C3.2 Defence against disease

Pathogens cause disease by entering and damaging a host.

A pathogen is a disease-causing organism or particle. Bacteria, viruses, fungi and protists reproduce or use host cells in ways that disrupt tissues, release toxins or trigger damaging inflammation.

classify the pathogen; route of entry/transmission; host process disrupted; resulting signs.

A respiratory virus enters droplets, infects airway cells and spreads before the immune response clears it.

Pathogen presence is not identical to symptoms: dose, host susceptibility and immune response also affect disease.

Skin and mucous membranes block entry.

Keratinised skin forms a physical barrier, while mucus traps particles and cilia move them away. Secretions such as lysozyme, tears and stomach acid add chemical protection.

barrier; trapped or killed agent; route out; limitation if the barrier is breached.

Mucus in an airway traps microbes and cilia move the mucus toward the throat, reducing access to lung tissue.

These are first-line defences, not antigen-specific memory responses.

Clotting seals a damaged blood vessel.

Platelets adhere to exposed tissue and release signals that activate clotting factors. A cascade converts fibrinogen to insoluble fibrin, forming a mesh that traps cells and limits blood loss.

damage → platelet plug → clotting cascade → fibrin mesh → repair/scab.

A cut exposes collagen; platelets accumulate, fibrin stabilises the plug and the sealed surface can begin to heal.

Clotting protects a wound but can be harmful if a clot forms inside an undamaged vessel.

Innate and adaptive immunity solve different problems.

Innate defences respond quickly using barriers, inflammation and phagocytes without tailoring receptors to one antigen. Adaptive immunity is slower initially but uses specific lymphocytes and memory.

compare speed; specificity; principal cells; memory; response on re-exposure.

A first infection may activate both systems, but a later exposure is controlled faster by memory lymphocytes.

Innate does not mean weak and adaptive does not mean immediate; the systems cooperate.

Phagocytes remove invaders by engulfing them.

Phagocytes follow chemical signals, bind a particle and enclose it in a vesicle. Lysosomes fuse with the vesicle, releasing enzymes and toxic chemicals that digest the contents.

chemotaxis → recognition → engulfment → phagosome/lysosome fusion → digestion.

A neutrophil surrounds a bacterium and destroys it inside a phagolysosome rather than releasing it back into tissue.

Phagocytosis is not the same as antibody production; it is a cellular innate response.

Lymphocytes provide specific immune recognition.

B and T lymphocytes carry receptors with particular complementary shapes. B cells can make antibodies; T cells coordinate responses or kill infected cells after activation.

antigen recognition; activation signal; B/T role; effector and memory outcome.

A T helper cell can activate a B cell whose receptor recognises the same pathogen antigen.

A lymphocyte is not activated merely because it is present; receptor match and co-signals matter.

An antigen is the feature an immune receptor recognises.

An antigen is a molecule or molecular region that can bind a specific antibody or lymphocyte receptor. Different pathogens display many antigens, so one response may not cover all variants.

identify the molecular target; receptor match; response triggered; distinguish antigen from whole pathogen.

A viral surface protein can act as an antigen even though the virus itself contains many other molecules.

Antigen does not mean ‘foreign organism’ as a whole; it is a recognisable molecular feature.

B cells activate only after antigen-specific signals.

A B cell binds a matching antigen through its receptor and normally receives help from a T helper cell. These signals start clonal expansion and antibody production.

B-cell receptor binding; helper signal; clonal expansion; effector/memory branches.

Only the B-cell clone whose receptor fits a viral antigen expands, limiting antibody production to relevant targets.

Antigen binding alone is not a complete guarantee of activation; context and helper signals regulate the response.

Plasma cells are antibody factories made by clonal selection.

Activated B cells divide into clones. Plasma cells secrete large amounts of antibody, while some daughter cells become long-lived memory cells.

selection by receptor match → clonal expansion → plasma cells → antibodies; retain memory branch.

A plasma cell releases antibodies that bind repeated surface epitopes on the infecting bacterium.

