Immunology and disease: WJEC A level Biology notes

Lesson 1 of 24

Why is the human body described as a host?

These notes cover Option A, Immunology and disease, in WJEC A level Biology Unit 4: , Inheritance and Options. Each lesson follows the WJEC specification, and the exam tips come from BioWelsh analysis of WJEC past papers.

Your body is not just you. Trillions of live on your skin, in your mouth and nose, and above all in your gut. Because they live in or on the body and get food and shelter from it, the body is described as their .

Bacteria such as Escherichia coli live in the large intestine. They make vitamin K, which the body absorbs, and they are normally harmless there.
Bacteria and fungi on the skin use up space and nutrients, so harmful find it hard to settle. This is called competitive exclusion.
Tiny mites live in the hair of the face and eat dead skin cells.
Some organisms are parasites, for example tapeworms in the gut and fleas or lice on the skin. They benefit while the is harmed.

Most of these organisms live in a balance with each other and with us. Trouble starts when the balance is upset: a harmless reaches the wrong part of the body (for example E. coli in the bladder), its numbers rise too far, or it starts releasing . can upset the balance too, because killing the normal gut bacteria lets other , such as Clostridioides difficile, multiply.

Lesson 2 of 24

What do the key terms about disease mean?

The specification lists fifteen terms that you must be able to define. Examiners reward short, precise definitions, so learn them as a set and notice the pairs that are easy to confuse.

The key terms about disease and what each one means
Term	Meaning
	Able to cause disease. A is an organism that causes disease.
	Able to be passed from one individual to another.
	A person or animal that is infected and can pass the on, but has no symptoms.
	A long-term of a , usually with few or no symptoms, that is a constant source of infection.
	Always present in a or area, at a steady, predictable level.
	A large, rapid increase in the usual number of cases in an area.
	An that spreads over a very wide area, across many countries or continents.
	An organism that carries a and transmits it to another organism, for example a mosquito.
	A molecule made by a that causes damage or disease.
	A molecule, usually a protein on a cell surface, that triggers an immune response and the production of .
	A protein () made by that binds to one specific .
	Forms of the same that have different surface , so different are needed.
	A preparation of weakened or killed , or inactivated that stimulates an immune response and without causing the disease.
	A substance, first made by , that kills bacteria or stops them growing, without harming human cells.
	When a is no longer affected by a drug that used to kill it or stop its growth.

How an outbreak can grow

1) : steady low level in one area
2) : a sudden large rise in cases in an area
3) : the spreads across many countries

Lesson 3 of 24

How is cholera caught, prevented and treated?

is a disease of the small intestine caused by a bacterium, cholerae. It is in parts of Asia and Africa where water supplies and sewage treatment are poor, and it breaks out as after floods, earthquakes and wars damage them.

The scanning electron micrograph below shows cholerae.

Black and white electron micrograph of a dense mass of short rod-shaped cells, many of them gently curved, lying in all directions and overlapping. A scale bar of 1 micrometre is at the bottom left; each cell is about 1 to 3 micrometres long. — Scanning electron micrograph of *Vibrio cholerae*, the bacterium that causes cholera. Photo: Ronald Taylor, Tom Kirn and Louisa Howard, Dartmouth Electron Microscope Facility, Copyrighted free use.

Each bacterium is a short rod with a gentle curve, often described as comma-shaped.
The scale bar at the bottom left is 1 µm, so each cell is only 1 to 3 µm long.
cholerae is , so it has a thin wall inside an outer membrane.

People catch by swallowing water or food contaminated with faeces that contain the bacteria. The bacteria attach to the lining of the small intestine and release . The makes the epithelial cells pump chloride ions out into the gut through channel proteins, and water follows by . The result is severe watery diarrhoea, so the person loses water and salts very quickly and can die of dehydration within hours.

Cholera at a glance
Feature	Cholera
Type of organism	Bacterium (): cholerae
Source of infection	Water or food contaminated with faeces from infected people or
Tissue affected	Epithelium of the small intestine
of transmission	Faecal-oral route, mainly through drinking water
Prevention	Clean water, sewage treatment, hand washing and food hygiene; an oral of killed bacteria, given in two doses, for people at high risk
Treatment	Replace water and salts: oral rehydration solution, or a drip into a vein in severe cases. shorten the illness but do not replace fluids.

also gave us one of the first pieces of epidemiology. In 1854 a London doctor, John Snow, plotted deaths on a street map and found they clustered round one water pump. When the pump was put out of use, new cases fell, which supported his idea that spreads through water rather than through bad air.

Lesson 4 of 24

How does tuberculosis spread and how is it controlled?

is caused by the bacterium Mycobacterium tuberculosis. It is one of the leading causes of death from a single agent in the world, and cases are still reported every year in the UK.

The light micrograph below shows M. tuberculosis after an acid-fast (Ziehl-Neelsen) stain.

