Systemic meningococcal disease

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Abstract
Neisseria meningitidis may cause clinical pictures which range from self-limiting meningococcaemia to lethal circulatory collapse. Most cases develop a distinct meningitis. The clinical pictures can now be described at a molecular level linking symptoms to biochemical events. The bacterial growth is compartmentalized, which is reflected in the levels of lipopolysaccharide and mediators in the blood and the cerebrospinal fluid. The intensity of the inflammatory response is closely associated with the clinical symptoms. Important pro-inflammatory mediators including tumour necrosis factor a, interleukin 1, interleukin 6 and interleukin 8, all participate in the inflammatory response. Anti-inflammatory principles, notably interleukin 1 receptor antagonist, interleukin 10 and soluble tumour necrosis receptors I and II, are elicited concomitantly. The contact activation system in plasma comprising the coagulation, fibrinolytic, complement and kallikrein-kinin systems are all activated in a dose-dependent manner. The underlying cause of the variable growth rate of meningococci in the circulation is presently not understood.

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