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At least 19 recordsLinked to original sources

PubMed1992

The effect of surgical trauma on the bacterial translocation from the gut.

Bacterial translocation is the passage of viable bacteria from the lumen of the gastrointestinal tract through the intestinal mucosa to other sites. It is believed that bacterial translocation may lead to infection and septicemia. The purpose of this study was to determine what factors in experimental surgical trauma lead to bacterial translocation. Two-month-old Wistar albino rats were divided into five groups: (A) control; (B) anesthesia (ether inhalation); (C) anesthesia and surgery (median laparotomy and transient compression of the intestines); (D) fasting only; and (E) anesthesia, surgery, and fasting. After 48 hours, ileum, mesenteric lymph nodes, and blood were cultured for aerobic and anaerobic organisms. In each group the number of animals with bacteria overgrowth was calculated. The incidence of bacterial translocation to mesenteric lymph nodes and blood in groups B and D were similar to the controls (P greater than .01). There was a significant increase in the number of animals with bacterial translocation in groups C and E (P less than .001). The majority of translocating bacteria were E coli.

Animals↗

PubMed1992

[Bacterial translocation in Crohn disease].

Bacterial translocation is the passage of viable endogenous bacteria from the gastrointestinal tract to mesenteric lymph nodes and other internal organs. The aim of this work was to study bacterial translocation in patients operated on for Crohn's disease. Twenty-eight patients, mean age 29 years, not having received any antibiotics since at least 8 days, presenting with ileal (n = 12), ileo-colonic (n = 14) or colonic (n = 2) Crohn's disease were studied. In 25 out of 28 cases (89%) indication for surgery was strictures inducing an upper small bowel distension in 9 out of 25 patients. Mesenteric lymph nodes and liver biopsies, portal blood samples and peritoneum swabs were harvested after laparotomy and before gut opening. Bacterial translocation, defined as the presence of intestinal bacteria in at least one of the specimens, was present in 8 out of 28 patients. This was found in lymph nodes draining surgical territories in 7 out of 8 cases. Bacterial strains involved in translocation included E. coli (n = 5), Enterococcus (n = 3), Clostridium perfringens (n = 2), Proteus (n = 2), and Bacteroides fragilis (n = 1). The rate of translocation differed neither according to Crohn's disease site nor with perforating or non perforating type of the disease. Five out of 9 patients operated on for strictures with proximal distension had a translocation. In conclusion, bacterial translocation was identified in 29% of patients operated on for Crohn's disease in this series. Distension of the intestine proximal to a digestive stricture could favor the occurrence of bacterial translocation in Crohn's disease.

Adolescent↗

PubMed1985

Bacterial translocation from the intestines.

Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal (GI) tract through the mucosal epithelium to other sites, such as the mesenteric lymph nodes, spleen, liver and blood. This paper reviews results from animal models utilized to obtain information concerning the defense mechanisms operating in the healthy host to confine bacteria to the GI tract. Gnotobiotic and antibiotic-decontaminated mice colonized with particular bacteria demonstrated that the indigenous GI flora maintains an ecologic equilibrium to prevent intestinal bacterial overgrowth and translocation from the GI tract. Studies with athymic (nu/nu) mice, thymus-grafted (nu/nu) mice, neonatally thymectomized mice, and mice injected with immunosuppressive agents demonstrated that the host immune system is another defense mechanism inhibiting bacterial translocation from the GI tract. Ricinoleic acid given orally to mice disrupted the intestinal epithelial barrier allowing indigenous bacteria to translocate from the GI tract. Thus, bacterial translocation from the GI tract of healthy adult mice is inhibited by: (a) an intact intestinal epithelial barrier, (b) the host immune defense system, and (c) an indigenous GI flora maintaining ecological equilibrium to prevent bacterial overgrowth. Deficiencies in host defense mechanisms act synergistically to promote bacterial translocation from the GI tract as demonstrated by animal models with multiple alterations in host defenses. Bacterial translocation occurred to a greater degree in mice with streptozotocin-induced diabetes, mice receiving nonlethal thermal injury, and mice receiving the combination of an immunosuppressive agent plus an oral antibiotic than in mice with only a primary alteration in host defenses. The study of bacterial translocation in these complex models suggests that opportunistic infections from the GI tract occur in discrete stages. In the healthy adult animal, bacterial translocation from the GI tract either does not occur or occurs at a very low level and the host immune defenses eliminate the translocating bacteria. Bacterial translocation does take place if one of the host defense mechanisms is compromised, such as a deficiency in the immune response, bacterial overgrowth in the intestines, or an increase in the permeability of the intestinal barrier. In this first stage, the bacteria usually translocate in low numbers to the mesenteric lymph node, and sometimes spleen or liver, but do not multiply and spread systemically.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

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.

