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.

Blood clotting rapidly seals a cut in the skin, limiting blood loss and pathogen entry.

Platelets at damaged tissue release clotting factors that start a cascade. The cascade produces thrombin, which rapidly converts soluble fibrinogen into insoluble fibrin strands.

Cut → platelet activation and clotting-factor release → cascade → thrombin → fibrinogen converted to fibrin → fibrin mesh traps erythrocytes → clot seals wound.

At a skin cut, the fibrin mesh stabilizes the platelet plug and traps red blood cells, forming a clot that can dry into a protective scab.

Thrombin converts fibrinogen to fibrin; it is not the mesh itself. Further clotting-factor details are outside this objective.

Innate immunity responds to broad pathogen categories and remains essentially unchanged during life; adaptive immunity targets particular antigens and forms memory.

Phagocytes can engulf unfamiliar bacteria immediately, while a later exposure to the same antigen triggers a faster antibody response from retained adaptive memory cells.

Innate does not mean weak, and adaptive does not mean immediate. For this objective, no innate component other than phagocytes needs to be named.

Phagocytes control infection by leaving the blood, moving amoeboidly to infected tissue, recognizing pathogens, engulfing them and digesting them.

Chemical signals guide phagocytes to an infection site. The flexible cell membrane changes shape during amoeboid movement and encloses a recognized pathogen by endocytosis in a vesicle.

Blood → amoeboid movement into infected tissue → pathogen recognition → endocytosis/phagosome → lysosome fusion → lysosomal enzymes digest pathogen.

A neutrophil leaves a capillary, crawls through tissue, encloses a bacterium and digests it after lysosomes fuse with the phagosome.

Phagocytosis is an innate cellular response, not antibody production. Engulfment contains the pathogen; lysosomal enzymes perform digestion.

Lymphocytes are adaptive immune cells that circulate in blood and are also concentrated in lymph nodes, where antigen-specific cells cooperate to produce antibodies.

An individual has a very large number of B lymphocytes with different receptors. Each B-cell clone is capable of making one specific type of antibody, so the population collectively recognizes many antigens.

Location: blood and lymph nodes. Diversity: many B-cell specificities. Cooperation: antigen-specific helper T cells help activate matching B cells, which can form antibody-secreting cells.

Only the small B-cell population with receptors complementary to a viral surface antigen is selected to produce antibodies against that antigen.

One B cell does not make every antibody. Large population diversity plus cooperation between lymphocytes creates the adaptive repertoire.

An antigen is a recognition molecule that can bind a specific antibody or lymphocyte receptor and trigger antibody production.

Most antigens are glycoproteins or other proteins and are located on the outer surface of a pathogen, where immune receptors can encounter them.

Antigen = molecular target, not the whole pathogen. Complementary receptor binding selects an antigen-specific response; different surface antigens select different lymphocyte clones.

Erythrocyte surface antigens from an incompatible blood group can stimulate antibody binding and production after transfusion, causing dangerous cell agglutination or destruction.

An antigen is not automatically an entire foreign organism. It is a recognizable molecule or molecular region, commonly a surface protein or glycoprotein.

An antigen-specific B lymphocyte is activated only after it interacts directly with its matching antigen and receives contact-dependent help from an activated helper T lymphocyte specific to the same antigen.

The two matching signals confirm antigen identity before the B cell divides. After activation, the B cell can produce antibody-secreting plasma cells and retained memory cells.

Specific antigen binds B-cell receptor → helper T cell activated by the same antigen contacts B cell → B cell activates → clonal expansion → plasma and memory cells.

A B cell recognizing one viral protein receives help only from a helper T cell activated by that same antigen type, preventing an unrelated B-cell clone from expanding.

Direct antigen binding alone is not sufficient in this model, and helper T-cell contact must be antigen-matched. Unactivated B cells do not yet secrete large antibody quantities.

