Pearson Edexcel International A Level Biology: Adaptive Immunity and Antibiotics (YBI11) – Revision Notes

These are condensed notes for statements 6.10 to 6.15 of the Pearson Edexcel International Advanced Subsidiary/Advanced Level Biology specification (YBI11), Issue 2, including Core Practical 14. Topic 6 belongs to International A2 (IA2); Topics 1 to 4 are International AS (IAS). There are no tiers. Read the study guide for full explanations and use the practice questions to test yourself. The course hub, printable checklist and free diagnostics cover the rest of the course.

6.10 Lymphocytes at a glance

Cell	Made from	Key job	Remember
B effector (mostly plasma cells)	Selected B cell	Secrete antibody	Lots of rough ER; one antibody type
B memory	Selected B cell	Wait; divide on second exposure	Long-lived; no antibody now
T helper	Selected T cell	Release cytokines	Activates B cells, T killer cells and phagocytes
T killer	Activated T cell	Destroy infected or abnormal cells	Needs direct contact; perforin damages the membrane
T memory	Selected T cell	Make T helper and T killer cells fast	Long-lived

Sequence in steps

1. Antigen-presenting cell shows the antigen.
2. Matching T helper cell binds (clonal selection) and divides (clonal expansion).
3. T helper releases cytokines.
4. B cell with matching receptor divides, forming plasma cells and B memory cells.
5. T killer cells are activated and attack infected cells.
6. Memory cells remain.

Humoral means antibodies in body fluids (B cells). Cell-mediated means whole cells doing the killing (T cells).

Primary against secondary response

	Primary	Secondary
Lag before antibody appears	Long	Short
Peak antibody	Low	Much higher
Cause	Few matching cells to find and clone	Many memory cells already selected
Symptoms	Often	Rarely

Small reminder. If a primary peak is 6 AU and a secondary is 90 AU, the secondary is 90 / 6 = 15 times higher.

6.11 Four types of immunity

	Active (own antibodies, memory cells)	Passive (antibodies given)
Natural	Catching and recovering from an infection	Placenta (fetus); breast milk
Artificial	Vaccination	Injected antibodies (antivenom, tetanus immunoglobulin)

Must-know distinctions

• Active: slow, long-lasting, memory cells present.
• Passive: immediate, short-lived, no memory cells, antibodies are broken down.
• Vaccine: antigen without disease. Booster: second dose giving a secondary response.
• Use passive treatment when protection is needed straight away, such as after a snake bite or an infected wound.

6.12 Evolutionary race: evasion mechanisms

Chain of reasoning: a pathogen variant escapes a defence, so it survives and reproduces, so its alleles spread, so the defence becomes less effective, so hosts with better responses survive, and the cycle repeats.

Mechanism	Example	Why it works
Antigenic variation	Influenza virus	Memory cells do not recognise the changed antigen
Destroying T helper cells	HIV	Loss of coordination of B and T cells
Surviving inside macrophages	Mycobacterium tuberculosis	Avoids digestion
Latency	Viruses in a dormant state	Few antigens shown
Capsule	Some bacteria	Antigens covered, so phagocytes bind less well
Antibiotic resistance	MRSA	Selection by antibiotic use

When you answer, state the example, the mechanism and the effect on the immune response (three linked points).

6.13 Antibiotics

	Bacteriostatic	Bactericidal
Effect	Stops growth and reproduction	Kills bacteria
Example	Tetracycline (blocks bacterial protein synthesis)	Penicillin (stops cell wall formation, causing lysis)
Viable count	Stays level	Falls
Needs immune system?	Yes, to clear bacteria	Less dependent

• Antibiotics target bacterial features: cell wall, ribosomes. They do not act on viruses.
• Resistance: random mutation, then selection by antibiotic, then spread of the allele to offspring and other bacteria by plasmids.
• Turbidity includes dead cells, so only viable counts show killing.

6.14 Core Practical 14 in steps

1. Disinfect bench; wash hands.
2. Spread a standard volume of safe, non-pathogenic bacteria on sterile nutrient agar to make a lawn.
3. Place different antibiotic discs with sterile forceps, plus a control disc in sterile water.
4. Tape the lid in two places only; invert; incubate (for example 25 °C, 24 to 48 hours).
5. Measure the diameter of each clear zone; repeat.
6. Autoclave or disinfect everything.

Item	Detail
Independent variable	Type of antibiotic
Dependent variable	Diameter or area of clear zone
Controlled	Bacterial density, agar depth, disc size, concentration, temperature, time
Why invert?	Condensation drips onto the lid, not onto the agar
Why not seal fully?	To avoid anaerobic conditions in which harmful bacteria might grow
Zone area	π r² with r = half of the diameter

Small reminder. Zone diameter 18 mm: r = 9 mm; area = π × 9² = 254 mm² (to 3 significant figures). Subtract the disc area if you want the clear area only; a 6 mm disc has area π × 3² = 28.3 mm², so 254 − 28.3 = 226 mm².

Evaluation points. Larger zone means more inhibition, but molecule size affects diffusion; the zone does not show bacteriostatic or bactericidal action; repeats allow a mean.

