Meningococcemia pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Pathophysiology
- Transmission through respiratory secretions from a nasopharyngeal carrier case-patient.
- Shock is due to lipooligosaccharide which is a potent toxin. This toxin initiates release of inflammatory cytokines, reactive oxygen radicals, prostaglandins, arachidonic acid, complement activated products, platelet aggregating factor, and perhaps nitric oxide.
- The bacteria attach to and multiply on the mucosal cells of the nasopharynx.
- In a small proportion (less than 1%) of colonized persons, the organism penetrates the mucosal cells and enters the bloodstream.
- The bacteria spread by way of the blood to many organs. In about 50% of bacteremic persons, the organism crosses the blood–brain barrier into the cerebrospinal fluid and causes purulent meningitis. An antecedent upper respiratory infection may be a contributing factor.