Fungal infections: terbinafine resistance: practice question

A Dermatology 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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Dermatology · Fungal infections: terbinafine resistance

Sample item

In India, many patients with extensive tinea corporis and cruris show poor response to terbinafine. What is the main mechanism of resistance in these dermatophytes?

APoint mutations in the squalene epoxidase geneBLoss of cell wall chitinCEfflux of fluconazole aloneDAbsence of ergosterol in the membrane

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

The answer and the reasoning

A. Point mutations in the squalene epoxidase gene

Recalcitrant dermatophytosis, often due to Trichophyton mentagrophytes/interdigitale genotype VIII (T. indotineae), commonly shows mutations in squalene epoxidase, the target of terbinafine. Itraconazole is the usual alternative.

Option by option

A. Point mutations in the squalene epoxidase gene (correct)
Correct. Squalene epoxidase mutations reduce binding of terbinafine.
B. Loss of cell wall chitin
Chitin loss is not the main mechanism of resistance here.
C. Efflux of fluconazole alone
Efflux of fluconazole alone does not explain terbinafine failure.
D. Absence of ergosterol in the membrane
Dermatophytes do have ergosterol, which is why azoles are active.

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 Dermatology question

What is the answer to this Dermatology question?

The best answer is A, Point mutations in the squalene epoxidase gene. Recalcitrant dermatophytosis, often due to Trichophyton mentagrophytes/interdigitale genotype VIII (T.

Why is "Loss of cell wall chitin" not the answer?

Chitin loss is not the main mechanism of resistance here.

Why is "Efflux of fluconazole alone" not the answer?

Efflux of fluconazole alone does not explain terbinafine failure.

Why is "Absence of ergosterol in the membrane" not the answer?

Dermatophytes do have ergosterol, which is why azoles are active.

What concept does this question test?

It tests Fungal infections: terbinafine resistance in Dermatology. indotineae), commonly shows mutations in squalene epoxidase, the target of terbinafine. Itraconazole is the usual alternative.

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 Fungal infections: terbinafine resistance?

Learn each condition by its primary lesion, site and signature sign. Then use the flashcards and the other Dermatology 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.