Communicable diseases, disease prevention and the immune system — OCR A-Level Biology

A pathogen is an organism or agent that causes disease and can be passed between hosts. Learners must distinguish the main types affecting animals and plants. In animals the key groups are bacteria (for example the bacterium causing tuberculosis), viruses (for example HIV), fungi (for example ringworm) and protoctists (for example the protoctist causing malaria). In plants the key groups are fungi (for example the fungus causing black sigatoka in bananas), bacteria (for example the bacterium causing ring rot in potatoes), viruses (for example tobacco mosaic virus) and protoctists (for example the protoctist causing potato blight). Recognise that each type differs in structure and replication, so treatment differs: antibiotics act on bacteria but not on viruses. A multiple-choice question may ask which group a named example belongs to, or which type is not a pathogen of plants.

Transmission is how a pathogen leaves one host or reservoir and reaches a susceptible host, where it must then enter and establish infection. For animals, teach direct contact (touching, body fluids, sexual contact), droplet and airborne routes (sneezing, coughing, aerosols), faecal–oral contamination of food and water, vectors such as mosquitoes and ticks, and indirect fomites. For plants, teach soil contamination, wind and water dispersal of spores, animal and insect vectors, and mechanical transfer on tools or hands. Link each route to a concrete example: Plasmodium via female Anopheles mosquitoes, or potato blight spores spread by wind and rain splash. Distinguish transmission from entry and from the body's defences, and note that overcrowding, poor sanitation and climate raise transmission risk.

Plants defend against pathogens with physical and chemical barriers. Physical defences include the waxy cuticle, cellulose cell walls, bark, and stomatal closure or guard-cell responses that limit entry. Chemical defences include antimicrobial compounds such as tannins, alkaloids and terpenoids, plus enzymes and the oxidative burst. Some tissues respond to infection by producing callose to thicken walls and block spread, and by localised cell death (hypersensitive response) that isolates the pathogen. Teach learners to separate prevention of entry (barriers) from responses after entry (chemicals, callose, cell death), and to avoid importing animal immune ideas such as antibodies or phagocytes as plant defences. A useful example is the thickened cuticle and antimicrobial compounds of many leaves.

Teach the primary non-specific defences that prevent pathogen entry: skin, mucous membranes, expulsive reflexes, blood clotting, wound repair and inflammation. The skin is a physical barrier; its outer layer of dead keratinised cells and sebum inhibit microbial growth. Mucous membranes line body openings and trap pathogens in mucus, which is then removed by cilia. Expulsive reflexes such as coughing, sneezing, vomiting and diarrhoea eject pathogens. Blood clotting seals wounds to prevent entry. Wound repair involves inflammation, which increases blood flow and brings phagocytes to destroy pathogens. Learners must be able to name each defence and explain how it acts non-specifically against a range of pathogens.

Phagocytes are white blood cells that engulf and digest pathogens by phagocytosis. Neutrophils have a lobed nucleus and granular cytoplasm; macrophages are larger, with a rounded or kidney-shaped nucleus, and act as antigen-presenting cells. In phagocytosis the phagocyte is attracted to chemicals from the pathogen, binds it, and the cell-surface membrane invaginates to enclose the microorganism in a vesicle called a phagosome. Lysosomes fuse with the phagosome and release hydrolytic enzymes (lysozymes) that digest the pathogen. Soluble digestion products are absorbed into the cytoplasm. In macrophages, antigens from the digested pathogen are displayed on the cell-surface membrane, helping to activate other immune responses. MCQ items test recognition of these structural features and the correct ordered sequence of phagocytosis, so learn the stages and the organelle roles precisely.

This practical requires you to examine a prepared blood smear under a light microscope and produce an accurate, labelled biological drawing of the cells you observe. First focus on low power, then increase magnification to find a suitable field. Identify red blood cells (small, numerous, biconcave, no nucleus) and white blood cells such as neutrophils (lobed nucleus, granular cytoplasm) and lymphocytes (large rounded nucleus, little cytoplasm). When drawing, use a sharp pencil, draw clear continuous lines, keep proportions correct, and do not shade. Label the cell types and visible structures such as the nucleus and cytoplasm. Add a title and state the magnification. Your drawing is assessed on accuracy, correct proportions, clean lines and correct labelling, so plan the layout before starting and keep the drawing large enough to show detail.

Specific immunity depends on lymphocytes, each with a surface receptor of one shape. B lymphocytes mature in bone marrow, carry antibody-like receptors and, once activated, divide and differentiate into plasma cells that secrete antibodies and memory cells that persist. T lymphocytes mature in the thymus. Helper T cells carry receptors that bind antigen presented by phagocytes and then release cytokines that stimulate B cells and cytotoxic T cells. Cytotoxic T cells recognise infected or abnormal cells and destroy them. So B cells act mainly through secreted antibody, while T cells act mainly through cell contact and signalling. A question may ask you to match a cell to its structure, its role or its mode of action, or to spot a mismatched pairing.

