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PubMed1992

Bacterial translocation from the gastrointestinal tract.

Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal tract to extraintestinal sites, such as the mesenteric lymph node complex, liver, spleen, kidney, and blood. The major mechanisms promoting bacterial translocation in animal models are: (a) disruption of the ecologic equilibrium to allow intestinal bacterial overgrowth, (b) deficiencies in host immune defenses, and (c) increased permeability of the intestinal mucosal barrier. These mechanisms can act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. Studies are presented of attempts to delineate the mechanisms promoting bacterial translocation utilizing animal models of intestinal bacterial overgrowth, immunosuppression, T-cell deficiencies, solid tumors, leukemia, diabetes, endotoxemia, hemorrhagic shock, thermal injury, bowel obstruction, bile duct ligation, protein malnutrition and parenteral nutrition. Also described are the use of selective antibiotic decontamination or nonspecific macrophage immunomodulators in attempts to reduce bacterial translocation from the gastrointestinal tract.

Animals↗

PubMed1993

The effect of rejection and graft-versus-host disease on small intestinal microflora and bacterial translocation after rat small bowel transplantation.

Bacterial translocation and the development of sepsis after small bowel transplantation may be promoted by immunological damage to the intestinal mucosa or by quantitative and qualitative changes in intestinal microflora. This study assessed the effects of rejection, graft-versus-host disease (GVHD) and immunosuppression on intestinal microflora and bacterial translocation after heterotopic rat small bowel transplantation. Isografts, allografts with and without CsA immunosuppression, and the semi-allogeneic parent to the F1 hybrid GVHD model were studied. Intestinal microflora in graft and host loops and bacterial translocation to host organs and the graft mesenteric lymph node were determined. Bacterial colonies were counted and individual colonies identified using API 20E nutrient and fermentation indicator techniques. Colony counts in isografts and allografts were significantly higher than in the native intestine, whereas there was a massive overgrowth in the native intestine in the GVHD group. The species profile for the host and graft loops was similar in animals that had received isografts, allografted animals receiving CsA, and animals undergoing GVHD. However, there was a large increase in Staphylococcus epidermidis in animals with rejection. Bacterial translocation was not detected in isografted animals, but was observed in all other animal groups, with S. epidermidis being the most prevalent organism. These findings demonstrate that rejection and GVHD are associated with shifts in intestinal microflora toward potentially pathogenic organisms and that bacterial translocation into recipient tissues poses a major threat for the development of sepsis.

Animals↗

PubMed2001

The effects of pentoxifylline treatment on bacterial translocation after hemorrhagic shock in rats.

Bacterial translocation is thought to be responsible for infectious complications after hemorrhagic shock. The aim of this study was to investigate the effects of pentoxifylline treatment on bacterial translocation in animals subjected to hemorrhagic shock. Thirty-one Wistar albino rats (280-360 g) were divided into three groups: sham (n=10), shock (n=11), and shock-pentoxifylline (n=10). Blood was not withdrawn from sham rats. Shock rats were subjected to 30 min of shock followed by reinfusion of shed blood. Shock/pentoxifylline rats received pentoxifylline after reinfusion of shed blood. After hemorrhage and reinfusion (24 h), the mesenteric lymph nodes, liver, spleen, and blood samples were evaluated using quantitative microbiological techniques, and the numbers of colony-forming units were compared between groups. Cecum was removed to evaluate the bacterial population. Ileum and cecum were examined histologically. The incidence of bacterial translocation was higher in the shocked rats (63%) than in the sham shock rats (10%). Pentoxifylline reduced the incidence of shock-induced bacterial translocation to 0%. Cecal bacterial levels were significantly higher in the shock rats than in the sham and shock/pentoxifylline rats. The histological damage caused by hemorrhagic shock was prevented by pentoxifylline treatment. In conclusion, the hemorrhagic shock triggered translocation of bacteria to the mesenteric lymph nodes, spleen, liver, and blood of rats. Pentoxifylline treatment just after shed blood transfusion significantly attenuated this phenomenon.

Animals↗

PubMed2001

Bacterial translocation in neonatal rats: the relation between intestinal flora, translocated bacteria, and influence of milk.

