Endotoxin promotes the translocation of bacteria from the gut

Experiments were performed in mice to determine whether endotoxin could cause bacteria normally colonizing the gut to spread systemically, a process termed bacterial translocation. Endotoxin given intraperitoneally promoted bacterial translocation in a dose-dependent fashion from the gut to the mesenteric lymph node (MLN). The incidence of bacterial translocation to the MLN was similar whether the endotoxin was administered intramuscularly or intraperitoneally, although the number of bacteria colonizing the MLN was greater with intraperitoneal endotoxin. The incidence and magnitude of endotoxin-induced bacterial translocation were similar between CD-1 and C3H/HeJ (endotoxin-resistant) mice, indicating that bacterial translocation is not prevented by genetic resistance to endotoxin. Thus, it appears that the gut may serve as a reservoir for bacteria causing systemic infections during endotoxemia.     

Endotoxin induces bacterial translocation and increases xanthine oxidase activity

Previously, we documented that endotoxin induces bacterial translocation from the gut and that inhibition or inactivation of xanthine oxidase activity reduces endotoxin-induced bacterial translocation. Consequently, experiments were performed to correlate endotoxin-induced bacterial translocation with changes in intestinal mucosal structure and xanthine dehydrogenase and oxidase activity. Segments of the jejunum, ileum, cecum, proximal colon, distal colon, and liver were harvested from ICR mice 24 hr after IP administration of E. coli 0111:B4 endotoxin (0.1 mg). Xanthine dehydrogenase and oxidase activities were measured in these samples and correlated with intestinal morphology. Bacteria translocated from the intestines to extraintestinal organs in 70% of the mice receiving endotoxin, while the organs of control mice were sterile (p less than 0.01). Endotoxin injured primarily the ileal and cecal mucosa and increased ileal and hepatic xanthine dehydrogenase and cecal oxidase activities (p less than 0.05). These results suggest that xanthine oxidase-induced mucosal damage plays a role in endotoxin-induced bacterial translocation.     

Endotoxin-induced bacterial translocation: a study of mechanisms

Previously, we documented that nonlethal doses of endotoxin cause the translocation (escape) of bacteria from the gut to systemic organs. The purpose of this study was to determine which portion(s) of the endotoxin molecule induces bacterial translocation and to examine the role of xanthine oxidase activity in the pathogenesis of endotoxin-induced bacterial translocation. Nonlethal doses of Salmonella endotoxin preparations (wild type, Ra, or Rb), containing the terminal portion of the core polysaccharide, induced bacterial translocation, whereas those preparations lacking the terminal-3 sugars (Rc, Rd, Re, or lipid A) did not induce bacterial translocation. Additionally, only those endotoxin preparations that induced bacterial translocation injured the gut mucosa, increased ileal xanthine dehydrogenase and oxidase activity, and disrupted the normal ecology of the gut flora, resulting in overgrowth with enteric bacilli. Inhibition of xanthine oxidase activity by allopurinol prevented endotoxin (Ra)-induced mucosal injury and reduced the incidence of bacterial translocation from 83% to 30% (p less than 0.01). These results suggest that endotoxin-induced bacterial translocation requires the presence of the terminal core lipopolysaccharide moiety and that xanthine oxidase-generated oxidants are important in the pathogenesis of endotoxin-induced mucosal injury and bacterial translocation.     

Experimental study of the effects of splenectomy and partial splenectomy on bacterial translocation.

BACKGROUND: The aim of this study is to evaluate the effect of splenectomy and partial splenectomy in a burn-induced bacterial translocation model and to study Kupffer cell (KC) morphology and number. METHODS: Mice were divided into sham-burn and burn groups. Each group was also subdivided to sham-splenectomy, partial-splenectomy, and splenectomy subgroups. At day 0, operations were performed. At the postoperative 10th day, a sham burn or burn injury was made in all animals. Twenty-four hours later, cultures for bacterial translocation were obtained and livers were evaluated for the quantity and morphology of KCs. RESULTS: Burned-splenectomized animals had significantly decreased bacterial translocation when compared with sham-splenectomized animals (p = 0.031). Interestingly, in both the sham-burned and burned groups, splenectomy subgroups had significantly higher numbers of KCs compared with partial-splenectomy and sham-splenectomy subgroups (p<0.00000). Burn injury caused a significant decrease of KC numbers in all subgroups compared with their correspondent sham-burned subgroups (p<0.05). CONCLUSION: Results revealed that splenectomy decreases bacterial translocation and also increases the number of KCs.     

