IB Biology · Theme C Interaction and interdependence · Organisms
C3.2 Defence against disease
Skin and mucous membranes keep pathogens out; clotting seals the gaps. Inside, phagocytes give a broad innate response, and lymphocytes give a specific adaptive one with memory. Antibiotics, vaccines and herd immunity are how we help, and resistance and zoonoses are how it goes wrong.
Compiled from the IB Biology guide (first assessment 2025, updated May 2026 for 2028) and our question bank ·
Specialist review in progress
· How these pages are made
Assessed in Paper 1A (multiple choice), Paper 1B (data-based) and Paper 2 (short and extended response). IB Biology guide (first assessment 2025, updated May 2026 for 2028).
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C3.2.1 Pathogens cause infectious disease, and observation beat germ theory to it
A pathogen is a disease-causing organism: viruses, bacteria, fungi and protists.
Archaea are not known to cause human disease.
An infectious disease is caused by a pathogen and can be transmitted.
Careful observation brings progress before mechanisms are known.
Semmelweis cut childbed fever with hand-washing; Snow removed the Broad Street pump handle in the London cholera outbreak.
Students often think archaea cause disease like bacteria. In fact none is known to cause disease in humans.
Students often think control needs the pathogen identified first. In fact Semmelweis and Snow acted on patterns, decades earlier.
C3.2.2 Skin and mucous membranes stop pathogens getting in
Primary defences stop pathogens entering; immune responses act once they are inside.
Skin is a physical barrier: tough, dead outer cells.
Skin is a chemical barrier: sebum keeps the surface at low pH, inhibiting growth.
Mucous membranes line airways, gut, reproductive tract and eyes; their mucus traps pathogens.
Students often think skin is only a physical barrier. In fact sebum makes it chemical too.
Students often think mucus is made only during infection. In fact sebum and mucus are produced continuously, a standing defence.
C3.2.3 Clotting seals a cut
Platelets adhere to damaged vessels and release clotting factors.
A cascade follows: each step activates many molecules of the next, so it is fast.
The enzyme thrombin converts soluble fibrinogen to insoluble fibrin.
The fibrin mesh traps erythrocytes, forming a clot.
Students often think fibrin is always in the blood. In fact fibrinogen circulates; thrombin makes fibrin only at damage.
Students often think blood clots because of air. In fact clotting factors from platelets start the cascade.
C3.2.4 Innate is broad and fixed; adaptive is specific and learns
The innate system responds to broad categories of pathogen.
It does not change over a lifetime; the response is the same every time.
The adaptive system, based on lymphocytes, responds to particular pathogens.
It builds memory, so later responses are faster and more effective.
Students often think the innate system improves with each infection. In fact only the adaptive system builds memory.
Students often think the adaptive response is faster. In fact innate is fast; adaptive takes days on first exposure.
C3.2.5 Phagocytes engulf and digest pathogens
Phagocytes leave capillaries by amoeboid movement and crawl to infection sites.
They recognise pathogens as foreign and engulf them by endocytosis into a vesicle.
Lysosomes fuse with the vesicle; their enzymes digest the pathogen.
One phagocyte can engulf many kinds of pathogen.
Students often think phagocytes stay in blood. In fact they squeeze out between capillary cells into tissue.
Students often think the pathogen enters the cytoplasm. In fact it stays inside a vesicle until digested.
C3.2.6 Lymphocytes cooperate to make antibodies
Lymphocytes circulate in blood and are held in lymph nodes.
B-lymphocytes and helper T-lymphocytes cooperate to produce antibodies.
There are very many different B-lymphocytes; each makes one specific antibody.
An antibody binds one antigen, helping eliminate the pathogen.
Students often think B-cells design an antibody after seeing the antigen. In fact each B-cell's antibody is fixed beforehand; the matching ones are selected.
Students often think lymph nodes are only filters. In fact they contain large numbers of lymphocytes.
C3.2.7 Antigens are the foreign molecules that trigger the response
An antigen is a molecule recognised as foreign that triggers antibody production.
Most are glycoproteins or other proteins on a pathogen's outer surface.
Erythrocytes carry antigens too, differing between blood groups.
Transfused into a different blood group, they can stimulate antibodies; blood must be matched.
Students often think antigens are the body's attack molecules. In fact antigens are foreign; antibodies are the response.
Students often think only pathogens have antigens. In fact red blood cells carry them, which is why blood groups matter.
C3.2.8 Helper T-cells switch B-cells on
2028 guide: scope reduced — Reported (unverified secondary source) that the 2028 guide no longer requires the detailed T-cell activation mechanism. The 2025 guidance requires that the helper T-cell must itself have been activated by the same type of antigen; q14 rests on that detail and is tagged 2025 only. q13, the concepts and the misconceptions test only the two requirements for B-cell activation (specific antigen plus helper T-cell contact), which the statement itself still demands, so they remain valid for both guides. Candidates sitting May/Nov 2026 or 2027 exams still need the fuller 2025 scope.
A helper T-lymphocyte makes no antibody but is needed to activate B-cells.
Helper T-cells are antigen-specific.
B-cell activation needs direct contact with its specific antigen and contact with a helper T-cell.
That helper T-cell must have been activated by the same antigen.
Students often think a B-cell starts secreting on meeting its antigen. In fact it also needs helper T-cell contact.
Students often think T-cells secrete antibodies too. In fact only B-cells, as plasma cells, do.
C3.2.9 Activated B-cells multiply into a clone of plasma cells
Only a small number of B-cells match any one antigen.
An activated B-cell divides by mitosis to form a large clone.
The cells differentiate into plasma cells that secrete antibody in quantity.
All cells in the clone make the same antibody.
Students often think one activated B-cell makes enough antibody. In fact it must first divide into a clone.
Students often think a clone makes several antibodies. In fact it is genetically identical and makes one type.
C3.2.10 Memory cells are why immunity lasts
Immunity is the ability to eliminate an infectious disease from the body.
It comes from long-lived memory cells, not from antibodies persisting.
Memory cells secrete nothing while the pathogen is absent.
On re-exposure they divide fast into plasma cells: more antibody, sooner.
