cellular mechanisms that result in symptoms of cholera

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    • #17052
      tesla93
      Participant

      Hi all,

      I”m trying to understand how cholera symptoms are developed, and all I know so far is that the cholera toxin (CT) is responsible for the main symptom of cholera, which is secretory diarrhea. More specifically, CT is an A-B5 subunit-type exotoxin released in the small intestine, but I can’t really find how specific cellular mechanisms that cause this and other symptoms (nausea, dehydration, vomiting, muscle cramps). Thanks for looking!

    • #113005
      tesla93
      Participant

      Just wanted to add in…one of the mechanisms is direct stimulation of chloride secretion by enterocytes, which is a result of the cholera toxin, but I don’t really understand what this is/I can’t find much information on it. This mechanism is responsible for secretory diarrhea

    • #113080
      naachiz
      Participant

      Cholera is an acute Diarrhoeal disease caused by V. Cholerae. It is seen in many countries of the world mainly the poor third world countries. Libya has no epidemic cases since 1970. Cholera is no longer the dreaded disease of the past because we can prevent deaths with Oral Rehydration Salt solution.

      You can read more about Cholera on these slides;
      http://in.docsity.com/en-docs/Cholera_- … re_Slides_

    • #113190
      MarkHolland
      Participant

      Cholera symptoms and signs include a rapid onset of copious, smelly diarrhea that resembles rice water and may lead to signs of dehydration.For example, vomiting, wrinkled skin, low blood pressure, dry mouth, rapid heart rate.

      Thanks

      🙁

    • #113224
      adithya528
      Participant

      The cholera toxin (CTX or CT) is
      an oligomeric complex made up
      of six protein subunits: a single
      copy of the A subunit (part A),
      and five copies of the B subunit
      (part B), connected by a disulfide
      bond. The five B subunits form a
      five-membered ring that binds to
      GM1 gangliosides on the surface
      of the intestinal epithelium cells.
      The A1 portion of the A subunit
      is an enzyme that ADP-ribosylates
      G proteins, while the A2 chain fits
      into the central pore of the B
      subunit ring. Upon binding, the
      complex is taken into the cell via
      receptor-mediated endocytosis.
      Once inside the cell, the disulfide
      bond is reduced, and the A1
      subunit is freed to bind with a
      human partner protein called
      ADP-ribosylation factor 6 (Arf6).
      [13] Binding exposes its active
      site, allowing it to permanently
      ribosylate the Gs alpha subunit of
      the heterotrimeric G protein. This
      results in constitutive cAMP
      production, which in turn leads
      to secretion of H2O, Na+, K+, Cl−,
      and HCO3− into the lumen of the
      small intestine and rapid
      dehydration. The gene encoding
      the cholera toxin is introduced
      into V. cholerae by horizontal
      gene transfer. Virulent strains of
      V. cholerae carry a variant of
      temperate bacteriophage called
      CTXf or CTXφ.

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