BACKGROUND: A high incidence of bacterial translocation in neonates results not only from immaturity of host-defense functions, but also from the dominant colonization of aerobic bacteria in the intestine. Bacterial colonization develops differently among breast-fed, formula-fed, premature, and full-term infants. The purpose of this study was to examine the incidence of bacterial translocation and to identify the translocated bacterial species, relating these findings to the intestinal microflora and to the type of feeding in neonatal rats. METHODS: Animals were divided into three groups: breast-fed normal pups (MR group), formula-fed pups fed via an intragastric cannula implanted esophageally (AR group), and breast-fed pups after the removal of the cannula (Sham group). Artificial rearing was achieved using a machine feeding system. Culture and identification of the bacteria in the intestine, mesenteric lymph nodes, liver, portal blood, and lungs were made using a simplified version of Mitsuoka's method. RESULTS: At 14 days of age, the dominant bacteria in the feces of the MR and Sham Groups were Enterobacteriaceae, Lactobacillus, and Enterococcus, but Enterobacteriaceae and Clostridium were significantly more common in the AR group than in the MR group. The dominant bacteria in the mesenteric lymph nodes were Enterobacteriaceae, Lactobacillus, and Staphylococcus. The extent of systemic bacterial translocation decreased earlier in the Sham group than in the AR group. CONCLUSIONS: The frequency with which species of bacteria were cultured from mesenteric lymph nodes and other peripheral sites did not mirror the composition of the intestinal flora. Among the translocated bacteria, Staphylococcus may be especially hard to recognize and difficult for the host-defense systems to destroy. Breast-feeding inhibited systemic bacterial translocation in the suckling period of the rat.

Animal Feed↗

PubMed2003

Intraperitoneal administration of oxygenated perfluorochemical inhibits bacterial translocation associated with severe acute pancreatitis.

Bacterial translocation from gut has been assumed to be an infectious source in severe acute pancreatitis. The purpose of this study was to test the effect of intraperitoneal administration of oxygenated perfluorochemical on bacterial translocation associated with rat experimental acute necrotizing pancreatitis. Severe necrotizing pancreatitis was induced by retrograde injection of 3% sodium deoxycholate into the biliopancreatic ducts of male Wistar rats. Although mortality rate was not improved by the treatment, intraperitoneal administration of oxygenated perfluorochemical, perfulorodecalin reduced incidence of bacterial translocation to the mesenteric lymph nodes from 60% to 37% 12 hours after development of pancreatitis, and significantly reduced number of bacterial colonies detected after 24 hours. The treatment did not alter the villous height and crypt depth of the ileum. In this model for pancreatitis, however, accelerated apoptosis of the intestinal epithelium was detected histochemically by TUNEL staining and biochemically by DNA fragmentation ELISA, and the apoptotic changes were significantly suppressed by the treatment. These results indicate that intraperitoneal administration of oxygenated perfluorochemical inhibits apoptosis of intestinal epithelium and bacterial translocation induced in severe acute pancreatitis.

Animals↗

PubMed2000

The effect of interleukin-6 on bacterial translocation in acute canine pancreatitis.

BACKGROUND: Bacterial translocation from the gut to mesenteric lymph nodes and other extraintestinal sites is an important source of infection in acute pancreatitis. Impaired host immunity is known to promote bacterial translocation. Interleukin-6 (IL-6) is a multifunctional cytokine that regulates the immune response, acute phase reaction, and hematopoiesis. METHODS: Twenty-four mongrel dogs (18-29 kg) were studied in four equal groups. In Groups I and II, acute pancreatitis was induced by direct pressure injection of 4% taurocholate and trypsin into the pancreatic duct at laparotomy. Groups III and IV had only laparotomy. Group I and III dogs were given IL-6 (50 microg/kg/d, sq) daily starting 24 h after operation and Group II and IV dogs received an equal volume of saline administered at similar time. All animals had blood drawn for culture, complete blood count (CBC), platelets, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and amylase on d 0, 1, 4, and 7. On d 7, mesenteric lymph nodes (MLN), spleen, liver, pancreas, and cecum were harvested for pathology study and for cultures of aerobic and anaerobic bacteria. Quantitative cecal cultures of aerobic and anaerobic bacteria were obtained. RESULTS: All Group I and Group II dogs had severe pancreatitis. The increase of plasma CRP in Group I was sustained throughout treatment (1.3+/-0.3 on d 0 vs 3.1+/-0.3*, 3.0+/-0.3*, and 2.9+/-0.3* on d 1,4, and 7, respectively). Plasma CRP was increased in Group II on d 1 and d 4 (1.3+/-0.3 mg/dL on d 0 vs 3.6+/-0.3* mg/dL on d 1, and 3.1+/-0.3* on d 4, *p < 0.05). There were no differences in white blood cell (WBC) count, differential, platelets, and ESR between Groups I and II. Bacterial translocation to MLN was lower in Group I (1/6) than in Group II (6/6) (p < 0.05). All 6 dogs in Group II had bacterial spread to distant sites compared to 2 of 6 dogs in Group I (p = 0.066). Both MLN and other distant organ cultures were negative in Group III and only 1 of 6 MLN cultures was positive in Group IV. CONCLUSIONS: IL-6 treatment decreases bacterial translocation to MLN and may be beneficial in reducing septic complications in acute pancreatitis.