Because only a small number of B cells recognize a given antigen, an activated B cell divides repeatedly by mitosis to form a large clone.

Clonal expansion supplies enough plasma cells to secrete an effective quantity of one antibody type. Every plasma cell in the clone inherits the selected antibody specificity.

Rare matching B cell → activation → repeated mitosis → clone of genetically matching cells → many plasma cells secrete the same specific antibody; some cells can become memory cells.

A selected B cell responding to a bacterial surface antigen produces thousands of plasma-cell descendants, all releasing antibodies complementary to that antigen.

Antibodies are secreted in quantity by differentiated plasma cells, not by every inactive B cell. Mitosis increases cell number without changing specificity.

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 are chemicals that block processes in bacteria while having little or no effect on corresponding processes in eukaryotic host cells.

Selective targets include bacterial cell-wall synthesis or bacterial ribosomes. Human cells lack bacterial walls and their cytoplasmic ribosomes differ, allowing a susceptible bacterial infection to be treated without the same target effect on human cells.

Identify bacterial target → explain disrupted bacterial process → explain why eukaryotic cells lack or differ in that target → predict treatment only for susceptible bacteria.

An antibiotic that blocks bacterial peptidoglycan-wall synthesis can stop dividing bacteria, while human cells have no peptidoglycan wall to block.

Viruses have no bacterial cell wall, ribosome or independent bacterial metabolism; they replicate using host-cell machinery. Antibiotics therefore do not control viral infections.

Antibiotic exposure selects resistant bacterial variants, allowing strains resistant to several antibiotics to evolve and spread.

Resistance genes arise through mutation or are acquired from other bacteria. An antibiotic kills susceptible cells, while resistant survivors reproduce and pass resistance vertically or transfer genes horizontally.

Existing genetic variation → antibiotic selection → resistant survival → reproduction/gene transfer → resistance frequency rises → different resistance genes can accumulate in one multiresistant strain.

Repeated exposure to different antibiotics can successively select a pathogenic strain carrying resistance to several drug classes, leaving fewer effective treatments.

Antibiotics do not direct bacteria to mutate. Careful use—only when appropriate, with the prescribed agent and regimen—reduces unnecessary selection pressure but cannot make evolution impossible.

A zoonosis is an infectious disease that can transfer from another animal species to humans, through several different transmission routes.

Zoonoses are prevalent among human infectious diseases because humans interact with livestock, wildlife, food systems and vectors. Ecology and behaviour change the opportunities for cross-species exposure.

Animal origin does not guarantee efficient human-to-human spread. Identify the reservoir or animal link, the transfer route and whether onward human transmission occurs.

Vaccination stimulates immunity to a specific pathogen without causing the disease itself.

A vaccine supplies pathogen antigens directly, or supplies DNA or RNA sequences that host cells use to make the antigen. Adaptive immune activation produces specific effector cells and retained memory cells.

Antigen vaccine: antigen is delivered. Nucleic-acid vaccine: DNA/RNA code for antigen is delivered. Both expose the immune system to the target antigen and develop memory without the full infection.

After immunization, later exposure to the pathogen reactivates antigen-specific memory cells, producing a faster response that can prevent disease.

A vaccine does not need to contain a live pathogen. Protection is antigen-specific and may require multiple doses or boosters.

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.

COVID-19 data must be compared using consistent definitions, time windows and denominators, with percentage change and percentage difference chosen for different questions.

Use percentage change for movement from an earlier baseline to a later value. Use percentage difference to compare two values when neither is designated as the original baseline. Check whether counts, rates or proportions are being compared.

Cases rising from 100 to 130 gives percentage change = (30 ÷ 100) × 100 = 30%. Comparing rates 40 and 50 gives percentage difference = (10 ÷ 45) × 100 = 22.2% (3 s.f.).

A percentage is only interpretable with its denominator and context. Testing effort, case definitions, reporting delays, population size and time window can change apparent trends; association alone does not establish cause.