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Bacterial Sepsis (bacterial + sepsis)
Selected AbstractsGrowth hormone and insulin-like growth factor 1 levels and their relation to survival in children with bacterial sepsis and septic shockJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2004N Önenli-Mungan Objectives: Despite improved supportive care, the mortality of sepsis and septic shock is still high. Multiple changes in the neuroendocrine systems, at least in part, are responsible for the high morbidity and mortality. A reduced circulating level of insulin-like growth factor and an elevated level of growth hormone are the reported characteristic findings early in the course of sepsis and septic shock in adults. The aim of this study was to evaluate the changes of growth hormone/insulin-like growth factor 1 axis in sepsis and septic shock and investigate the relationship between these hormones and survival. Methods: Fifty-one children with sepsis (S), 21 children with septic shock (SS) and 30 healthy, age- and sex-matched children (C) were enrolled in this study. Growth hormone, insulin-like growth factor 1 and cortisol levels of the sepsis and septic shock groups were obtained before administration of any inotropic agent. Results: Growth hormone levels were 32.3 ± 1.5 µIU/mL (range 4,56), 15.9 ± 0.6 µIU/mL (range 11,28) and 55.7 ± 2.7 µIU/mL (range 20,70) in S, C and SS groups, respectively. The difference between the growth hormone levels of the S and C groups, S and SS groups, and C and SS groups were significant (P < 0.001). Non-survivors (54.7 ± 1.6 µIU/mL) had significantly higher growth hormone levels than survivors (29.4 ± 1.5 µIU/mL) (P < 0.001). Insulin-like growth factor 1 levels were 38.1 ± 2.1 ng/mL (range 19,100), 122.9 ± 9.6 ng/mL (range 48,250) and 22.2 ± 1.9 ng/mL (range 10,46) in the S, C and SS groups, respectively, and the difference between the insulin-like growth factor 1 levels of the S and C, S and SS, and C and SS groups were significant (P < 0.001). Non-survivors (8.8 ± 1.1 µg/dL) had significantly lower cortisol levels than survivors (40.9 ± 2.1 µg/dL) (P < 0.001). We detected a significant difference between the levels of cortisol in non-survivors (19.7 ± 1.8 µg/dL) and survivors (33.9 ± 0.9 µg/dL) (P < 0.01). Conclusions: There were elevated levels of growth hormone with decreased levels of insulin-like growth factor 1 in children during sepsis and septic shock compared to healthy subjects. In addition, there were even higher levels of growth hormone and lower levels of insulin-like growth factor 1 in non-survivors than in survivors. We think that both growth hormone and insulin-like growth factor 1 may have potential prognostic value to serve as a marker in bacterial sepsis and septic shock in children. As there is insufficient data in the paediatric age group, more studies including large numbers of patients and additionally evaluating cytokines and insulin-like growth factor binding proteins are needed. [source] Identification of single amino acid residues essential for the binding of lipopolysaccharide (LPS) to LPS binding protein (LBP) residues 86,99 by using an Ala-scanning libraryJOURNAL OF PEPTIDE SCIENCE, Issue 4 2002Dr O. Reyes Abstract Lipopolysaccharide binding protein (LBP) is a 60 kDa acute phase glycoprotein capable of binding to LPS of Gram-negative bacteria and facilitating its interaction with cellular receptors. This process is thought to be of great importance in systemic inflammatory reactions such as septic shock. A peptide corresponding to residues 86,99 of human LBP (LBP86,99) has been reported to bind specifically with high affinity the lipid A moiety of LPS and to inhibit the interaction of LPS with LBP. We identified essential amino acids in LBP86,99 for binding to LPS by using a peptide library corresponding to the Ala-scanning of human LBP residues 86,99. Amino acids Trp91 and Lys92 were indispensable for peptide,LPS interaction and inhibition of LBP,LPS binding. In addition, several alanine-substituted synthetic LBP-derived peptides inhibited LPS,LBP interaction. Substitution of amino acids Arg94, Lys95 and Phe98 by Ala increased the inhibitory effect. The mutant Lys95 was the most active in blocking LPS binding to LBP. These findings emphasize the importance of single amino acids in the LPS binding capacity of small peptides and may contribute to the development of new drugs for use in the treatment of Gram-negative bacterial sepsis. Copyright © 2002 European Peptide Society and John Wiley & Sons, Ltd. [source] Disseminated candidiasis secondary to fungal and bacterial peritonitis in a young dogJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2009Catherine L. Rogers DVM, DACVECC Abstract Objective , To describe a severe case of bacterial sepsis and disseminated candidiasis in a