Acute Disease↗

PubMed1991

Bacterial translocation.

The phenomenon of bacterial translocation, the movement of viable indigenous microorganisms across the intestinal epithelial barrier, has been recognized for almost 100 years. At the present time, the precise mechanism of microbial transport is unknown. Active epithelial uptake and phagocyte-mediated transport have been proposed as likely explanations for the extraintestinal movement of bacteria to mesenteric lymph nodes and distant organ sites. Translocation has been proposed as the pivotal process associated with intestinal origin portal sepsis in seriously ill and immunocompromised patients. While several etiologic factors can be implicated in the pathogenesis of bacterial translocation, the present clinical implications are based almost solely on studies of dogs, rats and mice. Present investigations continue to suggest a causal relationship between intestinal mucosal integrity and infection by indigenous gastrointestinal bacteria.

Animals↗

PubMed1996

Bacterial translocation and gut microflora in obstructive jaundice.

Bacterial translocation from the gut is implicated in the pathophysiology of complications associated with obstructive jaundice. Absence of intraluminal bile salts and their antiendotoxic effects may result in overgrowth of bacteria, promoting bacterial translocation. The large bowel is the largest source of gram negative bacteria but the small bowel is more permeable. This study investigated the effect of obstructive jaundice on bacterial translocation and on the indigenous luminal microflora at 3 sites in the gastrointestinal tract. Significant bacterial translocation was demonstrated following 7 d of bile duct ligation compared with control or sham operated groups. A qualitative disturbance of the caecal indigenous microflora was demonstrated in jaundiced rats. There was no 'site-to-site' variation in the indigenous microflora at the 3 intestinal sites studied. We conclude that experimental obstructive jaundice for 1 wk promotes bacterial translocation without significant quantitative disturbance of the intestinal microflora in the small intestinal or caecum.

Animals↗

PubMed1984

Assessment of mouse strain on bacterial translocation from the gastrointestinal tract.

The translocation of indigenous bacteria from the gastrointestinal tract to the mesenteric lymphnodes was compared in ten strains of mice. Indigenous Escherichia coli were cultured from the mesenteric lymphnodes of only two of the six mouse strains examined. Thus, spontaneous translocation of indigenous enteric bacteria across the intestinal barrier did not occur to any significant extent in any of the mouse strains examined. Since bacterial overgrowth in the gastrointestinal tract promotes bacterial translocation, bacterial translocation was tested in ten mouse strains including B10 series after antibiotic-decontaminated and subsequent colonization with streptomycin-resistant E. coli C25. E. coli C25 populated the ceca of the mice at levels of 10(8) to 10(9) per gram and translocated to 90-100% of the mesenteric lymphnodes with mean of 10(1.13) to 10(1.86) per mesenteric lymphnode. However, there were no significant differences between mouse strains as to the translocation incidence or the numbers of viable E. coli C25 per mesenteric lymphnode. Thus, genetic differences between mouse strains did not influence bacterial translocation from the gastrointestinal tract to the mesenteric lymphnodes.

Animals↗

PubMed1993

Bacterial translocation after thermal injury.

