Pathogens evolve fast. So have our defences — barriers, innate immunity, adaptive immunity, vaccines.
Every sub-topic below feeds at least one of these questions.
How do body systems recognize pathogens and fight infections?
What factors influence the incidence of disease in populations?
The required syllabus content for C3.2, in order. Each card is one lesson-sized checkpoint.
A disease-causing organism is known as a pathogen, although typically the term is reserved for viruses, bacteria, fungi and protists.
The skin acts as both a physical and chemical barrier to pathogens.
Sealing of cuts in skin by blood clotting
Differences between the innate immune system and the adaptive immune system
Infection control by phagocytes
Lymphocytes as cells in the adaptive immune system that cooperate to produce antibodies
Antigens as recognition molecules that trigger antibody production
Activation of B-lymphocytes by helper T-lymphocytes
Multiplication of activated B-lymphocytes to form clones of antibody-secreting plasma cells
Immunity as a consequence of retaining memory cells
Transmission of HIV in body fluids
Infection of lymphocytes by HIV with AIDS as a consequence
Antibiotics as chemicals that block processes occurring in bacteria but not in eukaryotic cells
Evolution of resistance to several antibiotics in strains of pathogenic bacteria
Zoonoses as infectious diseases that can transfer from other species to humans
Vaccines and immunization
Herd immunity and the prevention of epidemics
Evaluation of data related to the COVID-19 pandemic
A pathogen is a disease-causing organism. In humans they come from four groups: viruses, bacteria, fungi, protists. Archaea, unusually, cause no known human disease.
In 19th-century Vienna, Ignaz Semmelweis noticed that doctors who washed their hands had far lower rates of childbed fever in their patients. In London, John Snow mapped a cholera outbreak to a single contaminated water pump on Broad Street. Both used careful observation to make breakthroughs in disease control — long before pathogens were even identified microscopically.
Most pathogens never get inside. Physical, chemical and clotting barriers stop them at the boundary.
Physical: dense layer of dead cells. Chemical: sebaceous glands secrete lactic and fatty acids (acidic — inhibits bacteria); lysozyme enzymes digest bacterial cell walls; mutualistic skin bacteria outcompete pathogens.
Line nose, trachea, mouth, urogenital tract. Mucus traps pathogens; lysozyme kills them. Cilia in the airways sweep contaminated mucus toward the throat.
When skin is cut, platelets and damaged tissue release clotting factors → prothrombin → thrombin → fibrinogen → fibrin mesh → red blood cells trapped → clot forms and dries to a scab. Seals blood loss and pathogen entry.
Once a pathogen breaches the barriers, two distinct immune systems engage — one fast and generic, one slower and specific.
Responds to broad categories of pathogen — bacteria, viruses, fungi — in the same way regardless of species. Includes physical barriers and phagocytes. Doesn't improve with experience. Doesn't change over a lifetime.
Produces antibodies that recognise specific antigens on specific pathogens. Slow first time (days). Builds memory cells that mount a fast, strong response on future re-exposure. Becomes more effective over time.
Phagocytes patrol the body, recognise pathogens, engulf them, and digest them with lysosomal enzymes.
Lymphocytes are the soldiers of the adaptive immune system. Each one is specific for a particular antigen. You carry millions of different B-cell types, each potentially able to respond to a different antigen.
Two lymphocyte types involved in antibody production:
Antigens are usually glycoproteins or other proteins on the surface of pathogens. Specific antibodies recognise and bind to specific antigens.
The ABO antigens on your red blood cells are part of your "self". Transfuse a person with the wrong blood type and their immune system attacks the foreign antigens. Type O (no antigens) is universal donor; type AB (both A and B antigens) is universal recipient. Each person produces antibodies against the antigens not present on their own cells.
From pathogen entry to a clone of antibody-producing cells — and to long-lasting immunity.
Immunity comes from the memory cells. If the same pathogen invades again, memory cells trigger a fast, strong response — antibodies appear within hours, not days. Most pathogens are cleared before you notice symptoms.
HIV is special. It infects and kills helper T-cells — the very cells needed to coordinate the immune response.
HIV is transmitted through sharing of body fluids:
HIV specifically targets helper T-cells (CD4 cells). Over years, helper T-cell numbers fall. The immune system can't coordinate responses; the body loses the ability to produce antibodies and fight off opportunistic infections. The clinical state of severe immunodeficiency caused by HIV is called AIDS.
Antibiotics work by interfering with processes specific to bacteria — leaving eukaryotic host cells alone. That's why they kill bacteria but don't poison us.
Bacterial populations evolve resistance to antibiotics through natural selection. The more we use antibiotics, the more we drive resistance.
Some pathogenic bacteria are now resistant to multiple antibiotics — MRSA (methicillin-resistant Staphylococcus aureus), MDR-TB. Slowing this requires careful use of antibiotics: only when needed, full course every time, no veterinary overuse. Scientists are also screening chemical libraries (recently with AI) for novel antibiotic candidates.
Many infectious diseases of humans originated in other species — they're zoonoses. Different routes of transmission, all crossing the species boundary.
Vaccines contain antigens (or DNA/RNA encoding antigens) that stimulate the adaptive immune response without causing disease.
When you receive a vaccine, your immune system mounts a normal primary response — producing antibodies and memory cells against the antigen — without you ever encountering the live pathogen. If the real pathogen later infects you, memory cells trigger a strong, fast secondary response.
If a high enough proportion of a population is immune (through vaccination or previous infection), transmission can't sustain itself — even susceptible individuals are protected because the pathogen can't find new hosts. Some communicable diseases (smallpox, polio in most countries) have been eliminated or near-eliminated this way.
Scientists publish their findings for peer review. Media often report on research mid-evaluation, before consensus settles. Vaccines are rigorously tested; risks of side effects are minimal but never zero. Distinguishing "rigorously tested, overwhelmingly evidence-supported pragmatic truth" from "absolute certainty" is widely misunderstood — and consequential.
Working with pandemic data requires two related but distinct calculations — IB-named skills.
(|A − B| ÷ ((A+B)/2)) × 100. Used to compare any two values without designating one as the "original".
((new − old) ÷ old) × 100. Used when you have a baseline and want the magnitude of change relative to it. Can be positive (increase) or negative (decrease).
Example: 3716 deaths in Europe on 2 Feb 2022; 370 deaths on 30 May 2022. % change = ((370 − 3716) / 3716) × 100 = −90%. % difference = (|370 − 3716| / 2043) × 100 = 164%.
If you can't define one of these in a sentence, that's where to revise next.
“How do animals protect themselves from threats?”
“How can false-positive and false-negative results be avoided in diagnostic tests?”