Clinical microbiology and hospital infection control: plasmid-mediated colistin resistance: 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 · Clinical microbiology and hospital infection control: plasmid-mediated colistin resistance

Sample item

A urinary Klebsiella pneumoniae isolate is resistant to colistin. Sequencing shows a plasmid-borne gene encoding a phosphoethanolamine transferase. How does this confer resistance?

AIt methylates 16S rRNA at the aminoglycoside binding siteBIt changes the peptidoglycan precursor terminus to D-Ala-D-LacCIt hydrolyses the beta-lactam ring of carbapenemsDIt adds phosphoethanolamine to lipid A, reducing negative charge and polymyxin binding

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

The answer and the reasoning

D. It adds phosphoethanolamine to lipid A, reducing negative charge and polymyxin binding

Polymyxins such as colistin bind the negatively charged lipid A of the outer membrane. The mcr-1 gene modifies lipid A with phosphoethanolamine, lowering the charge and binding. Because mcr-1 is on a plasmid, colistin resistance can spread between enteric bacteria.

Option by option

A. It methylates 16S rRNA at the aminoglycoside binding site
16S rRNA methylation causes high-level aminoglycoside resistance.
B. It changes the peptidoglycan precursor terminus to D-Ala-D-Lac
D-Ala-D-Lac is the vancomycin resistance mechanism in enterococci.
C. It hydrolyses the beta-lactam ring of carbapenems
Beta-lactam ring hydrolysis is the mechanism of carbapenemases and does not affect colistin.
D. It adds phosphoethanolamine to lipid A, reducing negative charge and polymyxin binding (correct)
Correct. Phosphoethanolamine modification of lipid A reduces colistin binding.

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.

Questions about this Microbiology question

What is the answer to this Microbiology question?

The best answer is D, It adds phosphoethanolamine to lipid A, reducing negative charge and polymyxin binding. Polymyxins such as colistin bind the negatively charged lipid A of the outer membrane.

Why is "It methylates 16S rRNA at the aminoglycoside binding site" not the answer?

16S rRNA methylation causes high-level aminoglycoside resistance.

Why is "It changes the peptidoglycan precursor terminus to D-Ala-D-Lac" not the answer?

D-Ala-D-Lac is the vancomycin resistance mechanism in enterococci.

Why is "It hydrolyses the beta-lactam ring of carbapenems" not the answer?

Beta-lactam ring hydrolysis is the mechanism of carbapenemases and does not affect colistin.

What concept does this question test?

It tests Clinical microbiology and hospital infection control: plasmid-mediated colistin resistance in Microbiology. The mcr-1 gene modifies lipid A with phosphoethanolamine, lowering the charge and binding. Because mcr-1 is on a plasmid, colistin resistance can spread between enteric bacteria.

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 Clinical microbiology and hospital infection control: plasmid-mediated colistin resistance?

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.