IB Biology C3.2: Defence against disease worked solutions

A pathogen is the agent that causes an infectious disease, and it can be a virus, bacterium, fungus or protist (A). B describes an antigen, C describes the disease and D is wrong because many bacteria in the body are harmless.

Only the adaptive system builds a memory, so a later response is faster (B). Phagocytes, mucus and platelets are all innate, non-specific defences (A, C, D).

Sticky mucus traps pathogens and cilia sweep the mucus away (B). Antibody secretion, phagocytosis and clotting belong to the cellular defences inside the body, not to the barriers (A, C, D).

The phagocyte engulfs the bacterium by endocytosis into a vesicle, and lysosomes then release enzymes into the vesicle (A). B reverses the order, C has no diffusion or division, and D gives the phagocyte the job of a plasma cell.

The cascade activates the enzyme thrombin from inactive prothrombin, and thrombin turns soluble fibrinogen into insoluble fibrin (A). The other options reverse substrate and product.

An antibody has binding sites that fit one antigen shape only (A). They are not general (B), they are proteins made by plasma cells (C, D).

A helper T-cell activated by the same antigen makes contact with the B-cell and activates it (C). Plasma cells and memory cells are products of the activated B-cell, and the phagocyte is not the activator of the B-cell.

Antibiotics block processes that occur in bacteria, but a virus has no metabolism and uses the host cell, so there is nothing to block (B). Size, mutation rate and stimulating antibodies are not the reason (A, C, D).

A zoonosis passes from another animal to humans, as rabies does from a dog bite (B). The other three pass from person to person.

When enough of the population is immune, the pathogen cannot keep passing from person to person, so it seldom reaches the people who are not immune (B). Antibody is not transferred by the vaccine of others (A, C) and immune people do not destroy pathogens on their skin (D).

(a) Any three: platelets at the cut release clotting factors (1); a cascade converts inactive prothrombin to thrombin (1); thrombin converts soluble fibrinogen to insoluble fibrin (1); fibrin forms a mesh that traps red cells and platelets (1). (b) Without the factor the cascade fails and no clot forms (1), so bleeding continues and the open wound lets pathogens enter (1).

(a) Day 14 (1). (b) The peak after the first dose is 20 and after the second is 150 (1); 150/20=7.5 times (1). (c) The first dose produced memory cells that persist (1); on the second dose they are activated and divide quickly into many plasma cells (1); so more antibody appears sooner (3 units at 7 days after the first dose but 150 at 7 days after the second) (1).

(a) Any two: blood (1); semen (1); vaginal fluid (1); breast milk (1). (b) HIV infects and destroys helper T-cells, so their number falls (1); fewer B-cells are activated, so fewer plasma cells form (1); little antibody is made, so the person cannot control the pneumonia, which is an opportunistic infection typical of AIDS (1).

(a) The fragment acts as an antigen that triggers B-cells and helper T-cells, so antibody is made and memory cells form (1); it is not a whole living bacterium, so it cannot cause the disease (1). (b) The second dose meets the memory cells made by the first dose (1), so more memory cells and plasma cells form and protection is greater (1).

(a) 8/400\times100=2\% and 72/400\times100=18\% (1); 18-2=16 percentage points (1). (b) Some bacteria already carry a resistance gene from a random mutation (1); the antibiotic kills the susceptible bacteria and the resistant ones survive (1); the survivors divide and pass the gene on, so the resistant proportion rises (1). (c) Any one: use antibiotics only for bacterial infections; complete the full course; avoid unnecessary prescriptions (1).

(a) A helper T-cell activated by the antigen contacts a B-cell that has bound the same antigen (1); the activated B-cell divides by mitosis to form a clone (1); the clone includes plasma cells that secrete the specific antibody (1); some cells become memory cells (1). (b) Memory cells persist for a long time (1); on a second meeting with the antigen they respond quickly and strongly, so the bacterium is destroyed before disease develops (1).

(a) Q and R, because each passes from an animal to people (1). (b) Q is carried by mosquitoes that bite people (1); R is taken in with unpasteurised milk (1). (c) Heat-treat (pasteurise) the milk (1).

(a) 15\,000/20\,000\times100=75\% (1). (b) An immune person cannot pass the pathogen on, so the chain of transmission is broken (1); an infected person rarely meets a susceptible person, so the outbreak dies out (1). (c) Six in ten people are not immune (1), so an infected person meets many susceptible people and the disease keeps spreading (1).

(a) (2000-1250)/1250\times100=+60\% (1 for the method, 1 for the value with its sign). (b) The mean of the totals is (38\,000+24\,000)/2=31\,000 and the difference is 14\,000 (1); 14\,000/31\,000\times100\approx45\% (1). (c) A percentage scales the change to the size of the population, so a large and a small region can be compared fairly (1).

