Vibrio Cholerae Virulency

Cholera toxin binds to ganglioside on intestinal mucosal cell, which leads to ribosylation of the alpha subunit of Gs protein.

This results in the inhibition of the inherent GTPase activity and irreversible activation of G Protein. Therefore adenyl cyclase remains active and keep cyclic AMP levels high. This prevents absorption of salts from intestine leading to watery diarrhoea and loss of water from body.

Ref: Textbook of Biochemistry by DM Vasudevan, 5th Edition, Page 382

A i.e. ADP ribosylation

C i.e. Causes continued activation of adenylate cyclase

Cholera toxin (Al subunit) catalyzes ADP ribosylation of Gsa subunit and causes persistent activation of adenyl cyclaseQ. This results in elevation of cAMP, which activates protein kinase AQ and causes phosphorylation of CFTR and Na⁺ – H⁺ exchanger. This inturn leads to inhibition of Na⁺ absorption and enhancement of Cl secretion. Thus massive amounts of NaC1 accumulate inside intestine lumen contributing to liquid stools (watery diarrhoea) characteristic of cholera.

Ans. is ‘b’ i.e., Toxin action is cAMP mediated 

• V. cholerae produces cholera toxin, the model for enterotoxins, whose action on the mucosal epithelium is responsible for the characteristic diarrhoea of the cholera.

Ans. is ‘c’ i.e., Phage 

.  Cholera toxin production is determined by a filamentous phage integrated with bacterial chromosome.

Ans. is ‘a’ i.e., ADP ribosylation of G regulatory protein 

Ans. is ‘a’ i.e., cAMP 

.  Effects of cholera toxin (enterotoxin) are mediated by activation of adenylate cyclase which produces elevated levels of intracellular cAMP. Elevated levels of cAMP inturn cause an ouylowing of ions and water to the lumen of intestine producing watery diarrhea.

Ans. is ‘d’ i.e., Pathogenecity of 0-139 vibrio is due to 0 antigen 

Ans. is ‘c’ i.e., V. cholerae toxin

Ans. is `b’ i.e., To bind GM₁ ganglioside receptor 

Ans. A: Increase in c-AMP

Cholera toxin consists of an A subunit coupled to a B subunit: the A subunit consists of an Al domain containing the enzymatic active site, and an A2 domain while the B subunit contains five identical peptides that assemble into a pentameric ring surrounding a central pore.

This AB_; structure is closely related to the heat-labile enterotoxin (LT) from enterotoxigenic Escherichia coli, which causes diarrhoea, often in infants.

Symptoms begin when the massive secretion of water and sodium in the small intestine, a consequence of the activation of cyclic AMP, exceeds the resorptive capacity of the colon.

Ans. C: Bacteriophage

Bacteriophages have two main components, protein coat and a nucleic acid core of DNA or RNA.

Most DNA phages have double-stranded DNA, whereas phage RNA may be double or single-stranded. A filamentous bacteriophage transmits the gene that encodes the toxin for cholera.

Cholera toxin genetic element CTX constitutes the genome of a filamentous bacteriophage (CTXf).

The phage could be propagated in recipient V. cholerae strains in which the CTXf genome either integrated chromosomally at a specific site, forming stable lysogens, or was maintained extrachromosomally as a replicative form of the phage DNA.

Ans. is ‘a’ i.e., Heat labile toxin

Heat labile toxin of E. coli and cholera toxin resemble each other in their structure, antigenic properties and mode of action. Both act by activating adenyl cyclase in the enterocyte to form cyclic adenosine 5′ monophosphate (c AMP).

Heat stable toxin of E. coli acts by activation of cyclic guanosine monophosphate (c GMP) in the intestine.