Classifying Pathogens

• Q1 — C: Antifungals target ergosterol in fungal cell membranes — a molecule absent in bacteria and human cells. Antibiotics target peptidoglycan (bacterial cell walls) or bacterial ribosomes, which fungi do not have. Antivirals and anthelmintics are irrelevant to fungal biology.
• Q2 — B: Viroids are non-cellular, consist only of circular ssRNA, and infect plants only — they have no protein coat. Prions are non-cellular, consist only of misfolded protein (no nucleic acid), and cause neurodegenerative disease in animals only. They are different in composition and host range.
• Q3 — D: The spike protein binding to ACE2 is a host cell entry mechanism — it determines which host cells can be infected. Once bound, the virus can fuse with the cell membrane and inject its genome. This is an entry adaptation, not a transmission or immune evasion adaptation (though these may occur elsewhere in the viral life cycle).
• Q4 — A: Hookworm larvae actively burrow through intact skin using proteolytic enzymes and physical movement. This is host barrier penetration — a host entry adaptation. Soil is not a biological vector (it does not carry the larvae actively to a new host). The route is transcutaneous, not respiratory or faecal-oral at this stage.
• Q5 — C: Erwinia amylovora is a bacterium — a prokaryotic microorganism. Insects act as mechanical vectors (they carry the bacteria on their bodies), but the bacterium can also survive and reproduce in plant tissue independently. This distinguishes it from obligate vector-dependent pathogens like Plasmodium. It is not a fungus, macroorganism, or non-cellular pathogen.

SA1: (a) Plasmodium falciparum is a protozoan, classified as a microorganism. It is a unicellular eukaryote — it has a nucleus, mitochondria, and a complex life cycle involving both a mosquito vector and a human host. It is not a bacterium (it is eukaryotic) and not a virus (it is a living cell capable of independent metabolism). (b) Tobacco mosaic virus is a non-cellular pathogen (virus). It consists of an RNA genome enclosed in a protein coat (capsid) — it has no cell membrane, no cytoplasm, and cannot replicate without hijacking a host cell's machinery. (c) A tapeworm is a macroorganism — specifically a helminth (parasitic worm). It is a multicellular animal, visible to the naked eye, with a complex body structure including hooks, suckers, and proglottids. It is classified as a macroorganism, not a microorganism.

SA2: The bacterium Staphylococcus aureus uses surface proteins called fimbriae (or adhesins) that bind to fibronectin receptors on host epithelial cells. This molecular attachment prevents the bacterium from being washed away by mucus or fluid flow, allowing it to colonise the tissue surface before invading. The influenza A virus uses a surface glycoprotein called haemagglutinin, which binds specifically to sialic acid receptors on respiratory epithelial cells. This receptor-ligand interaction initiates endocytosis — the cell engulfs the bound virus, bringing it inside. Both pathogens use a surface molecule to bind a specific host cell receptor as the first step in host entry. However, the bacterial adhesin facilitates surface colonisation, while the viral haemagglutinin triggers active internalisation of the virus into the host cell.

SA3: HIV is a retrovirus — a non-cellular pathogen containing RNA and the enzyme reverse transcriptase, which converts its RNA into DNA for insertion into the host cell genome. Antiretroviral drugs (e.g. reverse transcriptase inhibitors) specifically block this enzyme. Antibiotics, antifungals, and anthelmintics do not affect reverse transcriptase — there is no relevant target. Influenza is also a non-cellular pathogen (virus), but it replicates differently — neuraminidase inhibitors (e.g. oseltamivir) block influenza's neuraminidase surface protein, preventing new viral particles from being released from infected cells. This mechanism is specific to influenza's neuraminidase; it has no effect on HIV or on a worm. Taenia solium (tapeworm) is a macroorganism — a multicellular helminth. Anthelmintic drugs (e.g. mebendazole) disrupt tubulin polymerisation in the worm, preventing cell division and glucose uptake. Tubulin-disruption has no relevance to viral replication. A single treatment cannot be effective against all three because each pathogen has fundamentally different biology — different structures, different replication mechanisms, and different metabolic processes — meaning each requires a drug that specifically targets its unique biology.