Absence of intestinal bile promotes bacterial translocation.

Previously, the authors documented that extrahepatic biliary obstruction promotes the systemic translocation of bacteria from the intestine to visceral tissues. The current experiments were performed to determine whether it was the absence of intestinal bile or the presence of biliary obstruction that promoted bacterial translocation. Four groups of rats were studied: 1) nonoperated controls (n = 20), sham common bile duct-ligated (n = 22), common bile duct-ligated (n = 25), and common bile duct-diverted (choledochovesical bypass) (n = 23). The sham-ligated group underwent laparotomy and manipulation of the portal region; whereas the ligated group had their common bile ducts ligated, while the choledochovesical group had a silastic tube placed from the common bile duct to the bladder. Seven days later, at death, the incidence of bacterial translocation was higher in the groups of rats subjected to common bile duct ligation (41%) or diversion (32%) than in the control (3%) or sham-ligated (5%) groups (P less than 0.05). Histologic sections of ileums of ligated and diverted animals both showed subepithelial edema. These findings suggest that it is primarily the absence of bile in the intestine that promotes mucosal injury and bacterial translocation and not biliary obstruction.     

Hyperbaric oxygen prevents bacterial translocation in thermally injured rats.

This study was designed to evaluate the effects of hyperbaric oxygen (HBO2) on intestinal microflora and bacterial translocation (BT) caused by experimentally induced thermal injury in rats. Rats were separated into four groups, namely, HBO2 group, thermal injury (TI) group, TI + HBO2 group, and control group. All groups were further separated into short-term (2 days) and long-term (7 days) treatment or injury groups. Control group was neither exposed to thermal injury nor was given any treatment. Thirty percent second-degree thermal burn was induced on the dorsal body part of the rats in TI groups. In the HBO2 groups, rats received HBO2 treatment either without TI or following TI induction, for 2 and 7 days, respectively. Sampling from tissues and portal vein was performed on day 3 in the short-term groups and on day 8 in the long-term groups. Samples were cultured for identification of bacteria and colony counts. HBO2 treatment significantly reduced the colony counts of endogenous microflora in distal ileum of healthy rats (p < .05), while TI significantly increased the colony counts of endogenous microflora in distal ileum in short and long-term TI groups (p < .05). Presence of bacterial translocation was proven by bacterial isolation in mesenteric lymph nodes, liver, spleen and blood. Both short- and long-term HBO2 treatment following TI significantly reduced the colony counts of intestinal microflora (p < .05) and prevented bacterial translocation almost completely. It is concluded that thermal injury causes both bacterial overgrowth within intestinal lumen and bacterial translocation across the intestinal wall. HBO2 administration prevents both bacterial overgrowth and translocation.     

Elemental diet-induced bacterial translocation can be hormonally modulated.

BACKGROUND: The authors have previously documented that feeding mice an elemental diet resulted in bacterial translocation (BT) that could be prevented by the provision of dietary fiber. To test whether the protective effect of fiber was related to the stimulation of trophic gut hormones, the effects of sandostatin and bombesin were tested. METHODS: Mice fed either chow or the elemental diet were stratified into several groups and the ability of bombesin (10 micrograms/kg, tid) or sandostatin (100 micrograms/kg bid) to modulate BT was examined. After 14 days, mice were sacrificed and BT, cecal bacterial population levels, mucosal protein, and small bowel weight was measured. Segments of the ileum and jejunum were examined histologically. RESULTS: Incidence of elemental diet-induced BT (75%) was reduced by fiber (9%) or the administration of bombesin (13%) (p < 0.01). Although sandostatin did not promote BT in chow-fed mice, it reversed the protective effect of fiber on BT (75%) (p < 0.01). CONCLUSION: Elemental diet-induced bacterial translocation can be modulated hormonally and the beneficial effects of fiber on diet-induced BT appears to be hormonally mediated.     

Transplantation of the intestines and bacterial translocation

Infections, sepsis and multiple organ failure syndrome are associated with high morbidity and mortality in human and experimental small bowel transplantation (SBTx). These complications are attributed to bacterial translocation demonstrated in animal and human studies. Bacterial translocation (BT) is defined as the passage of viable bacteria from the intestinal lumen to other tissues or organs. BT has been associated with different clinical and experimental situations, hemorrhagic shock, trauma, bowel obstruction, immunodepression, total parenteral nutrition, antibiotics. Although BT has been investigated in several small and large animal models of SBTx, precise information on the mechanisms involved are not available. It is possible that the operative procedure by itself may promote BT for the interaction of a number of factors such as preservation, ischemia/reperfusion, abnormal motility, lymphatic disruption and aberrant systemic venous drainage, acute or chronic rejection and antibiotic therapy. Furthermore, the potent immunosuppressive therapy used in these patients may augment the deleterious effects caused by BT. In this review we examined the existing literature concerning BT with particular regard to intestinal transplantation, to better understand the alterations in the symbiotic relationship between immunocompromised host and his gut microflora after SBTx.     

