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.     

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.     

实验鼠重症急性胰腺炎时奥曲肽对细菌易位影响的质粒标记研究

目的评价奥曲肽对重症急性胰腺炎（ｓｅｖｅｒｅａｃｕｔｅｐａｎｃｒｅａｔｉｔｉｓ,ＳＡＰ）及其细菌易位的治疗作用。方法已定殖含重组质粒的大肠杆菌大鼠８０只随机分为４组,每组２０只。在预防治疗组及其对照组,于诱导ＳＡＰ前先以４μｇ／ｋｇ静脉注射后继以６μｇ·ｋｇ－１·ｈｒ－１灌注１小时奥曲肽。在治疗组及其对照组,于诱导ＳＡＰ后０５小时先静脉注射４μｇ／ｋｇ,以后继续皮下注射８μｇ／ｋｇ,８小时一次共２４小时。２４小时后杀鼠取肠系膜淋巴结及腹水作培养,并用质粒ＤＮＡ分析和抗菌谱对细菌加以鉴定识别。结果在预防治疗组肠系膜淋巴结和腹水细菌易位发生率分别为５５％（１１／２０）和２０％（４／２０）,而在治疗组则分别为４７４％（９／１９）和１５８％（３／１９）,与各自对照组相比,都显著降低（Ｐ＜００５）。预防治疗组和治疗组病死率分别为０％（０／２０）和５％（１／２０）,与其对照组相比,也显著降低（Ｐ＜００５）。结论奥曲肽对ＳＡＰ及其细菌易位有治疗作用     

创伤及休克肠道细菌移位的研究

研究创伤失血性休克肠道细菌移位的发生率。设计兔创伤失血性休克试验模型，实验组３０只兔，腹部皮肤撕脱１００ｍｍ×９０ｍｍ，并行股动脉放血致休克，对照组１０只兔，腹部撕脱同实验组，不放血致休克。对照组术后１小时、３小时、５小时取标本均未发现肠道细菌移位，实验组术后１小时采标本已有肠道细菌移位，３小时、５小时组细菌移位达３０％。认为创伤失血性休克早期即有肠道细菌移位，并讨论了其临床意义     

Acute pancreatitis,bacterial translocation,and different octreotide regimens: An experimental study

Purpose  

To determine the effect of octreotide, octreotide with zinc, levamisole, and misoprostol on the bacterial translocation that develops in rats with acute pancreatitis (AP).     

Lethal burn-induced bacterial translocation: role of genetic resistance

Since genetic factors may influence outcome after trauma or during infection, the current experiments were performed to examine the resistance of three genetically different mouse strains to burn-induced bacterial translocation. Outbred ICR, inbred Balb/c, and inbred C57/B1 mice, with a normal or disrupted (monoassociated with Escherichia coli C25) GI tract microflora, were subjected to sham or actual 25% body burns. In Balb/c, but not ICR mice, replacing the normal intestinal microflora with E. coli C25 converted the thermal injury from a nonlethal (0% mortality) to a lethal (68% mortality) injury. The increased mortality of the burned Balb/c mice monoassociated with E. coli C25 was associated with a higher incidence (p less than 0.05) and magnitude (p less than 0.05) of E. coli C25 translocation from the GI tract. The C57/B1 mice were intermediate between the Balb/c and ICR strains, in that C57/B1 mice monoassociated with E. coli C25 had a higher mortality and greater E. coli C25 translocation than mice with a normal microflora after thermal injury. Thus the composition of the intestinal microflora as well as the genetic background of the host influence the susceptibility of the host to burn-induced bacterial translocation and survival.     