6.15 Hospital-acquired infections

Contributory cause	Practice that follows
Hands carry bacteria	Hand washing, alcohol gel, bare below the elbow
Vulnerable patients	Isolation, screening, cleaning
Devices and wounds	Aseptic technique; remove devices early
Overuse of antibiotics	Prescribe only when needed; test sensitivity; narrow-spectrum choice where possible; reserve certain antibiotics; audit

Infection rate = infections / patient-days × 1000. Percentage change = (new − old) / old × 100.

Worked reminders

Classify from counts. A culture begins at 2.0 × 10⁶ viable cells per cm³. After 8 hours, antibiotic X gives 2.1 × 10⁶ and antibiotic Y gives 4.0 × 10³.

X: (2.1 - 2.0) / 2.0 x 100 = +5 %, so growth has stopped: bacteriostatic
Y: (4.0 x 10^3 - 2.0 x 10^6) / 2.0 x 10^6 x 100 = -99.8 %: bactericidal

Compare antibiotics from zones. Mean zone diameters (disc 6 mm): antibiotic S 20 mm and antibiotic V 15 mm.

Area S = pi x 10^2   = 314 mm2
Area V = pi x 7.5^2  = 177 mm2
Clear area beyond the disc: S = 286 mm2, V = 148 mm2
S / V = 286 / 148 = 1.9 times

Notice that the diameters differ by a factor of 1.33 but the areas by 1.9. This is because area depends on the square of the radius.

Rate in a hospital. 48 infections in 16 000 patient-days is 3.0 per 1000 patient-days. After new rules, 27 infections in 15 000 patient-days is 1.8 per 1000. The fall is (3.0 − 1.8) / 3.0 × 100 = 40 %.

More must-know distinctions

Pair	Difference
Antibody and cytokine	Antibodies are proteins made by plasma cells that bind antigens. Cytokines are signalling molecules released by T helper cells (and other cells) that stimulate other immune cells
T helper and T killer	T helper coordinates by signalling. T killer destroys the infected cell directly
Clonal selection and clonal expansion	Selection picks the lymphocyte with the matching receptor. Expansion is its division by mitosis into a clone
Vaccination and antibody injection	Vaccination gives antigen, so you make antibodies and memory cells. Antibody injection gives ready-made antibodies
Resistance and tolerance	Resistance is a property of bacteria that survive antibiotics. It is not a change in the patient
Lytic and latent viruses	A lytic virus makes new virions and bursts the cell. A latent virus stays dormant in the host cell, showing few antigens

Short model answers

Explain why the second response to a vaccine is faster. B memory cells were made in the first response [1]. They are already selected for the antigen and are more numerous than the original matching cells [1]. They divide and form plasma cells quickly [1], so antibody appears sooner and reaches a higher level [1].

Explain how resistance spreads in a population of bacteria. A mutation gives a resistant allele [1]. Sensitive bacteria are killed by the antibiotic, leaving resistant individuals to reproduce with less competition [1]. Offspring inherit the allele, and plasmids can carry it into other bacteria [1].

Quick self-test

1. Name the cell type that releases cytokines to activate B cells and T killer cells.
2. Which B cell stays in the body, without secreting antibody, to respond later?
3. Classify the immunity of a baby given antibodies in breast milk.
4. Why does passive immunity not last?
5. Antibody titre rises from 4 AU to 60 AU in 8 days. Calculate the mean rate of increase.
6. By what factor does a titre of 60 AU exceed one of 4 AU?
7. State one feature of influenza that allows evasion of memory cells.
8. Give the difference between bacteriostatic and bactericidal antibiotics.
9. A clear zone has diameter 15 mm. Calculate the zone area in mm² to 3 significant figures.
10. A ward falls from 45 infections to 27. Calculate the percentage reduction.
11. Give one way that antibiotic prescription is controlled to slow resistance.

Answers

1. T helper cell.
2. B memory cell.
3. Natural passive.
4. No memory cells are formed and the antibodies are broken down.
5. (60 − 4) / 8 = 7 AU per day.
6. 60 / 4 = 15 times.
7. Surface antigens change by mutation (antigenic variation).
8. Bacteriostatic stops growth; bactericidal kills.
9. π × 7.5² = 177 mm².
10. (45 − 27) / 45 × 100 = 40 %.
11. Prescribe only when needed, test which antibiotic the bacteria are sensitive to, or reserve some antibiotics for resistant infections.

Where marks are usually lost

• Calling a plasma cell a memory cell, or saying that T cells make antibodies.
• Saying that antibodies “kill” pathogens, without saying they bind, neutralise or mark them for phagocytes.
• Treating passive immunity as producing memory cells.
• Using “adapt” or “become immune” for bacteria where mutation followed by selection is needed.
• Saying that a larger clear zone proves that the antibiotic kills bacteria.
• Forgetting the control disc, or not stating that the plate is inverted and taped in two places.
• Using the diameter in place of the radius when working out area.
• Describing hospital measures with no link to the cause they address.
• Comparing infection counts when the patient-days differ.

Official syllabus

Pearson Edexcel International Advanced Subsidiary/Advanced Level Biology (YBI11) specification, Issue 2, published by Pearson Education Limited.