Students often think first-infection antibodies last for life. In fact antibodies fade; memory cells survive.
Students often think memory cells trickle out antibody for years. In fact they wait, then divide into plasma cells when needed.
C3.2.11 HIV passes only in certain body fluids
HIV is a retrovirus infecting certain lymphocytes.
It transmits in blood, semen, vaginal secretions and breast milk.
Routes: unprotected sex, shared needles, unscreened transfusions, mother to child.
Not by casual contact, saliva, sneezing or insect bites.
Students often think HIV spreads by coughing or shared cutlery. In fact only body fluids passed directly transmit it.
Students often think mosquitoes carry HIV. In fact insects do not transmit it.
C3.2.12 HIV kills helper T-cells, and AIDS follows
HIV infects and kills helper T-lymphocytes, not all white cells.
Without them, B-cells cannot be activated to make antibodies.
AIDS develops, often years later, when the immune system can no longer cope.
The illnesses of AIDS are opportunistic infections by other pathogens.
Students often think HIV and AIDS are the same. In fact HIV is the virus; AIDS is the later syndrome.
Students often think HIV kills B-cells. In fact it kills helper T-cells, so B-cells cannot be activated.
C3.2.13 Antibiotics hit bacterial processes, which viruses do not have
An antibiotic blocks a process in bacteria but not in eukaryotic cells.
Targets include peptidoglycan wall synthesis and protein synthesis on 70S ribosomes.
So bacteria die or stop dividing while the patient's cells are unharmed.
Viruses have no walls, ribosomes or enzymes of their own; they use the host's.
Students often think antibiotics treat any infection. In fact viruses lack the processes antibiotics block.
Students often think antibiotics harm our cells too. In fact their targets exist only in bacteria.
C3.2.14 Resistance evolves by natural selection, so use antibiotics carefully
Resistance arises by random mutation or a gene acquired from another bacterium.
The antibiotic kills susceptible bacteria; resistant ones reproduce: natural selection.
Each antibiotic needs its own resistance; multiresistant strains have accumulated several.
Careful use, not prescribing for viruses or overusing in farming, lowers the selection pressure.
Searching chemical libraries, now with computer models, is a new technique yielding new antibiotics.
Students often think exposure makes individual bacteria resistant. In fact mutation comes first; the antibiotic selects survivors.
Students often think the patient becomes resistant. In fact the bacterial strain does.
C3.2.15 Many human diseases come from other animals
A zoonosis transfers from other animal species to humans; most emerging diseases are zoonoses.
Tuberculosis (Mycobacterium bovis) passes from cattle in unpasteurised milk; rabies enters by bite.
Japanese encephalitis reaches humans by mosquito from infected pigs and wading birds.
COVID-19 (SARS-CoV-2) crossed from another species, probably bats, then spread by droplets.
Students often think a zoonosis cannot spread person to person. In fact COVID-19 did; rabies rarely does.
Students often think all zoonoses are viral. In fact bovine tuberculosis is bacterial.
C3.2.16 Vaccines deliver antigens, not the disease
A vaccine stimulates immunity to a specific pathogen without causing the disease.
It contains antigens, or DNA or RNA coding for an antigen the person's cells then make.
The antigen activates specific lymphocytes, which form memory cells.
Immunisation is the process of making a person immune, usually by vaccination.
Students often think vaccines supply antibodies. In fact they supply antigens; your own immune system makes the antibodies.
Students often think mRNA vaccines alter your genes. In fact the mRNA is translated in the cytoplasm and broken down.
C3.2.17 Herd immunity protects those who cannot be vaccinated
Herd immunity: when enough of a population is immune, transmission is greatly impeded.
Members are interdependent: each immune person shields susceptible ones.
The percentage needed depends on how easily the disease spreads.
If coverage falls, the disease can return and epidemics occur.
Scientists publish so others can evaluate; media report before that finishes. Vaccine risks are minimal but not nil: pragmatic truth, not certainty.
Students often think herd immunity makes everyone immune. In fact the unvaccinated stay susceptible but are less exposed.
Students often think a safe vaccine has zero side effects. In fact the risk is tiny, not nil, and far outweighed by benefit.
C3.2.18 Percentage change and percentage difference
Percentage change = (final − initial) ÷ initial × 100; negative for a decrease.
Percentage difference compares two values when neither is the original.
Percentage difference = difference ÷ mean of the two × 100, unless a reference is named.
Dividing new by old gives new as a percentage of old, not the change.
Students often divide by the final value. In fact the initial value is the denominator for percentage change.
Students often use the sum as denominator. In fact percentage difference uses the mean, the sum divided by two.
Diagnostic a bearings check, not a test
10 questions, one per part of the topic where we can. Answer them, then see which statements you own and which to read.
1 Which statement about the organisms that cause infectious diseases in humans is correct?
Answer and reasoning
Viruses, bacteria, fungi and protists all include species that are human pathogens, but archaea are not known to be. — A disease-causing organism is a pathogen, and the term is typically reserved for viruses, bacteria, fungi and protists. Archaea, although they are prokaryotes, are not known to cause any diseases in humans.
Archaea, like bacteria, include many species that are human pathogens, because both groups are prokaryotes. — A student who treats 'prokaryote' as meaning 'germ' picks this. Being a prokaryote does not make an organism a pathogen; archaea are not known to cause any human disease.
Only bacteria and viruses cause infectious diseases in humans; fungi and protists do not cause any. — A student whose examples of infectious disease are all bacterial or viral picks this. Fungi and protists also include human pathogens, such as the causes of athlete's foot and malaria.
Any microorganism that lives on or inside the human body is, by definition, a pathogen and a cause of disease. — A student who equates microorganisms with 'germs' picks this. A pathogen is defined by causing disease; most microorganisms on the skin and in the gut cause none.
2 Sebaceous glands in the skin secrete sebum. Which statement explains how sebum contributes to the skin's role as a primary defence against pathogens?
Answer and reasoning
It thickens the dead outer layer of the skin, so that the physical barrier becomes much harder for pathogens to penetrate. — A student who sees the skin as a physical barrier only picks this. Sebum is an oily secretion; it does not add to the dead cell layer. Its contribution is chemical, through the low pH it maintains.
