Clinical pathophysiology of meningitis

Meningococcal meningitis generally has a better prognosis than septicaemia. Meningococci reach the brain from the bloodstream, implying that the patient's immune response has prevented bacterial proliferation in the blood and not suffered overwhelming sepsis. This is because organisms are handled differently in these patients, which is probably due to differences in their inflammatory response to infection as well as different bacterial characteristics.

Deaths do occur, however due to the severity of the inflammatory process within the brain.

Once bacteria penetrate the blood-brain barrier, endotoxin and inflammatory mediators initiate a CSF inflammatory response, causing leakage of protein and fluid out of the cerebral vasculature. In addition, the processes delineated in septicaemia occur in brain blood vessels, causing cerebral oedema and cerebral vascular thrombosis. As a consequence there is an increase in brain water content and an increase in intracranial pressure. Both the increased pressure and thrombosis may lead to a reduction in cerebral perfusion, and consequently cerebral infarction and sometimes brain death.



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