Pesticides and Genetic Engineering

Q1.1 — Trend description (2 marks)

In the release area, the wild Ae. aegypti population declined progressively from 100% of baseline at Week 0 to approximately 10% of baseline at Week 20 — a reduction of about 90%. The control area remained near 100% throughout. [1 mark for describing progressive decline; 1 mark for quantifying using graph values, e.g. ~90% suppression.]

Q1.2 — Why the decline is progressive (3 marks)

OX513A acts through the same basic mechanism as SIT — reproductive failure, not direct killing. Wild females that mate with OX513A males produce offspring carrying the self-limiting gene; those offspring die before adulthood [1]. This removes one generation's worth of offspring. The effect accumulates across generations: each successive generation has fewer wild males available, so a higher proportion of wild females' matings are with OX513A males, and each generation produces fewer wild offspring than the last [1]. The population thus declines progressively over multiple generations — not instantly, because many adult wild females are still alive and mating at Week 1, and not every mating is with an OX513A male initially [1].

Q1.3 — Rebound after Week 20 (3 marks)

The partial rebound after Week 20 is most likely because OX513A releases slow or cease — the self-limiting gene cannot establish in the wild population (offspring die, so the gene is not retained), meaning the suppressive effect depends on continued releases [1]. As the ratio of OX513A males to wild males decreases (if releases slow), more wild females mate with fertile wild males and the population begins to recover [1]. To prevent this rebound, releases would need to be sustained at a sufficient ratio (sterile/GM males substantially outnumbering wild males) on an ongoing basis, or other vector-control strategies used in combination [1].

Q2 — Cause-and-effect chain (5 marks)

Effect 1: The pyrethroid is lethal to most mosquitoes that contact the net — susceptible individuals are killed [1].

Effect 2: These sodium channel mutations provide a survival advantage — mosquitoes carrying them are less affected by the pyrethroid and survive net contact [1].

Effect 3: The mutation frequency increases in the surviving population — the proportion of individuals carrying the resistant allele rises with each generation [1].

Effect 4: Offspring inherit the resistance allele — over successive generations the resistant genotype becomes dominant in the population, so pyrethroid bed nets become progressively less effective [1].

Overall outcome: Widespread pyrethroid resistance develops in Anopheles mosquito populations, threatening the effectiveness of insecticide-treated bed nets — one of the most important malaria prevention tools globally — and undermining malaria control programs, particularly in sub-Saharan Africa [1].

Q3.1 — Wolbachia spread mechanism (2 marks)

Wolbachia is maternally inherited — infected females pass the bacterium to all of their offspring through their eggs [1]. Once a proportion of females in the population are infected, those females contribute infected offspring to every subsequent generation; and because infected females are replacing uninfected females over time, the Wolbachia prevalence increases with each generation without needing further releases, eventually approaching fixation in the population [1].

Q3.2 — Wolbachia vs SIT: advantage and limitation (2 marks)

Advantage of Wolbachia over SIT: Wolbachia self-propagates through the population (once established, no continuous releases are needed); SIT requires continuous large-scale rearing and release to maintain population suppression — it cannot self-sustain [1].

Limitation of Wolbachia compared to SIT: Wolbachia does not reduce mosquito population size — it only reduces vector competence (ability to transmit dengue). SIT can eradicate a population entirely. If reducing the absolute number of vectors is also important (e.g. for nuisance biting or vectors of other pathogens), Wolbachia alone does not achieve this [1].

Q3.3 — Is the "not GM" distinction meaningful? (3 marks)

The distinction is biologically meaningful in a narrow sense: no foreign DNA sequence is inserted into the mosquito's genome — the mosquito's own genome is unaltered. This differentiates it from GM approaches such as OX513A or gene drive, where the insect's genetic material is directly changed [1].

However, from a risk-assessment perspective, the distinction is less meaningful than it appears, because the ecological consequences of releasing Wolbachia-infected mosquitoes can still include ecosystem-level changes. If Wolbachia spreads to other insect species (it naturally infects many insect species) or if it alters ecological interactions (e.g. effects on predators, parasites of Ae. aegypti), unintended non-target effects could still occur even without DNA-level modification [1].

Furthermore, the key risk-assessment questions — Will this change persist in the wild? Can it spread beyond the target area? What are the long-term ecological effects? — are relevant regardless of whether the modification is at the DNA or microbial-infection level. The "not GM" label should not be used as a substitute for rigorous ecological risk assessment [1].

Q4 — Compare and contrast table (6 marks)

How it reduces disease transmission:
Chemical pesticides: kills adult vectors on contact (given).
SIT: sterile males mate with wild females → no viable offspring → vector population declines over generations → fewer vectors to transmit disease.
OX513A: GM males mate with wild females → offspring carry self-limiting gene and die before adulthood → same population-suppression mechanism as SIT but using genetic modification rather than radiation. [1]

Risk of resistance developing:
Chemical pesticides: High — pre-existing mutations conferring resistance survive selection pressure and increase in frequency through natural selection.
SIT — very low: wild females cannot detect sterile from fertile males by any sensory cue, so there is no selectable trait available for "resistance." No fitness advantage accrues to females that "avoid" sterile males.
OX513A: Very low — same logic as SIT; additionally, the self-limiting gene eliminates itself with each generation, so no accumulation occurs. [1]

Species specificity:
Chemical pesticides: Often broad-spectrum — pyrethroids also affect pollinators, aquatic invertebrates and other non-target insects when used as sprays (bed nets are more contained).
SIT: High — sterile males compete only for mates within their own species (given).
OX513A: High — Ae. aegypti cannot crossbreed with other species; self-limiting gene is confined to that species. [1]

Key limitation:
Chemical pesticides: Resistance evolution and non-target ecological effects (bioaccumulation, toxicity to pollinators).
SIT: Very expensive; requires continuous large-scale rearing and release; does not prevent re-invasion once stopped.
OX513A — requires continuous releases: the self-limiting gene dies with offspring who carry it; the gene cannot persist or accumulate in the wild population without ongoing releases. Once releases stop, suppression effect diminishes and the wild population recovers (as shown in Q1.3 rebound). [1]

Named example of successful use:
Chemical pesticides: Pyrethroid bed nets for malaria prevention across sub-Saharan Africa (though pyrethroid resistance is now widespread in Anopheles); DDT eradicated malaria from southern Europe and North America in 1950s–60s.
SIT: New World screwworm eradicated from North and Central America (eradication from continental USA by 1966; extended to Panama–Colombia border by 1991).
OX513A: Field trials in Jacobina, Brazil and Grand Cayman Islands showed 70–90% population suppression. [1]

Award 1 mark per complete and correct row, up to 6 marks total. Accept equivalent correct responses.