It carries antibodies out onto the skin surface, where they bind to any pathogens before these can penetrate into the skin. — A student who assumes every defence involves the immune system picks this. Sebum contains no antibodies; the primary defences are barriers that act without lymphocytes or antibodies.
It makes the skin surface a chemical barrier: its fatty acids keep the pH low, inhibiting the growth of many pathogens. — The skin acts as both a physical and a chemical barrier. The physical barrier is the tough outer layer of dead cells; the chemical barrier is the acidic surface maintained by the fatty acids in sebum, which inhibits the growth of many pathogens.
It is secreted only once the skin is infected, so it is part of the immune response rather than a barrier. — A student who thinks secretions appear only during infection picks this. Sebum is produced continuously, so the acidic surface is a standing barrier that is in place before any pathogen arrives.
3 Which statement correctly distinguishes the innate immune system from the adaptive immune system?
Answer and reasoning
Both systems build up a memory of the pathogens they meet, but the innate system does so faster because it does not need to be specific to each one. — A student who applies 'building up immunity' to the whole immune system picks this. Only the adaptive system builds a memory; the innate system does not change during an organism's life.
The innate system responds to broad categories of pathogen and does not change during life; the adaptive system is specific and builds a memory of pathogens. — This is the distinction the IB draws. The innate response (including phagocytes) is the same on every exposure, whereas the adaptive response is specific to particular pathogens and becomes more effective because a memory of pathogens encountered is retained.
The innate system is the specific one, with each phagocyte recognizing just a single type of pathogen, while the lymphocytes respond to broad categories of pathogen. — A student who has attached specificity to the wrong cells picks this. Phagocytes respond to broad categories of pathogen; it is the lymphocytes of the adaptive system that are specific.
The adaptive system responds faster than the innate system on first exposure to a pathogen, because a specific response is a more efficient response. — A student who assumes the more effective system must be the quicker one picks this. On first exposure the adaptive response takes days, because the few specific lymphocytes must be activated and multiply; the innate response is immediate.
4 Which statement about B-lymphocytes and antibodies is correct?
Answer and reasoning
Each B-lymphocyte examines the antigen it meets and then adjusts the shape of the antibody it makes so that it fits the antigen. — A student who reads 'adaptive' as tailoring picks this. The antibody a B-cell makes is fixed before it meets any antigen; the antigen selects the B-cells that already fit it.
A person has a very large number of different B-lymphocytes, and each of them makes a single specific type of antibody. — An individual has a very large number of B-lymphocytes that each make a specific type of antibody. The diversity of B-cells, not any tailoring by an individual cell, is what allows a specific response to almost any antigen.
Helper T-cells and B-lymphocytes both secrete antibodies, which is why they are said to cooperate in producing them. — A student who reads 'cooperate' as both making antibody picks this. Only B-lymphocytes produce antibodies; helper T-cells cooperate by activating them.
B-lymphocytes are found only in the blood; lymph nodes contain trapped pathogens but no lymphocytes at all. — A student who knows lymphocytes only as white blood cells picks this. Lymphocytes both circulate in the blood and are contained in lymph nodes, which is where many antigens meet them.
5 Which statement about the helper T-lymphocyte that activates a B-lymphocyte is correct?
Answer and reasoning
It can activate any B-lymphocyte that it contacts, whatever antigen that B-lymphocyte happens to be specific to. — A student who takes 'helper' to mean a general assistant picks this. Helper T-cells are antigen-specific, and a B-cell is activated only by a helper T-cell activated by the same type of antigen.
It must itself have been activated by the same type of antigen as the B-lymphocyte that it goes on to activate. — There are antigen-specific B-cells and antigen-specific helper T-cells. Activation of a B-cell requires contact with a helper T-cell that has also become activated by the same type of antigen, so the two cells respond to the same pathogen.
It secretes the antibody itself and then passes the finished antibody to the B-lymphocyte to release. — A student who thinks T-cells make antibodies picks this. Antibody is made only by B-cells; the helper T-cell activates the B-cell but produces no antibody.
It is not required, because a B-lymphocyte is activated as soon as it binds its specific antigen. — A student who holds the one-step model picks this. Antigen binding alone does not activate a B-cell; contact with an activated helper T-cell is also needed.
6 What is the basis of a person's immunity to a disease that they have previously had?
Answer and reasoning
Antibodies made during the first infection remain in the blood at a protective level for the rest of the person's life. — A student who equates immunity with antibodies picks this. Antibodies are proteins that are broken down over months; long-term immunity depends on memory cells, which can make more.
Memory cells are plasma cells that keep on secreting the antibody at a low rate for many years after the infection. — A student who attaches 'memory' to the antibody picks this. Memory cells do not secrete antibody while the pathogen is absent; they divide into plasma cells when the antigen reappears.
Phagocytes of the innate immune system learned to recognize the pathogen during the first infection and now destroy it faster. — A student who thinks the innate system improves picks this. Phagocytes respond in the same way every time; immunity is a property of the adaptive system, based on memory cells.
Memory cells that are specific to the pathogen survive long-term and can make the antibodies that are needed. — Immunity is the ability to eliminate an infectious disease from the body. It is due to the long-term survival of lymphocytes that are capable of making the specific antibodies needed to fight the infection; these are memory cells.
7 Which statement about the transmission of HIV is correct?
Answer and reasoning
HIV is transmitted in body fluids such as blood, semen, vaginal secretions and breast milk, for example through unprotected sex, shared needles or from mother to child. — HIV is transmitted in body fluids. The mechanisms include unprotected sexual intercourse, sharing of hypodermic needles, transfusion of unscreened blood or blood products, and transmission from mother to child across the placenta, during birth or in breast milk.
HIV is transmitted through the air by coughing, and by casual contact such as shaking hands, sharing cutlery or using the same toilet as an infected person. — A student who generalizes from colds and contact infections picks this. HIV is not present in sufficient quantity in saliva or on skin, does not survive outside the body and is not transmitted by these routes.
