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C3.2 Defence against disease

Defence against disease combines physical barriers, clotting, phagocytes, lymphocyte specificity, vaccination, antibiotics and evolutionary responses to pathogens across human populations.

Syllabus
First assessment 2025
Topic
C3.2
Level
HL

Learning objectives

C3.2.1Pathogens cause infectious diseases• Pathogens are disease-causing viruses, bacteria, fungi, protists, or parasites• Archaea are not currently known to cause human infectious diseasesC3.2.2Skin and mucous membranes• Keratinized skin, shedding, lysozyme, mucus, and cilia are primary defences• Mucous membranes protect respiratory and digestive surfacesC3.2.3Blood clotting• Platelets and damaged tissue release clotting factors at wounds• Thrombin converts fibrinogen to fibrin, trapping blood cells and sealing entry pointsC3.2.4Innate vs. adaptive immune system• Innate immunity is broad, rapid, and does not become more specific over life• Adaptive immunity is antigen-specific and produces memory cellsC3.2.5Phagocytes• Phagocytes use amoeboid movement to reach infection sites• They recognize, engulf, and digest pathogens using lysosomal enzymesC3.2.6Lymphocytes• B-cells produce antibodies after activation; T-cells assist or destroy infected cells• Lymphocytes originate in bone marrow and circulate through blood, lymph, and lymph nodesC3.2.7Antigens• Antigens are non-self molecules that trigger specific immune responses• They are often proteins or glycoproteins recognized by antibodies or lymphocyte receptorsC3.2.8B-lymphocyte activation• B-cells bind antigen, internalize it, and present it with MHC proteins• Helper T-cells activated by the same antigen stimulate B-cell activationC3.2.9Clones of plasma cells• Activated B-cells divide by mitosis through clonal selection• Plasma cells rich in rough ER secrete large amounts of one specific antibodyC3.2.10Immunity from memory cells• Memory B- and T-cells remain after the primary response declines• Re-exposure triggers faster, stronger secondary immunityC3.2.11HIV transmission• HIV is transmitted through infected blood, semen, vaginal fluids, or breast milk• Transmission risk depends on fluid exchange, barriers, and viral loadC3.2.12HIV infection and AIDS• HIV infects helper T-cells using CD4 receptors and reverse transcriptase• AIDS results when helper T-cell loss weakens antibody production and immune coordinationC3.2.13Antibiotics• Antibiotics block bacterial processes absent from eukaryotic cells• They do not treat viruses; antivirals target viral replication processesC3.2.14Antibiotic resistance evolution• Antibiotic use selects resistant variants that survive and reproduce• Multi-resistant strains arise through mutation, plasmids, and overuse of antibioticsC3.2.15Zoonoses• Zoonoses transfer from animal reservoirs to humans, sometimes through vectors• Examples include rabies, tuberculosis, Japanese encephalitis, and COVID-19C3.2.16Vaccines and immunization• Vaccines contain weakened/inactivated pathogens, antigens, or genetic instructions• Immunization produces active artificial immunity and memory cellsC3.2.17Herd immunity• Herd immunity indirectly protects susceptible people when many are immune• Thresholds depend on transmission route and pathogen contagiousnessC3.2.18COVID-19 pandemic data evaluation• Evaluate COVID-19 data using source reliability, trends, and controlled comparisons• Calculate percentage change, percentage difference, incidence, and vaccine efficacy

A Pathogen Starts an Infection; Damage Produces Disease

A pathogen is a disease-causing biological agent. Infection means that it has entered and established itself in a host; infectious disease is the harmful condition that can result.

Comparison of viruses, bacteria, fungi, protists, parasitic animals and archaea as possible or known pathogen groups.
Group Disease-causing examples?
viruses, bacteria, fungi, protists yes
parasitic animals, including helminths yes
archaea no human infectious disease is currently known

Viruses are pathogens but are not cells. Exposure also does not guarantee disease: entry, replication, host defence and tissue damage all affect the outcome.

