Bacterial translocation in D-galactosamine-treated rats in a burn model.

Bacteria and endotoxins can pass through the gut barrier under certain conditions. This process of bacterial translocation (BT) may occur after thermal injury in animals and is thought to play a role in the pathogenesis of septic complications in severely burned patients. The current study was performed to determine the role of endotoxin-related cytokines in the pathogenesis of burn-induced BT. Wistar rats were used in which enhanced sensitivity to TNF/LPS reactions was achieved by treatment with galactosamine (GalN). The GI tracts of these rats were antibiotic decontaminated with oral bacitracin and neomycin and were colonized with a neomycin resistant (NR)-Escherichia coli strain. The rats were divided into four groups, 30 per cent TBSA scald with GalN (Burn+GalN) pretreatment; 30 per cent TBSA scald without GalN (Burn); or sham injury with (GalN) and without GalN (Sham) pretreatment. On day 2, the animals were killed and liver, spleen, lung, heart and the peritoneal cavity were cultured. Blood samples were taken and the concentrations of LPS, TNF, IL-6 and ALAT were determined. Mortality was significantly increased in the Burn+GalN group compared to the other groups. In all groups, the incidences of BT were increased compared to the sham-treated group, although BT was most pronounced in the Burn+GalN group. In the latter group it was accompanied by highly elevated IL-6 and ALAT levels. The results of this study suggest that endotoxin mediators like TNF and IL-6 could play a role in the phenomenon of BT and that the function of the liver is an important clearing mechanism.

The role of systemic antibodies against intestinal Escherichia coli in the prevention of bacterial translocation of Escherichia coli in a burn model in mice.

Bacterial translocation (BT) from the gastrointestinal (GI) tract has been proposed to play a role in the pathogenesis of septic complications in severely burned patients. It is well known that severely ill patients such as thermally injured patients may acquire new potential pathogenic microorganisms in the GI tract. Because these patients have no antibodies directed against these acquired microorganisms, BT may be facilitated in these patients. To investigate this hypothesis in a burn model, a study was performed in which two groups of C3H-HeN mice underwent a different period of intestinal overgrowth by a single neomycin-resistant (NR) Escherichia coli strain after oral neomycin-bacitracin treatment. Group I underwent a short period (5 days) and group II experienced a long period (44 days) of intestinal overgrowth before a thermal injury was executed. Two days postburn, plasma antibody titers of IgA, IgG, and IgM isotype against NR E. coli were measured by indirect immunofluorescence (IIF) and BT to various organs was determined by culturing. Although there were no significant differences of BT to organs between the groups, the IgG antibody titer against the NR E. coli strain was significantly increased in group II. Antibody titers of IgA and IgM were not significantly different between the groups. Titers of plasma antibodies of IgG isotype against the intestinal NR E. coli did not correlate with BT. We conclude that increased IgG titers against the NR E. coli used are the result of a longer intestinal overgrowth period and are not associated with prevented or decreased BT.

Effect of polymyxin B on intestinal bacterial translocation in Pseudomonas aeruginosa wound-colonized burned mice.

Bacterial translocation (BT) from the gastrointestinal tract has been proposed to play a role in the pathogenesis of septic complications in severely burned patients. In a burn model the effect of a subtherapeutic dose of polymyxin B-sulfate (PB) at BT was examined in Escherichia coli-monoassociated mice with Pseudomonas aeruginosa-inoculated burn wounds. The BT incidence and number of translocating microorganisms to the spleen (p less than 0.01), liver (p less than 0.01), lung (p less than 0.05) and heart (p less than 0.05) were diminished significantly in the PB-treated versus the untreated group. Endotoxin in plasma was detectable in one of the 16 PB-treated versus 6 of the 17 control mice (p less than 0.05). The relation of Pseudomonas burn wound inoculation, BT, endotoxin and the endotoxin-neutralizing properties of PB will be discussed.