Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effective management of intra-abdominal infections requires a combination of preoperative preparation, antibiotic prophylaxis and appropriate surgical technique. Antibacterial prophylaxis should provide coverage of all likely pathogens, including aerobic and anaerobic organisms. Whereas antibacterial combination therapy is appropriate in certain situations, single-agent prophylaxis is appropriate for the majority of patients and ampicillin/sulbactam, with its broad-spectrum anti-aerobic/anti-anaerobic activity, is an attractive prophylactic option. Surgery involving the gastrointestinal tract provides a special challenge by virtue of its high, predominantly anaerobic, bacterial load. However, the requirement for prophylaxis varies depending upon the precise site of intervention. Biliary tract surgery requires prophylaxis in high-risk patients only, whereas hepatobiliary or pancreatic surgery requires prophylaxis in all patients. Gastroduodenal operations require prophylaxis in the presence of risk factors, such as abnormal gastric acidity or bleeding. Colorectal procedures present a high risk of anaerobic infection and sepsis, and require adequate prophylaxis combined with a thorough preoperative preparation designed to reduce considerably the bacterial load of the bowel. Where peritonitis does follow intra-abdominal surgery, patients should receive antibacterial therapy commensurate with the risk of serious infection. A small proportion of patients will be at risk of severe infection and will require triple-agent therapy. However, most patients are likely to develop mild-to-moderate infections only and can be treated with a single, broad-spectrum antibiotic agent, such as ampicillin/sulbactam, a beta-lactam/beta-lactamase inhibitor.
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PMID:New perspectives in antibiotic prophylaxis for intra-abdominal surgery. 1199 40

Group B Streptococcus (GBS) is a Gram-positive bacterium that causes sepsis and meningitis in neonates and infants. Although several GBS-associated virulence factors have been described, the mechanisms of GBS invasive disease are not well understood. To characterize additional virulence factors, a novel in vitro infection assay was developed using rat fetal lung explants. However, application of GBS to the system induced rapid lung tissue destruction associated with increased media acidity. Since lactic acid produced by other streptococci is an important virulence factor, we hypothesized that lactic acid contributed to the virulence of GBS. Spent growth media and neutralized-spent media were applied to explants and results indicated that neutralization of the media completely protected the tissue from degradation. These results were verified using multiple viability assays and with transformed cell lines. Furthermore, comparable spent media from Escherichia coli did not induce tissue cytotoxicity, suggesting that GBS produces organic acids in excess of other potential bacterial pathogens. Analysis of the spent media indicated that l-lactate levels reached approximately 70 mM, indicating that lactic acid is a major constituent of the metabolic acid produced by GBS. Treatment of explants with lactic acid alone produced dose-dependent tissue degradation, indicating that lactic acid is independently sufficient to induce target-tissue cytotoxicity. Finally, both spent media and 23.6 mM lactic acid produced dramatic tissue autofluorescence; the basis for this is currently unknown. These studies demonstrate that GBS-produced lactic acid is a potential virulence factor and may contribute to GBS invasive disease.
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PMID:Lactic acid is a potential virulence factor for group B Streptococcus. 1901 Apr 9

Catheter type, access technique, and the catheter position should be selected considering to the anticipated duration of PN aiming at the lowest complication risks (infectious and non-infectious). Long-term (>7-10 days) parenteral nutrition (PN) requires central venous access whereas for PN <3 weeks percutaneously inserted catheters and for PN >3 weeks subcutaneous tunnelled catheters or port systems are appropriate. CVC (central venous catheter) should be flushed with isotonic NaCl solution before and after PN application and during CVC occlusions. Strict indications are required for central venous access placement and the catheter should be removed as soon as possible if not required any more. Blood samples should not to be taken from the CVC. If catheter infection is suspected, peripheral blood-culture samples and culture samples from each catheter lumen should be taken simultaneously. Removal of the CVC should be carried out immediately if there are pronounced signs of local infection at the insertion site and/or clinical suspicion of catheter-induced sepsis. In case PN is indicated for a short period (max. 7-10 days), a peripheral venous access can be used if no hyperosmolar solutions (>800 mosm/L) or solutions with a high titration acidity or alkalinity are used. A peripheral venous catheter (PVC) can remain in situ for as long as it is clinically required unless there are signs of inflammation at the insertion site.
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PMID:Access technique and its problems in parenteral nutrition - Guidelines on Parenteral Nutrition, Chapter 9. 2004 83