Intact Skin Is a Layered Barrier

  • Keratinized cells form a tough, dry physical barrier.
  • Continuous shedding removes attached microbes.
  • Skin secretions create chemical conditions that inhibit many microbes.
Body map showing skin and the mucous membranes of the respiratory and digestive systems, with shedding, lysozyme, mucus and cilia.

A cut, bite or puncture bypasses this barrier. The defence is strongest while the surface remains intact.

Mucous Membranes Trap, Move and Damage Pathogens

Respiratory and digestive surfaces must exchange materials, so they cannot be sealed by thick dry skin. They use a trap-and-remove system instead.

Mechanism Protective result
mucus traps microbes and particles
cilia sweep trapped material toward the throat
swallowing or coughing removes material from the airway
lysozyme in tears, saliva and mucus hydrolyses bacterial cell-wall peptidoglycan

Mucus alone is not the complete defence: protection depends on capture + movement + removal or chemical damage.

A Fibrin Mesh Seals a Breached Barrier

Clotting limits blood loss and closes an entry route for pathogens.

  1. Damaged tissue and activated platelets start a cascade of clotting factors.
  2. The cascade produces thrombin from its inactive precursor.
  3. Thrombin converts soluble fibrinogen into insoluble fibrin.
  4. Fibrin fibres trap platelets and blood cells, forming a clot that dries into a scab.

The clot is not simply a pile of platelets: the fibrin network gives the seal its reinforcing mesh.

Innate Response Buys Time; Adaptive Response Learns the Target

Feature Innate immunity Adaptive immunity
onset rapid slower on first exposure
recognition broad pathogen patterns or damage one antigen specificity per selected clone
main cells here phagocytes B and T lymphocytes
memory no antigen-specific memory memory cells produce an improved secondary response

The systems cooperate. Innate cells contain infection and present antigens; adaptive cells add precise targeting and long-term memory.

Phagocytes Enclose a Pathogen Before Digesting It

chemical signals → amoeboid movement → receptor attachment → engulfment into a phagosome → lysosome fusion → enzymatic digestion

The pathogen is destroyed inside a membrane-bound vesicle. Lysosomal enzymes are contained, reducing damage to the phagocyte's own cytoplasm.

Sequence of phagocytosis from chemotaxis and receptor attachment through engulfment, lysosome fusion and digestion.

Lymphocytes Divide the Adaptive Response into Distinct Jobs

All lymphocytes arise from stem cells in bone marrow. B cells mature in bone marrow; T cells mature in the thymus. Mature cells circulate through blood and lymph and concentrate in lymph nodes.

Cell Core job after activation
helper T cell coordinates responses and activates matching B cells
killer T cell destroys infected body cells displaying its antigen
B cell forms plasma cells and memory B cells
plasma cell secretes one specific antibody

A resting B cell does not yet release large amounts of antibody; high-output secretion follows activation and differentiation into a plasma cell.

Complementary Binding Makes Recognition Specific

An antigen is a molecular structure recognized specifically by an antibody or lymphocyte receptor and capable of contributing to an immune response. Many are proteins or glycoproteins.

Recognition depends on complementary three-dimensional shape and chemical interactions. One selected lymphocyte clone therefore responds to a particular antigenic feature, not to every foreign molecule.

A pathogen antigen binding to a complementary antibody variable region and a matching B-cell receptor.

B-Cell Activation Requires a Matching Helper-T Signal

  1. A B-cell receptor binds its complementary antigen.
  2. The B cell internalizes and digests the antigen.
  3. Antigen fragments are displayed on MHC II proteins.
  4. An activated helper T cell recognizing the same antigen binds and delivers co-stimulation and cytokines.
  5. The B cell is fully activated.

The two linked recognition events act as a specificity check: the B cell captures the target, and a matching helper T cell confirms that response.

