HSC Exam Practice

Sample response. An infectious disease is a disease caused by a pathogen — an organism or agent that invades a host and causes harm — and that can be transmitted between hosts either directly or indirectly.

Marking notes. 1 mark for identifying causation by a pathogen; 1 mark for identifying transmissibility between hosts. Both required for full marks.

Sample response. Microorganisms are microscopic living cells capable of independent metabolism and, in some cases, independent reproduction — examples include bacteria (e.g. Mycobacterium tuberculosis causing tuberculosis) and protozoa (e.g. Plasmodium falciparum causing malaria). Non-cellular pathogens are not living cells and cannot metabolise or reproduce independently — examples include viruses (e.g. SARS-CoV-2 causing COVID-19) and prions (e.g. the misfolded protein causing BSE), both of which lack cell membranes, cytoplasm, and (in the case of prions) any nucleic acid.

Marking notes. 1 mark for correctly defining microorganism with a named example; 1 mark for correctly defining non-cellular pathogen with a named example; 1 mark for articulating a key structural difference (living cells vs non-cellular; ability to metabolise independently).

Sample response. (a) Plasmodium falciparum: microorganism (protozoan) — it is a single-celled eukaryote that can metabolise and reproduce (inside red blood cells); it is a living cell. (b) Prion causing BSE: non-cellular pathogen — it is a misfolded protein containing no nucleic acid, no cell membrane, and no cytoplasm; it is not a living organism. (c) Puccinia graminis: microorganism (fungus) — it is a eukaryotic organism with a cell wall and can reproduce; fungi are living cells classified under microorganisms.

Marking notes. 1 mark per correct category + feature pairing (max 3). Category alone without a justifying feature scores 0 for that entry.

Sample response. Antibiotics work by targeting structures or processes specific to bacterial cells — for example, inhibiting bacterial cell wall synthesis, disrupting the bacterial ribosome (70S subunit), or blocking bacterial DNA replication. Viruses are non-cellular: they have no cell wall, no cytoplasm, no ribosomes, and do not independently carry out the metabolic processes that antibiotics disrupt. Because there are no bacterial targets present in a virus or a virally infected host cell, antibiotics have nothing to act on and are completely ineffective. Antiviral drugs, which target virus-specific processes such as viral RNA replication or viral attachment to host cells, must be used instead.

Marking notes. 1 mark for identifying the cellular targets of antibiotics (cell wall synthesis, ribosome, bacterial DNA replication — accept any one); 1 mark for explaining that viruses lack these structures/processes (non-cellular: no cell wall, no bacterial ribosome, no independent metabolism); 1 mark for explicitly concluding that antibiotics therefore cannot act on viruses and that antivirals are required.

Sample response. Primary data is collected directly by the researcher — for example, contact tracing interviews conducted by epidemiologists during the COVID-19 outbreak, or serology surveys in which blood samples from a population are tested for antibodies. Secondary data is data collected by someone else and then used for analysis — for example, published WHO disease surveillance reports or historical death records used to reconstruct the 1918 influenza epidemic.

Marking notes. 1 mark for correctly distinguishing primary (researcher collects directly) from secondary (collected by another and reused), each with one named example. Both components required.

Sample response. The vast majority of the approximately 38 trillion bacterial cells in the human body are not pathogens — they are commensal or mutualistic organisms that cause no harm and in many cases are essential for health. Gut bacteria contribute to digestion, vitamin synthesis, and immune system development. Pathogenicity (the ability to cause disease) is a specific, rare characteristic — scientists estimate that only a tiny fraction of the approximately one trillion bacterial species on Earth cause human disease. Disease occurs only when a pathogen (a disease-causing organism or agent) enters the body in sufficient numbers and overcomes host defences. The mere presence of bacteria is therefore not sufficient to cause infectious disease.

Marking notes. 1 mark for correctly stating that most bacteria in the body are not pathogens (commensal/mutualistic); 1 mark for explaining that pathogenicity is a specific, uncommon characteristic — most bacterial species cannot cause disease; 1 mark for linking disease causation to the concept of a pathogen specifically (an organism that enters a host and causes harm) rather than to bacteria generally.

Sample response (a) — trend description (2 marks). From Week 1 to Week 4, confirmed new cases rose sharply from near zero to a peak of approximately 1,780. From Week 4 to Week 13, cases declined steeply and consistently, reaching approximately 45 new cases per week by Week 13 — a reduction of roughly 97% from peak. There is a slight secondary increase from Week 13 onwards (to approximately 250 by Week 17), indicating a smaller second wave beginning in mid-June.

Marking notes (a). 1 mark for correctly describing the initial rise to a peak (with approximate week and magnitude); 1 mark for correctly describing the subsequent steep decline with supporting figures or a percentage reduction estimate.

