Insecticide Resistance in Aedes aegypti: Selection, Drift, or Something Else?
Fogging with malathion against Aedes aegypti began in one parish in 2016. Researchers sampled larvae from drains in two towns 40 km apart - Port A, which is sprayed, and Port B, which is not - and tested 200 adults per site per year at a discriminating dose. Survival was 4% in Port A and 3% in Port B in 2016; by 2020 it was 61% in Port A and 5% in Port B. Resistance in this population is thought to be conferred mainly by a single autosomal allele (kdr) showing incomplete dominance: RR and RS survive the dose, SS die. Spraying continued every rainy season, and the same insecticide class was used throughout. A vector-control officer argues that the population has 'learned to resist' and proposes doubling the dose; a colleague argues the change is just genetic drift in a small population.
1. Using the 2020 Port A data and the stated genotype–phenotype relationship, estimate the frequency of the resistance allele, showing your working and stating your assumptions.
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Survival means having at least one R allele, so the survivors are RR plus RS and the dead are SS:
- Frequency of SS = 1 − 0.61 = 0.39
- Therefore q² = 0.39, where q is the S allele frequency
- q = √0.39 ≈ 0.62, so the R allele frequency p ≈ 0.38
For comparison, in 2016: 1 − 0.04 = 0.96 = q², q ≈ 0.98, so p ≈ 0.02. The resistance allele has gone from about 2% to about 38% in four years - far too fast for drift alone in a population of this size, and exactly the trajectory expected under strong directional selection.
Heterozygotes would be 2pq = 2 × 0.38 × 0.62 ≈ 47% of the population, so most resistant individuals are RS, not RR. That matters for management: incomplete dominance means selection acts on heterozygotes too, so resistance spreads faster than for a fully recessive allele.
Assumptions: Hardy–Weinberg equilibrium; survival reflects genotype alone; the discriminating dose kills all SS; no migration and no other resistance mechanism. Each is testable.
2. Explain the change in Port A using natural selection, and explain what the Port B data contribute to the argument.
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The kdr allele was already present at low frequency before spraying - mutation generates variation independently of need, and four years is far too short for a new mutation to reach 38%. Malathion then acted as a selective agent: SS individuals were killed or failed to reproduce, while RS and RR survived, reproduced and passed on R. Because resistance is incompletely dominant, RS individuals were also favoured, so the allele's frequency rose geometrically. The population did not 'learn'; the allele frequencies changed across generations.
Port B is the control. It was unsprayed, ecologically similar, and only 40 km away, so migration between towns is possible. If drift or a general environmental change were responsible, Port B should show a similar shift; it did not (3% → 5%). That supports selection by insecticide specifically, rather than drift, and argues against migration as the main source of R alleles in Port A - otherwise Port B's frequency would also have risen.
Residual caveat: the two towns differ in more than spraying (drain density, larval habitat, other pesticide use), so this is a natural experiment, not a controlled trial.
3. The officer proposes doubling the dose. Evaluate that proposal, and predict what would happen to the resistance allele if spraying stopped for three years.
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Doubling the dose is likely to make things worse. At 61% survival, the dose already discriminates poorly; raising it kills the remaining SS and the weaker RS, which removes susceptible alleles from the population and increases the selection differential for R. The result is faster fixation of resistance and, if the mechanism is metabolic rather than target-site, cross-resistance to other insecticides. Practice is to rotate modes of action, use the lowest effective dose, and integrate larval-source reduction so that selection pressure is not continuous.
If spraying stopped, the resistance allele would probably decline - but only slowly, and only if R carries a fitness cost. In the absence of insecticide, RR and RS individuals may develop more slowly, store less lipid or be less competitive, so SS would recover. The decline would be gradual because heterozygotes are common (~47%) and sheltered from selection. If the allele is effectively neutral in the untreated environment, it could persist for many generations, meaning resistance could return rapidly if spraying resumed. Monitoring survival annually at a discriminating dose is the only way to know, and the prediction should be treated as conditional rather than certain.