Animals↗

PubMed1990

Bacterial translocation in colorectal cancers.

Bacterial translocation, the passage of viable indigenous bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other internal organs, has been poorly studied in man to date. Pericolonic lymph nodes, liver, portal blood, and peritoneum specimens were harvested before antibiotics were administered during 20 operations for colorectal cancer and compared with those obtained in 20 operations for non colorectal conditions. Bacterial translocation, defined as the presence of intestinal bacteria in at least one of the specimens, was found in 13 patients (65 percent) in the colorectal cancer group as compared to 6 (30 percent) in the control group (p less than 0.05). The increased incidence of bacterial translocation in colorectal cancers was mainly due to the presence of bacteria in the pericolonic lymph nodes adjacent to the cancer. These findings suggest that intestinal bacteria translocate from the bowel lumen in a high proportion of patients with colorectal cancer and further stress the need for prophylactic antibiotics in colorectal cancer surgery.

Adenocarcinoma↗

PubMed1992

Zymosan-induced bacterial translocation: a study of mechanisms.

BACKGROUND AND METHODS: At nonlethal doses, zymosan induces a systemic inflammatory state and promotes bacterial translocation. This study was performed to investigate the mechanisms by which zymosan causes intestinal mucosal injury and bacterial translocation. Bacterial translocation to the mesenteric lymph node was measured 24 hrs after intraperitoneal challenge with saline or zymosan (0.1 mg) in normal (CD-1), congenitally macrophage-hyporesponsive (C3H/HeJ), complement-deficient (DBA/2), or mast cell-deficient (W/Wv) mice. Since zymosan-induced bacterial translocation may be mediated by xanthine oxidase-generated oxidants, bacterial translocation was measured in mice pretreated with the xanthine oxidase inhibitor, allopurinol. To further investigate the role of oxidants in zymosan-induced bacterial translocation, ileal and hepatic levels of xanthine oxidase, myeloperoxidase, conjugated dienes, malondialdehyde, and the antioxidants--superoxide dismutase, catalase, and glutathione peroxidase, were measured. RESULTS: Zymosan-induced mucosal injury and bacterial translocation occurred to a similar extent (p less than .05) in all four genetic strains of mice, but were reduced in the mice pretreated with allopurinol. Zymosan increased (p less than .03) ileal and hepatic xanthine oxidase activity, while reducing (p less than .01) antioxidant (catalase) activity. There was also evidence of hepatic, but not ileal, lipid peroxidation (conjugated diene) (p less than .05) and neutrophil sequestration (myeloperoxidase) (p less than .01). CONCLUSIONS: Zymosan-induced intestinal mucosal injury and bacterial translocation do not require complement activation, or the release of macrophage or mast cell products. They appear to be mediated by xanthine oxidase-generated products and associated with disruption of the normal ileal and hepatic oxidant-antioxidant balance.

Allopurinol↗

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↗

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↗

PubMed1987

Effect of starvation, malnutrition, and trauma on the gastrointestinal tract flora and bacterial translocation.

We have previously shown, in an animal model, that viable indigenous bacteria will cross the intact gastrointestinal (GI) mucosa and spread systemically, a process termed bacterial translocation, if the normal bacterial ecology of the gut was sufficiently disrupted to allow bacterial overgrowth or if the animals were severely immunosuppressed. Starvation or protein malnutrition disrupts the normal indigenous GI tract microflora and impairs host antibacterial defenses. Consequently, we tested the effect of the combination of starvation or protein malnutrition plus burn trauma in promoting bacterial translocation from the GI tract. Bacterial translocation was measured by quantitatively culturing the mesenteric lymph nodes, spleens, livers, blood, and peritoneal cavities of normal or burned (30% of total body surface area) CD1 mice deprived of food for three days or fed a low-protein (0.03%) diet. The effect of starvation or protein malnutrition on the gut microflora was determined by quantitatively measuring the levels of bacteria present in the ceca. Both starvation and protein malnutrition increased the cecal levels of gram-negative enteric bacilli and decreased the levels of lactobacilli and strict anaerobes. Surprisingly, neither starvation nor protein malnutrition promoted bacterial translocation, even though these animals lost over 20% of their body weight and the ecology of the gut microflora was disrupted. In fact, the protein-malnourished animals exhibited lower incidences of bacterial translocation than normally nourished animals when both groups were monoassociated with Escherichia coli C-25 or monoassociated and burned. Thus, it appears that protein malnutrition does not promote bacterial translocation, even when combined with burn trauma.

Animals↗

PubMed1991

Hemorrhagic shock and bacterial translocation in a swine model.

