Revise Defence against infectious disease for IB Biology (C3.2)

A pathogen is any organism or virus that causes disease. The major categories are bacteria (e.g. the cause of tuberculosis), viruses (e.g. influenza and HIV), fungi (e.g. athlete's foot) and protists or protozoa (e.g. the malarial parasite). A disease is described as infectious when the pathogen can be transmitted from one host to another — directly, or indirectly through water, food, air or a vector such as a mosquito. This is the feature that separates infectious diseases from non-infectious conditions like genetic disorders or vitamin deficiencies, which cannot be caught. The body's job is to keep pathogens out, and to find and destroy any that get in before they multiply enough to cause harm.

The primary defences are called non-specific because they act against any pathogen without needing prior exposure and without singling out a particular invader. The skin is the first physical barrier: its outermost layer is made of tough, dead, keratinised cells, forming a dry surface with a slightly acidic pH that inhibits microbial growth while the skin remains intact. Internal surfaces that cannot be dry and keratinised — the airways, gut and reproductive tract — are lined instead with mucous membranes, which secrete sticky mucus that traps pathogens; in the airways, cilia beat to sweep the trapped mucus up towards the throat, where it is swallowed. Many of these secretions, along with tears and saliva, contain the enzyme lysozyme, which digests bacterial cell walls. Swallowed pathogens then meet a further chemical defence: stomach acid, whose very low pH kills most of them before they can establish an infection.

When the skin is cut, the barrier is broken and pathogens have a route in, so the body seals the wound quickly by forming a clot. Platelets accumulate at the damaged site and release clotting factors, which set off a cascade of reactions. In outline, the inactive plasma protein prothrombin is converted to the active enzyme thrombin; thrombin then catalyses the conversion of the soluble plasma protein fibrinogen into insoluble fibrin. The fibrin forms a mesh of threads that traps platelets and blood cells, producing a clot that plugs the wound. This stops further blood loss and, crucially for this topic, closes off the entry point so that pathogens cannot get through the broken barrier.

If pathogens breach the primary barriers, phagocytes provide the next non-specific response. Phagocytes are white blood cells — macrophages are the classic example — that patrol the tissues and blood and engulf anything recognised as foreign. The process, phagocytosis, is a form of endocytosis: the phagocyte binds to the pathogen and surrounds it with its membrane, drawing it inside into a vesicle called a phagosome. A lysosome, packed with digestive enzymes, then fuses with the phagosome, and the enzymes break the pathogen down. Because a phagocyte responds to any foreign material in the same way and keeps no record of what it has met, phagocytosis is still part of the non-specific defence — powerful and immediate, but not targeted and without memory.

Pathogens that survive the non-specific defences are dealt with by the specific immune response, carried out by lymphocytes — a class of white blood cell distinct from phagocytes. What makes it 'specific' is that it targets one particular pathogen, recognised by its antigens. An antigen is a molecule, usually a protein on the pathogen's surface, that the immune system identifies as foreign. Each B-lymphocyte (B-cell) carries receptors for one specific antigen. When a B-cell meets its matching antigen it is activated and divides rapidly, and many of its daughter cells differentiate into plasma cells — antibody factories that secrete large quantities of one specific antibody into the blood. An antibody is a Y-shaped protein whose binding site is complementary in shape to that one antigen, so it binds only that antigen and no other. This is antibody-antigen specificity, and it works like the fit between an enzyme and its substrate: one antibody type does not work against a different pathogen. Once bound, antibodies help destroy the pathogen — for example by clumping pathogens together and marking them so that phagocytes engulf them more readily.

Producing a targeted antibody from scratch takes several days, which is why a first infection can make you ill before it is cleared — the primary response. The lasting benefit comes afterwards. When B-cells are activated, some of their daughter cells do not become plasma cells but persist in the body as memory cells. These carry the receptor for the same antigen and remain in the blood and lymph long after the infection has gone. If the same pathogen is ever encountered again, the memory cells recognise its antigen immediately and divide to form plasma cells very quickly, so antibodies are produced faster and in far greater quantity than before. This secondary response usually destroys the pathogen before it can multiply enough to cause symptoms — so the person is immune. This is immunological memory, and it is the basis of both natural immunity after infection and the immunity produced by vaccination.