Clonal Selection Amplifies One Useful Specificity

An antigen does not instruct a B cell to invent a receptor. It selects the rare pre-existing B cell whose receptor already binds it.

After activation Result
repeated mitosis a clone with the same antigen specificity
differentiation into plasma cells rapid secretion of large amounts of matching antibody
differentiation into memory B cells long-lived capacity for a faster later response

Plasma cells contain extensive rough endoplasmic reticulum and Golgi apparatus because antibodies are proteins made and exported in large quantities.

Antibodies Mark and Disable Targets Rather Than Killing Cells Themselves

Antibody binding can… Consequence
cover a toxin or viral attachment site neutralize its interaction with host cells
cross-link many targets agglutinate them into easier-to-clear clusters
coat a pathogen make recognition and engulfment by phagocytes easier

The antibody supplies specific binding. Clearance is then completed by phagocytes, complement and other immune mechanisms.

Memory Changes the Timing and Scale of the Next Response

Response Starting state Typical outcome
primary only rare matching naive cells are present slower clonal expansion; symptoms may develop
secondary many long-lived matching memory cells are present faster, larger response; pathogen may be controlled before disease

Memory cells do not provide a permanent high antibody concentration. They preserve ready-to-expand antigen-specific clones, so re-exposure starts farther along the response pathway.

Defence Is a Layered Route from Exclusion to Memory

keep out with skin and mucosa → seal breaches with fibrin → contain broadly with innate phagocytes → recognize specifically with lymphocytes → amplify selected clones → clear with antibodies and effector cells → remember with long-lived B- and T-cell clones

If this step fails… The immediate consequence is…
surface barrier easier pathogen entry
phagocytosis weaker early containment
helper-T coordination weaker B-cell and killer-T responses
clonal expansion too few specific effector cells
memory formation no improved response on re-exposure

Protection is not one reaction. It is a connected sequence of barriers, broad responses, specific selection and retained memory.

HIV Transmission Requires Both an Infectious Fluid and an Entry Route

Transmission becomes possible when enough HIV in blood, semen, vaginal or rectal fluid, or breast milk reaches susceptible tissue or the bloodstream.

Route Why transmission can occur
unprotected sexual contact infected fluid contacts vulnerable mucosa or damaged tissue
shared needles or contaminated blood virus enters blood directly
pregnancy, birth or breastfeeding maternal virus can reach the child

HIV is not transmitted by intact-skin contact, sharing food, toilets, coughing, or insect bites. Risk depends on fluid + access + viral load, not on ordinary social contact.

HIV Converts Its RNA into DNA Inside Helper T Cells

attachment to CD4 and co-receptors → entry and uncoating → reverse transcriptase copies viral RNA into DNA → viral DNA integrates into host DNA → host machinery produces new virus

Integration lets viral information persist in the cell. Replication and immune attack progressively reduce functional helper T cells.

HIV attaches to a CD4-bearing helper T cell, releases RNA, uses reverse transcriptase to make viral DNA and integrates that DNA before immune coordination declines.

AIDS Is the Consequence of Lost Immune Coordination

HIV is the virus. AIDS is an advanced syndrome diagnosed when HIV has caused severe immune damage, indicated by very low CD4 helper-T-cell counts and/or characteristic opportunistic disease.

fewer helper T cells → weaker activation of matching B cells and killer T cells → reduced antibody and cell-mediated responses → normally controlled pathogens and cancers can cause severe disease

A person can transmit HIV without having AIDS. Antiretroviral therapy suppresses viral replication and can prevent or greatly delay progression.

An Antibiotic Works Only If the Pathogen Has Its Target

Selective toxicity means disrupting a bacterial structure or process more than the patient's cells.

Bacterial target Why it can be selective
peptidoglycan wall synthesis human cells have no cell wall
70S ribosome function bacterial ribosomes differ from cytoplasmic human 80S ribosomes
bacterial DNA or metabolic enzymes key molecules can differ enough for selective inhibition

Viruses have no peptidoglycan wall, ribosomes or independent metabolism. Antibiotics therefore do not treat viral infections; antivirals target stages of viral entry or replication instead.

