title: Translocation of indigenous microflora in an experimental model of sepsis.
abstract: Translocation of viable bacteria from gut to bloodstream and other sterile body sites during shock has been demonstrated in several experimental and clinical studies. The factors causing translocation and its incidence at different stages of shock are not known. The aim of the study was to evaluate the importance of several factors causing translocation of indigenous microflora in an experimental model of septic shock based on intraperitoneal Escherichia coli sepsis in rats. Counts of inoculated E. coli and translocated bacteria in different locations, gut morphology and haematological values were evaluated at different stages of sepsis. Sepsis developed in all animals and E. coli achieved the highest counts in blood 6 h after inoculation. Translocation was commonest at 6 and 12 h after inoculation. Frequently translocating bacteria were lactobacilli, bifidobacteria, bacteroides and peptostreptococci. In early sepsis, translocation was associated with high E. coli counts in blood, yet in late sepsis the opposite correlation was present. Low infiltration by neutrophils in the ileum and decreased mitotic activity in the colon were associated with a high translocation rate. In early sepsis, translocation was associated with low lymphocyte counts, but in late sepsis, with low neutrophil counts. Translocation of bacteria (including anaerobes) that colonise the gut in high counts takes place during sepsis. Putative influencing factors such as activity of the primary disease (bacterial counts in blood), gut morphology or haematological values seem to have different impacts on translocation, depending on the stage of the disease.
authors.forename: P
authors.initials: P
authors.lastname: Naaber
authors.forename: I
authors.initials: I
authors.lastname: Smidt
authors.affiliation: Department of Microbiology, *Department of Anaesthesiology and Intensive Care and †Department of Anatomy, University of Tartu, Tartu, Estonia.
authors.forename: K
authors.initials: K
authors.lastname: Tamme
authors.affiliation: Department of Microbiology, *Department of Anaesthesiology and Intensive Care and †Department of Anatomy, University of Tartu, Tartu, Estonia.
authors.forename: A
authors.initials: A
authors.lastname: Liigant
authors.affiliation: Department of Microbiology, *Department of Anaesthesiology and Intensive Care and †Department of Anatomy, University of Tartu, Tartu, Estonia.
authors.forename: H
authors.initials: H
authors.lastname: Tapfer
authors.forename: M
authors.initials: M
authors.lastname: Mikelsaar
authors.affiliation: Department of Microbiology, *Department of Anaesthesiology and Intensive Care and †Department of Anatomy, University of Tartu, Tartu, Estonia.
authors.forename: R
authors.initials: R
authors.lastname: Talvik
mesh_terms: D000818:Animals; D016470:Bacteremia / Q000382:microbiology; D018988:Bacterial Translocation; D001439:Bacteroides / Q000502:physiology; D001644:Bifidobacterium / Q000502:physiology; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000502:physiology*; D004927:Escherichia coli Infections / Q000382:microbiology*; D006321:Heart / Q000382:microbiology; D006801:Humans; D007413:Intestinal Mucosa / Q000382:microbiology / Q000473:pathology; D007668:Kidney / Q000382:microbiology; D007777:Lactobacillaceae / Q000502:physiology; D008099:Liver / Q000382:microbiology; D008168:Lung / Q000382:microbiology; D008198:Lymph Nodes / Q000382:microbiology; D010462:Peptostreptococcus / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012772:Shock, Septic / Q000382:microbiology*; D013154:Spleen / Q000382:microbiology