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)

A 58 year old Chinese male, one week after arriving in Canada from Hong Kong, presented with acute abdominal pain and diarrhoea which was rapidly followed by Escherichia coli infection causing septicaemia and meningitis. His past history revealed bronchial asthma for 15 years treated with steroids. At laparotomy, 7 days after the onset of symptoms, he was found to have extensive haemorrhagic infarction of the small bowel and right colon. Examination of the fibrosed mesenteric vessels revealed numerous filariform larvae of Strongyloides stercoralis, within the walls, and in all layers of bowel wall. The role of the parasite in the production of obliterative arteritis in this fatal case of haemorrhagic enteropathy is discussed. Clinical strongyloidiasis, in uncomplicated cases, varies from mild to severe with gastroenteritis, nausea, colicky abdominal pain, electrolyte imbalance and symptoms of malabsorption syndrome (MARCIAL-ROJAS, 1971). In malnourished individuals and patients with debilitating infections, either newly acquired or asymptomatic latent infection with S. stercoralis can assume severe dimensions (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). Similarly, in patients on steroid (CRUZ et al., 1966; WILLIS and MWOKOLO, 1966; NEEFE et al., 1973) and immunosuppressive therapy for lymphomatous diseases or deficient in immune response (ROGERS and NELSON, 1966; RIVERA et al., 1970), systemic strongyloidiasis is often fatal. The increased frequency of auto-infection in such patients with a breached immune barrier is, however, unclear. Further complications of this infection due to severe enterocolitis result in sepsis, bacteraemia and meningitis (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). This paper presents a fatal case of S. stercoralis infection which illustrates an uncommon if not unique, mechanism in its production of haemorrhagic enteropathy leading to sepsis and death.
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PMID:Fatal bowel infarction and sepsis: an unusual complication of systemic strongyloidiasis. 122 84

Escherichia coli hemolysin has been implicated as a pathogenicity factor in extraintestinal E. coli infections including sepsis. In the present study the effects of intravascular administration of hemolysin were investigated in isolated blood-free perfused rabbit lungs. Low concentrations of the toxin in the perfusate (0.05-5 hemolytic units/ml, corresponding to approximately 5-500 ng/ml), caused a dose- and time-dependent release of potassium, thromboxane A2, and prostaglandin I2, but not of lactate dehydrogenase, into the recirculating medium, as well as a dose-dependent liberation of the prostanoids into the bronchoalveolar space. These events were paralleled by a dose-dependent pulmonary hypertension, and studies with different inhibitors collectively indicated that the vasoconstrictor response was mediated predominantly by pulmonary thromboxane generation. In addition, E. coli hemolysin elicited a protracted, dose-dependent increase in the lung capillary filtration coefficient, which was independent of the prostanoid-mediated pressor response and resulted in severe pulmonary edema formation. We conclude that E. coli hemolysin can elicit thromboxane-mediated pulmonary hypertension combined with severe vascular leakage in isolated lungs in the absence of circulating inflammatory cells and humoral mediator systems, mimicking the key events in the development of acute respiratory failure in states of septicemia.
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PMID:Thromboxane-mediated hypertension and vascular leakage evoked by low doses of Escherichia coli hemolysin in rabbit lungs. 250 Apr 55

Systemic infection with Escherichia coli significantly decreased feed intake, slowed growth of the whole body and skeletal muscles, and severely inhibited muscle protein accumulation in both chicks and rats. Treatment with naproxen (6-methoxy-alpha-methyl-2-naphthaleneacetic acid), an inhibitor of prostaglandin production, decreased weight losses of body and muscle, and significantly inhibited muscle protein wasting in infected chicks and rats. E. coli infection increased net protein degradation by 44.8% (P less than 0.05) and prostaglandin E2 production by 148% (P less than 0.05) in isolated extensor digitorum communis muscle from chicks on day 2 after infection. Naproxen treatment significantly decreased net protein degradation and prostaglandin E2 production in infected chicks to values seen in muscles of healthy controls. Quantitatively and qualitatively similar results were seen in isolated rat epitrochlearis muscle.
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PMID:Prostaglandin-dependent muscle wasting during infection in the broiler chick (Gallus domesticus) and the laboratory rat (Rattus norvegicus). 268 31

Since the age of nine weeks a red haired girl suffered from purulent dermatitis and recurrent, systemic E. coli infections. She had an excessive hyperimmunoglobulinemia E, as well as impaired granulocyte adherence and chemotaxis. Though a sepsis was evident, the granulocytes exhibited a random FITC-Concanavalin A fluorescence. In spite of intensive treatment with various antibiotics and several granulocyte transfusions the child died at the age of 2 years and 11 months. As shown by the FITC-Concanavalin A distribution, the hyperimmunoglobulinemia E may have caused a decreased membrane fluidity causing the impaired adherence and chemotaxis. This could explain the pathophysiology of the Job's Syndrome.
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PMID:[Membranes properties of granulocytes in Job's-Syndrome with E. coli-septicemia (author's transl)]. 611 94