Antibiotics Select Resistance; They Do Not Create It on Demand

  1. Mutation or acquired DNA creates heritable variation before treatment.
  2. The antibiotic kills or inhibits susceptible bacteria.
  3. Resistant bacteria survive more often.
  4. Survivors reproduce, so resistance alleles become more frequent.

An individual bacterium does not evolve because it ‘tries’ to survive. The population evolves as allele frequencies change across generations.

A bacterial population with susceptible and resistant variants is exposed to antibiotic; resistant survivors reproduce and can transfer a resistance plasmid.

Multi-Resistance Combines New Alleles, Gene Transfer and Selection

Process Contribution
mutation creates a new resistance allele
plasmid transfer moves resistance genes between bacteria, sometimes across species
reproduction passes genes to descendants
antibiotic exposure repeatedly favours carriers of useful resistance genes

Unnecessary prescribing, incorrect doses, poor infection control and routine agricultural use can increase selection or spread. They do not deliberately cause mutation; they make resistant lineages more likely to survive and transmit.

A single bacterium can accumulate several resistance genes, producing a strain for which multiple treatments fail.

Zoonoses Cross from Animal Reservoirs by Different Routes

Route Example
direct contact or bite rabies
food, droplets or close animal exposure bovine tuberculosis
arthropod vector Japanese encephalitis via mosquitoes
spillover followed by sustained human transmission COVID-19, with probable animal origin

A reservoir maintains the pathogen in nature. A vector carries it between hosts. They may be different organisms and should not be used as synonyms.

Animal reservoirs pass zoonotic pathogens to humans directly or through a vector, with examples including rabies, bovine tuberculosis, Japanese encephalitis and COVID-19.

Different Vaccine Platforms Converge on Antigen Presentation

Platform What enters the body How antigen appears
attenuated or inactivated pathogen whole modified pathogen its antigens are processed and presented
subunit or toxoid selected antigenic material antigen is taken up by antigen-presenting cells
mRNA or DNA vaccine genetic instructions host cells make the antigen, then display or release it

All routes aim to activate matching helper T cells, B cells and often killer T cells without the uncontrolled disease caused by the pathogen. Clonal expansion then forms effector and memory cells.

Genetic vaccines do not alter the purpose of the response: they change how antigen is supplied, not the antigen-specific logic of adaptive immunity.

Vaccination Is Active Artificial Immunity

Immunity Source Memory formed?
active natural infection exposes the person to antigen usually
active artificial vaccination exposes the person to antigen safely usually
passive natural maternal antibodies cross placenta or enter milk no
passive artificial prepared antibodies are injected no

Active means the person's own lymphocytes respond and form memory. Passive means ready-made antibodies arrive from elsewhere, giving immediate but temporary protection.

Vaccination is called artificial because the exposure is deliberately provided—not because the antibodies or memory cells are artificial.

Herd Immunity Works by Breaking Transmission Chains

When many people are immune, an infected person is less likely to contact a susceptible person. Transmission chains end more often, indirectly reducing exposure for people who are not immune.

There is no universal threshold. It depends on contagiousness, route of transmission, vaccine effectiveness, duration of immunity, behaviour and how evenly immunity is distributed.

Population protection lowers risk; it does not guarantee that every susceptible individual is safe.

Transmission networks showing many immune people interrupting spread, compared with continued spread when few people are immune.

Choose the Measure That Matches the Question

% change=new−originaloriginal×100\%\text{ change}=\frac{\text{new}-\text{original}}{\text{original}}\times100

% difference=∣A−B∣(A+B)/2×100\%\text{ difference}=\frac{|A-B|}{(A+B)/2}\times100

I=NPI=\frac{N}{P}

VE=Iu−IvIu×100VE=\frac{I_u-I_v}{I_u}\times100

Question Measure
How far did one value move from its baseline? percentage change
How different are two values with no baseline? percentage difference
How quickly are new cases arising? incidence
How much lower is incidence in vaccinated people? vaccine efficacy

Use incidence or risk, not raw case counts, when group sizes or observation time differ. Here, Iᵤ and Iᵥ are incidences in unvaccinated and vaccinated groups.

