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Bacterial translocation consequential to intestinal bacterial overgrowth provokes aggravation of mortality by sepsis

Increasing evidence from experimental and clinical studies has eluded to the 'intestinal hypothesis of sepsis', which is based on bacterial or endotoxin translocation from the intestinal lumen to the extra-intestinal sites, thus generating an exacerbated inflammatory response leading to the aggravation of the pre-existing sepsis state or to the onset of sepsis. Nevertheless, growing acceptance of the 'intestinal hypothesis' was mainly triggered by indirect rather than concrete scientific evidence. In this study we examined the role of the association of bacterial translocation with varying severity of sepsis states, monitoring mortality and recovery of translocated bacteria in several host compartments using a rat model of bacterial translocation (BT) and sepsis (S).


BT groups: midline laparotomy was performed on Wistar rats under ketamine + hydroxychloral anesthesia (4:1). Rats were inoculated with 10 ml 107/1010 cfu/ml Escherichia coli R-6 (n = 20/group) by oroduodenal catheterization, which was confined to the small intestine by ligation of both the duodenum and ileum. S groups: inoculation of 107/109/1010 cfu/ml/100 g body weight Enterobacter cloacae 89 into the portal vein (n = 20/group). BT + S groups: 1010 BT + 107/109 S (n = 20/group). From 10 animals of each group, samples of mesenteric lymph node, liver, spleen and blood were collected 2 hours post inoculation and cultured in MacConkey agar medium. The remaining animals in each group were observed for mortality for 30 days (n = 10/group).


BT-107/1010 did not cause death and only 1010 inoculum promoted BT (mean = 1.8 × 105 cfu/g tissue). S-107 was not lethal, but promoted a transient bacteremia state, S-109 was LD85 within 25 hours, and S-1010 showed LD100 within 5 hours. Bacterial recovery from these groups/g tissue were, at the most, 104 cfu at S-107, 107 cfu at S-109 and 108 cfu at S-1010. BT-1010 in combination with S-107 showed significantly increased mortality (LD50 within 32 hours) as compared with BT-1010 (LD0) and S-10 (LD0) alone (P < 0.05), and the mortality rate was statistically similar to the severe sepsis group (S-109). In addition, the association of BT-1010 + S-109 also provoked a significant increase in mortality (LD100 within 13 hours) as compared with BT-1010 (LD0) and S-109 (LD85 within 25 hours) in terms of length of time to cause mortality (P < 0.05). Besides, sepsis in combination with BT showed a decreased rate of translocation in all groups as compared with the BT group alone. Overall data demonstrated significant deleterious synergistic effects of BT in combination with all states of sepsis, suggesting that translocation of bacteria through the gut-associated lymphoid system (GALT) favors the activation of the host systemic inflammatory response, even though the total quantification of internalized bacteria in the host compartments did not change at all by the addition of the BT process. Therefore, BT appears to provoke an exacerbated inflammatory state due to the bacterial challenge to the GALT during their traffic through mesenteric lymphatic tissue rather than the quantitative physical presence of the bacteria in the systemic compartment, therefore suggesting a distinctive GALTrelated host inflammatory response associated with the BT phenomena.

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Menchaca-Diaz, J., Silva, R., Figueiredo, L. et al. Bacterial translocation consequential to intestinal bacterial overgrowth provokes aggravation of mortality by sepsis. Crit Care 7, P28 (2003).

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  • Mesenteric Lymph Node
  • Bacterial Translocation
  • Bacterial Overgrowth
  • Enterobacter Cloaca
  • MacConkey Agar