In this study the authors show that viable E. coli from a patient with severe diarrhea can multiply and predictably induce fluid secretion in canine duodenal segments. As with human cholera, this is accompanied by an increase in mucosal adenyl cyclase activity without demonstrable histopathologic changes. Additionally, the potential of the control organisms to produce net fluid secretion without adenyl cyclase activation may define the limits of this model, but it also suggests that redistribution into the upper small bowel of normal colonic flora could play a role in the pathogenesis of other diarrheal states. Controlled studies with sterile cell free culture filtrates show that a brief exposure of canine jejunum to the enterotoxin from the E. coli causes simultaneous activation of mucosal adenyl cyclase and secretion of isotonic fluid. In contrast to the slow, prolonged action of cholera toxin, the onset of and recovery from both changes with E. coli enterotoxin occur within ten minutes. At submaximal doses the active enterotoxin can be shown to disappear from the small bowel.
|Original language||English (US)|
|Number of pages||10|
|Journal||Transactions of the Association of American Physicians|
|State||Published - Jan 1 1973|
ASJC Scopus subject areas