Splenectomy influences endotoxin-induced bacterial translocation

To determine whether splenectomy affects the antibacterial defenses of the gut, experiments were performed using bacterial translocation (BT) as a marker of intestinal barrier failure. The incidence of BT was measured 8 days after splenectomy or sham-splenectomy in mice receiving or not receiving endotoxin (0.1 mg IP). Splenectomy does not appear to promote BT from the gut, since the incidence of bacterial translocation after splenectomy or sham-splenectomy (5%) were not different. A second experiment was performed to determine whether the resistance to endotoxin-induced BT was modified after splenectomy. The incidence of endotoxin-induced BT was 73% in the unoperated control group, 59% in the sham-splenectomy group, but 23% in the splenectomy group (p less than 0.002). Thus, splenectomy but not sham-splenectomy increased the resistance of otherwise healthy mice to endotoxin-induced BT.     

Abdominal radiation causes bacterial translocation

The purpose of this study was to determine if a single dose of radiation to the rat abdomen leads to bacterial translocation into the mesenteric lymph nodes (MLN). A second issue addressed was whether translocation correlates with anatomic damage to the mucosa. The radiated group (1100 cGy) which received anesthesia also was compared with a control group and a third group which received anesthesia alone but no abdominal radiation. Abdominal radiation lead to 100% positive cultures of MLN between 12 hr and 4 days postradiation. Bacterial translocation was almost nonexistent in the control and anesthesia group. Signs of inflammation and ulceration of the intestinal mucosa were not seen until Day 3 postradiation. Mucosal damage was maximal by Day 4. Bacterial translocation onto the MLN after a single dose of abdominal radiation was not apparently dependent on anatomical, histologic damage of the mucosa.     

Increased transperitoneal bacterial translocation in laparoscopic surgery

Background: The indications for laparoscopic surgery have expanded to include diseases possibly associated with peritonitis such as appendicitis, perforated peptic ulcers, and diverticulitis. The safety of carbon dioxide (CO₂) pneumoperitoneum in the presence of peritonitis has not been proved. Our previous investigations demonstrated increased bacteremia associated with CO₂ insufflation. In effort to clarify the relative effects of intraabdominal pressure and type of gas, this study was designed to measure bacterial translocation with different gases at different pressures of pneumoperitoneum. Methods: For this study, 110 rats were given intraperitoneal bacterial innoculations with Escherichia coli and equally divided into five groups of 20 animals each. The study groups included a control group with no pneumoperitoneum administered (n = 30), insufflation at a commonly used pressure of 14 mmHg with helium (n = 20) and CO₂ (n = 20), and low insufflation at 3 mmHg with helium (n = 20) and CO₂ (n = 20) in an effort to minimize influences related to pressure. Blood cultures were checked at 15-min intervals for the first 45 min, then hourly thereafter for a total of 165 min after peritoneal inoculation with 2 × 10⁷ E. coli. Results: There is increased risk of bacterial translocation in comparing groups that underwent pneumoperitoneum with those that did not in the rat peritonitis model. Furthermore, these findings are dependent on the presence or absence of gas, but not necessarily on the type of gas used for insufflation. In the low-pressure groups of both gases (helium and CO₂), bacterial translocation was significantly increased, as compared with the control group. Low pressure also was associated with increased bacterial translocation, as compared with high pressure, but beyond 30 min of insufflation, no significant differences were apparent. Conclusions: The risk of bacterial translocation in the E. coli rat peritonitis model is increased with insufflation using CO₂ or helium, and this effect is more significant at lower pressures (3 mmHg) than at higher pressures (14 mmHg). However, no clinically applicable conclusions regarding the relative effects from type of gas or insufflation pressures could be confirmed.     

Tissue antioxidant capacity and bacterial translocation in parenteral nutrition. Experimental study

Alterations in the antioxidant system (AS) has been observed during total parenteral nutrition (TPN). Light exposure or changes in the composition of TPN may affect this deleterious effect. On the other hand, bacterial translocation (BT) is frequent under TPN and may be related to AS. The aim of the study was to determine the adverse effect of standard and glutamine-enriched (GE) TPN, with or without light exposure, on the AS, and its relationship to BT. Forty-nine adult Wistar rats underwent central venous cannulation and were randomly assigned to one of five groups: Sham (n = 16): chow and water ad libitum and saline i.v. TPN (n = 10): had standard TPN. TPN(-) (n = 8): standard TPN without light-exposure. GTPN (n = 8): GE TPN. GTPN(-) (n = 7): GE TPN without light exposure. After 10 days, glutation reduced (GSH) was determined in liver and kidney. Mesenteric lymph nodes, peripheral and portal blood samples were cultured for BT. Comparing to Sham rats, TPN groups had statistically significant lower GSH levels, but there were no differences between standard or GE groups nor with or without light exposure groups. Sham animals had 12% BT. Significantly higher BT (p < 0.05) was found in TPN rats: 70% in TPN group, 88% in TPN(-) group, 86% in GTPN(-) animals and only 50% in GTPN group (p = 0.06 vs TPN group). To conclude: 1. TPN reduces antioxidant capacity and induces BT. 2. Glutamine supplementation or light protection do not improve tissue antioxidant capacity under TPN. 3. Glutamine supplementation tends to reduce BT only in the presence of light. 4. Absence of light exposure does not improve BT TPN-related.     

