Humanity is only susceptible to Vibrio cholerae in natural circumstances, mainly through contaminated water or food material transmitted through the mouth. Under certain conditions, into the small intestine of Vibrio cholerae, rely on the motion of flagella through the mucus layer of the mucosal surface of the likely by pili role adhesion on the intestinal epithelial cells and multiply rapidly in the mucosal surface, after a short incubation period after abrupt onset. The bacteria invade intestinal epithelial cells and intestinal glands do not, do not invade the bloodstream, multiply and produce only in the local cholera toxin, this toxin on the mucosal epithelial cells of the midgut gland intestinal fluid excessive secretion in patients with vomiting and diarrhea, diarrhea the material was "Mi Ganshui like" and contains a lot of Vibrio, this disease-oriented typical characteristics.
The nature of the cholera toxin is a protein, not heat, 56 ° C for 30 minutes to destroy its activity. Sensitive to protease trypsin resistance. The toxin is a toxin, has strong antigenicity. This toxin is now able to highly purified crystalline, still maintaining strong biological activity. The pathogenic mechanism of cholera toxin as follows: The toxin consists of two sub-units of the A and B, the A subunit into A1 and A2 , two peptide chains, both rely on disulfide chain connection. A subunit is the toxic unit, wherein the the A1 peptide chain having an enzyme activity, the the A2 peptide chain binding to the B subunit involved in receptor-mediated endocytosis in the indexable role. B subunit is the binding unit can specifically recognize the receptor on the intestinal epithelial cells. A toxin molecule consists of an A subunit and 4 ℃ 6 B subunit composition of the polymer. Cholera toxin acts on a receptor on the intestinal membrane surface (by the ganglioside GM1), its B subunit binds to the receptor, the toxin molecule allosteric A fine unit enters the cells, the activation of the A1 peptide chain, thereby activating adenylyl cyclase (AC), adenosine triphosphate (ATP) into cyclic adenosine (cAMP), intracellular cAMP concentration, leading to intestinal mucosal cell function greatly hyperthyroidism, so a lot of fluids and electrolytes into the intestine occurs severe vomiting and diarrhea, dehydration and salt loss, metabolic acidosis can occur due to a large number of blood circulation failure, and even shock or death.