Vibrio Cholerae - infected person, treatment options
October 11, 2006 6:25pm CST
I am a student writing a paper,i want to know about what happens from the time a person is infected with vibrio cholerae, treatment and possible diagrams to trace the path of cholera toxin through the cell,identify specific cellular targets, destinations for the toxin. Also, how researchers can take advantage of cholera toxin to study cellular signaling and other cellular organelles, process
30 Mar 07
It is caused by a specific bacterium, Vibrio cholerae. When an adequate quantity of the bacteria has passed into the stomach in food they accumulate and begin to produce toxins in the body. The cholera toxin has the unpleasant ability to affect the cells of the gastrointestinal tract so that the affected person doesn't just get ordinary diarrhoea, but also starts to lose very large quantities of fluid. It is this fluid loss that can be very serious. Here are some tips:- Take only boiled water or water that has been sterilised or treated in another way. Hot coffee and tea, fizzy water are usually safe enough to drink. Boil unpasteurised milk before you take it. Avoid ice cubes in drinks. Food must be properly prepared and still hot when it is served. Avoid raw fruit and vegetables, unless you peel it yourself. n' also raw fish and shellfish.
• United States
18 Oct 06
Treatment Cholera can be treated by tetracycline. Also, water and electrolyte replacement are necessary. Vaccine is available, but it is short-lived. Vibrio Cholerae is a gram negative bacterium with a curved-rod shape that causes cholera in humans. It and other species of the genus Vibrio belong to the gamma subdivision of the Proteobacteria. There are two major strains of V. cholerae, classic and El Tor, and numerous other serogroups. V. cholerae colonizes the gastrointestinal tract, where it adheres to villous absorptive cells via pili, and secretes a Binary toxin, called cholera toxin (CT). The two CT subunits are named A and B, and are synthesised in a 1:5 ratio. B subunits bind and internalize A subunits, which are processed to A1. The A1 form catalyses ADP ribosylation from NAD to the regulatory component of adenylate cyclase, thereby activating it. Increased adenylate cyclase activity increases cyclic AMP (cAMP) synthesis causing massive fluid and electrolyte efflux, resulting in diarrhea. CT is encoded by the ctxAB genes on a specific filamentous bacteriophage. Transduction of this phage is dependent upon bacterial expression of the Toxin Coregulated Pilus (TCP), which is encoded by the V. cholerae pathogenicity island (VPI). VPI is generally only present in virulent strains and is laterally transferred. VPI was originally thought to encode a filamentous phage responsible for transfer. This theory was discredited by a study of 46 diverse V. cholerae isolates which found no evidence of VPI phage production. The generalized transduction phage CP-T1 has been shown to transduce the entire VPI which is then integrated at the same chromosomal location. Also, VPI has been shown to excise and circularize to produce pVPI via a specialised mechanism involving VPI-encoded recombinases. It is not known whether pVPI is involved in CP-T1 transduction or if it is perhaps a component of an alternative VPI mobilization mechanism. The bacterium was first isolated as the cause of cholera by Italian anatomist Filippo Pacini in 1854, but his discovery was not widely known until Robert Koch, working independently thirty years later, publicized the knowledge and the means of fighting the disease. hope this site provides with additional information http://textbookofbacteriology.net/cholera.html