Enterococcus faecalis Exacerbates Burn Injury-Induced Host Responses in Rats

Abstract

Pathophysiology of burn injury with complications of gram-positive infections is not well characterized. We have developed an in vivo rat model to study the effects of burn injury along with intra-abdominal inoculation of Enterococcus faecalis. We hypothesized that although burn injury or E. faecalis inoculation by itself may not induce significant pathophysiological responses, the combination of the two can lead to adverse pathophysiological consequences. Sprague-Dawley rats were divided into 4 groups: group 1(C), controls; group 2(B), burn injury on 30% total body surface area; group 3(EF), intra-abdominal implantation of bacterial pellet impregnated with E. faecalis; group 4(B+EF), burn injury plus bacterial pellet implantation. The mortality was 25% and 60% on day 1 and 2 in Group 4(B+EF), respectively; no significant mortality was observed in other groups. In group 4(B+EF), metabolic acidosis, respiratory alkalosis, and a hyperdynamic state developed on day 1, and metabolic and respiratory acidosis and a hypodynamic state on day 2. There were no significant alterations in metabolic or hemodynamic measurements in other groups. Intestinal microvascular permeability to albumin on day 1 and 2 was increased in group 4(B+EF). In group 2(B), microvascular permeability was not increased significantly. Although the permeability was increased on day 1 in group 3(EF), it declined on day 2. The metabolic and hemodynamic alterations were correlated with increased intestinal microvascular permeability to albumin. E. faecalis appeared to be involved in initiating a vicious cycle of burn injury-mediated disruption of intestinal integrity along with metabolic and hemodynamic derangements.

Differential effector responses by circulating/blood and tissue/peritoneal neutrophils following burn combined with Enterococcus faecalis infection

“…Such priming of neutrophils with burn injury could be due to one or more of the known mediators generated during the course of burn injury. In our recent studies, we have documented that superimposition of E. faecalis infection on burn injury caused an eruption of host mortality not seen with either individual challenge (Goto et al ., ; Samonte et al ., ). We hypothesized that the Enterococcus bacteria, and/or factors related to these organisms, aggravate burn‐induced modulations in host defense by PMNs and thereby contribute to host morbidity and mortality.…”

“…The results of our previous studies indicated a significant mortality in burn combined with E. faecalis infection (~60%). Burn or E. faecalis alone did not produce significant mortality (Goto et al ., ; Sayeed, ). The animals succumbed to death in B + EF group may have died from fulminant sepsis, bacterial translocation, or bacteremia; however, in this study we did not make any attempt to find the cause of death.…”

“…We have found that depleting circulating/blood neutrophils in burn rats reduces bacterial translocation (Fazal et al ., ; Sir et al ., ). We have also found that the combined injury (B + E. faecalis (EF)) worsens mortality and morbidity (Goto et al ., ; Samonte et al ., ). Based on these previous studies, we hypothesized that the burn combined with E. faecalis infection will alter the effector response of extravasated tissue/peritoneal neutrophils.…”

Mechanisms of postburn intestinal barrier dysfunction in the rat: Roles of epithelial cell renewal, E-cadherin, and neutrophil extravasation*

“…These findings, along with the slow initial BrdU incorporation shown here, could be related to hemodynamic changes resulting in the slowed postburn blood flow in the mesenteric vascular bed, which would restrict the transport of BrdU from the intraperitoneal cavity to the intestinal crypts by circulating blood (16,26). This effect may be compounded by increased postburn vascular permeability (21,26). The late appearance of BrdU immunopositive cells up to 18 hrs postinjection in burn rats could also be the result of slow delivery and/or clearance as a result of slow blood flow (16,21,26).…”

“…This effect may be compounded by increased postburn vascular permeability (21,26). The late appearance of BrdU immunopositive cells up to 18 hrs postinjection in burn rats could also be the result of slow delivery and/or clearance as a result of slow blood flow (16,21,26).…”