HIV is transmitted by blood-feeding insects such as mosquitoes, in the same way as the virus that causes Japanese encephalitis is transmitted. — A student who knows HIV is in blood and that mosquitoes carry some viruses picks this. HIV does not replicate in mosquitoes and is not transmitted by insect bites.
HIV can only be transmitted by a person who has already developed AIDS, because before that stage the virus is not present in body fluids. — A student who treats HIV and AIDS as the same thing picks this. A person with HIV is infectious from soon after infection, often for years before AIDS develops.
8 Why do antibiotics fail to control infections caused by viruses?
Answer and reasoning
Viruses are far smaller than bacteria, so antibiotic molecules are too large to bind to them or to enter them effectively. — A student who reaches for size as the explanation picks this. The reason is biochemical: an antibiotic blocks a bacterial process, and a virus has no equivalent process to block, whatever its size.
Antibiotics would destroy the human cells inside which viruses replicate, so they cannot safely be used against a viral infection. — A student who thinks antibiotics damage human cells picks this. Antibiotics are selective for bacterial processes and do not harm eukaryotic cells; they fail against viruses because there is nothing for them to act on.
They do not fail: antibiotics kill viruses as well as bacteria, only more slowly, so a longer course is needed for a viral infection. — A student who sees antibiotics as general anti-infection drugs picks this. Antibiotics have no effect on viruses at any dose or duration, because viruses lack the processes that antibiotics block.
Viruses have no metabolic processes of their own; they use those of the host cell, which antibiotics do not block. — Antibiotics are chemicals that block processes occurring in bacteria but not in eukaryotic cells. A virus has no cell wall, no ribosomes and no metabolism of its own: it reproduces using the eukaryotic host cell's processes, which antibiotics leave untouched.
It is a zoonosis: SARS-CoV-2 is thought to have transferred to humans from another species recently, and it then spread widely between people. — COVID-19 is an infectious disease that has recently transferred from another species. Once in humans, SARS-CoV-2 spread from person to person by respiratory droplets, causing a pandemic with profound consequences for human health, societies and economies.
It is a zoonosis, which means that every case of COVID-19 was caught directly from an infected animal rather than from another person. — A student who thinks a zoonosis must come from an animal each time picks this. Zoonosis refers to the original transfer from another species; COVID-19 then spread between humans, which is what made it a pandemic.
It is not a zoonosis, because SARS-CoV-2 arose within the human population, and diseases only very rarely transfer from animals to humans. — A student who thinks zoonoses are rare picks this. Most newly emerging human infections are zoonoses, and SARS-CoV-2 is thought to have come from another species, most probably bats.
It is not a zoonosis, because it spreads from person to person by respiratory droplets rather than by animal bites or insect vectors. — A student who defines zoonoses by a bite or vector route picks this. A zoonosis is defined by transfer from another species, not by the route; the modes of infection are varied.
10 For measles, transmission in a population is greatly impeded once about 95% of people are immune. A community's vaccination coverage falls from 96% to 85%. Which statement correctly describes a consequence?
Answer and reasoning
The unvaccinated people remain immune too, because herd immunity continues to protect the whole population permanently once it has been reached. — A student who takes 'immunity' literally picks this. Unvaccinated people were never immune; they were shielded by the high immune fraction, and that shield weakens as coverage falls.
Only the people who chose not to be vaccinated are affected, because each person's vaccination status affects only their own risk of infection. — A student who sees vaccination as a purely personal choice picks this. Falling coverage also endangers infants and people who cannot be vaccinated, who depended on others to block transmission.
People who are not immune, including those who cannot be vaccinated, are at greater risk because chains of transmission are no longer broken. — Members of a population are interdependent in building herd immunity. If a sufficient percentage is immune, transmission is greatly impeded; below that level the virus can pass from case to case, and everyone who is susceptible, whatever the reason, is more likely to be exposed.
There is no consequence, because measles was eliminated from the community while coverage was above 95% and so cannot return. — A student who thinks herd immunity removes a pathogen for good picks this. Herd immunity only impedes transmission while the immune percentage stays high; measles can be reintroduced and spread once coverage falls.
Read the ones marked not yet in Learn, then Verify.
Verify confirm before you go
20 more questions. Every wrong answer here is a real misconception, and you see why it is wrong straight away.
1 In 1854 John Snow recorded the addresses of people who died of cholera in Soho, London, and found that the deaths clustered around one public water pump. The pump handle was removed and the outbreak subsided. At that time the germ theory of disease had not been established. What does this episode illustrate about how science makes progress?
Answer and reasoning
A disease can be controlled only once the microorganism that causes it has been identified in the laboratory. — A student who assumes explanation must precede action picks this. The pump handle was removed, and deaths fell, decades before a bacterium was generally accepted as the cause of cholera; the observed pattern alone justified the action.
Careful observation of a pattern in the data can lead to effective control of a disease before its cause is known. — Snow acted on the pattern of deaths, not on knowledge of the pathogen, and the control measure worked. Careful observation during the Vienna childbed fever and London cholera epidemics led to breakthroughs in the control of infectious disease decades before the bacteria responsible were generally recognized.
Once Snow's conclusion had been published, it was certain and did not need to be evaluated by other scientists. — A student who thinks publication settles a claim picks this. Snow's conclusion was contested for years and gained acceptance only as other evidence accumulated; publication starts evaluation rather than ending it.
Science progressed here by proving that every microorganism in the pump water was a pathogen that had to be removed. — A student who treats all microorganisms as pathogens picks this. The episode showed only that something in the pump water caused cholera; most microorganisms in water are harmless, and the progress lay in acting on the observed pattern, not in identifying any microorganism.
2 Which sequence correctly describes the events that seal a cut in the skin?
Answer and reasoning
Platelets release clotting factors; a cascade produces thrombin; thrombin converts fibrin to fibrinogen; fibrinogen then traps erythrocytes. — A student who believes fibrin is the form that circulates picks this reversed sequence. Fibrinogen is the soluble circulating protein; thrombin converts it to insoluble fibrin, which forms the mesh.
Platelets stick to each other and to the edges of the cut, forming a solid plug that is itself the clot; no plasma proteins are involved at all. — A student who has learned only that 'platelets help clotting' picks this. Platelets start the process by releasing clotting factors, but the clot is a mesh of fibrin, made from the plasma protein fibrinogen, trapping erythrocytes.