Simple intestinal obstruction causes bacterial translocation in man

Indirect clinical evidence has accumulated indicating that the gut may be a reservoir for microorganisms causing systemic infection in man. Our experimental results, in a variety of animal models, demonstrate that bacteria can translocate across the mucosal barrier and cause systemic infections. To determine directly whether bacterial translocation occurs in man, we cultured mesenteric lymph nodes (MLNs) obtained at laparotomy from 42 patients, none of whom were clinically infected. Ten (59%) of 17 patients with intestinal obstruction (none of whom had necrotic bowel) had bacteria in their MLNs, in contrast to one (4%) of 25 patients operated on for other reasons. The most common bacteria cultured from the MLNs was Escherichia coli. Thus, it appeared that simple intestinal obstruction of the colon or small bowel in the absence of necrotic bowel was associated with bacterial translocation.     

A model of bacterial translocation in neuroblastoma-bearing mice

PURPOSE: The aim of this study was to establish a model of bacterial translocation (BT) in neuroblastoma-bearing mice. METHODS: A suspension of 1 x 10(6) cells of the murine neuroblastoma cell line C1300 was injected subcutaneously into the thighs of 8-week-old female A/J mice, which were then killed after 7, 14, and 21 days. Some of the mice were given 1-microm or 2-microm fluorescein-labeled latex beads in their drinking water for 7 days before being killed. Mesenteric lymph nodes (MLNs) were aseptically removed and cultured for 72 hours at 37 degrees C. Segments of distal ileum were obtained for histologic examination. Samples of venous blood were obtained for laboratory tests. RESULTS: Tumors were found at the injection sites on days 14 and 21 after C1300 injection. Although tumors were not found in 7 days, significantly high number of 1-microm latex beads were detected in MLNs compared with the control, and the number increased with tumor growth. The number of 2-microm latex beads was significantly higher on days 14 and 21. The percentage of mice with MLN cultures positive were significantly higher on day 14, and the percentage increased along with tumor growth. On day 21 after C1300 injection, body weight loss and anemia were observed, and histologic findings of the terminal ileum showed mucosal edema and villous thinning. Serum levels of interleukin (IL)-6 were significantly higher in mice killed 14 and 21 days after injection. CONCLUSIONS: The results suggest that BT from the gut to MLNs may occur in neuroblastoma C1300-bearing mice, and it increases along with tumor growth. Even in the early stage of malignancy, particles as small as 1 microm may translocate from the gut to MLNs.     

Water-soluble ethylhydroxyethyl cellulose prevents bacterial translocation induced by major liver resection in the rat.

Enteric bacteria might act as pathogens, translocating across the intestinal barrier to extraintestinal sites after major liver resection. In the current study, water-soluble ethylhydroxyethyl cellulose (EHEC) was administered before hepatectomy to evaluate the influence on bacterial translocation induced by major liver resection, phagocytic capacity by visceral and circulating macrophages, enteric bacterial population, and bacterial adherence on the intestinal surface in rats subjected to sham operation or to 70% or 90% hepatectomy. Oral or intravenous (IV) administration of EHEC reduced the incidence of bacterial translocation to mesenteric lymph nodes (MLN) and blood after major liver resection. Oral EHEC appeared more effective than IV administration in protecting against bacterial translocation to MLN in animals with 90% hepatectomy. Ethylhydroxyethyl cellulose (oral and IV) significantly diminished intestinal macrophage uptake capacity of 125I-labeled, heat-killed Escherichia coli as compared with animals without EHEC administration. Overgrowth or colonization of enteric bacteria after major liver resection could be prevented by oral or IV EHEC. Adherence of 14C-labeled, alive E. coli on the intestinal mucosa decreased after EHEC treatment in animals subjected to major liver resection. Systemic arterial pressure and intestinal blood flow markedly decreased from 1 hour and on after 90% hepatectomy. Intravenous administration of EHEC did not improve these alterations. Bacterial hydrophobicity and surface negative charge were significantly reduced 1 hour after bacterial culture with EHEC. Thus, EHEC appears to be a potent agent preventing translocation of enteric bacteria from the gut after major liver resection, by altering the surface characters of enteric bacteria, balancing the enteric microflora, inhibiting bacterial attachment onto the intestinal surface, and blocking phagocytosis by intestinal macrophages.     

