Green neutrophilic inclusions in meningococcal sepsis

2020 ◽  
Author(s):  
Louisa Shackleton ◽  
Dario Melotti ◽  
Catherine Leddy ◽  
Siobhan Glavey ◽  
Patrick Thornton ◽  
...  
Keyword(s):  
Meningococcal Sepsis

Disseminated intravascular coagulation in meningococcal sepsis

2003 ◽  
Vol 23 (03) ◽  
pp. 125-130 ◽  
Author(s):  
S. Zeerleder ◽  
R. Zürcher Zenklusen ◽  
C. E. Hack ◽  
W. A. Wuillemin
Keyword(s):  
Organ Dysfunction ◽  
Disseminated Intravascular Coagulation ◽  
Skin Necrosis ◽  
Multiple Organ ◽  
Meningococcal Sepsis ◽  
Multiple Organ Dysfunction ◽  
Intravascular Coagulation ◽  
Therapeutic Concepts ◽  
New Therapeutic Concepts ◽  
Coagulation And Fibrinolysis

SummaryWe report on a man (age: 49 years), who died from severe meningococcal sepsis with disseminated intravascular coagulation (DIC), multiple organ dysfunction syndrome and extended skin necrosis. We discuss in detail the pathophysiology of the activation of coagulation and fibrinolysis during sepsis. The article discusses new therapeutic concepts in the treatment of disseminated intravascular coagulation in meningococcal sepsis, too.

Severe, but completely reversible heart failure in an adult with meningococcal sepsis

2001 ◽  
Vol 56 (4) ◽  
pp. 255-257
Author(s):  
Kees JANSSENS ◽  
Vida FIRSOVAITE ◽  
Johan DE SUTTER
Keyword(s):  
Heart Failure ◽  
Meningococcal Sepsis

scholarly journals MyD88-Dependent Signaling Affects the Development of Meningococcal Sepsis by Nonlipooligosaccharide Ligands

2006 ◽  
Vol 74 (6) ◽  
pp. 3538-3546 ◽  
Author(s):  
Laura Plant ◽  
Hong Wan ◽  
Ann-Beth Jonsson
Keyword(s):  
Inflammatory Responses ◽  
Innate Immune ◽  
Meningococcal Sepsis ◽  
Wild Type ◽  
Microbial Infections ◽  
In The Wild ◽  
Myeloid Differentiation Factor ◽  
Dependent Pathway ◽  
Meningococcal Strain

ABSTRACT The Toll-like receptors (TLRs) and the adaptor myeloid differentiation factor 88 (MyD88) are important in the innate immune defenses of the host to microbial infections. Meningococcal ligands signaling via TLRs control inflammatory responses, and stimulation can result in fulminant meningococcal sepsis. In this study, we show that the responses to nonlipooligosaccharide (non-LOS) ligands of meningococci are MyD88 dependent. An isogenic LOS-deficient mutant of the serogroup C meningococcal strain FAM20 caused fatal disease in wild type C57BL/6 mice that was not observed in MyD88−/− mice. Fatality correlated with high proinflammatory cytokine and C5a levels in serum, high neutrophil numbers in blood, and increased bacteremia at 24 h postinfection in the wild-type mice. Infection with the parent strain FAM20 resulted in fatality in 100% of the wild-type mice and 50% of the MyD88−/− mice. We conclude that both LOS and another neisserial ligand cause meningococcal sepsis in an in vivo mouse model and confirm that meningococcal LOS can act via both the MyD88- dependent and -independent pathways, while the non-LOS meningococcal ligand(s) acts only via the MyD88-dependent pathway.

scholarly journals A Case of Meningococcal Sepsis and Meningitis with Complement 7 Deficiency in a Military Trainee

2013 ◽  
Vol 45 (1) ◽  
pp. 94 ◽  
Author(s):  
Sung Hoon Sim ◽  
Jung Yeon Heo ◽  
Eui-Chong Kim ◽  
Kang-Won Choe
Keyword(s):  
Meningococcal Sepsis

scholarly journals Does Dexamethasone Helps in Meningococcal Sepsis?

2017 ◽  
Vol 71 (3) ◽  
pp. 173 ◽  
Author(s):  
Ilir Tolaj ◽  
Hamdi Ramadani ◽  
Murat Mehmeti ◽  
Hatixhe Gashi ◽  
Arbana Kasumi ◽  
...  
Keyword(s):  
Meningococcal Sepsis

Dissecting the effects of lipopolysaccharides from nonlipopolysaccharide molecules in experimental porcine meningococcal sepsis

2010 ◽  
Vol 38 (6) ◽  
pp. 1467-1474 ◽  
Author(s):  
Bernt C. Hellerud ◽  
Erik W. Nielsen ◽  
Ebbe B. Thorgersen ◽  
Julie K. Lindstad ◽  
Anne Pharo ◽  
...  
Keyword(s):  
Meningococcal Sepsis

scholarly journals Complement Activation and Complement-Dependent Inflammation by Neisseria meningitidis Are Independent of Lipopolysaccharide

2004 ◽  
Vol 72 (6) ◽  
pp. 3344-3349 ◽  
Author(s):  
Tom Sprong ◽  
Anne-Sophie W. Møller ◽  
Anna Bjerre ◽  
Elisabeth Wedege ◽  
Peter Kierulf ◽  
...  
Keyword(s):  
Neisseria Meningitidis ◽  
Complement Activation ◽  
Oxidative Burst ◽  
Whole Blood ◽  
Meningococcal Sepsis ◽  
Necrosis Factor Alpha ◽  
Chemokine Production ◽  
Inflammatory Protein ◽  
Activation Products ◽  
Factor Alpha

ABSTRACT Fulminant meningococcal sepsis has been termed the prototypical lipopolysaccharide (LPS)-mediated gram-negative septic shock. Systemic inflammation by activated complement and cytokines is important in the pathogenesis of this disease. We investigated the involvement of meningococcal LPS in complement activation, complement-dependent inflammatory effects, and cytokine or chemokine production. Whole blood anticoagulated with lepirudin was stimulated with wild-type Neisseria meningitidis H44/76 (LPS+), LPS-deficient N. meningitidis H44/76lpxA (LPS−), or purified meningococcal LPS (NmLPS) at concentrations that were relevant to meningococcal sepsis. Complement activation products, chemokines, and cytokines were measured by enzyme-linked immunosorbent assays, and granulocyte CR3 (CD11b/CD18) upregulation and oxidative burst were measured by flow cytometry. The LPS+ and LPS− N. meningitidis strains both activated complement effectively and to comparable extents. Purified NmLPS, used at a concentration matched to the amount present in whole bacteria, did not induce any complement activation. Both CR3 upregulation and oxidative burst were also induced, independent of LPS. Interleukin-1β (IL-1β), tumor necrosis factor alpha, and macrophage inflammatory protein 1α production was predominantly dependent on LPS, in contrast to IL-8 production, which was also markedly induced by the LPS− meningococci. In this whole blood model of meningococcal sepsis, complement activation and the immediate complement-dependent inflammatory effects of CR3 upregulation and oxidative burst occurred independent of LPS.

CD46 accelerates macrophage-mediated host susceptibility to meningococcal sepsis in a murine model

2016 ◽  
Vol 47 (1) ◽  
pp. 119-130 ◽  
Author(s):  
Xiao Wang ◽  
Ding Zhang ◽  
Mikael Sjölinder ◽  
Yi Wan ◽  
Hong Sjölinder
Keyword(s):  
Murine Model ◽  
Host Susceptibility ◽  
Meningococcal Sepsis
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