Hemorrhagic shock-induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation

Experiments were performed to determine whether bacterial translocation (BT) after hemorrhagic shock is due to a reperfusion injury mediated by xanthine oxidase-derived oxidants. Rats were subjected to 30 minutes of shock (30 mm Hg) followed by reinfusion of shed blood. Twenty-four hours after hemorrhage and reinfusion, the mesenteric lymph node, liver, and spleen were harvested from each animal for bacterial culture, and the ileum and cecum were examined histologically. Sham-shocked (control) rats were instrumented, but blood was not withdrawn. The incidence of BT was higher in the shocked rats (61%) than in the sham-shocked animals (7%) (p less than 0.01). Allopurinol (50 mg/kg, administered orally), a competitive inhibitor of xanthine oxidase, reduced the incidence of shock-induced BT to 14% (p = 0.02). Similarly, rats fed a tungsten-supplemented molybdenum-free diet, which inactivates xanthine oxidase, reduced shock-induced BT to 10% (p = 0.02). The histologic damage cause by hemorrhagic shock was prevented by blocking xanthine oxidase activity. Thus hemorrhagic shock-induced bacterial translocation from the gut appears to be mediated by oxidants generated by activation of the xanthine oxidase system.     

The gut as a portal of entry for bacteremia. Role of protein malnutrition.

The current studies were performed to determine the influence of malnutrition alone or in combination with endotoxemia in promoting bacterial translocation from the gastrointestinal tract. Bacterial translocation did not occur in control, starved (up to 72 hours), or protein-malnourished (up to 21 days) mice not receiving endotoxin. Bacterial translocation to the mesenteric lymph nodes (MLNs) occurred in 80% of control mice 24 hours after receiving endotoxin (p less than 0.01). However, the combination of malnutrition plus endotoxin was associated with a higher incidence of translocation to the systemic organs (p less than 0.01), and higher numbers of bacteria per organ (p less than 0.01), than was seen in normally nourished mice receiving endotoxin. Additionally, mice that were protein malnourished were more susceptible to the lethal effects of endotoxin than were control animals, and the mortality rate was directly related to the degree of malnutrition (R2 = 0.93) (p less than 0.05). Histologically, endotoxin in combination with protein malnutrition resulted in mechanical damage to the gut mucosal barrier to bacteria. Thus, in the mice that were protein malnourished the spread of bacteria from the gut could not be controlled nor could translocated bacteria be cleared as well as normally nourished mice receiving endotoxin. These results support the concept that under certain circumstances the gut may serve as a clinically important portal of entry for bacteria.     

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.     

Incidence of bacterial translocation in four different models of experimental short bowel syndrome

The outcome of patients with short bowel syndrome is influenced for factors such as the length of remnant intestine or the presence or absence of ileocecal valve (ICV). Gram-negative sepsis, the main cause of mortality in this group of children, is probably due to bacterial translocation (BT), because after gut resection there are a number of circumstances that favour its occurrence, being the most known intestinal dismotility, bacterial overgrowth, loss of gut-associated lymphoid tissue, total parenteral nutrition (TPN) and fasting related mucosal atrophy. The aim of this experimental controlled study was to test the incidence of BT after four different types of gut resection, in animals fed orally or receiving TPN. Hundred and three adult Wistar rats bred and raised in our facilities according to European Union Regulations were randomly divided in six groups:--Group 1 (n = 26): non-manipulated animals, served as a control.--Group 2 (n = 14): 80% non-lethal small bowel resection, fed orally.--Group 3 (n = 15): same resection as group 2 but including ICV. Rat chow ad libitum.--Group 4 (n = 27): non-resected fasting animals receiving all-in-one TPN solution.--Group 5 (n = 11): same resection as group 2, but fasting and receiving TPN--Group 6 (n = 10): 90% small bowel resection, including cecum and ICV, fasting and TPN. The animals were maintained for 10 days in individual metabolic cages, and, at the end of the experiment, were bled by portal and cardiac puncture. Mesenteric lymph nodes, peripheral and portal blood samples were cultured for BT. Non-manipulated rats (group 1) had lower BT incidence (8%) than resected ones (groups 2, 3, 5 and 6, 93%, 60%, 91%, 60%, p < 0.05) or animals non-resected, receiving TPN (group 4.51%, p < 0.05). When resection included ICV in orally fed rats BT index was also lower (group 3 vs group 2.60% vs 91%, p < 0.05). In TPN resected animals a drop was also found in BT when ICV and cecum were added to small bowel resection (group 6 vs group 5.60% vs 91%, p < 0.05). In conclusion: 1. Gut resection is associated to a high degree of BT, even if the animals are fed orally. 2. Resection including ICV, produced less BT. 3. TPN-related BT was shown in half of the animals non resected. 4. TPN-resected rats had also less BT when ICV and cecum were removed.     