消化道重建术后肠道细菌移位的临床研究

目的：探讨消化道重建术后肠黏膜屏障损伤与肠道细菌移位（BT）及BT与术后全身炎症反应综合征（SIRS）的关系。方法：选择60例择期行消化道重建术的患者,于术前和术后1、3、5 d采集外周血,进行血浆二胺氧化酶及全血细菌DNA检测。全血DNA提取后进行PCR扩增,采用的靶基因为大肠杆菌特异性β半乳糖苷酶基因和16SrRNA基因。观察患者至术后10 d以监测SIRS情况。结果：术前PCR检测全血细菌DNA均为阴性,术后共有14例阳性。23例患者术后发生SIRS,其中12例患者PCR阳性。PCR阳性组SIRS发生率为85.7%（12/14）,阴性组为23.9%（11/46）（P〈0.01）。术后出现SIRS的患者PCR阳性率为52.2%（12/23）,无SIRS组为5.4%（2/37）（P〈0.01）。PCR阳性的患者血浆二胺氧化酶浓度较PCR阴性者明显升高（P〈0.01）,有SIRS的患者血浆二胺氧化酶较无SIRS患者明显升高（P〈0.01）。结论：消化道重建术后BT与肠黏膜屏障损伤密切相关,术后SIRS与BT密切相关。PCR技术可早期诊断细菌移位,对术后SIRS有较好的早期预警价值。     

Abdominal radiation causes bacterial translocation

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

Splenectomy influences endotoxin-induced bacterial translocation

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

大鼠急性胰腺炎肠道细菌易位的实验研究

目的本实验是观察大鼠急性胰腺炎后经胃肠道给予庆大霉素或谷氨酰胺对肠道细菌易位的影响。方法结扎封闭群 Wistar 大鼠的胆管,制成急性胰腺炎模型。分假手术组、急性胰腺炎组、庆大霉素组和谷氨酰胺组4组,各组又分5个亚组,分别于术后24、48、72、96和144小时处死动物。无菌下取回盲部淋巴结、胰腺、脾、肝、门静脉血和盲肠内容做细菌培养、计数。胰腺和小肠组织做病理检查。结果表明大鼠急性胰腺炎发生后,肠系膜淋巴结细菌数和阳性率明显增高,与门静脉血比较有显著差异。庆大霉索组盲肠内容和肠系膜淋巴结的大肠杆菌数明显减少,革兰氏阳性菌明显增多。谷氨酰胺组盲肠内容和肠系膜淋巴结的细菌数均显著减少。结论大鼠急性胰腺炎发生后早期肠道细菌易位主要经肠系膜淋巴途径。经胃肠道给予谷氨酰胺可防止肠道内细菌易位,减少胰腺感染的发生。     

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.     

Immunosuppression and intestinal bacterial overgrowth synergistically promote bacterial translocation

Gram-negative, enteric bacilli of the indigenous gastrointestinal tract microflora translocated primarily to the mesenteric lymph nodes in mice given either oral penicillin G sodium or clindamycin hydrochloride. These bacteria also translocated to the mesenteric lymph nodes in mice injected with cyclophosphamide or prednisone. However, in mice treated with the combination of an oral antibiotic plus an immunosuppressive drug, the translocating bacteria spread systemically to the peritoneal cavity. When the treatment with clindamycin and prednisone was extended to 12 days, the mice died of lethal sepsis beginning eight days after treatment. Thus, the combination of intestinal bacterial overgrowth and host immunosuppression synergistically promoted bacterial translocation from the gastrointestinal tract that resulted in lethal sepsis.     

谷氨酰胺二肽抑制小肠移植细菌易位的实验研究

目的观察甘氨酰谷氨酰胺(Gly-Gln)二肽对猪自体节段性小肠移植细菌易位的抑制作用。方法白色杂种猪10只行自体节段性小肠移植后随机分成2组:STPN 组(n=5),术后行标准全肠外营养 TPN 28天,GTPN 组(n=5)行与STPN 组等氮等热量强化 Gly-Gln(3%)的 TPN 28天。观察受体血浆 Gln 浓度及移植小肠粘膜 Gln 含量,移植小肠系膜淋巴结、肝、脾细菌数量和移植小肠对乙三胺五乙酸(~(99m)Tc-DTPA)的通透性。结果术后28天,GTPN 受体血浆 Gln 浓度和移植小肠粘膜 Gln 含量均高于 STPN 组,GTPN 组肠系膜淋巴结、肝、脾细菌数量(5.52±1.04,5.96±1.08,5.96±1.43LogCFU/g组织)明显低于 STPN 组(3.01±1.28,3.16±1.32,3.24±1.27Log CFU/g 组织),术后二组移植小肠通透性均增加,但GTPN 组明显高于 STPN(24.01±7.44%Vs7.77±3.04%,P<0.01)。结论 Gly-Gln 能提高受体血浆 Gln 浓度,维持移植小肠粘膜 Gln 含量,降低肠道通透性和细菌易位。     

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

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