Total parenteral nutrition promotes bacterial translocation from the gut

Bacterial translocation from the gut may be the primary event in many disease processes. The purpose of this study was to examine the route of nutrient administration on bacterial translocation from the gut. Each of 90 female Fischer rats underwent placement of a central venous catheter and was randomized to one of three groups. Group I (control) received food and water ad libitum. Group II received standard TPN solution orally from a bottle sipper and drank the solution ad libitum. Group III underwent TPN via the central catheter by pair feeding of the animals with group II. Animals were fed for 2 weeks, and liver, spleen, mesenteric lymph nodes, blood, and cecum were aseptically obtained for culture. A statistically significant difference (p less than 0.014) was found between translocation rates of parenterally fed animals compared with enterally fed animals. Two thirds of the animals (18/27) fed parenterally had culture-positive mesenteric lymph nodes compared with one third (9/27) of the enterally fed group and none (0/30) of the control group. A statistically significant increase in the cecal bacterial count was demonstrated in the animals fed the TPN solution, independent of route. Parenteral nutrition promotes bacterial translocation from the gut by increasing the cecal bacterial count and impairing intestinal defense.     

Effect of total parenteral nutrition plus morphine on bacterial translocation in rats.

OBJECTIVE: This study tested the hypothesis that gut stasis induced by parenteral morphine sulfate (MS) leads to enhanced bacterial translocation in rats on total parenteral nutrition (TPN). SUMMARY BACKGROUND DATA: TPN and MS are common adjuncts in the care of critically ill patients. TPN is known to provoke a variable degree of translocation. MS induces gut stasis with an accompanying bacterial overgrowth. The effect of these two treatments in combination on translocation is not known. METHODS: Rats were provided with central and subcutaneous lines for the continuous infusion of nutrients and drugs, respectively. Intestinal transit was assessed by the caudal movement of a fluorescent marker intubated into the proximal duodenum. Quantitative bacteriology was carried out from various segments of the gut and from ileocecal mesenteric lymph nodes (MLN), spleen, liver, and systemic blood obtained by cardia puncture on sacrifice at 96 hours. RESULTS: Transit was unchanged by TPN alone but prolonged when given in combination with MS. Bacterial overgrowth was also enhanced by MS and increased the bacterial translocation to MLN from 50% of animals with TPN, to 100% in those receiving both TPN and MS; the colony-forming units per MLN increased from 33 +/- 14 with TPN alone to 2079 +/- 811 (STD) with TPN plus MS. Furthermore, no bacteria were found at systemic sites with TPN alone, but in 93.3% of animals receiving TPN and MS. In a subgroup of rates provided with glutamine in TPN, the TPN plus MS effects on translocation were not reversed. CONCLUSIONS: These observations demonstrate the important role that morphine plays in promoting translocation, presumably by disrupting fasting motility and enhancing bacterial overgrowth.     

Glucan and glutamine reduce bacterial translocation in rats subjected to intestinal ischemia-reperfusion.

Intestinal ischemia/reperfusion (I/R) may induce bacterial translocation (BT). Glutamine (GLN)-enriched nutrition decreases BT. However, little is known about the effect of glucan (GL) in BT. This study investigated the combined effect of GL/GLN on BT, intestinal damage, and portal blood cytokines in animals under I/R. Four groups of 10 rats each were subjected to 60 min of intestinal ischemia and 120 min of reperfusion. The control group (group 1) received only rat food/water, group 2 received glutamine via gavage, group 3 received subcutaneuos soluble (1, 3)-d-glucan, and group 4 received GL + GLN. A sham group (group 5) served as a normal control. Bacterial cultures of ileum, mesenteric lymph nodes (MLN), liver and lung biopsies, histological changes of ileum, and serum cytokines variables were examined after I/R. Data were analyzed by analysis of variance (ANOVA) and the Newman-Keuls test. Results showed that GLN, GL, and GL/GLN significantly reduced BT to MLN, liver, and lung. BT was more attenuated after GL treatment than GLN (P < .05). Rats treated with both GL and GLN exhibited lower bacterial colony counts than the ones treated only with GLN or GL. Severe mucosal damage on histological findings was shown in group 1, but these findings were significantly ameliorated (P < .05) in groups 3 and 4. Tumor necrosis factor (TNF)-a and interleukin (IL)-6 levels in portal serum were significantly reduced and IL-10 was increased by GL and GLN treatment. In conclusion, the use of GL was more effective than GLN in reducing BT, intestinal damage, and cytokine levels after I/R. Additionally, the combination of GL and GLN improved results.