C3.2 Defence against infectious disease

You are surrounded by pathogens, yet most of the time you stay healthy — because the body has layered defences against infectious disease. For C3.2 it helps to picture those layers in order: first barriers that keep pathogens out, then a fast but general innate response, and finally a slower, highly specific adaptive response that also remembers past infections. Add the medical applications — vaccination and antibiotics — and you have the whole topic. Throughout, the recurring theme is specificity versus speed, and how the immune system manages both.

Barriers and the first line of defence

The body’s first defence is to stop pathogens entering at all. The skin forms a tough physical barrier, and where the body must be open to the environment — the airways, gut and other tracts — mucous membranes trap microbes in sticky mucus. These defences are non-specific: they act against any pathogen.

Chemical defences support the barriers: stomach acid kills many ingested microbes, and enzymes such as lysozyme in tears and saliva break down bacterial cell walls. Beneficial skin and gut microbiota add further protection by competing with pathogens for space and nutrients. If the skin is cut, blood clotting rapidly seals the wound, both stemming blood loss and preventing pathogens from entering through the breach.

Innate immunity: a fast, general response

If pathogens get past the barriers, the innate immune system responds quickly but without targeting a specific pathogen. Central to it are phagocytes, white blood cells that engulf and digest pathogens by phagocytosis: the phagocyte surrounds the microbe, takes it into a vesicle, and destroys it with enzymes.

Damaged or infected tissue also triggers inflammation: blood vessels widen and become more permeable, bringing more blood and more phagocytes to the site, which is why infected areas become red, warm and swollen. This response is the same regardless of which pathogen is present — it is fast and broad rather than precise, buying time for the slower adaptive response to develop.

Adaptive immunity, antibodies and memory

The adaptive immune system is slower to start but highly specific. It depends on lymphocytes, white blood cells that recognise a particular antigen — a molecule, usually a protein on a pathogen’s surface, that the immune system identifies as foreign.

One key group, the B-lymphocytes, produce antibodies: proteins that bind specifically to one antigen, marking the pathogen for destruction or neutralising it. When a lymphocyte meets its matching antigen it divides rapidly to produce many identical cells (clonal selection). Crucially, some become long-lived memory cells. If the same pathogen returns, these cells mount a much faster and stronger secondary response, so the person is immune. This memory is the basis of long-term immunity and of how vaccines work.

Vaccination and antibiotics

Vaccination uses immunological memory deliberately. A vaccine contains a harmless form or fragment of a pathogen (its antigens). It triggers a primary immune response and the formation of memory cells without causing the disease. If the real pathogen is later encountered, the rapid secondary response prevents illness. When a high enough proportion of a population is vaccinated, transmission is interrupted — herd immunity — protecting even those who are not immune.

Antibiotics treat bacterial infections by targeting features of bacterial cells, such as cell-wall synthesis, that human cells lack — which is also why antibiotics do not work against viruses. Their overuse has driven the evolution of antibiotic resistance: resistant bacteria survive treatment, reproduce and spread, so resistance increases through natural selection. This is why completing prescribed courses and avoiding unnecessary antibiotic use matter so much.