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Critical advances in the understanding and treatment of acute bacterial meningitis follow the recognition that proteins within the bacterial cell wall are responsible for inciting the acute inflammatory response, even in the absence of viable bacteria
Although many molecules may be involved, lipopolysaccharide in the walls of gram-negative organisms and techoic acid in the walls of gram-positive microorganisms activate brain microglia, leading to a cascade of inflammatory changes resulting in cortical microvascular permeability with diffuse cerebral edema, resulting in increased intracranial pressure
Recognition of this inflammatory cascade has lead to the use of less bacteriolytic antibiotics as well as concomitant high dose corticosteroid administration during the acute phases of bacterial meningitis