Malaria is caused by several different species of Plasmodium, a protozoan parasite. Plasmodium resistance to the common drugs used to treat malaria has increased in recent years.

In a scientific study, Plasmodium samples were analyzed in blood drawn from a large number of infected patients before drug treatment and subsequently from the subset of infected patients with drug-resistant Plasmodium. DNA sequences of four different Plasmodium genes thought to be involved in resistance were compared between samples from patients with drug-sensitive Plasmodium and patients with drug-resistant Plasmodium.

Which of the following best supports the hypothesis that preexisting mutations confer drug resistance?

Question

Malaria is caused by several different species of Plasmodium, a protozoan parasite. Plasmodium resistance to the common drugs used to treat malaria has increased in recent years.

In a scientific study, Plasmodium samples were analyzed in blood drawn from a large number of infected patients before drug treatment and subsequently from the subset of infected patients with drug-resistant Plasmodium. DNA sequences of four different Plasmodium genes thought to be involved in resistance were compared between samples from patients with drug-sensitive Plasmodium and patients with drug-resistant Plasmodium.

Which of the following best supports the hypothesis that preexisting mutations confer drug resistance?

BlackTom AI · Accepted Answer

Presence of resistance-associated mutations in pre-treatment samples indicates standing genetic variation that natural selection can act on once drugs are used. Relevant concepts: mutation creates allelic variants; standing genetic variation means some individuals already carry alleles that confer a trait; selection pressure (drug treatment) increases the frequency of alleles that confer survival; de novo mutation means the allele appears only after selection begins.

Step-by-step reasoning:
1. The study compares DNA sequences from many infected patients before any drug treatment and from the subset whose infections are drug-resistant after treatment. This design tests whether resistance-associated alleles existed before drugs were applied.
2. If the same mutations that are common in resistant isolates are also detectable in pre-treatment samples, those mutations existed prior to drug exposure. That is direct evidence of preexisting (standing) mutations rather than mutations that arose only after drug use.
3. Once drug treatment begins, parasites carrying those preexisting resistant alleles have a selective advantage and increase in frequency—explaining observed resistance in treated populations.
4. Conversely, if those mutations were absent in pre-treatment samples and only appeared after therapy, that would support de novo mutation during/after treatment rather than preexistence.

Why the correct answer is correct:
- It explicitly states that resistance-associated mutations are detectable in samples collected prior to antimalarial use. That observation is the hallmark of preexisting variation being responsible for resistance once selection occurs.

Why the other options are incorrect:
- Option 1 (same mechanism resulted from accumulation of new mutations) implies independent de novo evolution rather than preexisting alleles; it contradicts evidence of detection before drug use.
- Option 2 (resistance reversed by inhibitor of a pump) describes a mechanism or therapeutic reversal but does not demonstrate that mutations preexisted before drug exposure.
- Option 3 (continued use leads to increased resistance) describes selection pressure increasing resistance but does not distinguish whether resistance alleles were preexisting or newly arisen.

Conclusion: The best support for preexisting mutations conferring drug resistance is that some resistance-associated mutations are detectable in Plasmodium samples collected prior to antimalarial drug use, which matches the provided correct answer.

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