The primary immune response follows first exposure to an antigen. It is slow because the few lymphocytes with a matching receptor must be selected, then divide and differentiate. Antibody concentration rises gradually and may take days, and memory cells are produced. On later exposure to the same antigen, memory B and T cells respond quickly, so the secondary response is faster, larger and longer-lasting, with a higher antibody concentration. Memory cells also mean the person is often immune to that pathogen. A question may ask you to compare the two responses, interpret a graph of antibody concentration against time, or identify which features belong to the secondary response.

Antibodies are globular glycoproteins of the immunoglobulin family, secreted by plasma cells (differentiated B lymphocytes) in response to a specific antigen. Each antibody is a Y-shaped molecule of four polypeptide chains: two identical heavy chains and two identical light chains, held by disulfide bridges. The variable regions at the tips of the two arms form the antigen-binding sites, giving each antibody two identical binding sites and a shape complementary to one specific antigen. The constant regions are the same within a class and allow recognition by phagocytes and complement. General functions: binding to antigen to neutralise pathogens or toxins, marking them for destruction, and forming antigen–antibody complexes that can be destroyed by phagocytosis. Binding is specific and reversible.

This outcome requires an outline of three ways antibodies act. Opsonins are antibodies (or complement proteins) that bind to the surface of a pathogen, marking it so phagocytes can recognise and engulf it more readily — opsonisation. Agglutinins are antibodies that bind to antigens on several pathogens at once, clumping them together so large complexes form; this reduces the number of separate targets and makes phagocytosis more efficient. Anti-toxins are antibodies that bind to toxins produced by pathogens, neutralising them so they cannot bind to host cell receptors and cause harm. In each case the antibody binds specifically to its antigen; the difference lies in the consequence of binding — enhanced phagocytosis, clumping, or toxin neutralisation.

Immunity can be classified on two independent axes. Active immunity arises when the person's own immune system responds and produces antibodies and memory cells, giving slow onset but long-lasting protection; it occurs naturally after infection or artificially through vaccination. Passive immunity arises when antibodies are acquired ready-made rather than produced by the recipient, giving immediate but short-lived protection because no memory cells form; it occurs naturally across the placenta or in breast milk, and artificially through injection of antibodies such as antivenom. Because the two axes are independent, four combinations exist: natural active (infection), artificial active (vaccination), natural passive (maternal antibodies) and artificial passive (injected antibodies).

An autoimmune disease occurs when the immune system fails to distinguish self from non-self and mounts an immune response against the body's own tissues. Self-tolerance normally prevents this, so autoimmunity reflects a breakdown in that recognition. The immune attack may involve antibodies directed at self antigens or T cells attacking self cells, and the resulting damage produces the symptoms. Examples include type 1 diabetes, in which beta cells of the pancreas are destroyed so insulin production falls, and rheumatoid arthritis, in which the immune system attacks joint tissues causing inflammation. A question may ask for the definition, a named example, the mechanism of self-recognition failure, or the consequence for a specific tissue, so identify which is being tested.

Vaccination works by introducing a harmless form of an antigen so the adaptive immune system makes a primary response and, crucially, memory B and T cells. On later exposure to the real pathogen, memory cells give a faster, stronger secondary response that destroys the pathogen before symptoms develop. Vaccines may contain killed pathogens, attenuated live pathogens, toxoids, isolated antigens or subunit components. A vaccination programme protects a population, not just individuals: high uptake reduces the number of susceptible hosts so the pathogen cannot spread easily, giving herd immunity. This can prevent epidemics and protect people who cannot be vaccinated, such as the very young, immunocompromised patients or those with allergies. Low uptake or antigenic variation can allow outbreaks.

Medicines come from several sources. Many were originally discovered in plants: aspirin from willow bark, digoxin from foxgloves and quinine from cinchona. Microorganisms are a major source of antibiotics, for example penicillin from the fungus Penicillium, and bacteria such as Streptomyces yield many antibiotics. Some medicines are derived from animals, such as insulin historically from animal pancreas, and others are now made synthetically or by genetic engineering, for example human insulin produced by modified bacteria. Soil and marine organisms are being screened for new drugs. Understanding these sources helps explain why antibiotic resistance and loss of biodiversity matter. MCQ items test whether you can match a medicine or group of medicines to its correct source category, so classify each option as plant, microorganism, animal, synthetic or recombinant.

Antibiotics treat bacterial infection by targeting bacterial structures or processes, such as cell-wall synthesis or protein synthesis, that human cells lack. Benefits: they cure or control infections like tuberculosis and sepsis, reduce complications and transmission, and enable surgery and immunosuppression. Risks: they do not affect viruses, so misuse for viral illness is ineffective; side effects range from gut disturbance to allergic reaction; and selection pressure favours resistant bacteria. Overuse and incomplete courses increase resistant strains such as MRSA, and broad-spectrum drugs can disrupt normal flora. Managing risk means prescribing only when a bacterial cause is likely, choosing the narrowest effective agent, completing the course and applying infection-control measures.