Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental Escherichia coli septicaemia-peritonitis model was adapted to immunosuppressed mice. The mice were made neutropenic by a sublethal dose of cyclophosphamide, which resulted in a 100-fold increase in their susceptibility to intraperitoneal injection of E. coli O18:K1. A lethal infection could be prevented by passive immunisation with anti-K1 capsular or anti-O18 LPS antibodies but not with anti-J5 bacterial antibodies. The anti-K1 and anti-O18 antisera were able to increase the LD50 of the E. coli challenge by factors of 50 and 5, respectively. The role of non-specific, lipopolysaccharide (LPS)-mediated resistance to infection was also investigated in this model, in which only long-living phagocytic cells such as macrophages are believed to be functional. Pretreatment of mice with LPS was shown to prevent growth of the bacterial challenge in the peritoneal cavity and blood and to result in a five-fold increase in the LD50 of the challenge strain. These findings suggest an important role for macrophages as effector cells in defence against E. coli infection.
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PMID:Experimental Escherichia coli peritonitis in immunosuppressed mice: the role of specific and non-specific immunity. 327 82

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

The release profiles of interleukin 1 (Il-1) and tumor necrosis factor (TNF) were studied during experimental Escherichia coli septicemia and peritonitis with and without a preceding (-48 h) moderate trauma (femur marrow nailing). The trauma alone did not induce significant Il-1 or TNF liberation to plasma. During septicemia, a rapid IL-1-rise (+30 min) and subsequent normalization (+120 min) was seen. A previous trauma delayed (30 min), but accentuated (2x) and prolonged (> 4 h) the Il-1 response. During peritonitis, a delayed (30 min) but otherwise similar Il-1-response was observed. TNF levels rose rapidly (+30 min) in all animals, and remained high throughout the experimental period (6 h). The trauma did not influence the TNF response. We conclude that a synergism exists between trauma and infection with regard to the magnitude of the Il-1 response.
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PMID:The synergistic effect of trauma and infection on interleukin-1 but not tumor necrosis factor liberation during posttraumatic gram-negative septicemia. 848

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