Karmali Mohamed A
Laboratory for Foodborne Zoonoses, Health Canada, 110 Stone Road West, Guelph, Ontario, Canada, N1G 3W4.
Mol Biotechnol. 2004 Feb;26(2):117-22. doi: 10.1385/MB:26:2:117.
Shiga toxin-producing Escherichia coli (STEC), especially of serotype O157:H7, cause a zoonotic food or waterborne enteric illness that is often associated with large epidemic outbreaks as well as the hemolytic uremic syndrome (HUS), the leading cause of acute renal failure in children. After ingestion, STEC colonize enterocytes of the large bowel with a characteristic attaching and effacing pathology, which is mediated by components of a type III secretion apparatus encoded by the LEE pathogenicity island. Shiga toxins are translocated from the bowel to the circularoty system and transported by leukocytes to capillary endothelial cells in renal glomeruli and other organs. After binding to the receptor globotriaosylceramide on target cells, the toxin is internalized by receptor-mediated endocytosis and interacts with the subcellular machinery to inhibit protein synthesis. This leads to pathophysiological changes that result in HUS. Specific therapeutic or preventive strategies are presently not available. The recent sequencing of genomes of two epidemic E. coli O157 strains has revealed novel pathogenicity islands which will likely provide new insights into the virulence of these bacteria.
产志贺毒素大肠杆菌（STEC），尤其是O157:H7血清型，可引发一种人畜共患的食源性或水源性肠道疾病，这种疾病常与大规模的疫情爆发以及溶血尿毒综合征（HUS）相关，而HUS是儿童急性肾衰竭的主要病因。摄入后，STEC会在大肠的肠上皮细胞中定植，并呈现出特征性的黏附与抹除病理特征，这一过程由LEE致病岛编码的III型分泌系统的成分介导。志贺毒素从肠道转移至循环系统，并由白细胞运输至肾小球及其他器官的毛细血管内皮细胞。毒素与靶细胞上的受体球三糖神经酰胺结合后，通过受体介导的内吞作用被内化，并与亚细胞机制相互作用以抑制蛋白质合成。这会导致病理生理变化，进而引发HUS。目前尚无特异性的治疗或预防策略。最近对两株O157流行大肠杆菌菌株的基因组测序揭示了新的致病岛，这可能会为深入了解这些细菌的毒力提供新的见解。
