Info on host response to cholera (1 Viewer)

[lma0]

I have searched far and wide to try to find information about the host response to cholera.

My assessment is due this week and i need some sources on the above.

Please help, thanks in advance =]

 

[Undermyskin]

I'm the only one in my class to get the info from only one resource so I'm not sure if they are correct. (You know, we can't assess the reliability)

http://gsbs.utmb.edu/microbook/ch024.htm

 

[Nuggos]

V cholerae O1 and V cholerae O139 cause clinical disease by producing an enterotoxin that promotes the secretion of fluid and electrolytes into the lumen of the small intestine. The enterotoxin is a protein molecule composed of 5 B subunits and 2 A subunits. The B subunits are responsible for binding to a ganglioside (monosialosyl ganglioside, GM1) receptor located on the surface of the cells that line the intestinal mucosa.

http://emedicine.medscape.com/article/962643-overview#a0104

 

[Coookies]

^ only 4 years late... lol

 

[Nuggos]

aahhaha funny, but maybe someone else (like myself) is doing it atm you fuck! and that what i typed down is of extreme use.
So very kindly go drive your finger up your arse you slut!
many thanks

 

[Nuggos]

actually, pardon me i didnt realise you were a chick... makes sense now, why u posted that...
but what i dont get is why you arnt in the kitchen, or if u are i sure u have better things to be doing

 

[albeitunique]

Actually I'm doing it right now for an assessment due on friday. Thanks!

 

[useless stick]

When the bacteria for cholera is consumed the stomach acids usually kills most of them, however some will survive, even if it is only one bacteria. Since the small intestines have a slightly basic pH cholera can land their and undergo binary fission. It then begins to release a toxin called cholera toxin (pretty generic huh?) which modifies the g proteins activated by the protein linked receptors in the cell membrane. Ordinarily these g proteins (GTP) would stimulate the enzyme adenylyl cyclase to produce a secondary messenger called cAMP and then turn into an inactive form GDP, however this cholera toxin prevents the hydrolization of GTP to GDP causing GTP to constantly produce cAMP. Through having a high concentration of cAMP the small intestines secrete large amounts of water and salt back into the intestines instead of being reabsorbed. This results in vomiting and severe diarrhoea.

I got this information from the book Biology 5th edition by Reece, Campbell and Mitchell. Also I know there is a lot of weird terminology, however a quick Google search should be enough to clear up any confusions