Title: Gut translocation


Key words: gut translocation, lymphoid tissue, bacteria, Kupffer cells, immune defence, mesenteric lymph nodes, septicaemia, bowel microflora, stress, gastrointestinal disease, immature gut, neonatal surgery, pathogens, coagulase-negative staphylococcus, undernutrition, Gram-negative bacilli, digestive function, hypochlorhydria, gastric, pancreatic, liver pathology, dysbiosis, bowel obstruction, surgical intervention, E. coli, aerobic, anaerobic, bacterium, liver resection, portal clamping, inflammatory bowel disease, endotoxins, total parenteral nutrition, TPN, biliary flow, neonates, laparotomy, sepsis,  


Date: Oct 2006




Nutrimed Module:


Type: Article


Author: Morgan, G


Gut translocation

Gut translocation is the disruption of the natural barrier provided by the gut and related structures to invasion by pathogenic and potentially pathogenic bacteria. Such defence is provided by the immunological defence system in the gut associated lymphoid tissue (GALT), mesenteric lymph nodes and Kupffer cells of the liver. Breaching of this barrier leads to septicaemia, with potentially fatal consequences in the seriously ill. Gut, or bacterial, translocation, can occur in the presence of three precipitating factors:


1. Dysbiosis

Stress, severe illness, gastrointestinal disease, and undernutrition are all associated with changes in the bowel microflora. Prior to full colonisation of the immature gut in infants, it has been shown that, in neonatal surgical groups, the gut can be preferentially colonised by low-grade pathogens such as coagulase-negative staphylococci and, in the more compromised neonates, by potential pathogens such as aerobic Gram-negative bacilli such as E. coli. Amongst such groups, institution of these carrier states and an associated bacterial overgrowth precedes the development of gut translocation and septicaemia (Donnell 2002, van Saene 2003).


In the adult, H. pylori infection, hypochlorhydria, gastric, pancreatic, gallbladder and liver pathology, and inflammatory bowel disease can affect normal digestive function and lead to dysbiosis. Bowel obstruction leading to surgical intervention is the leading cause of dysbiosis and the ensuing bacterial translocation and septicaemia (Sedman 1994, Sagar 1995). In such series, both aerobic and anaerobic organisms have been isolated, E. coli being the most commonly identified bacterium (O’Boyle 1998). With portal clamping and liver resection operations, coagulase negative staphylococci have been more commonly identified and have been shown to spread via the mesenteric lymph nodes (Ferri 1997).


2. Breach of the gut mucosal barrier

Proliferation of pathogenic bacteria above a concentration of 105 orgs/cm2 promotes invasion and breach of the gut mucosal barrier and bacterial translocation (van Saene 2003). Other factors associated with damage to the intact mucosa, such as inflammatory bowel disease, surgery and shock – especially when accompanied with dysbiosis and nutritional deficiencies – will also predispose to gut translocation (Sedman 1994, Deitch 1996). Translocation is most favoured in the terminal ileum (van Saene 2004)


3. Immune system dysfunction

Defence against mucosal invasion by pathogenic bacteria is provided by the gut associated lymphoid tissue, mesenteric lymph nodes and the liver Kupffer cells. Endotoxins released by pathogenic bacteria such as aerobic gram negative bacteria and coagulase negative staphylococci have been shown to disrupt this immunological defence system (Billiar 1998, Alverdy 1992). The liver, in particular, plays an important role, acting through the portal circulation, removing any translocated bacteria that have not already been handled by the GALT and mesenteric lymph nodes so that they do not pass into the systemic circulation. It functions as a major organ of the immune system (Sheth 2001). In particular, endotoxins from pathogenic gut bacteria have been shown to incapacitate Kupffer cells in the liver (Marshall 1987, Billiar 1998). Suppression of liver immune function is a necessary antecedent of gut translocation (van Saene 2004)


More recently, total parenteral nutrition (TPN) has been shown to adversely effect gut immune function. Reduced gut motility and direct nutritional stimulation of the mucosa has been demonstrated to lead to mucosal atrophy and impairment of GALT, and lymph node and Kupffer cell function (van Saene 2003). Biliary flow is also impaired (Jawaheer 1995). These factors all favour intestinal dysbiosis. A direct effect on neutrophil phagocytic activity and immune function has also been demonstrated in infants receiving TPN, leading to increased susceptibility to invasion by coagulase negative staphylococci (Donnell 2002).


Review of the literature shows these factors to be cumulative and to lead to substantial incidences of morbidity in vulnerable groups such as neonates or those undergoing abdominal surgery. High carriage rates for gut pathogens have been reported with incidences of septicaemia caused by tranlocation of around 15% in neonates undergoing TPN (van Saene 2003) or in adult laparotomy cases (O’Boyle 1998). Attention to sepsis control, bowel management, nutrition, prophylactic and other measures is obviously called for against such a background.



1. Donnell SC, Taylor N, van Saene HKF, et al. (2002) Infection rates in surgical neonates and infants receiving parenteral nutrition; a five year prospective study. J Hosp Infect 52: 273-280

2. van Saene HKF, et al. (2003) Gut overgrowth with abnormal flora: the missing link in parenteral nutrition-related sepsis in surgical neonates. Eur J Clin Nutr 57: 548-553

3. Sedman PC, et al. (1994) The prevalence of gut translocation in humans. Gastoenterology 107: 643-9

4. Sagar PM, et al. (1995) Intestinal obstruction promotes gut translocation of bacteria. Dis Colon Rectum 38: 640-4

5. O’Boyle CJ, et al. (1998) Microbiology of bacterial translocation in humans. Gut 42: 29-35

6. Ferri M, et al. (1997) Bacterial translocation during portal clamping for liver resection. Arch Surg 132: 162-165

7. Deitch EA, Rutan R, Waymack JP (1996) Trauma, shock, and gut translocation. New Horizons 4: 288-9

8. van Saene HKF (2004) Lecture notes. Surrey University

9. Billiar TR, et al. (1988) Intestinal Gram-negative bacterial over- growth in-vivo augments the in-vitro response of Kupffer cells to endotoxin. Ann Surg 208: 532-40

10. Alverdy JC, Burke D (1992) Total parenteral nutrition: iatrogenic immuno-suppression. Nutrition 8: 359-365

11. Sheth K, Bankey P (2001) The liver as an immune organ. Curr Opin Crit Care 7: 99-104

12. Marshall JC, et al. (1987) Kupffer cell modulation of the systemic immune response. Arch Surg 122: 191-196

13. Jawaheer G, et al. (1995) Gall bladder contractility in neonates: effects of parenteral and enteral feeding. Arch Dis Child 72: F200-F202