Depending on the structure of the O-antigen, more than 150 serogroups are distinguished, among them the serogroups 01 and 0139 are the causative agents of the cholera. Virulence factors Virulence factors of V. cholerae include (i) cholera toxin, (ii) toxin coregulated pilus (TCP), (iii) adhesin factor (ACF), (iv) hemagglutination-protease (hap; mucinase), (v) neuramini-dase, and (vi) siderophores (Table 35-4). The high osmolarity of the intestinal fluid is balanced by large secre-tion of water, which overcomes the absorptive capacity of the lumen, eventually causing diarrhea (Fig. Cholera is a bacterial disease usually spread through contaminated water. These factors are responsible for intestinal colonization of V. cholerae and induction of fluid secretion, respectively. A small chromosome contains an integrin that captures and expresses antibiotic resistance cassettes. Hemagglutinin and prote-ase break mucin and fibronectin of the mucosa. The bacterium's natural habitat is brackish or saltwater where they attach themselves easily to the chitin-containing shells of crabs, shrimps, and other shellfish. It induces intestinal inflammation and also helps in releasing free vibrios from the bound mucosa to the intestinal lumen. Vaccination with killed cholera vaccine confers a short-lived protection. Biovar El Tor is resistant to polymyxin, agglutinates chicken red blood cells and hemolysates erythrocytes of ram, has a positive reaction of Foges-Proskauer and a hexamine test. The sequences of events leading to cholera are basically simple and confined to the gut. By continuing you agree to the use of cookies. Cholera toxin (CTx) pro-duced by V. cholerae is the key virulence factor of the bacteria. of sodium transport and activates the excretory chloride trans-port in the intestinal epithelial cells. Have nitrate reductase activity. Natural infections in cholera induce some degree of immunity for a short duration of 6–12 months. BACTERIAL FOOD POISONING: CAUSES, SYMPTOMS, TREATMENTS, RECOVERY. The enzyme destroys neuraminic acid,thereby increasing toxin receptors for the. Cholera vibrios possess O- and H-antigens. Pathogenesis of cholera. In sea water - up to 47 days, in river water - from 3-5 days to several weeks, in the soil - from 8 days to 3 months, in feces - up to 3 days, on raw vegetables - 2-4 days. Infection due to V. choleraebegins with the ingestion of contaminated water or food. Rabbit ileal loop test was one of the classical methods developed by De and Chatterjee in 1952. The enzyme splits mucus and fibronectin as well as subunit of the cholera toxin. Cholerogen binds to a specific receptor of enterocytes - ganglioside. V. Cholerae 0139 on phenotypic signs refers to the biologist El Tor. These are also responsible for increase in its resis-tance to human serum in vitro and development of bacte-remia occasionally seen during the infection caused by the bacteria. Vibrio are highly susceptible to acids and gastric acidity provides an effective barrier against small doses of cholera vibrios. The fluid is redistributed from the interstitial to the intravascular space. In the crypt region of epithelial cells, C1- ions are strongly isolated, and in the villus region, absorption of Na + and Cl- is difficult, which is the osmotic basis for isolating water into the intestine. The pathogenesis and virulence of the bacteria are due to an enterotoxin it produces—cholera toxin (CT). Rabbit ileal loop test was one of the classical methods developed by De and Chatterjee in 1952. Adenosine triphosphate regulates through the ion pump the secretion of water and electrolytes from the cell to the lumen of the intestine. Demonstration of histological changes in adrenal tumor (Y1) cells, elongation of Chinese hamster ovary cells, and activation of lipolysis in rat testicular tissue. Toxin coregulated pilus: The pili help in adherence ofV. pathogenesis of cholera Cholera strains vary in toxigenicity, and variations in host resistance probably explain the infrequency of more than one case in a family. Cholera is a toxin-mediated disease. Ter is coordinately expressed with the CT gene. The last decades have been marked by a remarkable increase in our knowledge of the structure, regulation, and function of biofilms formed under laboratory conditions. The mechanism of action of CT is discussed in this chapter at a later stage.

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