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Meningococcemia is notorious for evasion of the host immune system and its rapid progression to fulminant disease, and serves as a unique model for pediatric sepsis. Illness severity is determined by complex interplays among host, pathogen, and environment. The inflammatory host response, including proinflammatory and anti-inflammatory responses in innate and adaptive immunity, skews toward a proinflammatory state. This leads to endothelial dysfunction and activation of the hemostatic response, which may lead to disseminated intravascular coagulation. This article reviews the pathogenesis of sepsis, in particular the inflammatory and hemostatic response in meningococcal sepsis.
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Boeddha et al. (2020) studied this question.
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