Bacterial translocation is proposed as an explanation for sepsis associated with hemorrhagic shock. This study attempted to document these events in a large animal model. Male swine were randomly assigned to control (n = 10) or experimental (n = 10) groups. Animals were anaesthetized, and the bladder, portal vein, and a mesenteric lymphatic vessel cannulated. Experimental animals were bled 40% of blood volume. Over the next six hours maintenance fluids were given, and cultures of portal blood and mesenteric lymph taken. Before the swine were killed, cultures were taken from portal and systemic blood, mesenteric lymph, and lymph nodes, and a portion of terminal ileum was resected for histologic study. Experimental animals experienced significant shock as demonstrated by changes in hemodynamic and biochemical variables. Cultures and histologic examination of the terminal ileum showed no significant difference between control and experimental animals. In an unresuscitated swine model, significant bacterial translocation was not demonstrated within six hours of hemorrhagic shock.

Animals↗

PubMed1989

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.

Animals↗

PubMed1989

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.

Animals↗

PubMed1990

Food without fiber promotes bacterial translocation from the gut.

To determine whether the route and/or composition of nutritional support alters intestinal barrier function (measured as bacterial translocation), rats were divided into three groups: food (controls), intravenous total parenteral nutrition (IV-TPN) fed, and oral total parenteral nutrition (ORAL-TPN) fed. Bacterial translocation did not occur in the rats that were fed normally, but did occur in 60% of the rats fed the IV-TPN or the ORAL-TPN diets for 7 days (p less than 0.05). Since both the IV-TPN and ORAL-TPN diets induced bacterial translocation and the TPN solution (28% glucose and 4.5% amino acids) lacks fiber, two additional groups of rats were fed orally 2.5 gm cellulose powder/day plus TPN solution by either the intravenous or the oral route. The addition of cellulose powder decreased the incidence of bacterial translocation to 8% in the group fed the ORAL-TPN diet and to 0% in the group fed the IV-TPN diet. Cellulose improved intestinal barrier function, even though it did not prevent bacterial overgrowth or the loss of mucosal mass in the rats fed the IV-TPN or ORAL-TPN diets. Cellulose powder appears to have prevented bacterial translocation primarily by preventing IV-TPN- or ORAL-TPN-induced alterations in mucosal structure. Thus the oral administration of this fiber maintains intestinal barrier function and prevents bacterial translocation even in the absence of oral nutrients.

Administration, Oral↗

PubMed1990

Effect of hemorrhagic shock on bacterial translocation, intestinal morphology, and intestinal permeability in conventional and antibiotic-decontaminated rats.

Bacterial translocation and ileal and cecal injury have been shown to occur 24 h after limited periods of hemorrhagic shock. The present studies were performed to determine the temporal sequence of mucosal injury, permeability, and bacterial translocation after hemorrhagic shock. The results indicated that bacterial translocation and mucosal injury have occurred by 2 h after a 30-min episode of shock (mean arterial pressure 30 mm Hg). Although the histologic extent of the intestinal mucosal injury was less at 2 h postshock than at 24 h postshock, at both times intestinal barrier function was lost as measured by permeability to horseradish peroxidase. Since the role of translocating bacteria in potentiating the loss of intestinal barrier function after shock is unclear, the second goal was to determine whether the extent of shock-induced mucosal injury and permeability could be reduced or abrogated by antibiotic decontamination of the gut. The extent of shock-induced mucosal injury and intestinal permeability was similar between rats with a normal gut flora (greater than 10(6) bacteria/g cecum) and antibiotic-decontaminated rats (less than 10(3) bacteria/g cecum) 2 h postshock, although the incidences of bacterial translocation were 67% and 0, respectively. Thus, shock-induced mucosal permeability and injury appear not to be directly related to the presence of translocating bacteria.

Animals↗

PubMed1992

The degree of bacterial translocation is a determinant factor for mortality after burn injury and is improved by prostaglandin analogs.

Bacterial translocation and related mortality rates were examined in previously transfused BALB/c mice that were gavaged with 14C radioisotope-labeled Escherichia coli before inflicting a 20% full-thickness flame burn. Radionuclide counts were measured in blood obtained by retro-orbital puncture 4 hours postburn, and survival was recorded for 10 days. Radionuclide counts in the blood correlated well with both radionuclide counts and numbers of viable bacterial in the tissues. Survivors had significantly less bacterial translocation as evidenced by blood radionuclide counts compared with nonsurvivors, and there was a significant inverse correlation between the degree of translocation and the length of survival. In the next experiment, the prostaglandin E (PGE) analogs misoprostol, enisoprost, or 16,16-dimethyl PGE2 were administered to transfused animals for 3 days before burn. Prostaglandin E analogs significantly reduced bacterial translocation as measured by blood radionuclide counts 4 hours postburn and improved survival. The data demonstrate that the intensity of bacterial translocation after burn injury is significantly associated with subsequent death. Improvement of survival by PGE analogs is associated with decreased bacterial translocation.