Cronobacter is associated with outbreaks of rare, but life-threatening cases of meningitis, necrotizing enterocolitis, and sepsis in newborns. This study was conducted to determine the effect of organic acids on growth of Cronobacter in laboratory medium and reconstituted powdered infant formula (PIF) as well as the bacteriostatic effect of slightly acidified infant formula when combined with neonatal gastric acidity. Inhibitory effect of seven organic acids on four acid sensitive Cronobacter strains was determined in laboratory medium with broth dilution method at pH 5.0, 5.5 and 6.0. Acetic, butyric and propionic acids were most inhibitive against Cronobacter in the laboratory medium. The killing effect of these three acids was partially buffered in reconstituted PIF. Under neonatal gastric acid condition of pH 5.0, the slightly acidified formula which did not exert inhibition effect solely reduced significantly the Cronobacter populations. A synergistic effect of formula moderately acidified with organic acid combined with the physiological infant gastric acid was visible in preventing the rapid growth of Cronobacter in neonatal stomach. The study contributed to a better understanding of the inhibitory effect of organic acids on Cronobacter growth in different matrixes and provided new ideas in terms of controlling bacteria colonization and translocation by acidified formula.
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PMID:Growth inhibition of Cronobacter spp. strains in reconstituted powdered infant formula acidified with organic acids supported by natural stomach acidity. 2366 63

Background and Objectives. Antacids are often prescribed to preterm infants due to misdiagnosis of gastro-oesophageal reflux. This suppresses gastric acidity, a major defence mechanism against infection. This study aims to determine if ranitidine and omeprazole use in very low birth weight (VLBW) neonates, <1500 grams, is associated with increased risk of late onset sepsis, necrotising enterocolitis (NEC), and mortality. Methods. Retrospective analysis was conducted on neonates, <1500 grams, born and admitted into the Neonatal Intensive Care Unit at The Canberra Hospital during the period from January 2008 to December 2012. Information regarding late onset sepsis, NEC, mortality, ranitidine/omeprazole use, and other neonatal/hospital factors was collected for each neonate. Results. 360 neonates were evaluated, 64 received ranitidine and/or omeprazole, and 296 had not. There were no statistically significant differences in incidence of late onset sepsis (OR = 0.52, CI = 0.24-1.1, and p = 0.117), NEC Stage 2 and above (OR = 0.4, CI = 0.05-3.2, and p = 0.7), or mortality (OR = 0.35, CI = 0.08-1.5, and p = 0.19) between the two groups. After adjusting significant differences in neonatal and hospital factors, risk of late onset sepsis was significantly lower in those that received ranitidine/omeprazole (OR = 0.28, CI = 0.13-0.65, and p = 0.003). Conclusions. Ranitidine and omeprazole use in VLBW preterm infants may not be associated with an increased risk of infection, NEC, and mortality.
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PMID:Morbidity and Mortality in Preterm Infants following Antacid Use: A Retrospective Audit. 2799 Jan 66

We report here the discovery of a polysaccharide, namely EUP1, with anti-inflammatory activity from the herb of Eucommia ulmoides Oliv. We separated three polysaccharide fractions from this herb based on acidity and screened them for their activity in modulating the phenotype of murine macrophages. Among them, EUP1 was the only fraction to exert such a function - it stimulated Raw 264.7 cells to express CD206 and a key anti-inflammatory cytokine interleukin-10. Having fully characterised EUP1 with a series of chromatographic and spectroscopic analyses, we evaluated its anti-inflammatory effects in both in vitro and in vivo inflammatory models. In the murine model of sepsis induced by lipopolysaccharide, administration of EUP1 effectively suppressed the expression of major inflammatory cytokines, alleviated lung injury and increased animal survival rate. In summary, EUP1, with a clearly elucidated chemical structure and solid anti-inflammatory activity, may become a valuable candidate for further development into an anti-septic therapeutic agent.
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PMID:Post-screening characterisation and in vivo evaluation of an anti-inflammatory polysaccharide fraction from Eucommia ulmoides. 2850 49

In host defense, it is crucial to maintain the acidity of the macrophage phagosome for effective bacterial clearance. However, the mechanisms governing phagosomal acidification upon exposure to gram-negative bacteria have not been fully elucidated. In this study, we demonstrate that in macrophages exposed to Escherichia coli, the thioredoxin-interacting protein (TXNIP)-associated inflammasome plays a role in pH modulation through the activated caspase-1-mediated inhibition of NADPH oxidase. While there was no difference in early-phase bacterial engulfment between Txnip knockout (KO) macrophages and wild-type (WT) macrophages, Txnip KO macrophages were less efficient at destroying intracellular bacteria in the late phase, and their phagosomes failed to undergo appropriate acidification. These phenomena were associated with reactive oxygen species production and were reversed by treatment with an NADPH oxidase inhibitor or a caspase inhibitor. In line with these results, Txnip KO mice were more susceptible to both intraperitoneally administered E. coli and sepsis induced by cecum ligation and puncture than WT mice. Taken together, this study suggests that the TXNIP-associated inflammasome-caspase-1 axis regulates NADPH oxidase to modulate the pH of the phagosome, controlling bacterial clearance by macrophages.
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PMID:Thioredoxin-Interacting Protein Promotes Phagosomal Acidification Upon Exposure to Escherichia coli Through Inflammasome-Mediated Caspase-1 Activation in Macrophages. 3178 Nov 21


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