Effect of stress and trauma on bacterial translocation from the gut

Previously, we established that bacteria contained within the gut can cross the GI mucosal barrier and spread systemically, a process termed bacterial translocation. Three models were used to extend this work: cold exposure (up to 16 hr at 4 degrees C), a nontissue injury stress model; femoral fracture-amputation, a trauma model; and thermal injury (30% third-degree burn), a trauma model with retained necrotic tissue. CD-1 mice either with a normal GI microflora or who were monoassociated with Escherichia coli C-25 were subjected to sham or actual stress or trauma. The animals were sacrificed at various times postinsult and the ceca, mesenteric lymph nodes (MLN), spleens, and livers were quantitatively cultured. Neither the incidence nor the magnitude of bacterial translocation was increased in the cold-exposed animals compared to control mice. The incidence of bacterial translocation to the systemic organs was higher in the animals with a normal flora receiving femoral fracture amputation (11%) (P less than 0.02) than in animals receiving a thermal injury (1%) or sham-injured control mice (0%). In contrast, the incidence of translocation to the liver or spleen was higher in burned mice monoassociated with E. coli C-25 (60%) (P less than 0.01) than in E. coli monoassociated mice sustaining femoral fracture amputation (17%). Stress alone (cold exposure) does not promote bacterial translocation; however, trauma, especially in combination with retained necrotic tissue, promotes bacterial translocation. Thus bacteria colonizing the gut can invade systemic organs after trauma, especially when the normal ecology of the gut flora has been disrupted.     

Genetic susceptibility to mucosal damage leads to bacterial translocation in a murine burn model

Since genetic factors may be important in host resistance to infections after thermal injury, we screened the susceptibility of three mouse strains (CD-1, Balb/c, and C57/bl) to thermally induced bacterial translocation from the GI tract. Bacteria translocated to the MLNs of Balb/c but not the CD-1 or C57/bl mice receiving 25% body burns. The increased incidence of bacterial translocation in the burned Balb/c mice appeared to be due to a burn-induced gut mucosal injury, since the intestinal mucosa of the Balb/c but not the CD-1 or C57/bl mice was damaged 24 hr after the thermal injury. The mucosal injury appears to be mediated, at least in part, by xanthine oxidase-generated oxygen-free radicals, since inhibition of xanthine oxidase activity with allopurinol, or inactivation of xanthine oxidase activity by a molybdenum-free tungsten diet, prevented the mucosal injury and reduced the extent of bacterial translocation.     

Endotoxin but not malnutrition promotes bacterial translocation of the gut flora in burned mice

Previously we have shown that under certain conditions, bacteria can pass through the intact epithelial mucosa to the mesenteric lymph nodes (MLN), liver, spleen, and bloodstream to cause infection, a process termed bacterial translocation. To extend these studies, we determined the influence of protein malnutrition and endotoxemia on bacterial translocation in burned (25% TBSA) and unburned mice. The results of these experiments documented that protein malnutrition did not promote bacterial translocation from the gut in either burned or unburned animals, although it did disrupt the normal indigenous gut flora. In contrast, a nonlethal dose of endotoxin (IP) promoted bacterial translocation to the mesenteric lymph nodes in burned and unburned mice, but only in burned mice did the bacteria translocate from the gut to other systemic organs (p less than 0.01). Furthermore, the mortality rate of mice receiving only endotoxin or burn was less than 10%, while the combination of endotoxin plus a thermal injury increased the mortality rate to 100% (p less than 0.01). These studies support the concept that bacteria may translocate from the gut to other organs and be a potential source of lethal infections after thermal injury.     

