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Meningococcal Sepsis (meningococcal + sepsis)

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Medical Sciences	40%

Selected Abstracts

Elevated sweat sodium associated with pulmonary oedema in meningococcal sepsis

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2004
M. Eisenhut
Abstract Background, We observed a temporary positive sweat test with sodium and chloride levels greater than 60 mmol L,1 following meningococcal septicaemia. Objective was to investigate whether this finding is reproducible and whether this disturbance in epithelial sodium transport is related to sepsis-induced pulmonary oedema. Materials and methods, Twenty-four children with a diagnosis of meningococcal septicaemia and 10 controls with noninfectious critical illness admitted to the Royal Liverpool Children's Hospital were included. Sweat collection was by pilocarpine iontophoresis in the acute phase of the illness (days 1,5) and on follow up. Sodium and chloride concentrations were determined by flame photometry. Results, In patients with meningococcal septicaemia, sweat sodium and chloride concentrations were significantly higher in the acute compared with the recovery phase, with a mean (SD) of 31·0 (14·6) mmol L,1 in the acute vs. 19·6 (10·2) mmol L,1 on recovery for sodium and 21·0 (12·1) mmol L,1 in the acute vs. 11·8 (4·9) mmol L,1 on recovery for chloride (P < 0·01, t -test, for sodium and chloride). Sweat sodium and chloride were significantly higher in patients with meningococcal disease compared with controls and in the acute phase in patients with septicaemia-related pulmonary oedema [mean (SD) sodium: 41·0 (15·4) mmol L,1 and chloride: 28·8 (14·3) mmol L,1] compared with septic patients without [mean (SD) sodium: 24·5 (10·1) mmol L,1 and chloride: 15·3 (7·9) mmol L,1] (P < 0·01 for sodium and chloride). Conclusions, This is the first study to provide in vivo evidence of reduced epithelial sodium transport in children with septicaemia and of its association with pulmonary oedema. [source]

Low utilisation of unactivated protein C in a patient with meningococcal septic shock and disseminated intravascular coagulation

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2003
A. Lignell
Background:, Activated protein C has recently been shown in a multicentre trial to significantly reduce mortality in patients with septic shock. There are also some case reports and minor studies demonstrating promising results with the unactivated form of protein C. However, in children with severe meningococcal infection, skin biopsies have demonstrated low expression of endothelial thrombomodulin and protein C receptors, suggesting low protein C activation capacity in severe meningococcal sepsis. Methods:, A patient with meningococcal septic shock was treated with two doses of the unactivated form of protein C, the first during intense activation of the coagulation system and the second during a phase of low grade or no activation. Repeated plasma samples were analysed for protein C concentration, which made it possible to compare pharmacokinetics and half-lives of the two administrations. A shorter half-life during intense coagulation was expected if there was an activation and consumption of the protein C administered. Results:, The calculated half-lives of protein C during intense and low grade activation were 32 h and 19 h, respectively, a magnitude similar to that reported in protein C-deficient patients without infection. Conclusion:, The result indicates that whole body utilisation of the unactivated protein C was low. Endothelial impairment of protein C activation does not seem to be restricted to the skin vessels only. [source]

Non-lipooligosaccharide-mediated signalling via Toll-like receptor 4 causes fatal meningococcal sepsis in a mouse model

CELLULAR MICROBIOLOGY, Issue 3 2007
Laura Plant
Summary Meningococcal lipooligosaccharide (LOS) is a major inflammatory mediator of fulminant meningococcal sepsis and meningitis with disease severity correlating with circulating concentrations of LOS and proinflammatory cytokines. In this study we show that the proinflammatory response to live meningococci in a mouse model of sepsis involves TLR4, but can develop independently of the expression of LOS. This is supported by data showing that in vivo an isogenic LOS-deficient strain, lpxA, induced equivalent disease severity and similar proinflammatory responses as the serogroup C wild-type parent strain FAM20. This response was abolished in TLR4,/, mice, and neither the wild-type strain of meningococci nor the LOS-deficient mutant was able to cause fatal sepsis in these mice. Mouse survival correlated with low levels of cytokines and chemokines, the chemotactic complement factor C5a and neutrophil levels in blood at 24 h post infection. These data suggest that during meningococcal sepsis the recognition of one or more unidentified non-LOS component(s) by TLR4 is important in stimulating proinflammatory responses, and that fatality associated with meningococcal sepsis in mice is induced by the proinflammatory host response. [source]