HSC Exam Practice

Sample response. Vector control refers to strategies that reduce the spread of infectious disease by targeting the organisms (vectors) that transmit pathogens between hosts. One named example is the use of insecticide-treated bed nets (ITNs) containing pyrethroids to kill or repel Anopheles mosquitoes that transmit malaria.

Marking notes. 1 mark for defining vector control (strategies targeting organisms that transmit pathogens / disease vectors). 1 mark for a named, correct strategy (accept: pyrethroid spraying, DDT spraying, insecticide-treated nets, sterile insect technique, GM mosquito release, Wolbachia release, insect growth regulators applied to water bodies).

Sample response. Organophosphate insecticides (e.g. malathion) inhibit the enzyme acetylcholinesterase at nerve synapses. Acetylcholinesterase normally breaks down the neurotransmitter acetylcholine after it has transmitted a nerve impulse. When the enzyme is inhibited, acetylcholine accumulates at the synapse, causing continuous nerve stimulation (continuous firing of the nerve), which leads to paralysis and death of the insect.

Marking notes. 1 mark for identifying that organophosphates inhibit acetylcholinesterase. 1 mark for explaining that this prevents breakdown of acetylcholine at the synapse. 1 mark for stating the consequence: continuous nerve stimulation / firing, leading to paralysis or death.

Sample response. Pesticide resistance develops through natural selection, not because the pesticide induces mutations in mosquito DNA. Before any pesticide is applied, a small proportion of mosquitoes in the wild population already carry pre-existing mutations — for example, mutations that alter the structure of the sodium channel protein so that pyrethroids bind less effectively, or mutations that increase expression of detoxifying enzymes. These mutations arise spontaneously and exist in the population before pesticide exposure. When the pesticide is applied, susceptible mosquitoes (those lacking resistance mutations) are killed; resistant mosquitoes survive and reproduce. The resistance allele is heritable and is passed to offspring, so over successive generations the resistant genotype increases in frequency in the population. The pesticide acts as the selective pressure — it does not create the mutation but selects for individuals that already carry it.

Marking notes. 1 mark for identifying that resistance mutations pre-exist in the population before pesticide exposure (not caused by the pesticide). 1 mark for correctly describing natural selection: susceptible individuals die; resistant individuals survive and reproduce. 1 mark for stating that the resistance allele is heritable and increases in frequency across generations — linking this to the population-level outcome (progressively less effective pesticide).

Sample response. The sterile insect technique (SIT) works by mass-rearing the target insect species in a controlled facility, sterilising males using low-dose radiation (which disrupts sperm DNA without significantly affecting mating behaviour or competitiveness), then releasing them into the wild in numbers that substantially outnumber wild males. Wild females mate predominantly with sterile males and produce no viable offspring. Each generation produces fewer individuals than the last; if the release ratio is sustained, the wild population declines and can be eradicated from the target area. Resistance to SIT is very unlikely to develop because there is no selectable trait. In pesticide resistance, resistant individuals survive lethal pesticide exposure — their resistance mutation confers a direct survival advantage. In SIT, wild females cannot detect which males are sterile versus fertile; there is no sensory cue distinguishing them. A female that somehow "preferred" fertile males would need to be able to detect them, which is biologically impossible in species where SIT succeeds. Since no fitness advantage accrues to females with any particular mating preference, no resistance gene can be selected.

Marking notes. 1 mark for correctly outlining the mechanism of SIT (mass rearing → sterilisation → mass release; sterile males mate with wild females → no viable offspring → population declines). 1 mark for identifying the key reason SIT is so effective: release ratio (sterile males outnumber wild males). 1 mark for explaining why resistance is unlikely: females cannot distinguish sterile from fertile males, so there is no selectable trait. 1 mark for explicitly contrasting this with pesticide resistance: in chemical resistance, a mutation provides a measurable survival advantage that natural selection can act on; in SIT it cannot.

