Promotion by burn stress of the translocation of bacteria from the gastrointestinal tracts of mice

Abstract

A mouse burn model was established to test the effect of nonlethal thermal injury on the translocation of indigenous bacteria from the gastrointestinal (GI) tract to other organs. Specific pathogen-free (SPF) mice were given 15% or 30% total body surface area burns, and the mesenteric lymph nodes (MLNs), spleens, livers, blood, and peritoneal cavities were cultured for translocated bacteria at various time intervals. No viable aerobic, facultatively anaerobic, or strictly anaerobic bacteria of the indigenous flora grew in cultures from the MLNs of these mice. Consequently, SPF mice were antibiotic decontaminated and then colonized with Escherichia coli to develop a model in which E coli maintains abnormally high cecal population levels and translocates continuously to the MLN. These mice received 15% or 30% thermal burns four days after colonization with E coli. The incidence of bacterial translocation and the numbers of E coli translocating to the MLN, spleen, liver, blood, and peritoneal cavity increased with increasing burn area compared with controls. Mice receiving 15% burns could not clear intravenously challenged E coli from their bloodstream, MLN, or liver. Thus, burn stress promotes the translocation of bacteria from the GI tract to other organs to cause bacteremia.