OBJECTIVES: To review the mechanisms responsible for bacterial translocation after thermal injury. Areas investigated were the rate of bacterial translocation, blood flow to the gastrointestinal tract, potential of reversibility of mesenteric vasoconstriction, specific vasomediators responsible for postburn mesenteric vasoconstriction, potential reversal of gut mucosal atrophy with decreased translocation, and evidence of gut mucosal damage after thermal injury. DESIGN: Using three different animal models consisting of rats, sheep, and minipigs, the objectives were defined. Using the sheep model, the relationship of decreased mesenteric blood flow after thermal injury was defined along with rates of translocation, and the potential reversibility of the postburn mesenteric vasoconstriction and its effect on translocation. The effect of smoke inhalation and the combination of thermal injury and inhalation injury on rates of translocation are explained. Using minipigs, the role that thromboxane A2 plays on the postburn mesenteric vasoconstriction was defined by blocking thromboxane A2 synthesis with OKY046, a specific thromboxane synthetase inhibitor. Evidence of gut mucosal injury was determined using ornithine decarboxylase as an indicator of gut mucosal damage and subsequent repair in the minipig model. The rat model was used to demonstrate gut mucosal atrophy after thermal injury and the potential for reversal of atrophy with the use of bombesin, a specific gut mucosal growth stimulator. RESULTS: After thermal injury, there were significant decreases in mesenteric blood flow. There was also an increase in bacterial translocation. Selective infusion of nitroprusside into the cephalic mesenteric artery prevented the post-burn mesenteric vasoconstriction and attenuated bacterial translocation. Smoke inhalation and smoke inhalation with thermal injury resulted in mesenteric vasoconstriction and increased rates of bacterial translocation. OKY046 infusion prevented the postburn increase in mesenteric vascular resistance. There were increased concentrations of ornithine decarboxylase within the colonic mucosa, indicating a previous injury and the presence of ongoing repair. Likewise, there was gut mucosal atrophy after thermal injury with bacterial translocation. Treating with bombesin attenuates the postburn mucosal atrophy and prevents bacterial translocation. CONCLUSIONS: Thermal injury is associated with mesenteric vasoconstriction. This postburn mesenteric vasoconstriction results in damage to gut mucosa and allows for increases in bacterial translocation. The postburn mesenteric ischemia can be ameliorated with nitroprusside infusion, thus preventing translocation. Thromboxane A2 appears to be a major mediator of the postburn decrease in mesenteric blood flow. Likewise, prevention of postburn gut mucosal atrophy with bombesin attenuates bacterial translocation.

Animals↗

PubMed1994

Bacterial translocation following abdominal trauma in humans.

Bacterial translocation in humans has been identified only with small bowel obstruction and in trauma patients. Our aim was to determine whether the occurrence of bacterial translocation correlates with clinical outcome in trauma patients. All patients requiring exploratory celiotomy for abdominal trauma over a 2-month period were considered for the study. Gross fecal contamination of the abdomen was the only exclusion criterion. Five patients with small bowel injuries without obvious contamination were included. Patients received preoperative antibiotics. Once surgical hemostasis and injury repair were complete, two mesenteric lymph nodes were harvested--one for quantitative culture, the other for electron microscopic evaluation. Postoperatively, patients were monitored for infection via temperature, white blood cell (WBC) count, and, when indicated, chest X-ray (CXR) and culture. Statistical analysis utilized ANOVA (P < 0.05 significant) and linear regression. Sixteen patients were included in the study. Fifteen patients sustained penetrating abdominal trauma, one blunt. Six patients presented in Class I hemorrhagic shock, four in Class II, and two in Class III. The remaining four were not in hemorrhagic shock. Thirteen patients demonstrated bacterial translocation: one by culture alone, nine by electron microscopy, and three by both culture and electron microscopy. Statistical analysis of these three groups and patients without evidence of infection failed to reveal significant difference in average age, injury severity, hospital days, or incidence of postoperative infection. Bacterial translocation occurs following abdominal trauma in humans. Electron microscopic evaluation of mesenteric lymph nodes demonstrated that the incidence of translocation is greater than anticipated by culture alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Injuries↗

PubMed1995

Bacterial translocation from the gastrointestinal tract.

Bacterial translocation is defined as the passage of viable indigenous bacteria from the gastrointestinal tract to extraintestinal sites, such as the mesenteric-lymph-node complex, liver, spleen and bloodstream. Three major mechanisms promote bacterial translocation: intestinal bacterial overgrowth, deficiencies in host immune defenses and increased permeability or damage to the intestinal mucosal barrier.

Animals↗

PubMed2005

Cirrhotic rats with bacterial translocation have higher incidence and severity of hepatopulmonary syndrome.

