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Bacterial seeding

Bacterial seeding usually occurs by hematogenous spread. Organisms typically enter the meninges through the bloodstream, from other parts of the body. In patients without an identifiable source of infection, local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source.

Many meningitis-causing bacteria are carried in the nose and throat, often without symptoms in the carrier. Most meningeal pathogens are transmitted through the respiratory route, as exemplified by the fact that Neisseria meningitidis (meningococcus) is carried nasopharyngeally and by the nasopharyngeal colonization with Streptococcus pneumoniae (pneumococcus).

Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment, presumably by damaging mucosal defenses. Once inside the bloodstream, the infectious agent must escape immune surveillance (eg, antibodies, complement-mediated bacterial killing, and neutrophil phagocytosis). Subsequently, hematogenous seeding into distant sites occurs, including the CNS. The specific pathophysiologic mechanisms by which the infectious agents gain access into the subarachnoid space remain unclear.

Once inside the CNS, the infectious agents likely survive because host defenses (eg, immunoglobulins, neutrophils, complement components) appear to be limited in this body compartment. The presence and replication of infectious agents remain uncontrolled and incite a cascade of meningeal inflammation. This process of meningeal inflammation has been an area of extensive investigation in recent years that has led to a better understanding of meningitis pathophysiology.

Bacterial seeding results in increased permeability of the blood-brain barrier, cerebral edema, and the presence of toxic mediators in the CSF. Inflammations are characterized by polymorphonuclear cell infiltration and extensive fibrinous exudation, which extends throughout the CSF, basal cisterns, and cranial nerves. Acute leptomeningitis results in congestion and hyperemia of the pia-arachnoid and distention of the subarachnoid space by the exudates.

Once in the CSF, the paucity of antibodies, complement components, and white blood cells allows the bacterial infection to flourish. Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated events that result in increased permeability of the blood-brain barrier, cerebral edema, and the presence of toxic mediators in the CSF.

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