Blood at the cut is exposed to the air, which converts fibrinogen to fibrin; the fibrin mesh then traps the platelets and erythrocytes to seal the cut. — A student who thinks air triggers clotting picks this. The trigger is the release of clotting factors from platelets at the damaged site; clots form inside the body, with no air present, by the same cascade.
Platelets release clotting factors; a cascade produces thrombin; thrombin converts fibrinogen to fibrin; fibrin traps erythrocytes. — Clotting factors released from platelets start the cascade pathway, which results in rapid conversion of soluble fibrinogen to insoluble fibrin by thrombin. The fibrin mesh traps erythrocytes, forming the clot that seals the cut.
3 Fibrinogen circulates in the plasma of healthy people all the time, yet clots form only where a blood vessel has been damaged. Which statement best explains this?
Answer and reasoning
Thrombin, the enzyme that converts fibrinogen to fibrin, is produced by a cascade that starts only when platelets release clotting factors at a site of damage. — Fibrinogen is soluble and harmless while it circulates. Its conversion to insoluble fibrin requires thrombin, and thrombin is produced only at the end of the cascade pathway that the release of clotting factors from platelets initiates at the damaged site.
Fibrinogen is converted to fibrin only when it is exposed to the air at an open wound, so a clot cannot form inside a vessel that is intact. — A student who thinks air causes clotting picks this. Clots can and do form inside intact vessels when the cascade is triggered inappropriately; the trigger is damage and the release of clotting factors, not contact with air.
Fibrin is already present in the plasma, but its threads only become tangled into a mesh where the flow of blood is disturbed by damage. — A student who believes fibrin circulates ready-made picks this. The circulating protein is soluble fibrinogen; insoluble fibrin is produced only where thrombin has been generated by the cascade.
The cascade has so many steps that it is too slow to finish unless the blood is held still against the wall of a damaged vessel. — A student who reads 'cascade' as a delay picks this. The cascade amplifies the signal, which is why the conversion of fibrinogen to fibrin is rapid; its confinement to the wound is due to where the clotting factors are released.
4 A person is infected by the same strain of a virus twice, two years apart. The second time, the number of virus particles in the blood peaks at a much lower level and falls to zero in half the time. Which explanation is correct?
Answer and reasoning
Phagocytes of the innate immune system had learned to recognize this virus during the first infection, so they engulfed it faster the second time. — A student who credits the innate system with improvement picks this. The innate system does not change during an organism's life; phagocytes respond in the same way to a pathogen however often it is met.
Antibodies made during the first infection had stayed in the blood at their peak concentration for two years and destroyed the virus at once. — A student who equates immunity with persisting antibodies picks this. Antibodies are broken down over months, and the data show the virus still multiplied to a peak; what persists is memory cells, which produce a fresh and faster supply of antibody on re-exposure.
The adaptive immune system had retained a memory of the virus, so its specific response was faster and more effective the second time. — The adaptive system responds in a specific way to particular pathogens and builds up a memory of pathogens encountered, so the immune response becomes more effective. Memory cells from the first infection allowed antibody to be produced sooner and in greater quantity.
The phagocytes specific to this virus had multiplied during the first infection and were still present in large numbers. — A student who thinks phagocytes are specific picks this. Phagocytes respond to broad categories of pathogen and are not specific to one virus; the specific, multiplying, memory-forming cells are lymphocytes.
5 Which statement correctly describes how a phagocyte destroys a bacterium?
Answer and reasoning
It secretes enzymes from its lysosomes onto the bacterium, digesting it outside the cell, and then absorbs the soluble products. — A student who pictures the external digestion of fungi picks this. Phagocytes engulf the pathogen first; the lysosomal enzymes act inside a vesicle within the cell, not on the outside.
It lets the bacterium pass straight through its plasma membrane into the cytoplasm, where cytoplasmic enzymes break it down. — A student who thinks 'engulfing' means passing through the membrane picks this. Endocytosis encloses the bacterium in a membrane-bound vesicle; it never enters the cytoplasm freely, and the enzymes come from lysosomes.
It binds to the bacterium using a receptor specific to that strain and holds it until lymphocytes arrive to destroy it. — A student who thinks phagocytes are specific and only lymphocytes kill picks this. Phagocytes recognize broad categories of pathogen and destroy them themselves, by engulfing and digesting them.
It engulfs the bacterium by endocytosis and then digests it inside the cell, using the enzymes from its lysosomes. — Phagocytes recognize pathogens, engulf them by endocytosis so that the pathogen is enclosed in a vesicle, and digest them using enzymes from lysosomes that fuse with the vesicle.
6 A splinter carrying bacteria lodges in the connective tissue of a finger, some distance from the nearest capillary. Within hours the bacteria are being destroyed by phagocytes. Which statement describes how this happens?
Answer and reasoning
Phagocytes leave the capillary by amoeboid movement, crawl through the tissue to the bacteria, then engulf them by endocytosis and digest them. — Infection control by phagocytes includes amoeboid movement from blood to sites of infection, where the phagocytes recognize pathogens, engulf them by endocytosis and digest them using enzymes from lysosomes.
Phagocytes remain inside the capillary; tissue fluid carries the bacteria into the blood, where the phagocytes engulf and digest them. — A student who thinks 'white blood cells' stay in the blood picks this. Phagocytes move out of capillaries by amoeboid movement and go to the site of infection; the bacteria are destroyed in the tissue.
Phagocytes in the capillary secrete lysosomal enzymes into the tissue fluid, which diffuse to the splinter and digest the bacteria there. — A student who imagines external digestion picks this. Phagocytes do not release their enzymes into the tissue; they engulf the bacteria and digest them inside a vesicle using enzymes from lysosomes.
Only the few phagocytes that carry a receptor specific to this strain of bacterium respond to it; the rest ignore the infection. — A student who has transferred lymphocyte specificity to phagocytes picks this. Phagocytes belong to the innate system and respond to broad categories of pathogen, so any phagocyte reaching the splinter can engulf the bacteria.
