Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004610 (bacteremia)
 13,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Free radicals have been implicated in the pathogenesis of gram-negative bacterial sepsis. We assessed the effectiveness of antioxidants and chelators to alter oxidative injury in established severe experimental Escherichia coli septicemia. One hour after challenge by intraperitoneal injection of bacteria, 36 rabbits were treated with moxalactam and randomized in sets of three to receive either placebo, superoxide dismutase (SOD), or a combination of antioxidants and chelators consisting of SOD, sodium thiosulfate, alpha-tocopherol, deferoxamine, and diethyldithiocarbamate. Throughout the course of treatment, levels of bacteremia and endotoxemia were similar among the three experimental groups. Neither antioxidant-treated group was significantly different from the control group in mean arterial blood pressure, leukocyte count, platelet count, core temperature, blood lactate, oxygenation or survival. Arterial pH and [HCO3-] were significantly lower in the antioxidant combination group compared to the control and SOD groups (P less than .01). In this model, antioxidant and chelator therapy does not substantially ameliorate established septicemia.
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PMID:Effect of antioxidants in experimental Escherichia coli septicemia. 268 47

Escherichia coli septicemia is a common disease of young poultry and several species of mammals. Rabbit antiserum was prepared against iron-regulated outer membrane proteins of E. coli. Eighteen-day-old turkeys were passively immunized with antiserum and challenged by air sac inoculation of 1 X 10(6) to 2 X 10(6) CFU of E. coli O78:K80:H9. Turkeys injected with normal rabbit serum or saline solution before challenge served as controls. Fatalities (8 of 51 turkeys inoculated) occurred only in groups given saline solution or normal rabbit serum. The remaining turkeys were necropsied 96 h after challenge. Passive immunization with antiserum significantly (P less than 0.05) reduced the frequency of bacteremia at 96 h after challenge, the frequency of recovery of E. coli from air sacs, and the severity of gross lesions in inoculated birds as compared with birds given normal rabbit serum or saline solution.
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PMID:Passive immunization with antibodies against iron-regulated outer membrane proteins protects turkeys from Escherichia coli septicemia. 355 95

The lack of a primate model suitably reproducing clinical septic shock prompted an attempt to adapt a successful canine model to the Rhesus monkey. Animals were sedated wih 2 mg/kg Sernylan. Local anethesia for vascular catheter insertion was produced with 1% lidocaine. After baseline hemodynamic and blood measurements, the abdomen was entered and the cystic artery and duct were ligated and divided. A suspension of E. coli (ATCC 25922) was injected into the gallbladder, and the abdomen was closed. Sequential monitoring was performed every 12-24 hours until the animals expired. The first monkey was given 10(8) E. coli/kg, the dose used in the canine model. This animal expired during the first 24 hours with ATCC 25922 E. coli septicemia. The same outcome was seen in the next monkey with 10(6) E. coli/kg. Neither monkey exhibited a hyperdynamic circulatory status. Autopsies revealed no intraabdominal abscess or peritonitis. Three animals were given 10(4) E. coli/kg. One died within 24 hours, one died after 13 days, and one was a permanent survivor. Two had bacteremia but no abscess. None had a hyperdynamic circulatory status. In three other animals the cystic artery and duct were ligated and divided, but no E. coli was given. Survival varied from 11/2 to 21/2 days. None had a hyperdynamic circulatory status. All had bacteremia. Autopsies revealed no abscesses. In summary, the Rhesus monkey is exquisitely sensitive to endogenous and exogenous sources of bacteremia, which produce a hypodynamic circulatory status and death before peritonitis or intraabdominal abscess can develop. Thus, the ischemic, infected gallbladder preparation is an inadequate septic shock model in the Rhesus monkey.
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PMID:Another unacceptable model of primate septic shock. 676 Jul 3

Nitric oxide and vasoactive intestinal peptide (VIP) are potent vasodilators and postulated as inducers of hypotension. These mediators activate guanylate cyclase and adenylate cyclase, respectively, with subsequent biosynthesis of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) producing vascular smooth muscle relaxation and vasodilatation. Cyclic nucleotides and VIP were evaluated during Escherichia coli septicemia in two groups of rabbits; 1) sepsis alone and 2) sepsis and a competitive inhibitor of nitric oxide synthase, NG-monomethyl-L-arginine. Arterial blood was obtained for determination of bacteremia, lactic acidemia, nucleotides, nitrites, and VIP levels. Significant bacteremia, endotoxemia, tachycardia, lactic acidosis, and hypotension occurred in all animals (P < 0.005). Circulating blood levels of cGMP, nitrites, cAMP, and VIP (P < 0.005) increased with development of shock. The NG-monomethyl-L-arginine treated animals had less cGMP, nitrites, cAMP, and VIP produced (P < 0.01). Plasma cGMP levels remained stable, suggesting that stimulated phagocytes in whole blood were responsible for increased cGMP levels. Infusion of VIP produced profound hypotension and lactic acidemia. Results of these experiments provide definitive evidence that nitric oxide and VIP are mediators during septic shock and their messengers are cGMP and cAMP, respectively. In addition, phagocytic stimulation with increased production of cGMP may initiate shock, with these mediators acting synergistically to prolong hypotension.
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PMID:Cyclic nucleotides and vasoactive intestinal peptide production in a rabbit model of Escherichia coli septicemia. 753 47

Escherichia coli remains one of the most common etiologies of secondary peritonitis. CMY-2 is the most prevalent AmpC enzyme identified in nosocomial E. coli isolates causing bacteremia in Taiwan. This report is of a patient who underwent surgery for intestinal perforations due to blunt abdominal trauma and developed unexpected CMY-2-producing E. coli septicemia in the early postoperative period. The AmpC-type CMY-2 enzyme might partially contribute to the poor response to antimicrobial therapy of amoxicillin-clavulanic acid or flomoxef. Late changes in antibiotic therapy to an appropriate regimen of cefpirome based on the culture results did not result in a positive outcome and the patient died. Whether selection of an anti-AmpC regimen is appropriate as first-line treatment for traumatic abdomen-associated septicemia should be an area of further investigation in Taiwan.
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PMID:Early-onset septicemia due to CMY-2-producing Escherichia coli in a woman with blunt abdominal trauma. 2018 76