Antibodies are secreted by plasma cells, not by every B cell before activation.

Memory cells accelerate a second response.

Some activated B and T cells persist as memory cells. On re-exposure they respond more rapidly and strongly, often preventing noticeable disease.

primary exposure; memory formation; secondary exposure; faster/larger response.

A booster vaccine re-stimulates memory cells, producing protective antibody levels sooner than the first dose.

Memory is antigen-specific and can weaken; it does not make a person immune to every pathogen.

HIV spreads through particular body-fluid routes.

HIV transmission requires infected blood, semen, vaginal fluids or breast milk to reach susceptible tissue. It is not spread by casual contact, food sharing or intact skin.

source fluid; route of exposure; susceptible tissue; prevention barrier.

Sharing a contaminated needle can transfer infected blood directly into circulation, whereas a handshake cannot.

Transmission risk depends on exposure and viral load; a positive test does not identify the route by itself.

HIV can cause AIDS by reducing CD4 T cells.

HIV infects and progressively destroys CD4 helper T cells. As immune coordination falls, opportunistic infections and cancers become more likely; this clinical state is AIDS.

HIV entry/replication; CD4 decline; loss of coordination; opportunistic disease.

A person with low CD4 counts may develop an infection that a healthy immune system would normally control.

HIV infection and AIDS are not synonyms: treatment can delay or prevent progression to AIDS.

Antibiotics target bacterial processes.

Antibiotics inhibit bacterial structures or pathways such as cell-wall synthesis or ribosomes. They work only when the illness is caused by susceptible bacteria.

identify bacterial target; drug action; selective toxicity; treatment limit.

A cell-wall antibiotic can kill dividing bacteria while leaving human cells without bacterial walls largely unaffected.

Antibiotics do not cure viral infections and should not be judged by whether a fever has another cause.

Resistance spreads when antibiotics select variants.

A resistant bacterium survives a drug exposure, reproduces and passes resistance genes to descendants or other bacteria. Unnecessary or incomplete treatment increases selection pressure.

variation/gene; antibiotic exposure; survival; reproduction or transfer; population shift.

After a course removes susceptible bacteria, a resistant clone can multiply and dominate the remaining population.

The antibiotic does not ‘teach’ an individual bacterium to mutate; selection changes frequencies in the population.

Zoonoses cross from animal reservoirs into people.

A zoonosis is an infection naturally maintained in animals that reaches humans through contact, vectors, food or environmental spillover. Risk changes with ecology and behaviour.

reservoir; interface; transmission route; host jump; conditions increasing contact.

Deforestation can increase wildlife–livestock contact, creating more opportunities for a pathogen to reach people.

Animal origin alone does not prove a disease will spread efficiently between humans.

Vaccines create immune memory without the full disease.

A vaccine presents a safe form or component of an antigen, activating adaptive immunity and memory. Later exposure triggers a faster protective response.

antigen source; innate/adaptive activation; memory; later protection.

A booster raises antibody levels by reactivating memory cells rather than by causing the original infection.

Vaccination lowers risk and transmission but protection varies with pathogen, dose and population coverage.

Herd immunity protects some people indirectly.

When enough people are immune, an infectious case has fewer susceptible contacts and transmission chains are interrupted. The required coverage depends on pathogen transmissibility and mixing.

immune fraction; contact network; effective reproduction; vulnerable people left unprotected.

High measles vaccination coverage can prevent an imported case from reaching many susceptible people.

A simple percentage threshold is not universal; immunity may wane and coverage can be clustered unevenly.

Pandemic data need denominators and context.

Rates, case definitions, testing effort and time windows determine what disease data mean. Trends should be compared using consistent denominators and interpreted with uncertainty and confounders.

define numerator/denominator; check testing and reporting; compare like with like; separate correlation from cause.

More reported cases after testing expands may reflect detection as well as transmission, so positivity and hospitalisation add context.

A graph alone cannot establish causation or compare regions fairly if surveillance differs.