Sample response. OX513A is a self-limiting GM strain: males carry a self-limiting gene that causes offspring to die before adulthood unless the antibiotic tetracycline is present. In the wild environment (without tetracycline), offspring of OX513A × wild female matings die — the modification eliminates itself with each generation and cannot persist or accumulate in the wild population without continued releases. Gene drive mosquitoes use CRISPR-Cas9 to ensure the modified allele is inherited by nearly all offspring (not the Mendelian 50%). This allows the modification to spread rapidly through the entire wild population within a few generations and is intended to persist — potentially irreversibly — across the wild population rather than self-eliminating.

Marking notes. 1 mark for correctly explaining OX513A mechanism (self-limiting gene → offspring die without tetracycline → modification cannot persist). 1 mark for correctly explaining gene drive mechanism (CRISPR-Cas9 → near-100% inheritance → rapid population-wide spread). 1 mark for contrasting persistence: OX513A self-eliminates with each generation; gene drive is designed to persist and spread through the wild population (potentially irreversibly).

Sample response. SIT is most likely to succeed when: (1) the target species has females that mate only once in their lifetime (as in the New World screwworm), maximising the impact of each mating with a sterile male — a female that mates once with a sterile male produces no offspring for her entire reproductive life; and (2) the target area has geographic barriers (e.g. islands, isthmuses, mountain ranges) that limit re-invasion of wild individuals from outside the release zone, preventing the need to maintain permanent barriers indefinitely.

Marking notes. 1 mark per valid condition (max 2). Other acceptable responses: target species can be mass-reared cost-effectively in controlled facilities; sufficient release ratio can be maintained (sterile males substantially outnumber wild males); sufficient funding and political will exists to sustain releases over multiple generations.

Sample response (a). The kdr allele frequency increased progressively from approximately 0.18 in 2005 to approximately 0.86 by 2019 — a rise of approximately 0.68 (68 percentage points) over the 15-year study period. The trend is consistent and approximately linear, with the allele frequency roughly doubling between 2005 and 2011, then continuing to increase at a similar rate.

Marking notes (a). 1 mark for identifying the upward trend. 1 mark for quantifying the change using at least two values from the graph (e.g. ~0.18 in 2005 rising to ~0.86 in 2019; accept ±0.05).

Sample response (b). Pyrethroid-treated bed nets act as a persistent selective pressure on the An. gambiae population. Mosquitoes that contact the nets are exposed to pyrethroid. Those without the kdr allele have sodium channels that are sensitive to pyrethroid disruption and are killed or paralysed on contact. Mosquitoes that carry the kdr allele have an altered sodium channel structure that reduces pyrethroid binding, conferring a survival advantage — they survive net contact and proceed to reproduce. The kdr allele is heritable, so each generation has a higher proportion of kdr carriers than the last, as resistant individuals contribute more offspring to each successive generation. Over 15 years of continuous pyrethroid net use, this selection pressure has driven the kdr allele from a minority position (~18%) to near-fixation (~86%) in the sampled population.

Marking notes (b). 1 mark for identifying pyrethroid nets as the selective pressure that kills susceptible (non-kdr) mosquitoes. 1 mark for explaining the mechanism of kdr resistance (altered sodium channel structure → reduced pyrethroid binding → survival). 1 mark for explaining that kdr is heritable and increases in frequency each generation because resistant individuals survive and reproduce at higher rates. Award the third mark only if the answer connects the mechanism explicitly to the observed population-level trend in the data (from ~18% to ~86%).

Sample response (c). Consequence: as kdr allele frequency approaches fixation (~86% by 2019), pyrethroid-treated bed nets will become progressively less effective at killing An. gambiae on contact — reducing protection against malaria for communities relying on ITNs as their primary control measure, potentially causing a rebound in malaria transmission rates. Proposed modification: introduce insecticide rotation or a combination of active ingredients with different modes of action (e.g. switching some nets to bed nets treated with a different insecticide class such as chlorfenapyr, a pyrrole compound with a different mode of action, or combining pyrethroids with a synergist such as piperonyl butoxide to partially overcome kdr resistance). Alternatively, introduce Wolbachia-infected Ae. aegypti releases (for dengue control) or SIT for species-specific non-chemical suppression. Accept: any evidence-based, biologically sound modification with correct reasoning.

