Commensal bacteria do translocate across the intestinal barrier in surgical patients (original) (raw)
Related papers
Microbiology of bacterial translocation in humans
Gut, 1998
Background—Gut translocation of bacteria has been shown in both animal and human studies. Evidence from animal studies that links bacterial translocation to the development of postoperative sepsis and multiple organ failure has yet to be confirmed in humans.Aims—To examine the spectrum of bacteria involved in translocation in surgical patients undergoing laparotomy and to determine the relation between nodal migration of bacteria and the development of postoperative septic complications.Methods—Mesenteric lymph nodes (MLN), serosal scrapings, and peripheral blood from 448 surgical patients undergoing laparotomy were analysed using standard microbiological techniques.Results—Bacterial translocation was identified in 69 patients (15.4%). The most common organism identified wasEscherichia coli (54%). Both enteric bacteria, typical of indigenous intestinal flora, and non-enteric bacteria were isolated. Postoperative septic complications developed in 104 patients (23%). Enteric organisms...
Bacterial translocation: Overview of mechanisms and clinical impact
Journal of Gastroenterology and Hepatology, 2007
Bacterial translocation (BT) is a phenomenon in which live bacteria or its products cross the intestinal barrier. Gut translocation of bacteria has been shown in both animal and human studies. BT and its complications have been shown clearly to occur in animal models, but its existence and importance in humans has been difficult to ascertain. We review the mechanisms of BT and its clinical impact based on the current literature.
Cellular Microbiology, 2005
Intestinal bacteria play an etiologic role in triggering and perpetuating chronic inflammatory bowel disorders. However, the precise mechanisms whereby the gut microflora influences intestinal cell function remain undefined. Therefore, the effects of the nonpathogenic prototype translocating Escherichia coli , strain C25 on the barrier properties of human T84 and Madine-Darby canine kidney type 1 epithelial cells were examined. T-84 cells were also infected with commensal E. coil , strains F18 and HB101, and enterohaemorrhagic E. coli , serotype O157:H7. Strains F18 and HB101 had no effect on transepithelial electrical resistance (TER) of T84 monolayers. By contrast, epithelial cells infected with strain C25 displayed a time-dependent decrease in TER, preceded by an altered distribution of the cytoskeletal protein alpha-actinin, comparable to infection with E. coli O157:H7. E. coli C25 infection also led to activation of nuclear factor k k k k B (NFk k k k B), interleukin-8 secretion and alterations in localization of claudin-1, but not zona occludens-1 or claudin-4, in T84 cells. There were adherent C25 bacteria on the intact apical surface of infected T84 cells, while mitochondria appeared swollen and vacuolated. These novel findings demonstrate the ability of a translocating commensal bacterium to adhere to and modulate intestinal epithelial barrier function and to induce morphological changes in a manner distinct from the known enteric pathogen, E. coli O157:H7.
Critical assessment of the methods used for detection of bacterial translocation
Pediatric Surgery International, 2004
Aim Bacterial translocation (BT) can be demonstrated by blood and lymph node cultures and also by polymerase chain reaction (PCR) detection of DNA of enteric bacteria. Aiming at investigating BT after gastrointestinal operations we assessed it on two endpoints after ischemia–reperfusion (IR) or sham operation (SO). Methods 2 groups of 200-g Brown Norway male rats were treated as follows: SO animals (n=12) had laparotomy alone and IR animals (n=12) had successively 15 min clamping of the portal vein and the mesenteric artery. Half the animals in each group were killed on postoperative (p.o.) day 2 the other half on p.o. day 7. Under sterile conditions regional lymph nodes and vena cava and portal vein blood samples were recovered and cultured for aerobes and anaerobes. Escherichia coli β-galactosidase DNA was assessed in blood samples by PCR. The findings in the two groups were compared by means of χ2 tests. Results Post-hepatic (peripheral blood) BT was detected by cultures of gram-negative bacteria in 16% and 0% of SO and IR animals, respectively, on p.o. day 2 and in 16% and 50% on p.o. day 7. These differences were not significant (ns). E. coli DNA was found in one SO rat. Pre-hepatic BT (portal blood and/or lymph nodes) of gram-negative bacteria was found in 16% and 33%, respectively, on day 2 and in 16% and 16% on day 7 (ns). However, if gram-positive cultures were taken into account, the figures were 66% and 66% on day 2 and 66% and 83% on day 7 (ns). No anaerobes could be cultured. Conclusions (1) BT is frequent in surgically manipulated animals. (2) To limit the assessment of BT to Enterobacteriaceae is probably misleading, since consistent amounts of gram-positive bacteria are found in the pre-hepatic territory. (3) PCR tests limited to E. coli DNA alone are likely incomplete. (4) Short periods of vascular clamping do not increase BT on the two endpoints selected in comparison with SO animals.
