Hart C A, Batt R M, Saunders J R
Department of Medical Microbiology, University of Liverpool, UK.
Ann Trop Paediatr. 1993;13(2):121-31. doi: 10.1080/02724936.1993.11747636.
Since the mid-1940s, Escherichia coli has been recognized as a cause of diarrhoea. Subsequently it has been shown that at least five different pathogenic mechanisms are used to cause disease. Enterotoxigenic E. coli (ETEC) and enteropathogenic E. coli (EPEC) produce a noninflammatory diarrhoea, whereas enteroinvasive E. coli (EIEC), enterohaemorrhagic E. coli (EHEC) and enteroaggregative E. coli (EAggEC) produce an inflammatory diarrhoea. ETEC are a major cause of diarrhoea in infants (up to three episodes per year) and travellers. They produce diarrhoea by attaching to the small intestinal mucosa and elaborate one or both of heat labile and heat stable toxins. EPEC attach firmly to the intestinal mucosa leading to dissolution of the brush border by inducing vesiculation of the microvilli. This process is known as attaching-effacement, and in the jejunum and ileum results in a loss of brush border disaccharidase enzymes and a large area of absorptive surface. EPEC are a major cause of summer diarrhoea in infants and neonatal diarrhoea. EIEC attach to colonic enterocytes, penetrate by an endocytotic mechanism and replicate therein. This results in necrosis and stripping of large areas of colonic mucosa and a dysentery similar to but usually less severe than Shigella dysentery. EHEC produce attaching-effacement to the terminal ileal and colonic mucosa and release the toxins, verocytotoxin (VT) 1 or 2. These kill colonic enterocytes and produce haemorrhagic colitis. In addition, VT can damage vascular endothelial cells, leading to haemolytic uraemic syndrome. The role of EHEC in diarrhoea in children in the tropics is not known. The most recently described group are the EAggEC. They damage and blunt colonic villi by haemorrhagic necrosis, although the precise pathogenic mechanisms are unclear. EAggEC are a major cause of chronic diarrhoea in children. Although certain O-serotypes are associated with the different enteropathic E. coli, serotyping is not sufficiently specific or sensitive for use as a diagnostic tool. Specific diagnosis is expensive and time consuming and depends upon demonstration of the pathogenicity trait, and the pathogenicity gene(s) or their gene product(s). At present, to undertake such testing is not recommended for routine diagnosis but is most useful when surveys of the aetiology of acute and chronic diarrhoea are undertaken.
自20世纪40年代中期以来，大肠杆菌一直被认为是腹泻的病因。随后发现，至少有五种不同的致病机制可引发疾病。产肠毒素大肠杆菌（ETEC）和肠致病性大肠杆菌（EPEC）引起非炎性腹泻，而侵袭性大肠杆菌（EIEC）、肠出血性大肠杆菌（EHEC）和肠集聚性大肠杆菌（EAggEC）引起炎性腹泻。ETEC是婴儿（每年多达三次发作）和旅行者腹泻的主要病因。它们通过附着于小肠黏膜并分泌热不稳定毒素和热稳定毒素中的一种或两种来引起腹泻。EPEC牢固地附着于肠黏膜，通过诱导微绒毛形成小泡导致刷状缘溶解。这个过程称为黏附-抹平，在空肠和回肠会导致刷状缘双糖酶丢失和大面积吸收表面丧失。EPEC是婴儿夏季腹泻和新生儿腹泻的主要病因。EIEC附着于结肠上皮细胞，通过内吞机制侵入并在其中复制。这会导致大片结肠黏膜坏死和脱落，引发类似于志贺菌痢疾但通常较轻的痢疾。EHEC在回肠末端和结肠黏膜产生黏附-抹平并释放毒素，即志贺毒素（VT）1或2。这些毒素会杀死结肠上皮细胞并导致出血性结肠炎。此外，VT可损伤血管内皮细胞，导致溶血尿毒综合征。EHEC在热带地区儿童腹泻中的作用尚不清楚。最近描述的一组是EAggEC。它们通过出血性坏死破坏并使结肠绒毛变钝，尽管确切的致病机制尚不清楚。EAggEC是儿童慢性腹泻的主要病因。虽然某些O血清型与不同的肠致病性大肠杆菌有关，但血清分型作为诊断工具不够特异或敏感。特异性诊断昂贵且耗时，取决于致病特性以及致病基因或其基因产物的证明。目前，不建议将此类检测用于常规诊断，但在进行急慢性腹泻病因调查时最为有用。