Previous data from our laboratory have demonstrated that glucan administration significantly alters the course of a variety of experimentally induced infectious diseases. In view of the increasing incidence of gram-negative infections, studies were initiated to evaluate the effect of intraperitoneal glucan therapy on Escherichia coli-induced peritonitis and sepsis. Male ICR/Tex mice were injected intraperitoneally with glucan or dextrose on days 5 and 3 prior to intraperitoneal challenge with 1.0 x 10(8) E. coli. Glucan administration resulted in a significant enhancement of survival. Evaluation of the mechanism of protective action of glucan revealed that both the glucan and dextrose control groups showed an equivalent level of blood-borne E. coli at early periods. At 6 hours after challenge the glucan group showed a significant decrease in blood-borne E. coli. In contrast, the dextrose control group demonstrated progressive bacteremia. A significant depression of phagocytic activity occurred in E. coli-infected mice as compared with control mice that were not exposed to the bacterial challenge. The enhancement in phagocytic function observed in glucan-treated control mice was unaltered in E. coli challenged, glucan-treated mice. The possible importance of hyperfunctional macrophages in reduction of mortality from E. coli sepsis was denoted by methyl palmitate-induced reversal of the glucan hyperfunctional state. Methyl palmitate-treated glucan injected mice were not protected against E. coli infection. These data denote that the intraperitoneal administration of glucan significantly modifies the course of E. coli-induced peritonitis and bacteremia due, in part, to glucan-induced enhancement of macrophage function.
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PMID:Immunotherapeutic modification of Escherichia coli--induced experimental peritonitis and bacteremia by glucan. 633 16

Three patients with severe liver and renal failure admitted to the Infectious Diseases Department of the Alessandria for suspected leptospirosis in the second half of 1979 are presented. In one case, the agent responsible was Leptospira icterohaemorrhagiae AB Wjnberg strain, in another Gram-negative sepsis, and in the third acute pancreatitis associated with serious Escherichia coli infection. An account is given of the peritoneal dialysis technique that led to successful resolution of the serious liver and renal failure.
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PMID:[Possibilities and current technics of dialysis in leptospirosis with severe renal damage]. 667 99

The effect of muramyldipeptide (MDP), N-acetylmuramyl-L-alanyl-D-isoglutamine [MDP(Ala)], and its analogs on bacterial infection was studied using the experimental model of sepsis infection in mice. Injection of MDP(Ala) gave mice definitive protection against E. coli infection, but only partial protection against P. aeruginosa or K. pneumoniae infection. Several factors influencing the protective activity of MDP(Ala) on E. coli infection were studied, and it was demonstrated that the activity was induced by various routes of administration of MDP(Ala), including the oral route, and was markedly influenced by the bacterial inoculum size. It was also shown that the effective dose of MDP(Ala) was 100 micrograms per mouse for intraperitoneal, intravenous or subcutaneous injections and 1,000 microgram per mouse when administered orally. Furthermore, the optimal interval between MDP-treatment and infection was 24 hr when the treatment was carried out before infection. Clearance of bacterial cells in blood was observed after E. coli infection in mice treated with MDP(Ala). The efficacy of MDP(Ala) and two analogs, N-acetylmuramyl-L-valyl-D-isoglutamine [MDP(Val)] and N-acetylmuramyl-L-seryl-D-isoglutamine [MDP (Ser)], was evaluated for the E. coli infection; MDP(Val) was proven to be slightly less active than MDP(Ala), and MDP(Ser) to be the least effective, although MDP(Val) or MDP(Ser) was reported to have higher adjuvanticity than MDP (Ala) for the development of delayed-type hypersensitivity.
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PMID:Stimulation of nonspecific host resistance to infection induced by muramyldipeptides. 703 43