Total parenteral nutrition-induced changes in gut mucosal function: atrophy alone is not the issue.

BACKGROUND. Total parenteral nutrition (TPN) has been implicated in gut atrophy and breakdown of barrier function leading to bacterial translocation (BT) in animals. BT during TPN, however, is not found consistently, and it has therefore been suggested that macromolecular permeability may occur independently of BT during TPN. METHODS. Male Sprague-Dawley rats were administered isocaloric standard TPN enterally, parenterally, or split equally between the two routes or allowed food ad lib. A second group of rats was administered isocaloric TPN with and without 4% lipids, and changes in gut barrier function were assessed by measuring lactulose permeability. RESULTS. Rats receiving TPN both enterally and parenterally maintained histologic intestinal structure to the same degree as rats fed enterally and those allowed food. Although parenteral feeding led to significant gut atrophy and cecal bacterial overgrowth, BT was not increased. Gut permeability to lactulose, however, was increased significantly in the TPN groups. Lipid content did not affect outcome. CONCLUSIONS. These results suggest that gut atrophy, BT, and permeability to macromolecules are not necessarily related. Gut-origin septic states during TPN or trauma may be caused by an increased escape of macromolecules from the gut, and BT may be an end result rather than a primary cause of such septic episodes.     

急性坏死性胰腺炎并发感染防治方法的实验研究

目的 观察不同方法对急性坏死性胰腺炎（ＡＮＰ）并发感染的防治效果。方法 用胰管逆行注入法复制犬和大鼠ＡＮＰ模型,将大鼠随机分为非治疗组和中药、微生态、导泻、选择性肠道脱污染（ＳＤＤ）和生长抑素５个治疗组,观察胰、肠组织学、肠上皮细胞间连接结构、肠通透性、肠道菌群、脏器细菌移位率和病死率的变化。结果 中药清胰汤、双歧杆菌合剂和ＳＤＤ能明显改善肠道屏障的肠通透性,减轻细菌移位,降低病死率,单纯导泻效果     

Thermal injury promotes bacterial translocation from the gastrointestinal tract in mice with impaired T-cell-mediated immunity

We have shown previously that after thermal trauma viable bacteria will cross the intact gastrointestinal mucosa (bacterial translocation) to invade the mesenteric lymph nodes and other organs if the normal indigenous microflora is disrupted, allowing bacterial overgrowth. To determine whether T-cell-mediated immunity (T-CMI) was important in preventing translocation after thermal injury in animals with an intact normal flora, conventional (+/+), athymic (nu/nu), and heterozygous (nu/+) mice receiving a 30% third-degree burn were killed at various intervals after burn and their organs cultured. Bacterial translocation did not occur in control or burned specific pathogen-free mice with intact T-CMI but did occur in athymic mice with deficient T-CMI. Both the incidence of positive organs and the numbers of translocated bacteria per gram of organ were increased after thermal injury. Bacterial overgrowth was not responsible for these findings, since the levels of cecal enteric bacteria were not different between the burned and nonburned groups. Since translocation occurred to a greater extent in athymic burned mice than control athymic mice, it appears that a thermal injury promotes translocation by impairing other host defense systems in addition to the T-CMI.     

Prostaglandin E1 maintains structural integrity of intestinal mucosa and prevents bacterial translocation during experimental obstructive jaundice.