Antigens are proteins made by lymphocytes that bind to pathogens and mark them for destruction by the phagocytes. — A student who has swapped the two 'anti-' words picks this. The molecules made by lymphocytes that bind to pathogens are antibodies; antigens are the molecules on the pathogen that they bind to.
Antigens are toxins released by a pathogen into the blood, and it is these toxins that the antibodies must neutralize. — A student who merges antigens with toxins picks this. An antigen is a molecule on the surface of the pathogen that is recognized as foreign; a pathogen has antigens whether or not it produces toxins.
Most antigens are glycoproteins or other proteins, usually located on the outer surface of a pathogen. — Antigens are recognition molecules that trigger antibody production. Most are glycoproteins or other proteins, and they are usually located on the outer surfaces of pathogens, where they can be recognized by the immune system.
Antigens are found only on pathogens; molecules on the surface of human cells do not act as antigens. — A student who defines antigens by their source picks this. Antigens on the surface of human erythrocytes stimulate antibody production if transfused into a person with a different blood group.
8 A patient of blood group A is mistakenly transfused with erythrocytes from a donor of blood group B. Which statement explains why the patient's immune system responds to the transfused cells?
Answer and reasoning
Human cells carry no antigens of their own; the response is to bacteria that contaminated the donated blood while it was being collected. — A student who thinks only pathogens have antigens picks this. Erythrocytes carry surface glycoproteins that differ between blood groups, and these act as antigens in a recipient of a different group.
Antigens made by the patient's immune system attack the donor erythrocytes, and this attack is what is meant by the patient responding to the transfusion. — A student who has swapped antigen and antibody picks this. The attacking molecules made by the patient are antibodies; the antigens are the surface glycoproteins on the donor erythrocytes that are recognized as foreign.
The donor erythrocytes release toxins into the patient's plasma, and it is these toxins that act as the antigens stimulating antibodies. — A student who equates antigens with toxins picks this. Erythrocytes release no toxins; the antigens are glycoproteins fixed on the surface of the transfused cells.
The B antigens on the surface of the donor erythrocytes are foreign to the patient, so they stimulate antibody production. — Antigens on the surface of erythrocytes may stimulate antibody production if transfused into a person with a different blood group. The group B erythrocytes carry a surface antigen that the group A patient's immune system recognizes as foreign.
9 In an experiment, B-lymphocytes specific to an antigen were cultured with that antigen and no other cells. No antibody was produced. When helper T-lymphocytes were added to the culture, antibody production began. What does this show?
Answer and reasoning
A B-lymphocyte is activated to produce antibodies only when it both binds its specific antigen and makes contact with a helper T-lymphocyte. — B-cells produce antibodies only when they have been activated, and activation requires both direct interaction with the specific antigen and contact with a helper T-cell. Antigen alone was not sufficient; adding the helper T-cells supplied the missing requirement.
Binding of the antigen alone should have activated the B-lymphocytes, so the first culture must have been set up incorrectly. — A student who holds the one-step story picks this. The first culture behaved as expected: antigen binding is necessary but not sufficient, and without helper T-cell contact no activation occurs.
The antibody in the second culture was secreted by the helper T-lymphocytes, which make antibody when they meet an antigen. — A student who thinks T-cells make antibodies picks this. Helper T-cells secrete no antibody; their role is to activate the B-cells, which then produce it.
The helper T-lymphocytes showed the B-lymphocytes the shape of the antigen so that they could then design an antibody to fit it. — A student who imagines antibodies being designed picks this. The B-cells in the culture already made an antibody that fitted the antigen; what they lacked was activation by a helper T-cell.
10 After a person is exposed to a new pathogen for the first time, several days pass before antibodies against it can be detected in the blood. Which statement best explains this delay?
Answer and reasoning
A single activated B-cell can make all of the antibody required, but several days are needed for one cell to synthesize and secrete that much protein. — A student unaware of how few B-cells match any antigen picks this. One cell cannot supply enough antibody; the delay is the time taken for the activated B-cells to multiply into a clone of plasma cells.
The activated B-cells must first divide to produce plasma cells that make a range of different antibodies, and it takes days to make a set that fits the pathogen. — A student who expects variety from a clone picks this. Mitosis produces genetically identical plasma cells that all make the same antibody, the one that fitted the antigen; the delay is multiplication, not variety.
Few B-cells are specific to the antigen; after activation they must divide by mitosis to form a clone of plasma cells before enough antibody is made. — There are relatively small numbers of B-cells that respond to a specific antigen. To produce sufficient quantities of antibody, activated B-cells first divide by mitosis to produce large numbers of plasma cells capable of producing the same type of antibody, and this multiplication takes days.
The B-cells need several days to study the antigen and modify their antibody genes until the antibody they make fits the antigen's shape. — A student who thinks antibodies are designed to order picks this. The B-cells that respond already make an antibody that fits; the antigen selects them, and the delay is the time needed to produce a clone of plasma cells.
11 A person with untreated HIV infection eventually becomes unable to produce antibodies against new pathogens, even though tests show that B-lymphocytes are still present in their blood in substantial numbers. Which statement explains this?
Answer and reasoning
HIV infects and kills the B-lymphocytes that make the antibodies, so the cells that are needed for antibody production are no longer present in the blood. — A student who reasons backwards from the lost antibodies to the cell that makes them picks this. The stem states that B-cells are still present in substantial numbers; it is the helper T-cells that HIV destroys.
HIV infects and kills helper T-lymphocytes, and without contact with an activated helper T-cell a B-lymphocyte cannot be activated to make antibodies. — Only certain types of lymphocyte are infected and killed by HIV, principally helper T-cells. Because B-cell activation requires contact with an activated helper T-cell, the reduction in helper T-cells limits the ability to produce antibodies even though the B-cells themselves survive.
Antibodies are secreted by the helper T-lymphocytes, so when HIV destroys these cells the production of all antibodies stops. — A student who thinks T-cells make antibodies picks this. Helper T-cells produce no antibody; they activate the B-cells, and it is the loss of that activation that stops antibody production.
