OxfordAQA A Level Biology: The Causes of Disease — Practice Questions

These are original questions written for Marlbridge, in the style and at the standard of the examination. They are not reproduced past-paper questions — examination boards hold copyright in their own papers. Use these alongside the official past papers available free from your board.

Related: The Causes of Disease study guide, The Causes of Disease revision notes

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Section A

1. Name the two mechanisms by which a pathogen can cause disease in a host. [2]

2. Name the three interfaces through which a pathogen can enter a mammal’s body. [3]

Section B

3. Explain, using a named example, how a pathogen can cause disease predominantly through toxin production rather than direct cell damage. [4]

4. A student writes: “Viruses and bacteria both cause disease by directly destroying host cells.” Explain why this statement is not always accurate. [4]

5. Data show that countries with higher average smoking prevalence also have higher rates of both coronary heart disease and cancer.

(a) State the conclusion this data is consistent with. [1] (b) Explain why this correlation alone does not prove that smoking causes these diseases. [3] (c) Suggest one other variable that should be considered before drawing a firm conclusion. [1]

6. Explain why coronary heart disease and cancer should not be treated as though they share identical risk factors. [3]

7. Explain how the gas-exchange system can act as an interface for a pathogen to enter the body, using a named example of an airborne pathogen. [3]

8. A researcher wants to investigate whether a specific dietary risk factor is linked to coronary heart disease incidence, using data collected at the level of whole countries. Explain one limitation of using country-level data for this purpose. [3]

9. Explain the difference between a risk factor and a cause, using coronary heart disease as your example. [3]

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Answers

1. Cell damage — direct destruction of host tissue by the pathogen [1]. Toxin production — the pathogen releases a chemical substance that disrupts normal cell or tissue function, sometimes at a site distant from the infection [1].

2. The digestive, reproductive and gas-exchange systems [3 — 1 mark each].

3. The bacterium responsible for tetanus causes disease almost entirely through toxin production [1]. The toxin it releases affects the nervous system, causing sustained muscle spasms [1], while the bacterium itself does relatively little direct destruction of host tissue [1]. This contrasts with pathogens that cause disease mainly by directly destroying the cells they infect [1].

4. The statement is not always accurate because toxin production is a separate mechanism from cell damage — some pathogens cause disease mainly by releasing a chemical substance that disrupts cell or tissue function, sometimes far from the site of infection, rather than by directly destroying host cells [1] [1]. For example, a pathogen causing disease through toxin production (such as the tetanus bacterium) does relatively little direct tissue destruction compared with a pathogen that replicates inside and ruptures host cells [1] [1].

5. (a) The data is consistent with smoking being a risk factor for coronary heart disease and cancer [1]. (b) A correlation shows only that two variables change together, not that one causes the other [1]. Other variables that differ between the countries compared — such as diet, average age, access to healthcare, or genetic factors — could also explain the difference in disease rates [1], so establishing causation requires additional evidence — since deliberately assigning people to smoke for years would be unethical and impractical, this comes from large prospective observational (epidemiological) studies that statistically adjust for confounders, a clear dose-response relationship (more smoking, more disease), and a well-understood biological mechanism linking smoking to the disease, rather than from a controlled experiment [1]. (c) Any valid variable, e.g. dietary fat intake, physical activity levels, age distribution, or access to healthcare [1].

6. The specification treats coronary heart disease and cancer as having their own specific, and not necessarily identical, sets of risk factors [1] — for example, a factor strongly linked to one condition is not automatically a risk factor for the other [1]. Treating the two conditions as though they share identical risk factors risks applying evidence about one disease incorrectly to the other, rather than citing the specific risk factor evidence relevant to the disease named in the question [1].

7. The gas-exchange system is a boundary between the body and the external environment through which airborne pathogens can enter [1]. Example: a respiratory virus (such as one causing a respiratory infection) is inhaled and makes contact with the cells lining the airways or lungs, entering the body at this interface [1] [1].

8. Country-level data averages together very different individuals and sub-populations within each country, so it cannot show whether the individuals with the highest exposure to the risk factor are actually the individuals developing the disease [1]. Confounding variables that also differ between countries — such as diet, genetics, smoking rates or healthcare access — may explain the pattern instead of, or as well as, the risk factor being investigated [1], so a correlation at country level provides weaker evidence of an individual-level causal link than a study designed to control for these other variables [1].

9. A risk factor is a variable statistically associated with an increased likelihood of developing a disease, without necessarily being proven to cause it directly [1] [1]. A cause is a factor shown, through additional evidence such as a controlled study or an understood biological mechanism, to actually produce the disease [1]. For coronary heart disease, a high-fat diet is a well-established risk factor, but confirming it as a cause (rather than simply a correlate) requires evidence beyond incidence data alone [1].

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Where marks are usually lost

• Describing pathogens as causing disease only through direct damage, omitting toxin production as a separate mechanism.
• Failing to name a specific interface (digestive, reproductive, gas-exchange) when explaining how a pathogen enters the body.
• Treating a correlation between a lifestyle factor and disease incidence as proof of causation, without naming another variable that could also explain the pattern.
• Discussing coronary heart disease and cancer as though they share identical risk factors.
• Making a general claim (“pathogens cause disease”) without naming a specific pathogen and the mechanism it uses.