Bacteriology: toxin mechanisms: practice question

A Microbiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Microbiology · Bacteriology: toxin mechanisms

Sample item

A traveller develops watery diarrhoea from enterotoxigenic Escherichia coli that produces only the heat-stable toxin (ST). What is the intracellular mechanism responsible for the fluid secretion?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. Activation of guanylate cyclase C, raising intracellular cGMP

The heat-stable toxin of ETEC binds guanylate cyclase C on enterocytes and increases cGMP, which inhibits sodium absorption and stimulates chloride secretion. The heat-labile toxin and cholera toxin instead ADP-ribosylate the Gs protein and raise cAMP. Shiga toxin inhibits the 60S ribosomal subunit, and clostridial toxins inactivate Rho proteins.

Option by option

  • A. Activation of guanylate cyclase C, raising intracellular cGMP (correct)

    Correct. ST raises cGMP through guanylate cyclase C activation.

  • B. Inactivation of Rho GTPases

    Rho GTPase inactivation is caused by Clostridium difficile toxins.

  • C. Inhibition of 60S ribosomal subunit, causing cell death

    Inhibition of the 60S ribosome is the action of Shiga toxin.

  • D. ADP-ribosylation of Gs protein, raising cAMP

    Raised cAMP through Gs ADP-ribosylation is the mechanism of LT and cholera toxin.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Microbiology question

What is the answer to this Microbiology question?

The best answer is A, Activation of guanylate cyclase C, raising intracellular cGMP. The heat-stable toxin of ETEC binds guanylate cyclase C on enterocytes and increases cGMP, which inhibits sodium absorption and stimulates chloride secretion.

Why is "Inactivation of Rho GTPases" not the answer?

Rho GTPase inactivation is caused by Clostridium difficile toxins.

Why is "Inhibition of 60S ribosomal subunit, causing cell death" not the answer?

Inhibition of the 60S ribosome is the action of Shiga toxin.

Why is "ADP-ribosylation of Gs protein, raising cAMP" not the answer?

Raised cAMP through Gs ADP-ribosylation is the mechanism of LT and cholera toxin.

What concept does this question test?

It tests Bacteriology: toxin mechanisms in Microbiology. The heat-labile toxin and cholera toxin instead ADP-ribosylate the Gs protein and raise cAMP. Shiga toxin inhibits the 60S ribosomal subunit, and clostridial toxins inactivate Rho proteins.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Bacteriology: toxin mechanisms?

Make a one-line identity card for each organism: shape and stain, defining test, toxin, disease and drug. Then use the flashcards and the other Microbiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.