Vaishnavi C
Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Indian J Med Microbiol. 2013 Oct-Dec;31(4):334-42. doi: 10.4103/0255-0857.118870.
Bacterial translocation is the invasion of indigenous intestinal bacteria through the gut mucosa to normally sterile tissues and the internal organs. Sometimes instead of bacteria, inflammatory compounds are responsible for clinical symptoms as in systemic inflammatory response syndrome (SIRS). The difference between sepsis and SIRS is that pathogenic bacteria are isolated from patients with sepsis but not with those of SIRS. Bacterial translocation occurs more frequently in patients with intestinal obstruction and in immunocompromised patients and is the cause of subsequent sepsis. Factors that can trigger bacterial translocation from the gut are host immune deficiencies and immunosuppression, disturbances in normal ecological balance of gut, mucosal barrier permeability, obstructive jaundice, stress, etc. Bacterial translocation occurs through the transcellular and the paracellular pathways and can be measured both directly by culture of mesenteric lymph nodes and indirectly by using labeled bacteria, peripheral blood culture, detection of microbial DNA or endotoxin and urinary excretion of non-metabolisable sugars. Bacterial translocation may be a normal phenomenon occurring on frequent basis in healthy individuals without any deleterious consequences. But when the immune system is challenged extensively, it breaks down and results in septic complications at different sites away from the main focus. The factors released from the gut and carried in the mesenteric lymphatics but not in the portal blood are enough to cause multi-organ failure. Thus, bacterial translocation may be a promoter of sepsis but not the initiator. This paper reviews literature on the translocation of gut flora and its role in causing sepsis.
细菌易位是指肠道内的固有细菌穿过肠黏膜侵入通常无菌的组织和内脏器官。有时，炎症化合物而非细菌是导致临床症状的原因，如在全身炎症反应综合征（SIRS）中。脓毒症与SIRS的区别在于，脓毒症患者可分离出病原菌，而SIRS患者则不能。细菌易位在肠梗阻患者和免疫功能低下患者中更为常见，是随后发生脓毒症的原因。可引发肠道细菌易位的因素包括宿主免疫缺陷和免疫抑制、肠道正常生态平衡紊乱、黏膜屏障通透性、梗阻性黄疸、应激等。细菌易位通过跨细胞和细胞旁途径发生，可通过肠系膜淋巴结培养直接测量，也可通过使用标记细菌、外周血培养、微生物DNA或内毒素检测以及不可代谢糖的尿排泄间接测量。细菌易位可能是健康个体中经常发生的正常现象，不会产生任何有害后果。但当免疫系统受到广泛挑战时，它就会崩溃，导致远离主要病灶的不同部位出现脓毒症并发症。从肠道释放并通过肠系膜淋巴管而非门静脉血携带的因素足以导致多器官功能衰竭。因此，细菌易位可能是脓毒症的促进因素，但不是起始因素。本文综述了关于肠道菌群易位及其在导致脓毒症中作用的文献。
