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Pathophysiology
The brain is naturally protected from the body's immune system by a barrier the meninges create between the bloodstream and the brain. Normally, this protection is an advantage because the barrier prevents the body from attacking itself. However, in meningitis, the barrier can become a problem; once bacteria or other organisms have found their way to the brain, they are somewhat isolated from the immune system and can spread.
When the body tries to fight the infection, the problem can worsen; blood vessels become leaky and allow fluid, white blood cells, and other infection-fighting particles to enter the meninges and brain. This process, in turn, causes brain swelling and can eventually result in decreasing blood flow to parts of the brain, worsening the symptoms of infection.[7]
Depending on the severity of bacterial meningitis, the inflammatory process may remain confined to the subarachnoid space. In less severe forms, the pial barrier is not penetrated, and the underlying parenchyma remains intact. However, in more severe forms of bacterial meningitis, the pial barrier is broken, and the underlying parenchyma is invaded by the inflammatory process. Thus, bacterial meningitis may lead to widespread cortical destruction, particularly when left untreated.
Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process in bacterial meningitis and account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose in patients with this disease.
Exudates extend throughout the CSF, particularly to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resultant hearing loss), obliterating CSF pathways (causing obstructive hydrocephalus), and inducing vasculitis and thrombophlebitis (causing local brain ischemia).
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