrospinal fluid remain unclear. What does appear clear, however, is that a high-grade bacteremia is necessary, with more than 102 organisms/mm3 of blood to enable meningeal seeding. The organisms which cause meningitis appear to exhibit tropism for the meninges. This may be partly due to bacterial adhesive structures such as fimbriae which bind the circulating bacteria to receptors on the choroid plexus and cerebral capillary endothelial cells, thus facilitating bacterial translocation into the cerebrospinal fluid.

Other organisms, particularly those which may proliferate in the intracellular environment, such as the mycobacteria (including Mycobacterium tuberculosis) and salmonellae, may enter the cerebrospinal fluid despite having been phagocytosed by circulating monocytes or polymorphs. It is thought that these organisms may cause meningitis by entering the cerebrospinal fluid by normal white cell trafficking.

After penetrating the blood-brain barrier and entering the subarachnoid space, bacterial multiplication may proceed rapidly as the cerebrospinal fluid is a relatively poor immune environment. The cerebrospinal fluid contains low concentrations of specific antibody and complement components, and thus has a poor capacity for opsonization and bactericidal activity. In addition, bacterial capsular polysaccharide is antiphagocytic.

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