BACKGROUND: Bacterial translocation, that is, extra-intestinal dissemination of gut bacteria, occurs in approximately 50% of humans and rats with cirrhosis and plays a significant role in enhanced tumor necrosis factor-alpha (TNF-alpha) production. The authors' previous studies have indicated that prevention of bacterial translocation with norfloxacine or inhibition of TNF-alpha with pentoxifylline treatment decreased both the incidence and severity of hepatopulmonary syndrome by attenuating the induction of pulmonary intravascular macrophages in cirrhotic rats. In the present study the hypothesis was tested that the cirrhotic rats with bacterial translocation had higher TNF-alpha production, higher level of sequestration of macrophages in pulmonary vessels, and increased incidence and severity of hepatopulmonary syndrome. METHODS: Rats were studied 5 weeks after common bile duct ligation or sham operation. Bacterial translocation was defined by positive mesenteric lymph node cultures. Hepatopulmonary syndrome was assessed by measurements of alveoloarterial oxygen difference (AaPO(2)) and intrapulmonary shunt. The TNF-alpha concentration in plasma was measured by ELISA. Pulmonary intravascular macrophage sequestration was assessed by lung morphometric analysis. RESULTS: Bacterial translocation occurred in 48% of cirrhotic rats. Plasma concentrations of TNF-alpha and the percentage of vessels with pulmonary intravascular macrophages were higher in the cirrhotic rats with bacterial translocation. Rats with bacterial translocation also had a higher incidence (9% vs 63%, P < 0.01) and severity of hepatopulmonary syndrome, as indicated by higher levels of both AaPO(2) and intrapulmonary shunt. CONCLUSIONS: These results suggest that bacterial translocation may play a role in the pathogenesis of hepatopulmonary syndrome by inducing pulmonary intravascular macrophages through TNF-alpha upregulation.

Animals↗

PubMed2005

Bacterial translocation: not a clinically relevant phenomenon in colorectal cancer.

The aim of this study was to identify the risk factors for bacterial translocation and to determine the clinical significance of bacterial translocation in patients with colorectal cancer. Mesenteric lymph node sampling was performed to identify the presence of bacterial translocation in 75 patients with colorectal cancer undergoing laparotomy. Bacterial translocation was identified in 29 patients (39%), with the most common organism being Escherichia coli (31%). Three factors for bacterial translocation were identified, including a preoperative low peripheral lymphocyte count, metastasis to lymph nodes, and invasion depth (= T3). Stepwise regression analysis, however, selected only = T3 [odds ratio (OR) 4.0, 95% confidence interval (CI) 1.2-13.5]. Altogether, 35% of patients with bacterial translocation developed septic complications, compared with 20% in patients without bacterial translocation. In the multivariate analysis, bacterial translocation was not an independent risk factor for infection, with an OR of 1.8 (95% CI 0.56-5.96). Systemic inflammatory response syndrome developed on the first day in 62% of patients with bacterial translocation, compared with 50% of patients without bacterial translocation. Adjusting for the other factors, bacterial translocation was not a significant risk factor in the occurrence of systemic inflammatory response syndrome after surgery (OR 1.1, 95% CI 0.37-3.29). We concluded that in patients with colorectal cancers bacterial translocation does occur and is increased in patients with deep invasion. However, it appears to be of no clinical significance.

Adolescent↗

PubMed2000

Bacterial translocation in patients undergoing abdominal aortic aneurysm repair.

BACKGROUND: Bacterial translocation occurs in humans and is associated with an increased incidence of septic morbidity. The aims of this study were to determine the prevalence of bacterial translocation in patients undergoing open abdominal aortic aneurysm (AAA) repair and to identify any association with postoperative septic complications. METHODS: This was a prospective observational study in which patients undergoing aneurysm repair were assessed for evidence of bacterial translocation by culture of a mesenteric lymph node (MLN), small bowel serosal exudate and thrombus within the aneurysm. All postoperative septic complications were recorded. RESULTS: A total of 51 patients was studied (40 men, 11 women; median age 72 years). Enteric bacteria were isolated from the MLNs of five patients (prevalence of bacterial translocation 10 per cent), one of whom also yielded growth from the serosal exudate. Septic morbidity occurred in four of five patients in whom bacterial translocation was identified, compared with nine of 46 in those without translocation (P = 0.013, Fisher's exact test, mid P). One patient in whom Escherichia coli was grown from the MLN developed an aortoenteric fistula, with a coliform species isolated from the graft. CONCLUSION: This study suggests that bacterial translocation occurs in patients undergoing AAA repair. It is associated with an increased incidence of postoperative septic morbidity and provides a possible mechanism for infection of prosthetic aortic grafts.