A Pandemic Comparison Is Only as Fair as Its Denominators

Before comparing groups, check:

  • the same case definition and testing access
  • population size or person-time at risk
  • the same observation period
  • age, prior infection and health differences
  • exposure patterns, circulating variants and time since vaccination
  • uncertainty, missing data and source reliability
Trial arm Cases Participants Risk
unvaccinated 185 15,210 1.216%
vaccinated 11 15,210 0.072%

VE=(1−0.059)×100=94.1%VE=(1-0.059)\times100=94.1\%

A correlation or group difference supports a causal claim only when design and confounding have been addressed. Report what the data measure—not more than they can show.

Control Disease by Targeting the Correct Stage

Stage in the disease system Control logic
reservoir or transmission route reduce contact, block vectors, use barriers and infection control
pathogen replication choose a treatment with a real pathogen-specific target
population evolution use antibiotics only when appropriate and limit spread of resistant strains
susceptible host vaccinate to build antigen-specific memory before exposure
population network raise and distribute immunity so transmission chains break
evidence and policy compare rates fairly, quantify effects and account for confounding

Ask three questions in order: Where is the causal bottleneck? Which intervention acts there? What evidence would show that it worked?

Effective disease control joins cellular mechanisms, evolutionary consequences and population data. A correct intervention aimed at the wrong stage—or supported by an unfair comparison—can still fail.

Pathogens cause infectious diseases

6 marks

Describe the cause, transmission and effects of malaria.

Skin and mucous membranes

3 marks

Describe how disease-causing bacteria are prevented from entering the body.

Blood clotting

7 marks

Explain how blood clotting occurs and the consequence for a person who has hemophilia.

Innate vs. adaptive immune system

1 mark

Distinguish between innate and adaptive immune response.

The graph shows the magnitude of the immune response after infection or after vaccination over time.

Phagocytes exam focus

4 marks

Describe how phagocytic leucocytes may act as a defence against disease.

Lymphocytes exam focus

7 marks

Explain how cells in the bloodstream cause a specific immune response.

Antigens exam focus

1 mark

What is a characteristic of antigens?

B-lymphocyte activation

7 marks

Explain the production of antibodies when a patient is infected with the TB bacterium.

Clones of plasma cells

1 mark

What is a role of activated B cells?

Immunity from memory cells

3 marks

Suggest possible reasons for the observed pattern of presence of antibodies in vaccinated mice.

The summer after vaccination, the prevalence of B. burgdorferi infection in tick nymphs collected on mice from the two sites was measured.

\cline { 2 - 5 } \multicolumn{1}{c|}{}State of infection of tick nymphs with B. burgdorferi
\cline { 2 - 5 } \multicolumn{1}{c|}{}Site 1Site 2
Host miceInfectedNot infectedInfectedNot infected
Control mice903155789
Vaccinated mice8728849121

HIV transmission

1 mark

How has the transmission of HIV been reduced?

HIV infection and AIDS

4 marks

Discuss the consequences of infection with HIV.

Antibiotics exam focus

3 marks

(i) Estimate the diameter of the zone of inhibition of chloramphenicol.
(ii) Distinguish between the action of tetracycline and penicillin on B. subtilis.
(iii) Suggest a reason for the result with disc X .

Antibiotic resistance evolution

9 marks

Explain how natural selection can lead to evolution using antibiotic resistance in bacteria as an example.

Zoonoses exam focus

1 mark

State the term used for an infectious disease that can transfer from other species to humans.

Vaccines and immunization

8 marks

Some prokaryotes cause infectious disease in humans. Explain the principles of vaccination.