Light micrograph of a pale blue, patchy background with about twenty thin red rods scattered across it. The rods are straight or slightly curved, some lying singly and a few in small groups. A darker blue band crosses the right side of the image. — *Mycobacterium tuberculosis* in a sample stained with the acid-fast Ziehl-Neelsen stain. Photo: CDC/Dr. George P. Kubica, Public domain.

The red rods are the bacteria. They are long, thin and slightly curved.
They stay red because their waxy cell wall keeps the red dye even when washed with acid and alcohol. This is why they are called acid-fast.
The blue background is other material in the sample, such as mucus and human cells, stained with a counterstain.

is spread through the air. When an infected person coughs or sneezes, tiny droplets carrying the bacteria are breathed in by others. It spreads most in crowded, poorly ventilated housing and among people whose immune systems are weakened, for example by HIV or poor nutrition. The bacteria mainly infect the lungs, where they form small damaged called tubercles. Many infected people carry bacteria for years with no symptoms, and the infection can become active later.

Tuberculosis at a glance
Feature	Tuberculosis
Type of organism	Bacterium: Mycobacterium tuberculosis
Source of infection	Droplets from people with active ; cattle with bovine can also be a source through milk
Tissue affected	Mainly the lungs; it can spread to lymph nodes, bones and other organs
of transmission	Airborne droplets (coughing and sneezing)
Prevention	, made from a weakened strain of a related bacterium, M. bovis; better housing and ventilation; and tracing contacts
Treatment	A course of several taken together for at least six months

Treatment takes so long because the bacteria grow very slowly and can hide inside cells. Several are given together because a bacterium is very unlikely to carry giving to all of them at once. Multi-drug strains, which no longer respond to the main drugs, are a growing problem. The gives good protection to young children but is less effective in adults, so in the UK it is now offered to babies and children at higher risk rather than to everyone.

Lesson 5 of 24

How was smallpox wiped out?

was caused by the variola virus, a large virus with DNA as its genetic material. It spread by droplets and close contact with an infected person or their bedding. The virus infected the respiratory tract, then spread in the blood and caused a rash of fluid-filled blisters over the skin. About a third of people with the severe form died, and survivors were often scarred or blinded.

The transmission electron micrograph below shows variola virus particles.

Black and white electron micrograph of four dark oval particles on a pale background. The lower left particle is the clearest: it has several outer layers and a darker dumbbell-shaped core in the middle. The other particles are darker and less sharply outlined. — Transmission electron micrograph of variola (smallpox) virus particles. Photo: CDC/Dr. Fred Murphy and Sylvia Whitfield, Public domain.

Each particle is oval to brick-shaped, among the largest of all viruses.
The dark dumbbell shape inside the lower left particle is the core, which holds the viral DNA.
The layers around the core are the proteins and membranes of the virus, which carry its .

There was never a cure, but there was an excellent , made from the live vaccinia virus, a close relative that causes only a mild infection. From 1967 the World Health Organisation (WHO) ran a worldwide programme: whenever a case was found, the patient was isolated and everyone around them was vaccinated, a method called ring . The last natural case was in 1977, and was declared eradicated in 1980. It is the only human disease ever to have been wiped out.

Why smallpox could be eradicated
Feature of smallpox	Why it helped
Only one , with little	One worked everywhere and kept working
The was highly	A single dose gave strong, long-lasting immunity
No animal	Once every human case was stopped, there was nowhere for the virus to survive
No ; the rash was easy to recognise	Every case could be found and isolated quickly
The freeze-dried was stable without a fridge	It could be taken to hot, remote areas

Lesson 6 of 24

Why does influenza keep coming back?

() is caused by the virus. It infects the epithelial cells lining the nose, throat and airways, causing fever, sore throat, cough and aching muscles. It spreads through droplets from coughs and sneezes, and from hands that touch contaminated surfaces and then the nose or mouth. Most people recover in a week, but kills many older and vulnerable people each winter.

The transmission electron micrograph below shows virus particles.

Black and white electron micrograph of about a dozen pale, roughly round particles of different sizes, grouped together. Each is surrounded by a thin dark ring with a short fuzzy fringe of spikes on the outside. — Transmission electron micrograph of influenza A virus particles, negatively stained. Photo: CDC/F. A. Murphy, Public domain.

The particles are roughly round but vary in shape, because each has a soft envelope taken from the membrane of the cell.
The fuzzy fringe around each particle is a layer of protein spikes in the envelope.
These spikes are the two surface : (H), which lets the virus enter a cell, and (N), which lets new particles leave.

The virus stores its as eight separate pieces of RNA. There are several subtypes of A, named by their H and N , for example H1N1 or H3N2. Birds and pigs carry many of these subtypes, so they are disease for new human strains.

The diagram below shows the two ways in which the surface of change.