16,16-Dimethylprostaglandin E2↗

PubMedDate not supplied

Effect of three liquid diets on cecal bacterial flora and bacterial translocation in mice.

Separate groups of mice were fed either standard rodent chow or one of three liquid diets (Impact, Isosource HN, Fibersource HN) for 14 days to determine the effects of these liquid diets on the cecal bacterial flora and on the incidence of bacterial translocation to the mesenteric lymph nodes. Liquid Isosource and liquid Fibersource had no noticeable effect on either the cecal bacterial flora or the incidence of bacterial translocation. Liquid Impact was associated with cecal bacterial overgrowth but had no effect on the incidence of bacterial translocation. Each of the liquid diets was then lyophilized and similarly fed to mice; none of the lyophilized diets had a noticeable effect on the cecal bacterial flora or the incidence of bacterial translocation. To test these liquid and lyophilized diets in stressed mice, separate groups of mice were again fed the various diets for 14 days but given parenteral Escherichia coli lipopolysaccharide (LPS) 24 h before being killed. None of the liquid or lyophilized diets had a noticeable effect on the cecal bacterial overgrowth noticed in LPS-treated chow-fed mice. Compared with chow-fed mice, the typically elevated LPS-induced bacterial translocation was even more elevated in mice fed liquid diet but was somewhat decreased in mice fed lyophilized diet. Thus, the modulatory effects of these liquid diets on the cecal flora and the incidence of bacterial translocation appeared to depend on the composition of the diet and on prior treatment with parenteral LPS.

Animals↗

PubMed1991

Endotoxin-induced bacterial translocation and mucosal permeability: role of xanthine oxidase, complement activation, and macrophage products.

BACKGROUND AND METHODS: Previously, we documented that nonlethal doses of endotoxin injure the intestinal mucosal barrier and promote bacterial translocation from the gut to systemic organs. The current study was performed to determine the role of cytokines and complement activation in the pathogenesis of endotoxin-induced mucosal injury and bacterial translocation, as well as to quantify the magnitude of endotoxin-induced intestinal mucosal permeability. RESULTS: The frequency of endotoxin-induced bacterial translocation was similar between normal outbred (88%), complement deficient (67%), and macrophage-hyporesponsive (55%) mice, indicating that neither complement nor macrophage activation is necessary for endotoxin-induced bacterial translocation to occur. As early as 2 hrs after endotoxin challenge, there was evidence of a greater than two-fold increase in ileal (p = .008) but not jejunal (p = .11) permeability as measured by the clearance of 51Cr EDTA. Both the increase in endotoxin-induced ileal permeability and the occurrence of bacterial translocation were largely prevented by pretreatment with allopurinol, a competitive inhibitor of xanthine oxidase. CONCLUSIONS: These results suggest that endotoxin-induced bacterial translocation, mucosal injury, and ileal permeability are mediated via activation of xanthine oxidase, and not through complement activation or the liberation of macrophage products.

Animals↗

PubMed1990

Oral glutamine reduces bacterial translocation following abdominal radiation.

The effect of dietary glutamine on bacterial translocation was studied in rats following administration of a single dose of abdominal radiation (1000 rad) that causes a reproducible mucosal injury and results in a high incidence of culture-positive mesenteric lymph nodes after radiation (XRT). Following XRT, rats received only the amino acid glutamine (3%, +GLN) in their drinking water or a control nonessential amino acid (glycine, -GLN). Diets were isonitrogenous and isovolumetric. Four days after XRT, rats were anesthetized and a laparotomy was performed. Mesenteric lymph nodes were sterilely excised and cultured. Arterial blood was also obtained for whole blood glutamine determination. Control rats received no XRT but received identical diets. In XRT rats who received the GLN-free diet, the incidence of culture-positive mesenteric lymph nodes was 89% (eight of nine rats) while in the radiated rats receiving the GLN-enriched diet, the incidence fell to 20% (P less than 0.05). In non-radiated control rats receiving GLN-enriched and GLN-depleted diets for 4 days, bacterial translocation occurred in zero of eight and one of eight rats, respectively (NS). Provision of glutamine to XRT rats resulted in higher blood levels of glutamine (408 +/- 25 microM in XRT +GLN vs 311 +/- 19 microM in XRT -GLN, P less than 0.05). In addition, provision of GLN maintained mucosal mass and reduced weight loss (P less than 0.05). The data lend further support to the hypothesis that glutamine helps maintain the gut mucosal barrier and thereby decreases the incidence of bacterial translocation following bowel injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