Immunity comes in two independent pairs, and combining them gives four categories. Active immunity is produced when your own lymphocytes meet an antigen and make antibodies and memory cells; it develops over time but lasts a long time, because the memory cells persist. Passive immunity comes from receiving ready-made antibodies from another source; it is immediate but temporary, because no memory cells are formed and the borrowed antibodies are gradually broken down. Cutting across this is whether immunity was acquired naturally or artificially. Natural active immunity follows recovery from an actual infection; artificial active immunity follows vaccination. Natural passive immunity is the transfer of a mother's antibodies to her baby across the placenta or in breast milk; artificial passive immunity is an injection of ready-made antibodies, for example the antivenom given after a venomous snakebite when there is no time to build a response.

A vaccine works by presenting the immune system with a pathogen's antigens in a form that cannot cause serious disease — a weakened (attenuated) or killed pathogen, a fragment of it such as a surface protein, or genetic instructions for the body to make that antigen itself. Because the antigens are still recognised as foreign, the body mounts a primary response and, crucially, forms memory cells, exactly as it would after a real infection — but without the danger of the disease. If the person later meets the actual pathogen, those memory cells trigger a rapid, large secondary response that destroys it before symptoms appear. This is active artificial immunity. Vaccination also protects the wider population through herd immunity: when a high enough proportion of people are immune, the pathogen can rarely find a susceptible host, so chains of transmission break down and even unvaccinated individuals — such as newborns or people who cannot be vaccinated for medical reasons — are indirectly protected.

Antibiotics are drugs that kill or inhibit bacteria by targeting features unique to bacterial cells — for example the enzymes that build the bacterial cell wall, or bacterial ribosomes, which differ from our own. Because these targets exist only in bacteria, antibiotics can harm the pathogen while leaving human cells unaffected. This same logic explains why antibiotics do NOT work against viruses: a virus is not a cell, has no cell wall or ribosomes of its own, and replicates inside the host's cells using the host's machinery — so there is nothing for the antibiotic to attack. Prescribing antibiotics for a viral illness such as a cold or flu therefore does no good, and it does real harm by promoting resistance.

Antibiotic resistance evolves by natural selection. Within a bacterial population there is variation, and by chance some individuals carry an allele that makes them resistant to a particular antibiotic. When the antibiotic is used, it kills the non-resistant bacteria but the resistant ones survive. These survivors reproduce — and because bacteria reproduce rapidly and can also pass resistance genes to one another — the resistant type comes to dominate the population. Over-prescribing antibiotics and not completing a full course both speed this up: the more often bacteria are exposed to the drug, and the more survivors are left behind by a half-finished course, the stronger the selection for resistance. The result is strains such as MRSA that ordinary antibiotics no longer treat.

C3.2 explanation questions are marked analytically: each distinct valid biological point is worth one mark. Answer marks (A) credit a correct step in the reasoning, error-carried-forward (ECF) means an earlier slip does not cost you the marks that follow if your method is written down, and equivalent wording is accepted provided the biology is unambiguous. Study how each mark below is tied to a specific, named idea rather than to loose phrasing - and note that hitting the memory-cell step is what turns a partial answer into full marks.

The ideas in C3.2 connect widely across the course. Antibody-antigen specificity is the molecular-recognition principle you meet again in enzyme-substrate binding and receptor signalling; immunological memory is the reason vaccination has controlled diseases that once killed millions; and antibiotic resistance is natural selection observed in real time, linking this topic straight to evolution and to one of the most pressing problems in modern medicine. Master the habit of writing immune explanations as a chain of distinct, named steps - antigen recognised, specific lymphocytes activated, antibodies and memory cells made, secondary response on re-exposure - and you have a template that answers almost any question this topic can ask.