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PubMed2006

[Clinical study on bacterial translocation in severe multiple trauma patients].

OBJECTIVE: To investigate bacterial translocation in severe multiple trauma patients using polymerase chain reaction (PCR) to detect the presence of bacteria in the blood. METHODS: Sixteen severe multiple trauma patients [injury severity score (ISS)>20] in surgery intensive care unit (SICU) were selected. Blood samples were collected 2, 24 and 48 hours after trauma for bacterial culture and microbial DNA detection. Meanwhile, plasma levels of D-lactate and lipopolysaccharide (LPS) in systemic circulation were determined. PCR was performed after DNA extraction, with target beta-lactosidase gene of E. coli and 16SrRNA gene of most pathogenic bacteria. All patients were observed within 30 days for infectious complications. D-lactate and LPS levels were determined in 63 patients before selective operation. RESULTS: Microbial DNA could be detected in blood as early as 2 hours following severe trauma, and altogether positive results were found in 10 patients (62.50%). All PCR-positive patients manifested sepsis, but none of the PCR-negative patients did (P<0.01). Bacterial DNA was discovered in 100.00% of sepsis patients and none in non-sepsis patients (P<0.01). Seventy percent of PCR-positive patients developed infectious complications, while none of PCR-negative patients did (P<0.01). The blood culture was positive only in 3 patients (18.75%), all of them were PCR-positive. E.coli DNA was found in 70.00% of all the PCR positive blood specimens. Systemic plasma concentration of D-lactate and LPS of all patients was significantly higher than that in control group, which consisted of 63 inpatients waiting for elective operations. Systemic plasma level of D-lactate showed a positive correlation with that of LPS (r=0.94, P<0.01). CONCLUSION: Intestinal bacterial translocation (most commonly E. coli) might occur early (2 hours) after severe trauma. Infection and sepsis have a close relationship with bacterial translocation. Detection of blood microbial DNA using PCR could reflect bacteria translocation and forecast imminent infection and sepsis.

Adolescent↗
PubMed2003

Role of bile in intestinal barrier function and its inhibitory effect on bacterial translocation in obstructive jaundice in rats.

BACKGROUND: Our previous study using genetically labeled Escherichia coli strain JNW14 revealed that obstructive jaundice promotes bacterial translocation in rats and that the absence of bile in the intestinal tract is considered to be a factor inducing bacterial translocation. The aim of this study was to investigate the role of bile and bile acids in intestinal barrier function against bacterial translocation. MATERIALS AND METHODS: Eight-week-old male specific-pathogen-free Wistar rats were subjected to ligation of their common bile ducts (CBDL). The CBDL rats were treated with bacitracin, neomycin sulfate, and streptomycin sulfate, and the intestinal tract was colonized with E. coli strain JNW14, which was genetically labeled with resistant markers against the above three antibiotics, to monitor the bacterial translocation. The rats were then administered saline, cholic acid (20 mg/100 g BW), taurocholic acid (TCA: 5-50 mg/100 BW), or bile (1.5-6 mL/day) via a duodenal catheter. The degree of bacterial translocation of E. coli strain JNW14 to the mesenteric lymph nodes was compared. Histopathological examination of the terminal ileum and intestinal permeability test using phenolsulfonphthalein was also performed. RESULTS: Both cholic acid and TCA showed no inhibitory effect on bacterial translocation at any of the doses tested in CBDL rats, although TCA significantly decreased the numbers of E. coli strain JNW14 in the cecum. However, bile administration reduced the numbers of E. coli strain JNW14 in the cecum and mesenteric lymph nodes in CBDL rats although the inhibitory effect was weak. The integrity and permeability of the intestinal mucosa were kept at normal levels by bile administration in CBDL rats whereas the morphological changes, such as villous atrophy, villous edema, and lacteal canal dilatation, were observed in other CBDL rats. CONCLUSION: Bile plays an important role in maintaining the intestinal barrier function to prevent the invasion of enteric bacteria to the underlying tissues, suggesting that the intestinal administration of bile to patients with obstructive jaundice is a useful way to reduce infectious complications by inhibiting bacterial translocation from the intestine to other organs.

Animals↗
PubMed2001

Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in rats.

Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP) and growth hormone (GH) has the ability to promote the intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. ANP was induced in rats by injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or placebo. Laparotomized animals without induction of ANP (sham operation [SO]) served as controls. At 24 hours after operation, blood was drawn for bacterial culture and determination of amylase, lipase, and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas, and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of 125I-labeled albumin from blood to intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcriptase-polymerase chain reaction (RT-PCR). Morphologic changes of pancreas and ileum were also analyzed. Administration of GH significantly decreased the serum amylase, lipase activities, plasma endotoxin level, and incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in pancreas and ileum was alleviated by GH treatment. Ileal mucosal thickness, villus height, and crypt depth in GH treatment rats were obviously increased compared with those of ANP rats. The intestinal permeability was markedly improved in the GH group versus the ANP group. GH treatment resulted in up-regulation of IGF-1 mRNA expression in ileum, but not in liver. These results suggested that exogenous GH had beneficial effects in maintaining the integrity of intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the up-regulation of IGF-1 mRNA in intestine by GH treatment.

Amylases↗
PubMed1996

Allopurinol and glutamine attenuate bacterial translocation in chronic portal hypertensive and common bile duct ligated growing rats.

BACKGROUND: Spontaneous bacterial infections and septicaemia result in morbidity and mortality in patients with portal hypertension and obstructive jaundice. AIM: The aim of this study in rats was to investigate the incidence of bacterial translocation in portal hypertension and obstructive jaundice, and to evaluate the effects of allopurinol and glutamine. METHODS: Rats were subjected to sham laparotomy (SL), portal hypertension (PH) by calibrated stenosis of the portal vein, and common bile duct ligation (CBDL). Animals of each group were either treated with allopurinol (50 mg/kg twice a week), glutamine (1 g/kg/d), and allopurinol and glutamine. RESULTS: After four weeks, significant bacterial translocation in the untreated PH and CBDL rats occurred. Intestinal mucosal malondialdehyde concentrations (MDA), as an indicator for lipid peroxidation, and myeloperoxidase activity (MPO) released from activated neutrophils were also significantly increased (p < 0.01). Allopurinol and glutamine in PH and CBDL rats improved bacterial translocation, and decreased MDA and MPO values (p < 0.01). CONCLUSION: In PH and CBDL rats significant bacterial translocation, ileal mucosal lipid peroxidation, and neutrophil derived MPO activity occurred. Allopurinol and glutamine significantly reduced bacterial translocation, as well as ileal mucosal MDA and MPO activities.

Allopurinol↗
PubMedDate not supplied

Bacterial translocation in experimental intestinal obstruction.

In this study, bacterial translocation to the mesenteric lymph nodes (MLN), liver and spleen and the histopathological changes in the intestine MLN, liver and spleen were investigated in Wistar Albino rats with intestinal obstruction. The subjects were divided into three main groups: the control group, simple obstruction group and loop obstruction group. Each group was further subdivided into two sub-groups: those who underwent repeat laparotomy at 12 h or at 24 h. No bacterial translocation was observed in the control group. The incidences of bacterial translocation to the MLN, livers and spleens of the rats with loop obstruction who underwent repeat laparotomy at 24 h were the highest. According to the cultured bacteria growth results, Escherichia coli was most abundant (48%). Most histopathological changes were observed in the MLN, livers, spleens and intestines of the rats with loop obstruction who underwent second laparotomy at 24 h.

Animals↗
PubMed1998

Non-protein energy overloading induces bacterial translocation during total parenteral nutrition in newborn rabbits.

The effect of energy intake provided by total parenteral nutrition (TPN) on the incidence of bacterial translocation and the relationship between TPN-induced cholestasis and bacterial translocation were investigated in newborn animals. Forty-six Japanese white newborn rabbits were divided into three groups: TPN-H group (high energy TPN; 280 kcal.kg-1.d-1), TPN-L group (low energy TPN; 180 kcal.kg-1.d-1), and a control group (breast fed). On day 8, they were all killed for investigation of the presence of bacterial translocation, for blood chemistry analysis, and for histological examination of the ileum. The incidence of translocation to any of mesenteric lymph nodes and liver and spleen was significantly higher in the TPN-H group (67%) than in both the TPN-L group (13%) and the control group (10%) (P < 0.01). No difference was seen in ileum morphology between the two TPN groups. Although the mean bilirubin level of the TPN-H group tended to be higher than the TPN-L group, whether or not bacterial translocation occurred was not found to be closely related to the degree of TPN-associated cholestasis. In conclusion, parenteral nonprotein energy overloadng increased the incidence of bacterial translocation in the newborn rabbit. However, bacterial translocation did not appear to be associated with the development of TPN-associated cholestasis.

Animals↗
PubMedDate not supplied

Octreotide inhibits hepatic fibrosis, bile duct proliferation and bacterial translocation in obstructive jaundice.

BACKGROUND/AIMS: The protective effect of octreotide on bacterial translocation, bile duct epithelial proliferation and hepatic fibrosis was studied in an experimental obstructive jaundice model. METHODOLOGY: Forty-five healthy Wistar albino rats were randomly divided into three groups. Group I (n = 15): Median laparotomy and common bile duct manipulation performed (Sham group). Group II (n = 15): Laparotomy and common bile duct ligation performed. Group III (n = 15): After laparotomy and common bile duct ligation octreotide (Sandostatin, sandoz) was given. Simultaneously group I and II received 3 cc 0.9% NaCl and group III received 20 micrograms/kg/daily octreotide subcutaneously every 8 hours during 9 days. Two days after the procedure all rats were opened under ether anesthesia and sterile conditions. Group I had simple laparotomy but group II and III also had common bile duct ligation by 5/0 prolene. Seven days after the surgery (9th day after treatment) all rats underwent laparotomy and tests for bacterial translocation, liver biochemical tests and histopathologic analysis of liver and small bowel were carried out. RESULTS: In group II cecal population levels of bacteria were significantly higher than group I and group III (p < 0.05). In group II there was also statistically significant bacterial translocation to the mesenteric lymph nodes. Pathological changes were found in terminal ileum samples in group II which seemed to improve in group III. Hepatocyte function was preserved with octreotide treatment which also significantly decreased bile duct proliferation and periportal fibrosis in response to biliary obstruction. CONCLUSIONS: This experimental study showed that octreotide is effective in preventing bacterial translocation, bile duct proliferation and hepatic fibrosis in obstructive jaundice.

Animals↗
PubMedDate not supplied

Effects of somatostatin analogues and vitamin C on bacterial translocation in an experimental intestinal obstruction model of rats.

The passage of viable endogenous bacteria and their products across the intact intestinal mucosal barrier, disseminating to the mesenteric lymph nodes, peritoneal cavity, spleen, liver, and circulation, is defined as bacterial translocation. Intestinal obstruction induces bacterial translocation due to mucosal disruption, motility dysfunction, and increased intestinal volume, leading to bacterial overgrowth. In a rat model of intestinal obstruction, the effects of both high-dose vitamin C (350 microg/kg), an antioxidant agent known to have a cytoprotective effect in ischemia-reperfusion injury, and somatostatin (20 microg/kg), a gastrointestinal antisecretory agent, in preventing bacterial translocation were studied. Both intestinal and liver samples from the rats was observed, and it was found that the rate of bacterial translocation was 100% in the control group, and only 43% for the rats who were given intraperitoneal vitamin C and somatostatin. The difference was statistically significant. In conclusion, we are convinced that vitamin C and somatostatin analogues may have protective effects against bacterial translocation in mechanical bowel obstruction.

Animals↗
PubMedDate not supplied

Adrenalin tolerance does not prevent bacterial translocation in a murine burn model.

Burn injury causes mesenteric vasoconstriction and bacterial translocation. Since catecholamines are powerful vasoconstrictors and elevated immediately after burn injury, we hypothesised that adrenaline tolerance might decrease burn-induced mesenteric vasoconstriction and bacterial translocation. Adrenaline tolerance was developed in Swiss albino mice. Adrenaline tolerant and control animals were subdivided into sham-burn and burn subgroups. 24 h after sham-burn or burn injury, specimens were obtained for microbiological evaluation. Also, in a separate group of adrenaline tolerant and control animals, superior mesenteric blood flow was measured. Burn injury increased bacterial translocation rate in both control (P = 0.001) and adrenaline tolerant groups (P = 0.0351). The caecal bacterial level increase was significant after burn injury in control groups (P = 0.0004) but was not significant in adrenaline tolerant animals (P = 0.743). Mesenteric blood flow was decreased significantly by burn injury in both control and adrenaline tolerant animals (P < 0.00001). The results showed that catecholamines do not mediate postburn mesenteric vasoconstriction or bacterial translocation.

Animals↗
PubMed2002

The effect of mesenteric lymphadenectomy and Kupffer cell depletion on bacterial translocation.

BACKGROUND: Infectious complications are associated with high morbidity in patients with short bowel syndrome and after small bowel transplantation. Bacterial translocation from the intestine is probably an essential factor in the genesis of these infections. In a model for bacterial translocation in the rat we examined the consequence of mesenteric lymphadenectomy and the depletion of Kupffer cells. MATERIALS AND METHODS: The effect of mesenteric lymphadenectomy was studied in two different models; in rats where a Thiry-Vella loop had been created from small bowel and in rats that had received a syngeneic small bowel transplant. To study the role of the Kupffer cells, rats with Thiry-Vella loops were treated intravenously with the Kupffer cell inhibitor gadolinium chloride. All animals were sacrificed on Day 3 postoperatively and the bacterial translocation to the mesenteric lymph nodes, liver, spleen, lung, and blood was evaluated. RESULTS: Removal of the mesenteric lymph nodes did not result in any increased bacterial translocation in animals with a Thiry-Vella loop. However, the inactivation of Kupffer cells with gadolinium chloride produced a more severe translocation to the liver, spleen, and lungs. After small bowel transplantation the bacterial translocation to the spleen was increased in animals without mesenteric lymph nodes. CONCLUSIONS: In the model of bacterial translocation from a defunctionalized loop of small bowel the inhibition of Kupffer cells will promote the systemic spread of the translocating bacteria. This indicates an important protective function of the Kupffer cells against translocating microbes.

Animals↗
PubMed2001

Bacterial translocation in a non-lethal rat model of peritonitis.

BACKGROUND: Bacterial translocation from the gut may occur under a variety of different clinical circumstances and has been implicated in the development of multiple organ failure. The aim of this study was to determine the distribution of bacterial translocation occurring in a model of chemically induced peritonitis. We also sought to document the degree of the associated immune and inflammatory response. METHODS: Though a midline laparotomy, rats were injected with 5 mg of zymosan (in 0.2 ml of saline) into the subomental space. After 4, 18, 24, 48 and 96 h, a number of endpoints evaluated: intraperitoneal cellular influx, TNF-alpha and interleukin-6 concentrations and myeloperoxidase activity. Bacterial cultures were initiated from the free peritoneal fluid, mesenteric lymph nodes, liver, lung, and kidney. Imprints were also made of the peritoneal mesothelial surface to determine its integrity. RESULTS: When comparing rats injected with zymosan with the controls, there was evidence of a peritoneal inflammatory response within 4 hours. Facultative gram negative bacteria were found to be growing in the mesenteric lymph nodes and in the peritoneal fluid at 48 h. Anaerobic organisms were also cultured from the peritoneal fluid at 48 h. No organisms were cultured from the liver, lung or kidneys. In addition there was a significant increase in intraperitoneal cell numbers (predominantly neutrophils, P < 0.05), myeloperoxidase activity (P < 0.05) and TNF-alpha and IL-6 concentrations (P < 0.05). There was extensive loss of the peritoneal mesothelial cells. The peritoneal inflammatory changes and bacterial translocation had resolved by 96 h. CONCLUSION: Bacterial translocation can be induced by the presence of an acute inflammatory focus in the peritoneal cavity. The translocation and inflammatory changes were associated with extensive loss of mesothelial cells. Nonetheless, these changes all resolved, indicating that the peritoneal cavity has a significant capacity to deal with such insults. A clearer understanding of the cellular and molecular events involved in the resolution phase could lead to improvements in the treatment of peritonitis.

Journal Article↗
PubMed2001

Effects of octreotide on intestinal transit and bacterial translocation in conscious rats with portal hypertension and liver fibrosis.

In cirrhosis, delayed intestinal transit may be responsible for increased endoluminal bacterial overgrowth and increased bacterial translocation. Octreotide has been reported to reduce intestinal transit. Therefore, we evaluated whether octreotide administration influences bacterial translocation in a model of liver fibrosis secondary to dimethylnitrosamine (DMNA) administration. Twenty-nine conscious rats were randomly assigned to three groups (sham rats + placebo as controls, DMNA + placebo, DMNA + octreotide, 1.5 microg/kg thrice daily subcutaneously), and including portal pressure, intestinal transit (radioactive method), and bacterial translocation were measured. Three of four variables measuring intestinal transit suggested a significant delay in intestinal transit in DMNA rats compared to controls (eg, cumulated radioactivity 50%: controls: 5.3+/-1.5, DMNA + placebo: 3.2+/-1.2, DMNA + octreotide: 2.7+/-1.9, P < 0.01). This delay tended to be enhanced by octreotide but the effect was only significant with one of the intestinal transit variables. Bacterial translocation was significantly increased in DMNA rats compared to controls but octreotide did not increase translocation [eg, germ count (log) in lymph nodes: controls: 3.1+/-3.6, DMNA + placebo: 12.3+/-4.4, DMNA + octreotide: 10.6+/-6.0, P < 0.001]. There was no significant correlation of portal pressure, intestinal transit, and bacterial translocation in this study. In conclusion, our results show that, although octreotide worsens delayed intestinal transit, it has no influence on the level of bacterial translocation.

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↗
PubMed2005

The effect of L-tryptophan on hemorrhagic shock induced bacterial translocation.

Hemorrhagic shock causes mucosal damage in intestine and it results in translocation of bacteria to distant organs. In this study, effects of various doses of L-Tryptophan on the prevention of bacterial translocation in hemorrhagic shock induced rabbits were investigated. This study was carried out on six groups, each was consisting of 10 rabbits. While any procedure was conducted on the rabbits in group 1 (as a control group), 1 x 10(10)Escherichia coli isolate were administered rabbits in the other groups by gavage. In groups 3, 4, 5, and 6, hemorrhagic shock was induced. After induction of hemorrhagic shock, 10, 50, and 200 mg/kg L-Tryptophan were intragastrically administered to animals in groups 4, 5, and 6, respectively. Blood and terminal ileum samples were taken to detect bacterial translocation by polymerase chain reaction and mucosal damage by histopathological examination at 24 h after hemorrhagic shock. The occurrence of bacterial translocation increased as well when intestinal bacterial intensity was increased (P < 0.05). The most intensive bacterial translocation was formed in group 3 as a result of the additive effect of hemorrhagic shock to bacterial augmentation. It was observed that bacterial translocation was significantly reduced in groups 5 and 6 that are 50 and 200 mg/kg L-Tryptophan were administered (P < 0.01). Histopathological changes on mucosa and submucosa support these results. As a result, we concluded that augmentation of intestinal bacterial intensity induces bacterial translocation, the addition of hemorrhagic shock to bacterial augmentation makes more excessive translocation and mucosal changes have effective roles in these events. L-Tryptophan decreased the intestinal mucosal damage and bacterial translocation induced by hemorrhagic shock, in a dose-dependent manner.

Animals↗
PubMed1995

[Bacterial translocation in a model of small intestine autotransplant in dogs].

BACKGROUND: Sepsis is the commonest complication of small bowel transplantation. These infections are presumably caused by bacterial translocation, due to splanchnic ischemia. AIM: To study bacterial translocation in the immediate postoperative period after a small bowel transplantation in dogs and to relate it to splanchnic ischemia. METHODS: Three groups of dogs were studied. In group A (n = 6) spontaneous episodes of splanchnic ischemia were monitored in the first 18 h of the postoperative period. In group B (n = 5), a 60 min ischemia was induced by superior mesenteric artery occlusion, two hours after small bowel transplantation. In group C (n = 5) a 60 min ischemia was induced by occlusion of mesenteric vein, two hours after transplantation. Bacterial translocation was assessed through bacterial cultures from the mesenteric vein and splanchnic ischemia with intramucosal pH measurement (a pH < 7.2 was considered indicative of ischemia). RESULTS: Twenty eight of 83 cultures were positive, specially for Gram negative bacilli. The incidence of positive cultures was 14% for group A, 17% for group B and 79% for group C (p < 0.01 compared to groups A and B). The higher incidence of bacterial translocation occurred during the first two hours after transplantation, when the lower intramucosal pH recordings were obtained. The percentage of positive cultures was 39% during periods of ischemia, compared to 24% during periods without ischemia (p = NS). CONCLUSIONS: Bacterial translocation occurs during the first two hours after intestinal transplantation, in concomitance with the lower intramucosal pH readings.

Animals↗
PubMed1997

The effects of vagotomy on bacterial translocation: an experimental study.

The effects of truncal vagotomy and proximal gastric vagotomy on bacterial translocation in rats were investigated in this experiment. The rats were divided into three groups. Only esophageal and gastric manipulations were performed in the control group (Group I). The anterior and posterior vagi were found and 0.5- to 1-cm pieces were taken out in the truncal vagotomy + pyloric dilatation group. In addition, pyloric dilatation was performed using a Fogarty catheter (Group II). The branches of the vagi, which lead to the rumen and corpus, were first tied with 5/O silk and then resected in the proximal gastric vagotomy group (Group III). All animals were sacrificed on the 7th day. Qualitative and quantitative tissue cultures of cecum, liver, spleen, mesenteric lymph node, and blood from vena cava were taken and a tissue sample from the ileum was obtained for histopathological examination with light microscopy. At the end of microbiologic study, the bacterial concentration on the cecal wall was 10.68 x 10(8) in the truncal vagotomy group, while it was 0.53 x 10(8) in the proximal gastric vagotomy group. Bacterial translocation was observed more in vagotomy groups than in control groups on the mesenteric lymph node, liver, and spleen. Bacterial translocation was greater in the truncal vagotomy group than in the proximal gastric vagotomy group (P < 0.05). Bacterial translocation was observed mostly in the liver, spleen, and mesenteric lymph node in the proximal gastric vagotomy group. No microorganisms could be cultured on systemic blood cultures. Cultures were positive only for one rat in the proximal gastric vagotomy group and for two rats in the truncal vagotomy group. At the end of histopathologic examination, when histopathologic parameters given for each rat were calculated, they were 5.44 +/- 2.12 in the truncal vagotomy group and 4.77 +/- 2.12 the in proximal gastric vagotomy group. The difference between these two groups was statistically significant (P < 0.05). Thus, there was damage to the intestinal wall in vagotomy groups, and it was greater in the truncal vagotomy group than in the proximal gastric vagotomy group. It was observed that bacterial translocation occurs after vagotomy, that this translocation occurs more after truncal vagotomy than after proximal gastric vagotomy, and that the translocation that occurred after vagotomies was not effective enough to create bacteremia.

Animals↗
PubMed2004

Head injury-associated bone fractures induce bacterial translocation: an experimental study.

OBJECTIVES: To determine whether long bone fractures cause bacterial translocation and to investigate the effect of concomitant head trauma on this process. DESIGN: An in vivo animal model. SETTING: Animal Laboratory, University of Mersin School of Medicine, Mersin, Turkey. SUBJECTS: Male Sprague-Dawley rats (n = 60). INTERVENTION: Sixty male Sprague-Dawley rats were divided into five groups: (1). anesthesia only (control group, n = 12); (2). anesthesia and tibia fracture (n = 12); (3). anesthesia, tibia fracture, and femur fracture (n = 12); (4). anesthesia, tibia fracture, femur fracture, and moderate head trauma (n = 12); and (5). moderate head trauma only (n = 12). After 24 hours, mesenteric lymph nodes, liver, spleen, ileum, and systemic blood samples were quantitatively cultured for aerobic organisms. MAIN OUTCOME MEASUREMENTS: Colony-forming unit per gram for bacteria count. RESULTS: The incidence of bacterial translocation was higher in groups that had fractures (4/12 in group 2; 5/12 in group 3) than in the control group (2/12); however, this did not reach statistical significance. There was a significant increase in the number of subjects with bacterial translocation in group 4 (9/12) compared with the control group and group 5 (3/12) (P = 0.0123, P = 0.0391). CONCLUSIONS: Multiple fractures of long bones associated with head injury promote bacterial translocation.

Animals↗