Giannella R A
Annu Rev Med. 1981;32:341-57. doi: 10.1146/annurev.me.32.020181.002013.
Acute bacterial diarrheal disease is a worldwide problem of enormous magnitude. In recent years a number of bacteria have been added to the list of recognized etiologic agents causing acute diarrheal disease. This was made possible by our increased understanding of the mechanisms by which such bacteria cause diarrhea and by the development of methods to detect these bacterial enteropathogens. We are now able to define an etiologic agent in 50-80% of cases of acute diarrhea, depending on the particular population. The bacterial agents recently incriminated as important causes of diarrhea include E coli Y. enterocolitica, B. cereus, C. fetus, V. parahemolyticus, and many other coliform organisms. Establishment of an enteric infection depends upon a complex interplay between host defense mechanisms and bacterial virulence factors adapted to overcome these defenses. Bacterial enteropathogens cause diarrhea primarily by elaborating enterotoxins (which also requires the organisms to adhere to the surface of the intestinal cell) and by invading the intestinal mucosa. The number of known bacterial enterotoxins has rapidly increased. Enterotoxins cause intestinal secretion and diarrhea by stimulating the adenyl cyclase system or the guanyl cyclase system and by other mechanisms yet to be defined. The ability of enterotoxigenic bacteria to adhere to the intestine involves a specific binding interaction between bacterial structures called pili or fimbriae and specific receptors on the surface of intestinal cells. Both bacterial pili and the intestinal receptors are under genetic control. A variety of other bacteria, Salmonellae, Shigellae, Y. enterocolitica etc, must invade the mucosa to cause diarrheal disease. The ability to invade is essential to the pathogenesis of disease and requires particular surface characteristics of the bacterium as well as the active participation of both the bacterium and the host cell. The bacteria probably elaborate substances that signal the host cell to initiate the invasive process, i.e. endocytosis. The mechanism by which invasive bacteria evoke intestinal secretion is uncertain but is probably a multifactorial process involving products elaborated by the mucosal acute inflammatory reaction and enterotoxins elaborated by the bacteria.
急性细菌性腹泻病是一个全球性的重大问题。近年来，一些细菌已被列入已确认的引起急性腹泻病的病原体名单。这得益于我们对这些细菌引起腹泻机制的深入了解以及检测这些肠道细菌病原体方法的发展。现在，根据特定人群的不同，我们能够在50%至80%的急性腹泻病例中确定病原体。最近被认定为腹泻重要病因的细菌病原体包括大肠杆菌、小肠结肠炎耶尔森菌、蜡样芽孢杆菌、胎儿弯曲杆菌、副溶血性弧菌以及许多其他大肠菌群生物。肠道感染的发生取决于宿主防御机制与适应克服这些防御的细菌毒力因子之间复杂的相互作用。细菌性肠道病原体主要通过产生肠毒素（这也要求细菌附着于肠细胞表面）和侵入肠黏膜来引起腹泻。已知的细菌肠毒素数量迅速增加。肠毒素通过刺激腺苷酸环化酶系统或鸟苷酸环化酶系统以及其他尚未明确的机制引起肠道分泌和腹泻。产肠毒素细菌附着于肠道的能力涉及被称为菌毛或纤毛的细菌结构与肠细胞表面特定受体之间的特异性结合相互作用。细菌菌毛和肠道受体均受基因控制。多种其他细菌，如沙门氏菌、志贺氏菌、小肠结肠炎耶尔森菌等，必须侵入黏膜才能引起腹泻病。侵入能力对于疾病的发病机制至关重要，需要细菌具有特定的表面特征以及细菌和宿主细胞的积极参与。细菌可能产生一些物质，向宿主细胞发出信号以启动侵入过程，即内吞作用。侵入性细菌引发肠道分泌的机制尚不确定，但可能是一个多因素过程，涉及黏膜急性炎症反应产生的产物和细菌产生的肠毒素。