The absence of bile in the gut lumen induces mucosal injury and promotes bacterial translocation (BT). Prostaglandin E (PGE) has a protective effect on the mucosal layer of the alimentary tract. We hypothesize that PGE1 may prevent BT by its beneficial action on the mucosa of the small bowel. Thirty Wistar albino rats were divided equally into 3 groups; Group 1 (control) underwent sham laparotomy, group 2 obstructive jaundice (OJ) and group 3 (OJ + PGE1) underwent common bile duct (CBD) ligation and transection. Groups 1 and 2 received; 1 mL normal saline and group 3 received 40 mg of the PGE1 analogue misoprostol dissolved in 1 mL normal saline administered by orogastric tube once daily. After 7 days, laparotomy and collection of samples for laboratory analyses were performed, including bacteriological analysis of intestine, mesenteric lymph nodes (MLNs), and blood, and histopathologic examination of intestinal mucosa to determine mucosal thickness and structural damage. Serum bilirubin and alkaline phosphatase levels confirmed OJ in all animals with CBD transection. The mucosal damage score was significantly reduced in jaundiced animals receiving PGE1 compared to jaundiced controls (2.15 +/- 0.74 vs 5.3 +/- 0.59; p < .00001) and mucosal thickness was greater (607 +/- 59.1 microm vs. 393 +/- 40.3 microm; p < .00001). The incidence of BT to MLNs decreased from 90% to 30% (p < .02) when jaundiced rats received PGE1. PGE1 treatment reduced the detection rate of viable enteric bacteria in the blood from 60% to 10% (p < .057). We conclude that administration of PGE1 provides protection against OJ-induced atrophy and damage of intestinal mucosa, and thereby prevents translocation of enteric bacteria to underlying tissues.     

Hemorrhagic shock-induced bacterial translocation: the role of neutrophils and hydroxyl radicals

We previously documented a relationship between xanthine oxidase activation, intestinal injury, and bacterial translocation (BT) in rats subjected to hemorrhagic shock. The current experiments were performed to determine the relative roles of hydroxyl radicals and neutrophils in the pathogenesis of shock-induced mucosal injury and BT. The incidence of BT was higher in the shocked rats (30 mm Hg for 30 min) than the sham-shock controls (87% vs 12.5%; p less than 0.01). Administration of the hydroxyl radical scavenger, dimethyl sulfoxide (DMSO), or the iron chelator, deferoxamine, reduced the incidence of BT from 87% to 20% and 40%, respectively (p less than 0.05). DMSO and deferoxamine appear to prevent shock-induced BT by blunting the magnitude of shock-induced mucosal injury. In contrast, neutrophil depletion did not prevent BT or protect the intestinal mucosa in shocked rats. Instead, the incidence of systemic spread of translocating bacteria past the mesenteric lymph nodes to the livers and spleens of the shocked rats was higher in the neutrophil-depleted rats (56%) than in any other group (p less than 0.01). Thus, shock-induced BT and intestinal injury appear to be mediated by oxidants (.OH) derived from xanthine oxidase, rather than granulocytes.     

Effect of growth hormone, epidermal growth factor, and insulin on bacterial translocation in experimental short bowel syndrome

BACKGROUND/PURPOSE: An adaptive process starts in the remaining intestine after massive resection, and several trophic factors including growth hormone (GH), epidermal growth factor (EGF), and insulin (INS) have been shown to have a positive effect on it. Bacterial translocation (BT) is frequent after extensive small bowel resection, but the effects of GH, EGF, or INS have not been investigated in experimental short bowel syndrome (SBS). This study tests the hypothesis that GH, EGF, or INS decrease BT in SBS in rats with parenteral nutrition (PN). METHODS: Thirty-eight adult Wistar rats underwent central venous cannulation and were assigned randomly to 1 of 4 groups receiving for 10 days 4 treatment regimes: (1) PN group (n = 10): fasting, all-in-one PN solution (300 mL/kg/24 h, 280 kcal/kg/24 h), 80% gut resection including ileo-cecal valve; (2) GH group (n = 9): fasting, same PN regime and resection, GH (1 mg/kg/d, subcutaneously); (3) EGF group (n = 9): fasting, PN, resection, EGF (150 microg/24 h intravenously); (4) INS group (n = 9): fasting, PN, resection, INS (1 UI/100 g/24 h subcutaneously). At the end of the experiment they were killed, and mesenteric lymph nodes (MLN) and peripheral and portal blood samples were recovered and cultured. Several fragments of intestine were taken to determine cell proliferation (PCNA index) and morphometric parameters (villous height, crypt depth). RESULTS: GH, EGF, and INS groups showed a 28%, 29%, and 30% increase in gut mucosal thickness, and PCNA index rose 21%, 20%, and 25%, respectively in comparison with PN controls. Bacterial translocation to peripheral blood was detected in 0% of PN animals and in 44%, 40%, and 28% of GH, EGF, or INS rats, respectively (P < .05). No differences were found in BT in MLN or portal blood among groups. CONCLUSION: Administration of GH, EGF, or INS improves gut mucosal structure in rats with SBS under PN, but, surprisingly, the incidence of BT detected in peripheral blood was increased rather than decreased in animals receiving these treatments.     

