Search PubMed⌕ Search

PubMed · 7583986

Multiple organ failure.

Abstract

Multiple organ failure remains a leading cause of death in surgical intensive care units. This review of multiple organ failure focuses on recent (1990 to 1992) laboratory and clinical advances related to diagnosis, prognosis, and therapy of multiple organ failure and is divided into three parts. First, it recasts multiple organ failure into the currently accepted terminology, ie, the multiple organ dysfunction syndrome. Second, it examines the strengths and weaknesses of three mechanistic hypotheses proposed for the clinical syndrome. The three hypotheses focus on the gut, molecular mediators, and the microvasculature. Third, it synthesizes those three mechanisms into a single paradigm; this unifying paradigm can serve as a framework in which to interpret subsequent laboratory and clinical advances.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T G Buchman. 1993. Multiple organ failure.. https://pubmed.ncbi.nlm.nih.gov/7583986/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Bacterial surface association of heat-labile enterotoxin through lipopolysaccharide after secretion via the general secretory pathway.

Heat-labile enterotoxin (LT) is an important virulence factor expressed by enterotoxigenic Escherichia coli. The route of LT secretion through the outer membrane and the cellular and extracellular localization of secreted LT were examined. Using a fluorescently labeled receptor, LT was found to be specifically secreted onto the surface of wild type enterotoxigenic Escherichia coli. The main terminal branch of the general secretory pathway (GSP) was necessary and sufficient to localize LT to the bacterial surface in a K-12 strain. LT is a heteromeric toxin, and we determined that its cell surface localization was mediated by the its B subunit independent of an intact G(M1) ganglioside binding site and that LT binds lipopolysaccharide and G(M1) concurrently. The majority of LT secreted into the culture supernatant by the GSP in E. coli associated with vesicles. Only a mutation in hns, not overexpression of the GSP or LT, caused an increase in vesicle yield, supporting a specific vesicle formation machinery regulated by the nucleoid-associated protein HNS. We propose a model in which LT is secreted by the GSP across the outer membrane, secreted LT binds lipopolysaccharide via a G(M1)-independent binding region on its B subunit, and LT on the surface of released outer membrane vesicles interacts with host cell receptors, leading to intoxication. These data explain a novel mechanism of vesicle-mediated receptor-dependent delivery of a bacterial toxin into a host cell.

Bacterial Toxins↗

Variation among Escherichia coli O157:H7 strains relative to their growth, survival, thermal inactivation, and toxin production in broth.

To estimate the potential outcomes of food processing on the fate of foodborne pathogens. variations in microbial parameters such as growth rate, survival time, thermal inactivation time, and toxin production must be known. Previous microbial studies using single strains or cocktails provide error estimates for the uncertainty of the experimental and statistical procedures, but not for variations among strains. In this study, the behavior of 17 strains of Escherichia coli O157:H7 were followed when placed in synthetic media that permitted growth, survival, or thermal inactivation. The parameter values were not rejected as being normal, lognormal, gamma, or Weibull distributions. The ratio of the standard deviation to mean (normal distribution) for the exponential growth rate was 0.16 and for the lag phase duration, it was 0.38. The ratios of times to achieve a 4-log10 reduction at two survival conditions were 0.39 and 0.46; ratios of thermal D values at 55 and 60 degrees C were 0.42 and 0.33, respectively. The ratio of the negative log10 of toxin production was 0.24. These distributions are larger than the coefficient of variations observed for experimental errors in single strain and cocktail experiments. This indicates the limitations in precision that predictions of future population numbers can have when the potential presence of all strains needs to be considered. This variation among strains is applicable whether predictions are made by traditional subjective and point estimates or by using models and risk assessments.

Bacterial Toxins↗

Clostridium difficile toxin A alters in vitro-adherent neutrophil morphology and function.

The effects of purified toxin A in vitro on the shape and function of polymorphonuclear leukocytes (PMNL) were examined. Toxin A induced changes in adherent PMNL shape from a compact spherical or pyramidal shape to a thin and rope-like shape. This change in shape was accompanied by rearrangement of the F-actin cytoskeleton into aggregates. Toxin A-treated PMNL exhibited increased adherence and expressed less L-selectin and more Mac-1, compared with untreated PMNL. In contrast to these proinflammatory actions, toxin A impaired both directed and non-directed PMNL migration in response to N-formylmethionylleucylphenylalanine. In addition, toxin A decreased the oxidative activity of adherent PMNL stimulated by recombinant human tumor necrosis factor-alpha. These effects could be explained by toxin A-induced glucosylation of the signaling small-size guanine 5'-triphosphate-binding proteins of the Rho family in human PMNL.

Bacterial Toxins↗