Interleukin-6 (IL-6) is a multipotential cytokine detected in the serum of patients or experimental animals undergoing bacterial sepsis. To date, the role of IL-6 in gram-negative sepsis models has been controversial. We have used IL-6-deficient mice to investigate the role of IL-6 during virulent Escherichia coli infection and in lipopolysaccharide (LPS)-induced mortality. In this report we describe an increased susceptibility of IL-6-deficient mice to E. coli infection in terms of mortality and accumulation of viable bacteria in tissues, indicating a protective role for IL-6 during the immune response against E. coli. In contrast, mortality rates of IL-6-deficient mice and control animals undergoing LPS-induced shock did not differ, indicating that IL-6 was inconsequential for survival in this model. Furthermore, we have shown that neutrophils were crucial for resistance to E. coli in normal mice. IL-6-deficient mice were unable to efficiently induce neutrophilia in the bloodstream immediately following challenge with E. coli, in contrast to a characteristic neutrophilia induced in control animals. Prophylactic treatment of the mutant animals with recombinant IL-6 protein reverted both the deficit of neutrophilia and the accumulation of bacteria in tissues. These data clarify the role of IL-6 as protective in virulent E. coli infection and suggest that the protective effect may be at least partially mediated through neutrophils.
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PMID:Interleukin-6 is required for a protective immune response to systemic Escherichia coli infection. 875 58

Escherichia coli hemolysin (HlyA) is a proteinaceous pore-forming exotoxin that is implicated as a significant pathogenicity factor in extraintestinal E. coli infections including sepsis. In perfused rabbit lungs, subcytolytic concentrations of the toxin evoke thromboxane-mediated vasoconstriction and prostanoid-independent protracted vascular permeability increase (11). In the present study, the influence of submicromolar concentrations of free arachidonic acid (AA) and eicosapentaenoic acid (EPA) on the HlyA-induced leakage response was investigated. HlyA at concentration from 0.02 to 0.06 hemolytic units/ml provoked a dose-dependent, severalfold increase in the capillary filtration coefficient (Kfc), accompanied by the release of leukotriene(LT)B4, LTC4, and LTE4 into the recirculating buffer fluid. Simultaneous application of 100 nmol/L AA markedly augmented the HlyA-elicited leakage response, concomitant with an amplification of LTB4 release and a change in the kinetics of cysteinyl-LT generation. In contrast, 50 to 200 nmol/L EPA suppressed in a dose-dependent manner the HlyA-induced increase in Kfc values. This was accompanied by a blockage of 4-series LT generation and a dose-dependent appearance of LTB5, LTC5, and LTE5. In addition, EPA fully antagonized the AA-induced amplification of the HlyA-provoked Kfc increase, again accompanied by a shift from 4-series to 5-series LT generation. We conclude that the vascular leakage provoked by HlyA in rabbit lungs is differentially influenced by free AA versus free EPA, related to the generation of 4- versus 5-series leukotrienes. The composition of lipid emulsions used for parenteral nutrition may thus influence inflammatory capillary leakage.
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PMID:Impact of arachidonic versus eicosapentaenoic acid on exotonin-induced lung vascular leakage: relation to 4-series versus 5-series leukotriene generation. 903 87

Nitric oxide (NO) is an important vasodilator that is produced by constitutive (cNOS) as well as inducible (iNOS) isoforms of nitric oxide synthase. The pore-forming hemolysin of Escherichia coli (HlyA), an important virulence factor in extraintestinal E. coli infections, was found to be a potent stimulator of NO liberation in isolated endothelial cells, and that it also causes thromboxane generation and related vasoconstriction in rabbit lungs. We investigated the effect of different concentrations of HlyA on pulmonary NO synthesis in buffer-perfused rabbit lungs. NO release into the alveolar as well as the intravascular compartment was monitored on-line by chemiluminescence detection of expired NO and by measurement of (peroxy-)nitrite/nitrate release into the perfusate. HlyA induced a pressor response and an immediate dose-dependent increase of exhalative and intravascular NO liberation, further enhanced by the addition of the NOS substrate L-arginine. The nonspecific NOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA), but not the iNOS selective inhibitors aminoguanidine and 2-(2-aminoethyl)-2-thiopseudourea-dihydrobromide, blocked the HlyA-evoked NO liberation into both the alveolar and the intravascular compartments. Enhancement of NO formation (L-arginine) slightly reduced, and inhibition of NO synthesis (L-NMMA) amplified greatly, the HlyA-elicited vasoconstrictor response. Inhibition of the pressor response by a thromboxane receptor antagonist did not interfere with the exotoxin-elicited NO formation. We conclude (1) that marked NO biosynthesis occurs in this model of the septic lung, (2) that the signal transduction in response to HlyA proceeds via activation of cNOS directly related to exotoxin activity and not to secondary changes in shear stress, and (3) that this vasodilator release mitigates the HlyA-induced pulmonary vasoconstriction. These findings may have important implications for therapeutic approaches using NOS inhibitors in sepsis.
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PMID:Nitric oxide biosynthesis in an exotoxin-induced septic lung model: role of cNOS and impact on pulmonary hemodynamics. 947 64


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