Marking notes (c). 1 mark for predicting a specific consequence of increasing kdr frequency (bed net ineffectiveness → reduced malaria protection / rebound in transmission). 1 mark for a plausible, evidence-based modification with correct biological reasoning. Accept any valid strategy with correct justification.

Sample response. The sterile insect technique (SIT) is the most ecologically clean and resistance-proof approach to vector population eradication currently in use, but its applicability is context-dependent and it has significant logistical limitations. The New World screwworm eradication program provides compelling evidence of SIT's potential at scale. The fly was eradicated from the continental United States by 1966 — the program at its peak released approximately 2 billion sterile flies per week from a single facility in Mission, Texas. By 1991, eradication was extended through Mexico and Central America, and a sterile fly barrier is now maintained at the Panama–Colombia border to prevent re-invasion. This represents the largest biological pest eradication in history, achieved without a single chemical pesticide application, and the screwworm has not caused significant livestock damage in North or Central America since. SIT succeeds in the screwworm case because of two biological vulnerabilities: female screwworm flies mate only once in their lifetime, so a single sterile mating renders a female reproductively inactive for life; and the program exploited geographic barriers (the Central American land bridge narrowing to the Panama–Darién bottleneck) that allowed a permanent biological barrier to be maintained. SIT is most likely to succeed when: (i) females mate once, maximising the per-mating impact of sterile males; (ii) geographic barriers limit re-invasion; (iii) the species can be mass-reared efficiently; and (iv) sustained funding and infrastructure are available. SIT's limitations are predominantly logistical and economic, not biological. It is far more expensive per unit area than pesticide application — rearing billions of insects per week requires substantial capital infrastructure. It produces no immediate effect (the population must decline across multiple generations before eradication is achieved). And it does not prevent re-invasion — the Panama barrier must be maintained indefinitely because screwworm persists in South America. Compared to chemical pesticides, SIT offers critical advantages: no risk of resistance development (wild females cannot detect sterile males, so no selectable trait exists), no chemical residues or bioaccumulation, and no non-target effects on other insect species. Compared to GM approaches (OX513A), SIT similarly cannot persist without ongoing releases, but does not face the regulatory and public-acceptance barriers associated with genetically modified organisms. Gene drive mosquitoes offer the prospect of self-sustaining population suppression or modification without ongoing releases, but face serious concerns about irreversibility and unintended spread. Overall, SIT is highly effective in appropriate contexts — where the biology of the target species and geography align — and its advantages over chemical pesticides in resistance risk, ecological safety, and long-term sustainability are compelling. Its high cost and logistical demands limit its application to situations where the disease or economic burden justifies the investment.

Marking notes. 1 mark — Uses specific screwworm evidence (eradication from continental USA by 1966; releases of ~2 billion sterile flies per week; extension through Central America; Panama–Colombia barrier). 1 mark — Correctly explains two or more conditions under which SIT is most likely to succeed (single-mating females; geographic barriers; mass-rearing feasibility; sustained release). 1 mark — Identifies specific limitations of SIT (cost; requires continuous releases; does not prevent re-invasion; slow population-level effect requiring multiple generations). 1 mark — Correctly compares SIT with chemical pesticides on resistance risk (SIT: no selectable resistance trait; pesticides: high resistance risk via natural selection) and ecological impact (SIT: no residues, no non-target effects; pesticides: can affect pollinators and aquatic invertebrates). 1 mark — Correctly compares SIT with at least one GM approach (OX513A or gene drive) on at least one criterion. 1 mark — Reaches an explicit evaluative conclusion that acknowledges context-dependence and trade-offs (not a simple "SIT is best" or "SIT is worst" statement).