Aged↗

PubMedDate not supplied

The effects of nitric oxide supplementation and inhibition on bacterial translocation in bile duct ligated rats.

Obstructive jaundice promotes bacterial translocation from the gut, but the role of nitric oxide is controversial in this process. We studied the effects of nitric oxide synthase substrate, L-arginine, and nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester, on bacterial translocation in bile duct ligated rats. The animals were randomized into five groups; control, sham, common bile duct ligation alone, nitric oxide inhibition, and nitric oxide supplementation. Obstructive jaundice was performed with common bile duct ligation. L-arginine or N(G)-nitro-L-arginine methyl ester was injected once daily for 14 days. Blood bilirubin level, liver histology, and bacterial translocation to the mesenteric lymph nodes as well as to the liver were assessed. The L-arginine supplemented group had the lowest bacterial translocation rate, but the most prominent hepatic fibrosis. Nitric oxide inhibition increased bacterial translocation to the mesenteric lymph nodes. Therefore, the administration of nitric oxide donor or inhibitor acts as a significant regulatory factor for bacterial translocation in obstructive jaundice.

Analysis of Variance↗

PubMedDate not supplied

P- and E-selectin blockade can control bacterial translocation and modulate systemic inflammatory response.

Bacterial translocation is an important phenomenon in clinical medicine and leads to an increase in patient morbidity and mortality by multiple organ failure. The selectin family plays an important role in the pathogenesis of inflammation, causing an increase in leukocyte-endothelium interactions and inducing a greater leukocyte's migration. This study considered the effect of a sulfo derivative of Sialyl-Lewis(X), GM 1998-016, that will block the P- and E-selectins interaction with a ligand, the Sialyl-Lewis(X), valuing the modulation of the systemic inflammatory response and the induced translocation. Seventy-five Wistar male rats were injected intraperitoneally with Zymosan A and treated with different doses of GM 1998-016 according to study groups. Measurements of values of qualitative and quantitative microbiology, neutrophil infiltration (myeloperoxidase), oxygen free radicals (superoxide anion, superoxide dismutase, catalase, and gluthatione peroxidase), and cytokines (tumor necrosis factor-alpha and interleukin-1beta) were taken at different times after Zymosan administration. A significant decrease of bacterial translocation, both local (MLN) and systemic (p < .05), was observed, with a decrease in the neutrophil infiltration (p < .001), the oxygen free radicals production (p < .01) and the studied cytokines (p < .01). In conclusion, GM 1998-016 showed a protective effect in an in vivo experimental model of bacterial translocation, downregulating the inflammatory response and the leukocyte-endothelium interactions.

Animals↗

PubMedDate not supplied

Bacterial translocation and enteral nutrition in humans: an outsider looks in.

PURPOSE: To assess the literature documenting the existence of bacterial translocation in humans, the effects of enteral nutrition on bacterial translocation in humans, and the hypothesis that enteral nutrition prevents bacterial translocation in humans. DATA IDENTIFICATION: Sources included Medline search, references from review articles, and references from animal and human studies. STUDY SELECTION: The goal was to include all animal and human studies directly addressing questions of bacterial translocation and nutritional status or nutritional support. DATA EXTRACTION: An attempt was made to briefly summarize methodology and findings of relevent studies. No general attempt was made to assess quality of individual studies. RESULTS OF DATA SYNTHESIS: Bacterial translocation is a well documented phenomenon in animal models. Starvation and malnutrition of themselves do not induce bacterial translocation, but may facilitate translocation in the presence of other systemic insults. Parenteral nutrition and many forms of enteral nutrition may induce and/or facilitate bacterial translocation. Chow and certain fiber sources seem protective. Moderate direct and several lines of indirect evidence support the existence of bacterial translocation in humans. There is no direct evidence and questionable indirect evidence suggesting that enteral nutrition prevents or modifies bacterial translocation in humans. CONCLUSIONS: The hypothesis relating enteral nutrition and bacterial translocation in critically ill patients remains attractive, but unproven.

Animals↗