Pearson Edexcel International A Level Biology: Adaptive Immunity, Immunisation and Antibiotics (YBI11)

This guide teaches adaptive immunity, immunisation and antibiotics for the Pearson Edexcel International Advanced Subsidiary/Advanced Level Biology specification (YBI11), Issue 2. It covers statements 6.10 to 6.15 of Topic 6, including Core Practical 14. Topics 1 to 4 are International AS (IAS) and Topics 5 to 8 are International A2 (IA2), so this material is A2. There are no tiers. Statement 6.9 (antigens, antibodies, plasma cells, macrophages and antigen-presenting cells) comes just before this unit, and the guide recaps only what you need from it. Pair it with the revision notes and the practice questions. The course hub and printable checklist show the rest of the course, and the free diagnostics show where to start.

What this guide covers

Statement	What you must be able to do
6.10	Explain the roles of B cells (B memory and B effector) and T cells (T helper, T killer and T memory)
6.11	Explain how immunity is gained: natural, artificial, active and passive
6.12	Explain how evasion mechanisms support the “evolutionary race” between pathogens and hosts
6.13	Distinguish bacteriostatic from bactericidal antibiotics
6.14	Core Practical 14: investigate the effect of different antibiotics on bacteria
6.15	Link the causes of hospital-acquired infections to codes of practice on prescribing and on hospital hygiene

6.10 B cells and T cells

Every lymphocyte carries receptors of one shape. When a lymphocyte meets an antigen that fits, it is selected, divides by mitosis and forms a clone (clonal selection and expansion). The antigen is often shown to it on the surface of an antigen-presenting cell such as a macrophage.

B cells (the humoral response)

• B effector cells are the cells that act. Most become plasma cells, which have extensive rough endoplasmic reticulum and secrete large amounts of a single antibody into the blood and tissue fluid.
• B memory cells do not secrete antibody now. They stay in the body for years, ready to divide and form new plasma cells if the same antigen returns.

T cells (the cell-mediated response)

Cell	Role
T helper	Binds the antigen on an antigen-presenting cell, divides, and releases cytokines. Cytokines stimulate B cells to divide and become plasma cells, activate T killer cells, and attract and activate phagocytes
T killer	Recognises cells showing the antigen, such as virus-infected cells or cancer cells, and destroys them by releasing substances such as perforin that damage the membrane
T memory	Long-lived. Forms T helper and T killer cells quickly on a second exposure

The secondary response

The first exposure is slow because very few lymphocytes fit the antigen, so they must be found and then cloned. Memory cells exist in much greater numbers than the original matching cells, and they respond to a lower dose. The second response therefore starts sooner, rises faster, peaks higher and lasts longer, often before symptoms appear.

Worked example: reading antibody data

Antibody concentration (arbitrary units, AU) after an antigen is given on day 0 and again on day 50:

Event	Result
First exposure	Antibody first detected on day 6; peak of 8 AU on day 16
Second exposure	Antibody 3 AU on day 51; peak of 104 AU on day 56

Fold difference in peaks = 104 / 8 = 13 times
Rate, first response  = (8 - 0) / (16 - 6)    = 0.8 AU per day
Rate, second response = (104 - 3) / (56 - 51) = 101 / 5 = 20.2 AU per day

Explain the difference: B memory cells formed after the first exposure are already selected, so no time is spent finding a matching B cell. They divide and form plasma cells at once, giving a faster rise, in this case 20.2 compared with 0.8 AU per day, and a higher peak.

6.11 Types of immunity

Immunity is active if you make your own antibodies and memory cells, and passive if you are given antibodies made by someone else. It is natural if it happens in everyday life and artificial if it is given as a medical treatment.

	Active	Passive
Natural	Infection with a pathogen, then recovery	Antibodies cross the placenta to the fetus; antibodies in breast milk, especially colostrum
Artificial	Vaccination (immunisation)	Injection of antibodies, for example antivenom or tetanus immunoglobulin

• Active immunity is slow to start, because the primary response must happen, but long-lasting, because memory cells form.
• Passive immunity works at once but is short-lived. The recipient’s B cells were never stimulated, so there are no memory cells, and the antibodies are broken down within weeks.
• A vaccine contains the antigen (for example a weakened pathogen, an inactivated pathogen, a treated toxin or a purified surface protein) but cannot cause the disease. It triggers a primary response, so memory cells are ready. A booster dose gives a secondary response and raises the level of memory cells.

6.12 The evolutionary race

Pathogens and hosts evolve in response to each other. A host with immune responses that work against a pathogen survives better. A pathogen variant that escapes those responses survives and reproduces better, and its alleles spread. Then the host’s defences become less effective, and so on. The theory is supported by the many different ways pathogens evade the immune system.

Evasion mechanism	Example and effect
Antigenic variation	Influenza viruses mutate so that surface proteins change. Memory cells from earlier infections no longer recognise the new antigens, so a new vaccine is needed
Attacking immune cells	HIV infects and destroys T helper cells, so the response cannot be coordinated
Surviving inside phagocytes	Mycobacterium tuberculosis is engulfed by macrophages but resists digestion and lives inside them
Hiding inside cells	Viruses that enter a latent state show few antigens, and so escape T killer cells
Masking antigens	Some bacteria have a capsule that covers surface antigens, so phagocytes bind less well

Bacterial resistance to antibiotics, described below, is the same process in action, with the antibiotic as the selection pressure.

6.13 Bacteriostatic and bactericidal antibiotics

An antibiotic is a chemical that harms bacteria and has little effect on human cells. Antibiotics act on features that bacteria have and human cells lack, such as the peptidoglycan cell wall, or on bacterial ribosomes.