Intestinal obstruction promotes gut translocation of bacteria
Diseases of The Colon & Rectum, 1995
Transl0cation of enteric organisms has been implicated as a possible source of sepsis in susceptible patients. Animal studies have suggested that intestinal obstruction promotes bacterial translocation from the gut lumen. The aim of this study was to study the prevalence of bacterial translocation in patients with and without intestinal obstruction. METHODS: Serosal scrapings, mescnteric lymph nodes, and peripheral blood cultures were obtained from 254 patients. Scrapings and nodes were homogenized and incubated aerobically and anaerobically. Full-thickness biopsies underwent villous height analysis. The clinical course was followed for at least six weeks. RESULTS: Bacterial translocation to mesenteric nodes occurred more frequently in patients with large bowel obstruction than in patients without obstruction (14 of 36 patients vs. 16 of 218 patients; P < 0.001). Both aerobic and anaerobic bacteria were found to translocate. The more distal the obstruction, the more likely anaerobic bacteria were to be identified. Translocation of bacteria predisposed to postoperative septic complications (P < 0.05). Villous height was not related to bacterial translocation. CONCLUSIONS: Gut translocation of bacteria is more common in patients with intestinal obstruction, and its association with septic complications appears to be of clinical significance.
Bacterial translocation: impact of probiotics
Food & Nutrition Research, 2004
There is a considerable amount of data in humans showing that patients who cannot take in nutrients enterally have more organ failure in the intensive care unit, a less favourable prognosis, and a higher frequency of septicaemia, in particular involving bacterial species from the intestinal tract. However, there is little evidence that this is connected with translocation of bacterial species in humans. Animal data more uniformly imply the existence of such a connection. The main focus of this review is to describe different ways to alter the luminal milieu to decrease bacterial translocation. It is possible to reduce absorption of endotoxin by administration of bile salts in obstructive jaundice. Increasing the oral intake of glutamine will reduce bacterial translocation in rats with radiation-induced gut injury. The bacterial microflora plays a very important role in maintaining the normal intestinal ecological environment and supplying preferred fuels to the intestinal wall, consequently supporting the intestinal barrier. Disruption of the balance of intestinal bacterial microflora may increase the incidence of bacterial translocation by modifying intestinal barrier function. Bacterial species such as enteric Gram-negatives and Gram-positive cocci are more prone to translocation, whereas lactobacilli seem to have a protective effect. Administration of live lactobacilli either orally or by enema will reduce translocation. The mechanisms underlying the decreased translocation are not obvious. One effect may be mediated via an action on the intestinal wall and its permeability. Recently, the results of three randomized studies on the use of L. plantarum in patients with pancreatitis, undergoing liver transplantation or upper gastrointestinal surgery have been published, which all indicate a potential role for lactobacilli in translocation. In conclusion, by altering the luminal content of bacteria it seems possible to reduce the incidence of secondary infections. The influence of the luminal milieu on bacterial translocation is not fully understood. There is convincing evidence from experimental studies, but only circumstantial evidence from clinical studies.
European Journal of Clinical Microbiology & Infectious Diseases, 2020
Adherent-invasive Escherichia coli (AIEC) has been implicated as a microbiological factor in inflammatory bowel disease (IBD) pathogenesis. These strains are defined by their ability to adhere to and invade intestinal epithelial cells, and to survive and replicate in macrophages. We postulated that AIEC strains may commonly inhabit the gut of healthy individuals (HI), cause extraintestinal infections, and be found in sewage treatment plants (STP) and surface waters (SW). A total of 808 E. coli strains isolated from HI; patients with community-acquired urinary tract infection (CA-UTI), septicaemia and urosepsis; STP; and SW, showing a diffuse adhesion pattern to Caco-2 cells were included in this study. Typing of the strains using a combination of RAPD-PCR and PhPlate fingerprinting grouped them into 48 common clones (CCs). Representatives of each CC were tested for the ability to invade Caco-2 cells, survive and replicate in macrophages, and for the presence of six virulence genes commonly found among AIEC strains. Twenty CCs were deemed AIEC based on their ability to survive and replicate in macrophages, while encoding htrA, dsbA and clbA genes. These CCs primarily originated from HI and CA-UTI patients but were also detected in secondary locations including STP and SW. Strains lacking intramacrophagic survival and replication abilities were regarded as diffusely adhering E. coli (DAEC). Certain clones of AIEC are common in the gut of HI whilst promoting CA-UTI. The survival and persistence of AIEC in STP and SW may have serious public health ramifications for individuals predisposed to IBD.
New Microbes and New Infections, 2015
Nosocomial infection is the infection that is mainly acquired during a hospital treatment or 2 environment. One such infecting agent Escherichia coli harbors many virulence genes that 3 enable it to become pathogenic causing damage to the host. The mechanism of the E.coli 4 virulence factors provenance to cause infection in host environments is not clearly 5 elucidated. We investigated the virulence and pathogenicity of E.coli affected by the host 6 environment. For this, the blood (N=78) and fecal (N=83) E.coli isolates were collected 7 from sepsis and non-sepsis patients respectively admitted to the ICU. The E.coli genomic 8 DNA was isolated and the phylogenetic grouping was conducted by Triplex PCR. The 9 occurrence of nine virulence genes among the all the isolates was confirmed by gene 10 specific PCR. The prevalence of E.coli in blood isolates was more in phylogenetic groups B2 11 and D as compared to A and B1, however in fecal isolates there was no significant 12 difference. The prevalence of 'Adhesin' and 'Toxin' (papG, sfa, afa, cnf1, hlyA) genes was 13 higher in blood as compared to fecal E.coli isolates. However, the prevalence of aer, traT 14 and PAI was similar as well as higher among both of these groups. These observations 15 indicate a role of external environment (hospital setting) on host susceptibility 16 (development of infection) in the fecal E.coli isolates thereby making the patient prone to a 17 sepsis condition.
