Adel Al Othman - 210119276

M335 Lab 21/4/2014

Homework 3
Write about Vibrio cholera toxins.

Vibrio cholera is a species of bacteria belonging to the Vibrio group of
Proteobacteria. This group contains gram negative, aquatic bacteria that employ a
fermentative metabolism and are usually pathogenic. Vibrio cholera is a foodborne
pathogen that is the cause of cholera disease in humans, and does not cause this disease in
other hosts. This disease is caused by cholera exotoxins which cause the loss of large
amounts of fluid from intestinal tissues, which in turn can cause death of the tissues from
dehydration and loss of electrolytes.
Cholera toxin is an AB toxin, consisting of a single A subunit and 5 B subunits. The B-
subunit contains the site by which the toxin binds specifically with a complex lipid called gan
glioside GM1, in the cytoplasmic membrane of epithelial cells. The A subunit is transferred in
e the cell, where it adds an ADPribose molecule to a protein called G protein. The ADP
ribosylation puts the G protein in an active state. The function of the G protein is to activate
the enzyme adenyl cyclase. Adenyl cyclase converts ATP to cyclic AMP (cAMP). With adenyl
cyclase continually active, the levels of cAMP increases in the cell. Cyclic AMP is a specific
mediator of a variety of regulatory systems in cells, including ion balance. The increased
cyclic AMP level blocks the normal transport of sodium from the lumen into the
bloodstream. It also brings about the secretion of chloride and bicarbonate ions into the
intestinal lumen.
Cholera can be treated by fluid replacement with solutions contains electrolytes and
other solutes to counter the dehydration effect. Also, expression of cholera enterotoxin
genes ctxA and ctxB is controlled by toxR. The toxR product is a transmembrane protein that
controls cholera A and B chain production, as well as controlling outer membrane proteins
and pili required for successful attachment and colonization of Vibrio cholera.
References:
- Brock Biology of Microorganisms; 13
th
edition; 2012; Madigan, Martinko, Stahl, Clark;
pg. 505, 524, 824, 834, 835