Chemotherapy: MRSA resistance mechanism: practice question

A Pharmacology 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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Pharmacology · Chemotherapy: MRSA resistance mechanism

Sample item

A surgical wound swab grows Staphylococcus aureus resistant to cloxacillin and cefazolin. What is the molecular basis of this resistance?

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

The answer and the reasoning

A. Acquisition of the mecA gene encoding a low-affinity penicillin-binding protein, PBP2a

Methicillin-resistant S. aureus carries mecA on the SCCmec element, which encodes PBP2a with poor affinity for nearly all beta-lactams except the anti-MRSA cephalosporins such as ceftaroline. Isolates are therefore treated with vancomycin, linezolid, daptomycin or teicoplanin. Penicillinase-resistant penicillins like cloxacillin are active against ordinary penicillinase-producing strains but not against MRSA.

Option by option

  • A. Acquisition of the mecA gene encoding a low-affinity penicillin-binding protein, PBP2a (correct)

    Correct. A target with low affinity lets cell wall synthesis continue despite the drug.

  • B. Loss of outer membrane porins that restrict drug entry

    Porin loss is a feature of Gram-negative bacteria, and S. aureus has no outer membrane.

  • C. Production of a plasmid-borne beta-lactamase that hydrolyses the beta-lactam ring

    Plasmid beta-lactamase gives penicillin resistance, but cloxacillin is stable against it.

  • D. Alteration of the D-Ala-D-Ala terminus to D-Ala-D-Lac

    A D-Ala-D-Lac terminus is the vancomycin resistance mechanism of enterococci.

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.

More Pharmacology questions

Questions about this Pharmacology question

What is the answer to this Pharmacology question?

The best answer is A, Acquisition of the mecA gene encoding a low-affinity penicillin-binding protein, PBP2a. Methicillin-resistant S.

Why is "Loss of outer membrane porins that restrict drug entry" not the answer?

Porin loss is a feature of Gram-negative bacteria, and S. aureus has no outer membrane.

Why is "Production of a plasmid-borne beta-lactamase that hydrolyses the beta…" not the answer?

Plasmid beta-lactamase gives penicillin resistance, but cloxacillin is stable against it.

Why is "Alteration of the D-Ala-D-Ala terminus to D-Ala-D-Lac" not the answer?

A D-Ala-D-Lac terminus is the vancomycin resistance mechanism of enterococci.

What concept does this question test?

It tests Chemotherapy: MRSA resistance mechanism in Pharmacology. aureus carries mecA on the SCCmec element, which encodes PBP2a with poor affinity for nearly all beta-lactams except the anti-MRSA cephalosporins such as ceftaroline. Isolates are therefore treated with vancomycin, linezolid, daptomycin or teicoplanin. Penicillinase-resistant penicillins like cloxacillin are active against ordinary penicillinase-producing strains but not against MRSA.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. 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 Chemotherapy: MRSA resistance mechanism?

Learn drugs as classes, then the exception in each class that an examiner would pick. Then use the flashcards and the other Pharmacology 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.