Scientific Reports
Rigottier-Gois & pascale serror enterococci are subdominant members of the human gastrointestinal microbiota. Enterococcus faecalis is generally harmless for healthy individuals, but it can cause a diverse range of infections in immunodeficient or elderly patients with severe underlying diseases. In this study, we analysed the levels of intestinal translocation of indigenous enterococci in C57BL/6, CF-1 and CX3CR1 −/− mice upon clindamycin antibiotic-induced dysbiosis. We found that C57BL/6 was the most permissive model for enterococcal translocation and that initiation of E. faecalis translocation coincided with a threshold of enterococcal colonisation in the gut lumen, which once reached, triggered E. faecalis dissemination to deeper organs. We showed that the extent to which E. faecalis clinical strain VE14821 competed with indigenous enterococci differed between the C57BL/6 and CX3CR1 −/− models. Finally, using a simplified gnotobiotic model, we observed E. faecalis crossing an intact intestinal tract using intestinal epithelial cells as one route to reach the lamina propria. Our study opens new perspectives for assessing the effect of various immunodeficiencies and for investigating mechanisms underlying enterococcal translocation. Enterococci are typical intestinal pathobionts. Although subdominant in the core intestinal microbiota and relatively harmless for healthy humans, under certain circumstances enterococci can cause infections such as bacteraemia, peritonitis, endocarditis, and urinary tract, wound, and device-related infections 1. The successful survival of enterococci in the hospital environment can be attributed to multidrug resistance and pathogenic traits. E. faecalis and E. faecium are the Enterococcus species most commonly associated with infection and vancomycin resistance. Enterococci are now ranked as the third most common type of nosocomial pathogen, with E. faecalis accounting for 60 to 80% of enterococcal infections 2,3. Despite increasing epidemiological evidence that intestinal domination by vancomycin-resistant enterococci (VRE) precedes human bloodstream infections 4-6 , it remains to be established whether E. faecalis blooming upon antibiotic treatment leads to translocation and subsequent human bloodstream infection. Pioneering work using mouse models highlighted the effect of antibiotic treatments on enterococcal colonisation and translocation 7,8. Enterococcal translocation has since been reported after antibiotic-induced dysbiosis, coinfection, severe inflammatory conditions, severe burn injuries and acute irradiation, and after disruption of intestinal mucosal barrier function in various mouse genetic backgrounds 8-16. Miyazaki et al. 10 showed that mice after treatment with antimicrobial agents and cyclophosphamide displayed increased susceptibility to VRE bacteraemia, leading to death in one-third of the mice following oral VRE inoculation. Amongst the 13 mouse lines tested under these conditions, C57BL/6 mice were identified as the strain most susceptible to VRE infection after oral inoculation. However, whether higher susceptibility of C57BL/6 mice correlates with a higher translocation efficiency remains to be established. Enterococcal translocation has also been investigated in some studies combining deficiency of mucosal immunity and intestinal dysbiosis 17,18. CX3CR1 −/− mice have been shown to display increased levels of bacterial translocation to the mesenteric lymph nodes, with Enterococcus being the predominant genus 18 .
Intestinal cell migration damage induced by enteropathogenic Escherichia coli strains
Brazilian Journal of Medical and Biological Research, 2018
Epithelial cell migration is an essential response to enteric pathogens such as enteropathogenic Escherichia coli (EPEC). This study aimed to investigate the effects of EPEC infection on intestinal epithelial cell migration in vitro, as well as the involvement of type III secretion system (T3SS) and Rho GTPases. Crypt intestinal epithelial cells (IEC-6) were infected with EPEC strains (E2348/69, DescF, and the LDI001 strain isolated from a malnourished Brazilian child) and commensal E. coli HS. Wound migration and cell death assays were performed at different time-points. Transcription and expression of Rho GTPases were evaluated using real-time PCR and western blotting. Overall, EPEC E2348/69 reduced migration and increased apoptosis and necrosis levels compared to EPEC LDI001 and E. coli HS strains. Moreover, EPEC LDI001 impaired cell migration at a higher level than E. coli HS and increased necrosis after 24 hours compared to the control group. The different profiles of virulence genes between the two wild-type EPEC strains, characterized by the absence of espL and nleE genes in the LDI001, might explain the phenotypic results, playing significant roles on cell migration impairment and cell death-related events. Moreover, the type III secretion system is determinant for the inhibition of intestinal epithelial cell migration by EPEC 2348/69, as its deletion prevented the effect. Active Rac1 concentrations were increased in E2348/69 and LDI001-infected cells, while the T3SS-deficient strain did not demonstrate this activation. This study contributes with valuable insight to characterize the mechanisms involved in the impairment of intestinal cell migration induced by EPEC.