HIV infects and destroys all types of white blood cell, so every part of the immune system, including antibody production, fails at once. — A student who pictures the whole immune system being wiped out picks this. HIV infects only certain lymphocytes; the B-cells in the stem are present but cannot be activated.
12 Two people infected with HIV were compared. Person X had 900 helper T-lymphocytes per mm³ of blood and no other infections. Person Y had 150 helper T-lymphocytes per mm³ and had developed pneumonia caused by a fungus that rarely causes disease in healthy people. Which conclusion is best supported?
Answer and reasoning
The pneumonia in person Y is caused directly by HIV, which has spread from the blood into the lungs as the infection has progressed. — A student who treats AIDS as a single disease caused by HIV picks this. The stem states that the pneumonia is caused by a fungus; it is an opportunistic infection that the weakened immune system cannot eliminate.
Person Y's B-lymphocytes have all been destroyed by HIV, which is why antibodies against the fungus have not been produced. — A student who assumes the antibody-producing cell must be the target picks this. The data are about helper T-cells, which HIV kills; B-cells survive but cannot be activated without them.
Person Y's loss of helper T-lymphocytes has limited antibody production and defence against infection, so an opportunistic infection has taken hold. — HIV kills helper T-cells, and a reduction in these lymphocytes limits the ability to produce antibodies and fight opportunistic infections. Person Y's low count and a fungal pneumonia that healthy people resist together indicate that AIDS has developed.
Person X cannot really be infected with HIV, because HIV and AIDS are the same condition and person X shows no symptoms of any disease. — A student who equates HIV with AIDS picks this. A person can carry HIV for years with a helper T-cell count high enough to prevent opportunistic infections; AIDS develops only when the count has fallen far.
13 Penicillin blocks the enzymes that build cross-links in the peptidoglycan cell wall of bacteria. A patient takes penicillin for a bacterial infection. Why does the drug kill the bacteria without harming the patient's own cells?
Answer and reasoning
Human cells have no cell wall and do not synthesize peptidoglycan, so the process that penicillin blocks does not occur in the patient's cells at all. — Antibiotics are chemicals that block processes occurring in bacteria but not in eukaryotic cells. Peptidoglycan cell wall synthesis is one such process: bacteria depend on it, eukaryotic cells do not carry it out, so penicillin is selective.
Penicillin does damage the patient's cells in the same way, but the patient has so many more cells that the loss is not noticeable. — A student who assumes any cell-killing drug is indiscriminate picks this. Penicillin's target does not exist in human cells, so it does not damage them; selectivity, not cell numbers, is the explanation.
Penicillin cannot reach the inside of human cells, so it only acts on bacteria, which live outside cells in the blood and tissues. — A student who explains antibiotic selectivity by where the drug can reach picks this. Selectivity is biochemical: human cells lack peptidoglycan and the enzymes that build it, so there is no target for penicillin whether or not the drug enters them.
The patient's cells have evolved resistance to penicillin, because humans have now been exposed to the drug for several generations. — A student who thinks resistance is a property of people picks this. Resistance evolves in bacterial populations under selection; human cells were never affected by penicillin, so there was nothing to become resistant to.
14 A hospital ward uses one particular antibiotic heavily. Over several years, an increasing proportion of the bacteria isolated from patients on the ward are found to be resistant to it. Which statement correctly explains this change?
Answer and reasoning
Repeated exposure to the antibiotic caused individual bacteria to develop resistance during their own lifetimes, and they passed on this acquired trait to their offspring. — A student who thinks resistance is a response to exposure picks this. The antibiotic does not cause resistance in an individual bacterium; it selects for bacteria that already carry a resistance mutation.
Random mutations had given a few bacteria resistance; the antibiotic killed the susceptible ones, so resistant bacteria survived, reproduced and became more common. — Resistance evolves by natural selection. Variation from random mutation (or acquired genes) exists before exposure; heavy use of the antibiotic removes the susceptible bacteria and leaves the resistant ones to reproduce, so the resistant proportion rises over time.
The patients on the ward gradually became resistant to the antibiotic, so it stopped working against the bacteria that were infecting them. — A student who locates resistance in the patient picks this. Resistance is a heritable property of the bacterial strain, which is why it is detected in bacteria isolated from patients.
The bacteria became resistant to every antibiotic at the same time, because a single mutation makes a bacterium generally tougher against all drugs. — A student who pictures a 'superbug' as generally hardier picks this. Resistance is specific to the process each antibiotic blocks; resistance to several drugs requires several separate genes or mutations.
15 Researchers screened a chemical library of thousands of compounds using a computer model trained to predict antibacterial activity. They identified a compound, structurally unlike any existing antibiotic, that killed several multiresistant strains of bacteria in the laboratory. Which statement is the best evaluation of this work?
Answer and reasoning
Because the compound kills multiresistant strains, bacteria will not be able to evolve resistance to it, since they have not previously encountered it. — A student who thinks resistance is a reaction to a drug's history picks this. Resistance arises by random mutation and selection; a new antibiotic will select for resistant variants just as older ones did.
Because the results have been published, the compound can be regarded as a proven antibiotic that is ready to be given to patients. — A student who thinks publication settles a claim picks this. Publication allows other scientists to evaluate the work; a laboratory result must survive further testing, including trials in humans, before use.
A new technique has opened a new avenue of research; the compound still needs testing, and careful use of antibiotics is still necessary. — The NOS point is that the development of new techniques, such as searching chemical libraries, can lead to new avenues of research and is yielding new antibiotics. A laboratory hit is a candidate, not a medicine, and any antibiotic will select for resistance if used carelessly.
Because new antibiotics can now be found by searching chemical libraries, there is no longer any need to limit the use of the existing antibiotics. — A student who sees discovery as the whole solution picks this. Every antibiotic in use selects for resistance, so careful use is still necessary to slow the emergence of multiresistant bacteria.
16 A farm worker develops tuberculosis after drinking unpasteurized milk from a cow infected with the bacterium Mycobacterium bovis. Which statement about this infection is correct?
Answer and reasoning
It is not a zoonosis, because zoonoses are transmitted only by animal bites or by insect vectors, not in food. — A student who generalizes from rabies and mosquito-borne diseases picks this. The modes of infection of zoonoses are varied; transfer in milk from an infected cow qualifies just as a bite does.
