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| Resource type: Journal Article DOI: 10.1016/j.surg.2012.06.022 ID no. (ISBN etc.): 0039-6060, 1532-7361 BibTeX citation key: Babrowski2013 View all bibliographic details |
Categories: BioAcyl Corp Creators: Babrowski, Fink, Romanowski Publisher: Elsevier Collection: Surgery |
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| Abstract |
BackgroundSecondary peritonitis continues to carry a high mortality rate despite the aggressive use of imaging, drainage, and antibiotics. Although host factors and microbial burden contribute to the outcome of peritonitis, we propose a role for bacterial virulence as a determinant of outcome from peritonitis. Bacterial virulence is an inducible trait that is activated in response to specific local “cues” that we have previously shown to be present in the mouse gut exposed to surgical stress and injury.
MethodsPseudomonas aeruginosa was harvested after its intestinal inoculation into the cecum of mice subjected to surgical injury (30% hepatectomy) or sham surgery (controls). Harvested strains were then injected into the peritoneum of noninjured (naïve) mice and mortality determined.
ResultsP. aeruginosa harvested from the intestines of surgically injured mice caused 100% mortality, whereas strains harvested from control mice caused no mortality. Among recovered strains, a distinct P. aeruginosa morphotype (wrinkled shape) was shown to cause lethal peritonitis compared to smooth-shaped strains, which were nonlethal. Wrinkled strains were associated with a tendency to elicit a more proinflammatory response in mice compared to smooth-shaped strains.
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| Notes |
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Recent large cohort studies comparing infection rates among surgical and nonsurgical patients have shown that not only are infections more frequent among surgical patients, but they are also more lethal.1,2 Even when controlling for comorbid conditions, surgical patients experience more frequent and severe infections despite being healthier than their comparative nonsurgical counterparts.2 This conclusion remains statistically valid even when surgical site infections are eliminated from the comparison, and suggests that surgical injury itself might shift the dynamics of the host pathogen interaction, resulting in a greater degree of infectious-related morbidity and mortality. Although current paradigms of the causes of surgical infection posit that infection develops merely as a result of the permissive effects of a dysfunctional immune system that is unable to contain or clear an invading pathogen, there is now increasing evidence that the ability of microbial organisms to dynamically sense host stress signals and respond with enhanced virulence governs the occurrence, course, and outcome of infection.3-8
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |