No abstract available.
*Bacterial Translocation ; Humans ; Liver Cirrhosis/*microbiology

Bacterial Translocation ; Humans ; Liver Cirrhosis ; microbiology

Early in 1962, after an extensive review including 312 cases of bacteremia in burn patients, we were surprised to find that there was about 30% of bacteremia in the patients who had no detectable microorganisms from repeated wound cultures, but blood cultures were usually positive for gut flora. From that time on the idea of gut-origin infection emerged. In following twenty years, a series of experiments were carried on in Wistar rats with 30% TBSA full-thickness burn. The results showed that the fluorescein labeled enteric microbes (Pseudomonas aeruginosa, Bacteroid fragilis and Candida albicans) could translocate through the stress injured intestinal wall and were recovered in visceral organs. The radioisotope 125I labeled endotoxin began to ascend in concentration in portal vein since 15 minutes postburn. Radioautography of liver sections demonstrated the labeled endotoxin granules. With the creation of minute mesenteric lymph fistulas, the clearance of endotoxin and TNFalpha was found to be significantly high in lymph fluid exited from the intestine. All above evidences indicated that the gut is a potential route of endogenous infection, and it also explained how did the patients manifest sepsis early after burn injury without a definite infectious focus. Now the concepts of gut-origin infection are commonly accepted, the measures like early enteral feeding for the protection of intestinal barrier has been established.
Bacteremia ; etiology ; Bacterial Translocation ; Burns ; microbiology ; Gastrointestinal Tract ; microbiology ; Humans

The bacterial translocation is defined as the passage of viable bacteria or its toxin from the lumen of the gastrointestinal tract through the intestinal mucosa to other site of host. It is believed that bacterial translocation may lead to systemic infection and septicemia. The purpose of this study was to determine what factors in experimental surgical trauma lead to bacterial translocation. Two-nonth-old Wistar albino rats were divided into three groups: A-control; B-anesthesia only and C-anesthesia and surgery. After 24 and 48 hours, caval blood, mesenteric lymph nodes, liver, lung and spleen were harvested aseptically and cultured for aerobic organism. To exclude the possibility of contamination during surgical manipulation and harvesting, swab culture of peritoneal surface was performed. The bacterial translocation seldom occurred 24 hours after surgical manipulation. There was a significant increase in the number of animals with bacterial translocation in group C, 48 hours after manipulation and harvesting, swab culture of peritoneal surface was performed. The bacterial translocation seldom occurred 24 hours after surgical manipulation. There was a significant increase in the number of animals with bacterial translocation in group C, 48 hours after surgical manipulation. The majority of translocating bacteria was E. coli.
Animals ; Bacteria ; Bacterial Translocation* ; Gastrointestinal Tract ; Intestinal Mucosa ; Liver ; Lung ; Lymph Nodes ; Rats ; Sepsis ; Spleen

OBJECTIVETo investigate the intestinal microflora status and bacterial translocation in rats after liver transplantation.

METHODSMale Brown-Norway (BN) rats were randomly divided into 4 groups: group I (n = 8) for liver transplantation; group II (n = 8) for simulated liver transplantation; group III (n = 8) for sham operation and group IV (n = 8) for normal group. Caecal bacterial counts, plasma endotoxin, intestinal mucosal ultrastructure and bacterial translocation to liver, spleen, kidney, and mesenteric lymph node were studied 24 h after surgery.

RESULTSThe numbers of Bifidobacterium and Lactobacillus per gram of wet feces were significantly decreased in group I compare with those in the group III and group IV, while Enterobacteriaceae and Enterococcus counts were increased markedly compare with those in the group III and group IV, but no different was found between group I and group II. Impaired intestinal mucosa integrity were found in the group I and group II. In group I, the levels of plasma endotoxin increased after the transplantation when compare with group III and group IV. Increased incidence of bacterial translocation to liver, spleen and mesenteric lymph node were also observed after the transplantation (compare with those in the group IV, P < 0.01; compare with those in the group III, P < 0.01, P < 0.01, P < 0.05, separately). The increased rate of the bacterial translocation in liver was also found in transplantation group as compare with group II (P < 0.05).

CONCLUSIONSLiver transplantation may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function, and this dysfunction might be caused by the process of intestinal ischemia-reperfusion injury in transplantation.

Animals ; Bacterial Translocation ; Endotoxins ; blood ; Intestines ; microbiology ; ultrastructure ; Liver Transplantation ; Male ; Random Allocation ; Rats

Acute pancreatitis is an inflammatory disease that is caused by various etiologies including gallstone, alcohol or hypertriglyceridemia. Although most cases of acute pancreatitis show self-limiting course, severe cases are still associated with significant morbidity and mortality. The pathogenic mechanisms of acute pancreatitis are not fully understood. However, it is a central dogma that premature intracellular activation of trypsinogen is the earliest pathologic event. Even though it remains unknown how intracellular trypsinogen activation can be caused by such diverse etiologies, this initial insult in pancreatic acinar cells lead to local inflammatory complications and a systemic response or death. Pathophysiologic mechanisms related to the progression of acute pancreatitis include microcirculatory injury, chemoattraction of inflammatory cells, release of pro-inflammatory cytokines, and bacterial translocation to pancreas and systemic circulation. Recently, several interesting transgenic mice model experiments shed a light in trypsin independent mechanism of local and systemic inflammation for progression of acute pancreatitis.
Acinar Cells ; Animals ; Bacterial Translocation ; Cytokines ; Gallstones ; Hypertriglyceridemia ; Inflammation ; Light ; Mice ; Mice, Transgenic ; Pancreas ; Pancreatitis ; Trypsin ; Trypsinogen

BACKGROUND/AIMS: Non-selective beta blockers (NSBBs) are currently the only accepted regimen for preventing portal hypertension (PHT)-related complications. However, the effect of NSBBs is insufficient in many cases. Bacterial translocation (BT) is one of the aggravating factors of PHT in cirrhosis; therefore, selective intestinal decontamination by rifaximin is a possible therapeutic option for improving PHT. We investigated whether the addition of rifaximin to propranolol therapy can improve hepatic venous pressure gradient (HVPG) response. METHODS: Sixty-four cirrhosis patients were randomly assigned to propranolol monotherapy (n=48) versus rifaximin and propranolol combination therapy (n=16). Baseline and post-treatment HVPG values, BT-related markers (lipopolysaccharide [LPS], LPS-binding protein [LBP], interleukin-6 [IL-6], and tumor necrosis factor α [TNF-α]), serological data, and adverse event data were collected. HVPG response rate was the primary endpoint. RESULTS: Combination therapy was associated with better HVPG response rates than monotherapy (56.2% vs 87.5%, p=0.034). In combination therapy, posttreatment BT-related markers were significantly decreased (LPS, p=0.005; LBP, p=0.005; IL-6, p=0.005; TNF-α, p=0.047). CONCLUSIONS: Rifaximin combination therapy showed an additive effect in improving PHT compared to propranolol monotherapy. These pilot data suggest that the addition of rifaximin to NSBBs could be a good therapeutic option for overcoming the limited effectiveness of NSBBs.
Bacterial Translocation ; Decontamination ; Fibrosis ; Humans ; Hypertension, Portal ; Interleukin-6 ; Pilot Projects* ; Portal Pressure* ; Propranolol* ; Tumor Necrosis Factor-alpha ; Venous Pressure

Vibrio vulnificus causes primary septicemia as a result of the consumption of contaminated seafood. The intestinal epithelial layer is the first host barrier encountered by V. vulnificus upon oral intake; however, epithelial translocation (invasion) of V. vulnificus has not been extensively studied. In this study, we investigated in vivo translocation of V. vulnificus using clinical (CMCP6) and environmental isolates (96-11-17M). And we analyzed physiological changes of intestinal epithelium concurrent with bacterial translocation by using polarized HCA-7 transwell culture system. The efficiency of epithelial translocation of 97-11-17M strains was significantly lower than that of pathogenic clinical isolate CMCP6 in a murine ligated ileal loop model. In an oral infection model, the survival rate was reciprocally related with efficacy of in vivo epithelial translocation. These results indicate that efficient translocation of V. vulnificus through intestinal epithelium is highly correlated with successful oral infection. We determined translocation of the bacteria from upper to lower chamber, changes of transepithelial electric resistance (TER) and cytotoxicity of the polarized HCA-7 cells to understand general features of V. vulnificus invasion. Bacterial translocation was accompanied by big decrease of TER (about 90%) and about 50% cytotoxicity of the epithelial cells. Taken together, these results indicate that V. vulnificus actively translocates the epithelium by destruction of epithelium and the efficiency of intestinal invasion by V. vulnificus is critical for successful oral infection. From this result, it is suggested that integrity of intestinal barrier is an important factor for susceptibility to oral infection of V. vulnificus.
Bacteria ; Bacterial Translocation ; Electric Impedance ; Epithelial Cells ; Epithelium ; Intestinal Mucosa ; Seafood ; Sepsis ; Survival Rate ; Vibrio vulnificus* ; Vibrio*

In this study, we investigated the effect of different values of intra-abdominal pressure on bacterial translocation. Twenty-four Wistar-Albino rats were divided into four groups. The animals belonging to the Control group were not subjected to any increased intra-abdominal pressure. In groups I, II and III, an intra-abdominal pressure of 14, 20, and 25 mmHg, respectively, was established by carbon dioxide pneumoperitoneum for a period of 60 minutes. Four hours after the pneumoperitoneum, all animals were sacrificed to evaluate the degree of bacterial translocation at this time. Liver, spleen and mesenteric lymph nodes were excised under sterile conditions. Bacterial growth was assessed using standard bacteriological techniques and compared statistically. The Kruskal-Wallis and Mann-Whitney U tests were used for the statistical analysis. Different amounts of bacterial growth were found in all of the animals subjected to increased intra-abdominal pressure, except for the controls. Bacterial translocation was detected at an intra-abdominal pressure of 14 mmHg but this finding was not statistically significant (p > 0.05). There was a significant increase in bacterial growth in animals subjected to an intra- abdominal pressure of 20 mmHg or above (p < 0.001). As a result, we found that bacterial translocation started when the intra-abdominal pressure reached a level of 14 mmHg. Patients should be closely monitored for septic complication risks following laparoscopic procedures in which the intra-abdominal pressure exceeds 20 mmHg.
Abdomen ; Animals ; *Bacterial Translocation ; Carbon Dioxide ; Laparoscopy/*adverse effects ; Pneumoperitoneum, Artificial/adverse effects ; Pressure ; Rats ; Rats, Wistar ; Splanchnic Circulation

This paper is to explore changes of intestinal mucosal barrier, intestinal flora, and bacterial translocation in rats with severe acute pancreatitis (SAP). Twenty four male SD rats were randomly divided into the control group (n = 10) and the experimental group (n = 14). The model of severe acute pancreatitis of rats was induced by the method of injecting adversely 5% sodium taurocholate into the common biliary-pancreatic duct. All of the rats were killed after 24 hours and the level of the serum amylase and the plasma endotoxin was determined after that. The pathological changes of pancreas and small intestine were observed through hematoxylin-eosin staining (HE staining) and the abdominal viscera bacterial translocation rates were tested. With the method of real-time polymerase chain reaction (RT-PCR) the quantity of the intestinal flora was analyzed. In the control group, the level of Escherichia coli, Lactobacillus and Bifidobacterium were 2.08 ± 1.29, 11.04 ± 7.55 and 12.21 ± 4.95, respectively. On the contrast, the level of Escherichia coli in the cecum contents was much higher (9.72 ± 3.58, P < 0.01), while the Lactobacillus number was decreased significantly (0.67 ± 0.34, P < 0.01), and the Bifidobacterium number was also decreased (4.59 ± 3.42, P < 0.05) in the experimental group, so the ratio of Bifidobacterium/Escherichia coli was reversed. Besides, in the experimental group, the plasma endotoxin positive rates and the bacterial translocation rates were much higher (P < 0.01 or P < 0.05) and the pathology scores of pancreas and small intestines were also significantly higher (P < 0.01) than those in the control group. These results indicated that in severe acute pancreatitis rats, the intestinal mucosal barrier was severely damaged and the dysbacteriosis occurs in the intestinal canal. And these might relate to the occurrence and development of multiple organ infection.
Animals ; Bacterial Translocation ; Endotoxins ; Intestinal Mucosa ; pathology ; Intestines ; microbiology ; Male ; Pancreas ; pathology ; Pancreatitis ; microbiology ; pathology ; Rats ; Rats, Sprague-Dawley