[The cholera syndrome - pathogenesis and pathogens (author's transl)].
The same pathomechanism underlies both classical cholera and the enteritides due to nonagglutinating (NAG) vibrios and a few types of E. coli. A heat-labile enterotoxin activates the adenocyclase. This stimulates the cells of the small intestine to secrete ions and water, the immune reaction in the intestine is retarded and the production of gastric juice is reduced. Neuraminidase potentiates these reactions by opening additional enterotoxin receptors. Endotoxin is a further pathogenetic factor. The individual pathogens can certainly be clearly distinguished microbiologically, but the possession of the same pathogenetic factors makes the transition seem rather fluid. For this reason it is certainly wrong to regard NAG vibrios as only harmless water vibrios.
D000262:Adenylyl Cyclases; D002771:Cholera / Q000209:etiology*; D003967:Diarrhea / Q000209:etiology; D004751:Enteritis / Q000209:etiology*; D004768:Enterotoxins; D004789:Enzyme Activation; D004926:Escherichia coli / Q000472:pathogenicity; D006801:Humans; D007413:Intestinal Mucosa / Q000503:physiopathology; D009439:Neuraminidase; D011453:Prostaglandins; D014733:Vibrio / Q000472:pathogenicity; D014734:Vibrio cholerae / Q000472:pathogenicity; D014883:Water-Electrolyte Imbalance / Q000209:etiology
D004768:Enterotoxins; D011453:Prostaglandins; D009439:Neuraminidase; D000262:Adenylyl Cyclases
Das Cholera-Syndrom-Pathogenese und Erreger