• Bacteriostatic antibiotics stop bacteria growing and reproducing but do not kill them. The host’s immune system has to clear the infection. Example: tetracycline, which blocks protein synthesis on bacterial ribosomes.
• Bactericidal antibiotics kill bacteria. Example: penicillin, which prevents the cell wall from being built, so water enters by osmosis and the cell bursts (lysis).

Antibiotics do not work on viruses, which have no cell wall and no metabolism or ribosomes of their own.

Worked example: classifying from viable counts

A culture starts at 5.0 × 10⁵ viable cells per cm³. After 6 hours: no antibiotic, 4.0 × 10⁷; antibiotic X, 5.2 × 10⁵; antibiotic Y, 1.0 × 10³.

No antibiotic: 4.0 x 10^7 / 5.0 x 10^5 = 80 times higher
X: 5.2 x 10^5 / 5.0 x 10^5 = 1.04, so no real change in viable cells
Y: (5.0 x 10^5 - 1.0 x 10^3) / 5.0 x 10^5 x 100 = 99.8 % fall

X stops growth, so it is bacteriostatic. Y reduces the number of living cells, so it is bactericidal. A turbidity reading could not show this, because dead cells still scatter light.

Antibiotic resistance

Mutation produces a resistant bacterium by chance. The antibiotic kills the sensitive bacteria, so the resistant ones reproduce with less competition. Resistance alleles pass to offspring and, by plasmids, to other bacteria. Methicillin-resistant Staphylococcus aureus (MRSA) is an example.

6.14 Core Practical 14: the effect of different antibiotics on bacteria

The specification gives only the aim. This is a standard method using discs.

1. Disinfect the bench. Work near a Bunsen flame or with sterile equipment, and wash your hands before and after.
2. Use a sterile pipette to put a measured volume of a broth culture of a safe, non-pathogenic bacterium onto a sterile nutrient agar plate. Spread it evenly with a sterile spreader to make a lawn.
3. Using sterile forceps, place discs of different antibiotics on the agar, spaced apart. Include a control disc soaked in sterile water.
4. Fix the lid with two short pieces of tape, not all round, and label the base. Invert the plate and incubate, for example at 25 °C for 24 to 48 hours.
5. Do not open the plate. Measure the diameter of each clear zone (zone of inhibition) with a ruler, and repeat.
6. Autoclave or disinfect all plates and equipment.

Variables to control: volume and density of bacteria, agar depth and type, disc size, antibiotic concentration, temperature and time.

Safe and ethical use: use harmless strains from a recognised supplier, never culture samples from people or surfaces, keep lids on, and dispose of material by autoclaving.

Worked example: zones of inhibition

Disc diameter is 6 mm. Zone diameters (including the disc), three repeats each: antibiotic P 22, 24 and 23 mm; antibiotic R 12, 13 and 14 mm; control 6 mm.

Mean P = (22 + 24 + 23) / 3 = 23.0 mm; radius 11.5 mm
Area of zone P = pi x 11.5^2 = 415 mm2
Mean R = 13.0 mm; radius 6.5 mm; area = pi x 6.5^2 = 133 mm2
Disc area = pi x 3^2 = 28.3 mm2
Clear area beyond the disc: P = 387 mm2, R = 104 mm2
P / R = 387 / 104 = 3.7 times

Antibiotic P is more effective at stopping growth under these conditions. The control has no zone, so the water did not stop growth. Zone size also depends on how fast the antibiotic diffuses, so do not compare molecules by zone alone. A zone cannot show whether an antibiotic is bacteriostatic or bactericidal: you would have to sample the zone and subculture it onto fresh agar. If bacteria grow, the antibiotic was bacteriostatic.

6.15 Hospital-acquired infections

Hospital-acquired infections (HAIs) are infections picked up in hospital. They are common because:

• Patients are weak, have open wounds or take medicines that suppress immunity.
• Devices such as catheters and ventilators give bacteria a way in.
• Many people are in close contact, and staff and visitors move between wards.
• Antibiotics are used heavily, which selects for resistant bacteria such as MRSA and Clostridioides difficile.

Codes of practice follow from these causes:

Cause	Control measure
Spread on hands	Hand washing or alcohol gel between patients; bare-below-the-elbow dress
Spread between patients	Isolation of infected patients; screening on admission; cleaning of surfaces and equipment
Entry through skin	Aseptic technique for procedures; sterile instruments; removing devices as soon as they are unneeded
Selection of resistant bacteria	Prescribe antibiotics only when needed; choose by testing which antibiotic the bacteria are sensitive to; follow the prescribed course; reserve some antibiotics for resistant infections; audit use

Worked example: comparing infection rates

A ward had 36 infections in 12 000 patient-days. After new hand hygiene and screening rules, it had 21 infections in 10 500 patient-days.

Before: 36 / 12 000 x 1000 = 3.0 per 1000 patient-days
After:  21 / 10 500 x 1000 = 2.0 per 1000 patient-days
Change: (3.0 - 2.0) / 3.0 x 100 = 33.3 % reduction

Using rates, not raw counts, is fair because the patient-days differ. The fall is consistent with the rules working, but other changes may have happened in the same period.

Common errors

• Writing that antibiotics kill viruses, or that bacteria “become immune” to antibiotics. Resistance arises by mutation and selection.
• Saying plasma cells are memory cells. B effector cells become plasma cells; B memory cells are a separate group.
• Describing passive immunity as stimulating memory cells.
• Claiming that a clear zone shows an antibiotic kills the bacteria.
• Measuring the zone radius when the method specifies diameter, or forgetting to square the radius.

Next, test yourself with the practice questions and the revision notes.

Official syllabus

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