title: 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.
authors.affiliation: Department of Surgery and Burn, Trauma Shock Institute, Loyola University Medical Center, Maywood, Illinois 60153, USA.
authors.forename: Masakatsu
authors.initials: M
authors.lastname: Goto
authors.forename: Victoria
authors.initials: V
authors.lastname: Samonte
authors.forename: Mehdi
authors.initials: M
authors.lastname: Khan
authors.forename: Farah
authors.initials: F
authors.lastname: Haque
authors.forename: Amit
authors.initials: A
authors.lastname: Goyal
authors.forename: Walid
authors.initials: W
authors.lastname: Al-Ghoul
authors.forename: Syed
authors.initials: S
authors.lastname: Raziuddin
authors.forename: Nadeem
authors.initials: N
authors.lastname: Fazal
authors.forename: Thyyar
authors.initials: T
authors.lastname: Ravindranath
authors.forename: R Lawrence
authors.initials: RL
authors.lastname: Reed
authors.forename: Richard L
authors.initials: RL
authors.lastname: Gamelli
authors.forename: Mohammed M
authors.initials: MM
authors.lastname: Sayeed
mesh_terms: D000418:Albumins / Q000378:metabolism; D000818:Animals; D002056:Burns / Q000097:blood / Q000150:complications* / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood; D013293:Enterococcus faecalis / Q000502:physiology*; D016908:Gram-Positive Bacterial Infections / Q000097:blood / Q000150:complications* / Q000382:microbiology* / Q000503:physiopathology; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007261:Infusions, Intra-Arterial; D019344:Lactic Acid / Q000097:blood; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012769:Shock / Q000097:blood / Q000150:complications
chemical_list: D000418:Albumins; D002245:Carbon Dioxide; D019344:Lactic Acid