(a) Day 5 (1). (b) (98-17)/98\times100=82.7\approx83\% decrease (1 for the method, 1 for the value). (c) Any two: masks reduced transmission (1); infected people isolated (1); many people became immune, so fewer susceptible people remained (1). (d) The fall begins the day after the rule, which fits the claim (1); but the rise had already slowed and the data show an association in time only, with no control town without the rule (1); herd immunity and isolation could produce the same pattern, so the data cannot show that masks caused the fall (1).

(a) 153/180\times100=85\% (1); 70/175\times100=40\% (1). (b) 85-40=45 percentage points (1). (c) The placebo group shows how many recover without the drug, so the effect of X can be separated (1); it controls for the effect of patients believing they have been treated (1). (d) The cure rate is much higher with X and the groups are fairly large (1); but the data do not say how patients were allocated, how severe the infections were or whether X had side effects (1); only one infection and one 7-day period were tested, so use for all patients is not yet justified (1).

(a) 40/20\,000\times100=0.2\% (1); 160/20\,000\times100=0.8\% (1). (b) (0.8-0.2)/0.8\times100=75\% (1 for the method, 1 for the value). (c) Any two: a placebo control group (1); large groups of the same size (1); the same follow-up period for both groups (1). (d) Any two: follow-up was only three months, so long-term protection is unknown (1); only adults took part (1); the data do not show whether the disease was less severe, or whether side effects occurred (1).

(a) Any six: platelets release clotting factors and thrombin converts fibrinogen to fibrin, so a clot seals the cut (1); phagocytes engulf bacteria by endocytosis (1) and lysosome enzymes digest them (1); a helper T-cell activates a B-cell that has bound the bacterial antigen (1); the B-cell divides by mitosis to form a clone (1); plasma cells secrete the specific antibody, which marks the bacteria for phagocytes (1); memory cells persist and give faster protection if the bacterium returns (1).

(a) As prescriptions rise from 300 to 900, the percentage of resistant samples rises from 8 to 36 (1). (b) Heavier antibiotic use kills susceptible bacteria and the resistant ones survive (1); they divide and pass on the gene, so the resistant share of the population rises (1). (c) The data show a positive association (1); only three countries are compared and other factors such as hygiene, sampling methods or use in farming are not controlled (1); a correlation does not prove a cause, though the mechanism of selection makes the link plausible (1).

(a) (900-140)/900\times100=84.4\approx84\% decrease (1 for the method, 1 for the value). (b) HIV destroys helper T-cells, and by year 8 few remain (1); fewer B-cells are activated by helper T-cells, so fewer plasma cells form (1); less antibody is secreted against the new infection (1). (c) The count falls from 320 to 140 between year 6 and year 8, crossing 200 (1).

(a) Any two: it has no metabolism of its own (1); it has no cell wall to block (1); it makes its proteins on host ribosomes, so there is no bacterial process to inhibit (1). (b) Ribosomes in the person's cells translate the mRNA into the viral surface protein (1); the protein acts as an antigen that activates helper T-cells and B-cells (1); the B-cells divide and some of the clone become memory cells (1). (c) A mutation changes the base sequence and so the amino acid sequence of the surface protein (1); the shape of the antigen changes, so antibodies and memory cells made against the old shape no longer fit (1); the virus can infect cells without being bound, so protection falls (1).

(a) (0.14-0.02)/0.02\times100=600\% (1 for the method, 1 for the value). (b) The population varied because a mutation produced the resistance allele (1); the antibiotic acted as the selection pressure, so resistant bacteria survived and reproduced more (1); they passed the allele to their offspring, so its frequency in the population rose (1). (c) Bacteria divide in minutes, so there are many generations in a short time (1); they reproduce by binary fission, so each survivor founds a resistant clone (1); resistance genes can also pass between bacteria, which insects do not do (1).

(a) The order of amino acids (primary structure) decides how the polypeptide folds (1); the folded shape forms a binding site that fits one antigen shape (1). (b) Ribosomes on rough ER make the antibody protein in large amounts (1); the Golgi apparatus processes it and packs it in vesicles (1); the vesicles fuse with the plasma membrane and release the antibody by exocytosis (1). (c) The clone arises by mitosis from one activated B-cell (1), so every cell has identical genes, including the gene for the same antibody (1); each cell therefore makes the antibody that fits the same antigen (1).

(a) The membrane has to bend round the bacterium and pinch off a vesicle (1); phospholipids can move sideways in the fluid bilayer, so it can change shape (1); the vesicle membrane can later fuse with the lysosome membrane (1). (b) Digestive enzymes break down proteins and other molecules, so free in the cytoplasm they would digest the cell itself (1); a lysosome keeps them enclosed until a vesicle with a target joins it (1). (c) Oxygen is small and non-polar and crosses by simple diffusion, down its concentration gradient, directly through the bilayer (1); a whole bacterium is far too large, so it is enclosed in a vesicle by endocytosis (1), which uses energy and changes the shape of the membrane (1).