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Association of Virulence Mechanisms with Specific Meningococcal Infections Specific disease manifestations of meningococcal infections have specific virulence and pathogenic mechanisms, as described below for fulminant meningococcemia and meningitis. Fulminant Meningococcemia Purpura Fulminans Fulminant meningococcemia is perhaps the most rapidly lethal form of septic shock experienced by humans. It differs from most other forms of septic shock by the prominence of hemorrhagic skin lesions (petechiae, purpura; see Fig. 52-5) and the consistent development of DIC. The dominant proinflammatory molecule in the meningococcal cell wall is the endotoxin or LOS, and the outer membrane that contains it is poorly tethered to the underlying peptidoglycan | Chapter 136. Meningococcal Infections Part 4 Association of Virulence Mechanisms with Specific Meningococcal Infections Specific disease manifestations of meningococcal infections have specific virulence and pathogenic mechanisms as described below for fulminant meningococcemia and meningitis. Fulminant Meningococcemia Purpura Fulminans Fulminant meningococcemia is perhaps the most rapidly lethal form of septic shock experienced by humans. It differs from most other forms of septic shock by the prominence of hemorrhagic skin lesions petechiae purpura see Fig. 52-5 and the consistent development of DIC. The dominant proinflammatory molecule in the meningococcal cell wall is the endotoxin or LOS and the outer membrane that contains it is poorly tethered to the underlying peptidoglycan. This structural peculiarity seems to account for the fact that meningococci shed LOS-containing membrane blebs as they grow. The bacteria can multiply to very high concentrations in the blood. The concentrations of endotoxin detected in the blood of patients with fulminant meningococcemia are 10- to 1000-fold higher than those found in the blood of patients with bacteremia due to other gram-negative bacteria. The bacteria and endotoxin-containing blebs stimulate monocytes neutrophils and endothelial cells which then release cytokines and other mediators that can activate many distant targets including other leukocytes platelets and endothelial cells. In addition meningococci can invade the vascular endothelium. When activated the endothelium produces molecules that can be procoagulant as well as adhesive for leukocytes. Patients with fulminant meningococcemia usually have extremely high blood levels of both proinflammatory mediators i.e. TNF-a IL-1 interferon Y IFN-y and IL-8 and anti-inflammatory mediators i.e. IL-1 receptor antagonist IL-1Ra soluble IL-1 receptors soluble TNF-a receptors and IL-10. The plasma of patients with meningococcal shock can decrease the responses of normal .