previously healthy dog. Case Summary , Fungal sepsis was identified in a 2-year-old dog following intestinal dehiscence 4 days after abdominal surgery. Septic peritonitis was identified at admission and evidence of dehiscence at the previous enterotomy site was found during an exploratory laparotomy. Both gram-positive cocci and Candida albicans were cultured from the abdominal cavity. Candida sp. was also subsequently cultured from a central venous catheter. Euthanasia was performed due to failure to respond to therapy. Fungal organisms, morphologically consistent with Candida spp., were found in the lungs and kidney on postmortem histopathologic examination indicating disseminated candidiasis. New or Unique Information Provided , Candida peritonitis is a well-recognized entity in humans and contributes to morbidity and mortality in critically ill patients. Abdominal surgery, intestinal perforation, presence of central venous catheters, and administration of broad-spectrum antibiotics are all considered to be suspected risk factors. This report describes the first known case of systemic candidiasis occurring secondary to Candida peritonitis and bacterial sepsis in a critically ill dog. [source] Factors Associated with Outcome in Foals with Neonatal Isoerythrolysis (72 Cases, 1988,2003)JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2008A.C. Polkes Background: Neonatal foals with isoerythrolysis (NI) often die, but the risk factors for death have not been identified. Objectives: To identify factors associated with outcome in foals with NI and to identify factors associated with death from liver failure or kernicterus in the same population. Animals: Seventy-two foals with NI examined at referral institutions. Methods: Retrospective case series. Information on signalment, clinical examination findings, laboratory testing, treatment, complications, outcome, and necropsy results were obtained. Results: The overall survival rate was 75% (54 of 72). Liver failure (n = 7), kernicterus (n = 6), and complications related to bacterial sepsis (n = 3) were the 3 most common reasons for death or euthanasia. The number of transfusions with blood products was the factor most strongly associated with nonsurvival in a multivariate logistic regression model. The odds of liver failure developing in foals receiving a total volume of blood products , 4.0 L were 19.5 (95% confidence intervals [CI]: 2.13,178) times higher than that of foals receiving a lower volume (P= .009). The odds of kernicterus developing in foals with a total bilirubin , 27.0 mg/dL were 17.0 (95% CI: 1.77,165) times higher than that of foals with a lower total bilirubin (P= .014). Conclusions and Clinical Importance: Development of liver failure, kernicterus, and complications related to bacterial sepsis are the most common causes of death in foals with NI. Foals administered a large volume of blood products are at greater risk for developing liver failure. [source] Antagonistic lipopolysaccharides block E. coli lipopolysaccharide function at human TLR4 via interaction with the human MD-2 lipopolysaccharide binding siteCELLULAR MICROBIOLOGY, Issue 5 2007Stephen R. Coats Summary Lipopolysaccharides containing underacylated lipid A structures exhibit reduced abilities to activate the human (h) Toll-like receptor 4 (TLR4) signalling pathway and function as potent antagonists against lipopolysaccharides bearing canonical lipid A structures. Expression of underacylated lipopolysaccharides has emerged as a novel mechanism utilized by microbial pathogens to modulate host innate immune responses. Notably, antagonistic lipopolysaccharides are prime therapeutic candidates for combating Gram negative bacterial sepsis. Penta-acylated msbB and tetra-acylated Porphyromonas gingivalis lipopolysaccharides functionally antagonize hexa-acylated Escherichia coli lipopolysaccharide-dependent activation of hTLR4 through the coreceptor, hMD-2. Here, the molecular mechanism by which these antagonistic lipopolysaccharides act at hMD-2 is examined. We present evidence that both msbB and P. gingivalis lipopolysaccharides are capable of direct binding to hMD-2. These antagonistic lipopolysaccharides can utilize at least two distinct mechanisms to block E. coli lipopolysaccharide-dependent activation of hTLR4. The main mechanism consists of direct competition between the antagonistic lipopolysaccharides and E. coli lipopolysaccharide for the same binding site on hMD-2, while the secondary mechanism involves the ability of antagonistic lipopolysaccharide,hMD-2 complexes to inhibit E. coli lipopolysaccharide,hMD-2 complexes function at hTLR4. It is also shown that both hTLR4 and hMD-2 contribute to the species-specific recognition of msbB and P. gingivalis lipopolysaccharides as antagonists at the hTLR4 complex. [source] | ||||||||||