Sample response (b) — strength and limitation (3 marks). Strength: mandatory case reporting provides systematic, regular national data on confirmed infections, allowing epidemiologists to track incidence over time and detect trends and epidemic curves (such as identifying the Week 4 peak) without needing to survey the population actively. Limitation: case reporting only captures confirmed diagnoses — people who are infected but asymptomatic, or who do not seek testing, are not counted. This means the true scale of transmission is almost certainly larger than the notified case count suggests, and the data underestimates actual spread.

Marking notes (b). 1 mark for the correctly identified strength with an explanation linking it to what case reporting reveals about transmission; 1 mark for the correctly identified limitation; 1 mark for explaining why the limitation means the data may underestimate true transmission.

Sample response (c) — serology survey interpretation (2 marks). The serology survey implies that case reporting substantially underestimated actual infection rates — only 33–50% of infections were captured by confirmed diagnoses. This is because case reporting depends on individuals being tested and diagnosed; asymptomatic infections or infections not leading to medical contact are missed. A serology survey is primary data: researchers directly collect and test blood samples from a population sample themselves, rather than analysing existing records.

Marking notes (c). 1 mark for explaining that the serology result implies case reporting is an underestimate of true transmission (because undetected infections are not captured); 1 mark for correctly classifying serology survey as primary data and explaining why (researchers directly collect the samples).

Sample response. The classification of a pathogen into the correct category is not merely an academic exercise — it directly determines what diagnostic tools are used, what treatments can be effective, and whether standard control measures (such as sterilisation) will work.

Bacteria are living prokaryotic cells with cell walls (peptidoglycan in most species), 70S ribosomes, and independent metabolic processes. Mycobacterium tuberculosis, the bacterial pathogen causing tuberculosis in humans, can therefore be targeted by antibiotics — for example, rifampicin inhibits bacterial RNA polymerase, and isoniazid disrupts cell wall synthesis. Because bacteria are living cells, diagnosis involves culturing them, staining (e.g. Ziehl–Neelsen for acid-fast bacteria like Mycobacterium), or PCR of bacterial DNA. The same category applies to plant pathogens such as Agrobacterium tumefaciens (crown gall disease), which is treated with bactericide or physical removal of the gall.

Viruses are non-cellular: they consist of nucleic acid (DNA or RNA) enclosed in a protein coat and cannot metabolise or reproduce without a host cell. SARS-CoV-2 (causing COVID-19) is a positive-sense single-stranded RNA virus. Because viruses lack the cellular structures targeted by antibiotics, these drugs have no effect. Antiviral agents (e.g. remdesivir, which inhibits viral RNA polymerase) or supportive care must be used. Diagnosis relies on PCR to detect viral RNA, or serology to detect antibodies — not cell culture in the same sense as bacteria. Tobacco mosaic virus (TMV), which infects plants, is similarly non-cellular and controlled through quarantine and resistant cultivar breeding rather than drugs.

Prions form the most extreme sub-category of non-cellular pathogens: misfolded proteins with no nucleic acid whatsoever. The prion causing BSE in cattle (and variant CJD in humans) cannot be destroyed by autoclaving, UV radiation, or standard disinfectants — because it has no lipid membrane and no enzymes to denature in the conventional sense. No drug treatment exists. Diagnosis requires post-mortem brain biopsy showing characteristic spongiform changes. Control relies entirely on surveillance and slaughter rather than treatment.

Fungi, such as Puccinia graminis (wheat stem rust), are eukaryotic cells with ergosterol-containing membranes, making them distinct from bacteria (no ergosterol) and viruses (no cells). Antifungal agents such as triazoles target ergosterol synthesis — they would be ineffective against bacteria or viruses. Human fungal pathogens such as Trichophyton species (causing tinea) require antifungal creams or systemic antifungals, not antibiotics.

Analysis: the pattern across all three categories shows that structural biology drives therapeutic strategy. Classification identifies which cellular or molecular targets exist in the pathogen — and therefore which class of treatment agent (antibiotic, antiviral, antifungal, antiparasitic) can exploit those targets. A misclassification would result in an ineffective treatment: prescribing antibiotics for influenza, or antivirals for a fungal infection. The lesson's category system is therefore not just descriptive — it is the diagnostic and therapeutic decision framework for infectious disease.

Marking notes. 1 mark — names and correctly classifies at least three pathogens into the correct category (microorganism sub-type, macroorganism, or non-cellular sub-type) with the disease each causes. 1 mark — explains the treatment rationale for bacterial diseases with reference to a specific mechanism (e.g. antibiotic targets cell wall or ribosome). 1 mark — explains why viruses cannot be treated with antibiotics and what is used instead, with a named example. 1 mark — explains a distinctive property of prions (no nucleic acid, cannot be sterilised) and links this to treatment impossibility. 1 mark — correctly compares the diagnostic approaches for at least two categories (e.g. culture vs PCR; post-mortem vs serology). 1 mark — applies the analysis to at least one plant pathogen (e.g. TMV, Agrobacterium, Puccinia) and its treatment/control approach. 1 mark — reaches an explicit analytical conclusion that links pathogen classification to treatment decision-making, framing classification as a diagnostic/therapeutic framework rather than merely a descriptive one.