It is not a zoonosis, because tuberculosis is a human disease that only occasionally infects cattle and other animals. — A student who assumes familiar diseases are purely human picks this. Mycobacterium bovis is a pathogen of cattle that transfers to humans, which is exactly what makes bovine tuberculosis a zoonosis.
It cannot be a zoonosis, because only viruses can cross from one species to another; bacteria stay in one host. — A student whose zoonosis examples are all viral picks this. Bacteria such as Mycobacterium bovis transfer between species too; zoonoses include bacterial as well as viral pathogens.
It is a zoonosis, because the pathogen has transferred from another species of animal to a human. — A zoonosis is an infectious disease that can transfer from other species to humans. Tuberculosis is one of the examples the IB names: Mycobacterium bovis infects cattle and can be transmitted to people in unpasteurized milk.
17 An mRNA vaccine against COVID-19 contains RNA with the sequence coding for the spike protein of SARS-CoV-2, packaged in lipid nanoparticles. Which statement correctly explains how it stimulates immunity?
Answer and reasoning
The RNA is translated into antibodies against the spike protein, which then circulate in the blood ready to bind to the virus. — A student who thinks vaccines supply antibodies picks this. The RNA codes for the antigen, not for antibodies; the person's own B-lymphocytes make the antibodies in response to it.
Cells translate the RNA into spike protein, an antigen that stimulates the adaptive immune system to form memory cells without causing disease. — Vaccines contain antigens, or nucleic acids with sequences that code for antigens, and stimulate the development of immunity to a specific pathogen without causing the disease. The person's cells make the spike protein, and the adaptive response to it leaves memory cells.
The RNA produces a weakened form of the whole virus inside the person's cells, giving a mild case of COVID-19 that generates immunity. — A student who thinks a vaccine is a mild dose of the disease picks this. The RNA codes for one protein only; no virus is assembled and the disease does not occur.
The RNA is copied into the DNA of the person's chromosomes, so that their cells will permanently carry and express the gene for the viral antigen. — A student who blurs RNA and DNA picks this. The mRNA is translated in the cytoplasm and then degraded; it does not enter the nucleus or alter the person's genome, and antigen production is temporary.
18 A news article reports a newly published study claiming that a vaccine causes a rare side effect, before other scientists have evaluated the study. Which response shows the best understanding of how science works?
Answer and reasoning
Accept the claim as established, because a study that has been published in a scientific journal has been proven to be correct. — A student who thinks publication is proof picks this. Publication begins evaluation by other scientists; a published claim is provisional until it has survived that scrutiny.
Conclude that the vaccine is unsafe, because a vaccine that is genuinely safe would carry no risk of side effects of any kind. — A student who treats safety as an absolute picks this. Risks of side effects are minimal but not nil; a rare side effect does not make a vaccine unsafe if the benefit greatly outweighs it.
Dismiss the claim without reading it, because vaccines are tested so rigorously that a side effect of any kind is impossible. — A student who confuses well-supported with certain picks this. Rigorous testing makes side effects very unlikely, not impossible; science offers pragmatic truths, and new evidence should be evaluated.
Treat the claim as provisional until other scientists have evaluated the study; vaccine risks are minimal but not nil. — Scientists publish so that others can evaluate their work, and the media often report while evaluation is still happening. Vaccines are tested rigorously and side effects are minimal but not nil, so a new claim deserves evaluation rather than immediate acceptance or dismissal.
19 In a country, the number of new COVID-19 cases recorded per day fell from 2000 in one week to 1600 in the following week. What is the percentage change in the daily number of cases?
Answer and reasoning
Fell by 20% — Percentage change = (final − initial) ÷ initial × 100 = (1600 − 2000) ÷ 2000 × 100 = −400 ÷ 2000 × 100 = −20%, a fall of 20%.
Fell by 25% — A student who divides the change by the final value picks this: 400 ÷ 1600 × 100 = 25%. Percentage change is measured relative to the initial value, 2000.
Fell by 22% — A student who applies the percentage difference formula picks this: 400 ÷ 1800 × 100 = 22%. Percentage difference uses the mean of the two values and is for comparing two groups; a change over time uses the initial value as the reference.
Fell by 80% — A student who divides the new value by the old value picks this: 1600 ÷ 2000 × 100 = 80% is the new figure as a percentage of the old one. The change is 80% − 100% = −20%.
20 In one week, region P recorded 640 COVID-19 hospital admissions per million people and region Q recorded 960 per million. Taking the mean of the two rates as the reference value, what is the percentage difference between the two regions' admission rates, to the nearest whole number?
Answer and reasoning
50% — A student who divides the difference by one of the values, as in a percentage change, picks this: 320 ÷ 640 × 100 = 50%. Neither region is the 'original', and the stem sets the mean, 800, as the reference.
40% — Percentage difference = difference ÷ mean × 100. The difference is 960 − 640 = 320 and the mean is (640 + 960) ÷ 2 = 800, so 320 ÷ 800 × 100 = 40%.
33% — A student who divides by the larger value picks this: 320 ÷ 960 × 100 = 33%. Percentage difference is symmetrical because it uses the mean of the two values, not either value alone.
20% — A student who divides by the sum of the two values picks this: 320 ÷ 1600 × 100 = 20%. The denominator is the mean, (640 + 960) ÷ 2 = 800, so the answer is twice this.
That was your twenty minutes. Real practice on C3.2 is past-paper questions marked against the mark scheme.
What the exam asks of C3.2
Paper 1A asks you to classify pathogens, recognise innate versus adaptive features, and identify steps in clotting or antibody production. Paper 1B gives COVID-19 or vaccination data and asks for percentage change or percentage difference, then interpretation. Paper 2 uses *outline*, *describe* and *explain*: explain how a B-cell is activated and produces antibody, explain antibiotic resistance as natural selection, discuss herd immunity. Expect *evaluate* on vaccine evidence: state what the data show and what remains uncertain.
Compiled from the IB Biology guide (first assessment 2025, updated May 2026 for 2028) and our question bank · Specialist review in progress. How these pages are made ·
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