Pathophysiology of meningococcal meningitis and septicaemia

Abstract

Neisseria meningitidis is remarkable for the diversity of interactions that the bacterium has with the human host, ranging from asymptomatic nasopharyngeal colonisation affecting virtually all members of the population; through focal infections of the meninges, joints, or eye; to the devastating and often fatal syndrome of meningococcal septic shock and purpura fulminans.

Figure 1

The inflammatory cascade in meningococcal septicaemia.

Figure 2

(A) The inflammatory, coagulation, and fibrinolytic pathways are linked at many levels, leading to organ failure and eventually death. (B) The coagulation and fibrinolytic pathways rely on the function of endothelial proteins and protein complexes. Dysfunctional regulatory mechanisms in meningococcal disease include endothelial (protein C pathway) and plasma (TFPI, antithrombin, PAI) factors.

Figure 3

Factors involved in intravascular thrombosis and purpura fulminans.