Vibrio Cholerae Essay

1083 words - 5 pages

Canada’s Cholera epidemic began in June of 1832 when a ship named The Carrick arrived from Ireland. A large number of passengers on the ship, all Irish immigrants to Canada, were sick with this disease. Because the majority of the population lived very close together and under poor conditions, the outbreak spread swiftly and infected many people very quickly. Entire communities quarantined themselves in hopes of preventing the spread of infection. Since Vibrio cholerae, the bacterium responsible for causing Cholera, is transmitted by the fecal-oral route, most commonly through water, they were not saved from contracting the infection.

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cholerae was the bacterium responsible for cholera.

V. cholerae is a gram-negative bacilli. It is a non-spore forming, facultatively anaerobic bacterium with a single polar flagellum for motility.3 It also contains an outer membrane composed of lipopolysaccharides (LPS), which is responsible for the O antigens on the bacterium. LPS also contains Lipid A, which is responsible for producing the endotoxin that causes disease in humans. Cholera is spread through contact with water contaminated with infectious feces. There are two main serotypes of V. cholerae that have been responsible for epidemics, O1 and O139.4 Serotype O1 is commonly known as El Tor, and has three distinct biotypes: Ogawa, which has antigens A and B; Inaba, which displays A and C antigens; and Hikojimo, which displays all three antigens. Serotype O139 displays a different O antigen.1 The El Tor strain of V. cholerae is more virulent than classic strains. More people who are exposed to the El Tor strain become infected than people who are exposed to another serotype.1 People also carry this strain for longer than normal.

This bacterium is able to survive high pH and salt concentrations, which allows it to successfully survive in the gastrointestinal tract of humans.4 V. cholerae has also been found within biofilms, which can make it hard to treat with antibiotics. V. cholerae causes infection in humans by secreting an enterotoxin which promotes the secretion of fluids and electrolytes by the small intestine.2 Although the bacterium produces a toxin, it does not invade the intestinal wall. The toxin is composed of many different polypeptide chains that together have two subunits, labelled A1 and A2, and five binding sites.5 It works by activating a toxin regulated pilus.2 After binding to receptors that can be found on the surface of many body cells, subunit A1 is released when the disulfide bond is broken down. It is then able to enter into the cell. A1 causes disease near the basolateral membrane where it targets the protein Guanine.5 Through constant activation of adenylate cyclase, the conversion from adenosine triphosphate to cyclic adenosine monophosphate is able to take place.5 The ultimate effect of this transformation is hypersecretion of potassium, bicarbonate,...

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