Granulocyte macrophage colony-stimulating factor improves survival in two models of gut-derived sepsis by improving gut barrier function and modulating bacterial clearance.

OBJECTIVE: The effect of recombinant murine granulocyte macrophage colony-stimulating factor (rmGM-CSF) on survival and host defense was studied using two clinically relevant models of infection that included transfusion-induced immunosuppression. SUMMARY BACKGROUND DATA: Granulocyte macrophage colony-stimulating factor improves resistance in several models of infection, but its role in transfusion-induced immunosuppression and bacterial translocation (gut-derived sepsis) has not been defined. METHODS: Balb/c mice were treated with 100 ng of rmGM-CSF or placebo for 6 days in a model of transfusion, burn, and gavage, or cecal ligation and puncture (CLP). Translocation was studied in the first model. RESULTS: Survival after transfusion, burn, and gavage was 90% in rmGM-CSF-treated animals versus 35% in the control group (p < 0.001). After CLP, survival was 75% in the rmGM-CSF group versus 30% in the control group (p = 0.01). Less translocation and better killing of bacteria was observed in the tissues in animals treated with rmGM-CSF. CONCLUSION: The ability of rmGM-CSF to improve gut barrier function and enhance killing of translocated organisms after burn injury-induced gut origin sepsis was associated with improved outcome. Granulocyte macrophage colony-stimulating factor also improved survival after CLP.     

Hemorrhagic shock induces bacterial translocation from the gut

Sepsis and multiple organ failure are common after hemorrhagic shock. The goal of the current experiments was to determine whether hemorrhagic shock would promote the translocation of bacteria from the gut to visceral organs. Twenty-four hours after being subjected to sham shock, or 30, 60, or 90 minutes of shock (30 mm Hg), rats were sacrificed and their organs quantitatively cultured for translocating bacteria. There was a direct relationship between the duration of hemorrhagic shock and the 24-hour mortality rate (p = 0.02). Bacteria did not translocate from the gut in the sham-shock rats, but did translocate to the mesenteric lymph nodes, livers, and spleens of the rats subjected to hemorrhagic shock (p less than 0.01). Rats subjected to 90 minutes of shock shock exhibited a greater degree of bacterial translocation than rats receiving 30 or 60 minutes of shock (p less than 0.05). The most common translocating bacteria were Escherichia coli and Enterococcus. Hemorrhagic shock injured the gut mucosa and caused subepithelial edema and focal areas of necrosis. Thus hemorrhagic shock followed by reinfusion of shed blood disrupts the gut barrier and allows indigenous bacteria normally contained within the gut to cause systemic infections.     

Gut bacterial translocation and postoperative infections: a prospective study in schistosomotic patients

BACKGROUND: Bacterial translocation (BT) across the intact intestinal mucosal barrier has been postulated as a source of sepsis in susceptible patients, including those with cirrhosis and portal hypertension. This condition has not been studied in hepatosplenic schistosomiasis, wherein portal hypertension and the presence of an immune deficiency state associated with the parasitic disease could predispose to BT into mesenteric lymph nodes (MLN). A study was conducted to determine the prevalence of aerobic bacteria in MLN (bacterial translocation) of patients with hepatosplenic schistosomiasis, and establish a possible association with postoperative infections. METHODS: In a series of 51 patients submitted to surgical treatment of schistosomotic portal hypertension with splenectomy and gastric devascularization, MLN were obtained from each patient at the beginning (MLN1) and at the end (MLN2) of the surgical procedure, and sent for bacteriological analysis. Prospective patient evaluation during the postoperative period correlated positive MLN cultures with infectious complications. RESULTS: The prevalence of aerobic bacteria was 17.6% at MLN1 and 27.5% at MLN2, however, this difference was non-significant (p = 0.24). Bacterial translocation to all MLN was 22.5%. Escherichia coli was the most frequent organism (26.1%, 6/23). The overall incidence of postoperative infections was 19.6% (10/51), with a significant association with the presence of positive cultures of MLN (p = 0.043). CONCLUSIONS: The findings of this study suggest that the presence of aerobic bacteria on MLN as a consequence of BT may play a role in the development of postoperative infectious complications, particularly in schistosomotic patients.