Diagram in two halves. On the left, headed antigenic drift, three virus particles labelled year 1, year 2 and year 3 are joined by arrows. Each particle is a circle with purple lines inside for RNA segments, surrounded by spikes with blue round heads for haemagglutinin and green square heads for neuraminidase. In year 2 one round head is white, and in year 3 two are white, showing spikes whose shape has changed slightly. Text explains that copying errors change the haemagglutinin a little each year, so a new vaccine is made each year. On the right, headed antigenic shift, a human virus H3N2 with blue round and green square heads and a bird virus H5N1 with red round and gold square heads both point into one oval host cell, for example a pig cell. An arrow leads from the cell to a new virus with red round heads and green square heads labelled new subtype H5N2. Text explains that RNA segments mix and the new combination can spread as a pandemic. A key is along the bottom. — Antigenic drift and antigenic shift in the influenza virus. Original BioWelsh diagram.

: the RNA is copied with no proofreading, so small build up. Each year the H and N spikes change a little.
from an earlier infection or fit the changed less well, so a new has to be made every year.
: when two different subtypes infect the same cell, for example a human virus and a bird virus in a pig, their RNA pieces are mixed in new virus particles.
The result is a new combination of H and N that nobody's immune system has met, which can spread quickly as a . in 1918, 1957, 1968 and 2009 began this way.

is controlled mainly by prevention: an annual for older people, young children and other groups at risk, good hygiene such as hand washing and catching sneezes in tissues, and staying away from others when ill. do not work against the virus, but they are used to treat bacterial infections, such as pneumonia, that can follow . Antiviral drugs can reduce symptoms if taken early.

Lesson 7 of 24

How is malaria transmitted and controlled?

is caused by Plasmodium, a single-celled protoctist. Five infect humans; Plasmodium falciparum causes most deaths and P. vivax is also common. is in many tropical and subtropical regions, becomes in wet seasons when mosquitoes breed, and kills hundreds of thousands of people a year, most of them young children in Africa.

The photograph below shows an Anopheles mosquito, the of .

Close-up sepia-toned photograph of a dark mosquito with very long, thin legs spread out on a smooth pale surface. Its slender body is tilted, with the long thin mouthparts pointing down towards the surface at the front and narrow wings folded over the back. — An *Anopheles* mosquito, the vector of malaria, resting on a pale surface. Photo: Edward McClellan, CDC, CC0.

The mosquito rests with its body tilted at an angle to the surface, which is typical of Anopheles.
The long, thin mouthparts at the front are used by females to pierce skin and suck blood.
Only the females feed on blood, which they need to make their eggs. The males feed on plant juices and , so they do not transmit .

The diagram below shows the life cycle of Plasmodium, which needs both a mosquito and a human.

Flow diagram in two shaded zones. The top zone, inside the female Anopheles mosquito, has three boxes joined by arrows from left to right: gametocytes taken in with a blood meal become gametes in the gut; gametes fuse, sexual reproduction, to form zygotes; zygotes develop into sporozoites, which move to the salivary glands. An arrow leads down into the bottom zone, inside the human, to a box reading sporozoites injected with saliva when the mosquito feeds. Arrows lead left to in liver cells, asexual reproduction makes thousands of merozoites, and then to merozoites invade red blood cells and reproduce asexually inside them. Curved arrows labelled repeats form a loop between that box and a box below reading red cells burst every 2 to 3 days, releasing merozoites, each burst brings a fever. An arrow from this box leads right to some merozoites develop into male and female gametocytes in the blood, and a dashed arrow labelled a mosquito feeds on an infected person leads from there back up to the first mosquito box. — The life cycle of *Plasmodium*, which causes malaria. Original BioWelsh diagram.

When an infected female mosquito feeds, she injects with her saliva.
The travel in the blood to the liver, enter liver cells and reproduce asexually, making thousands of .
invade red blood cells and reproduce asexually again. The red cells burst every two or three days, releasing more , and each burst brings a bout of fever.
Some develop into male and female . When another mosquito feeds, it takes them in, and they form gametes that fuse in its gut.
The zygotes develop into , which move to the mosquito's salivary glands, ready to infect the next person.

The light micrograph below is a stained blood smear from a person with P. falciparum .

Light micrograph of many pale beige round red blood cells, some overlapping. Many of the cells contain one or more tiny purple rings or dots, and a few contain three or four. There are no nuclei in the red blood cells. — Stained thin blood smear showing ring forms of *Plasmodium falciparum* in red blood cells. Photo: CDC/Dr. Greene, Public domain.

The pale discs are red blood cells, which have no .
The small purple rings and dots inside many of them are young parasites, called ring forms.
Some red cells contain two or more rings. Looking for these under the microscope is still the standard way to diagnose .

Ways to prevent malaria and why each one works
Measure	Why it works
Sleeping under insecticide-treated bed nets	Anopheles feeds at night, so nets keep mosquitoes off and the insecticide kills them
Spraying insecticide on indoor walls	Kills mosquitoes that rest on walls after feeding
Draining standing water	Removes the places where mosquitoes lay eggs and larvae develop
A film of oil on water, or fish that eat larvae	Larvae cannot breathe at the surface, or are eaten
Releasing sterile male mosquitoes	Females that mate with them lay eggs that do not hatch
Antimalarial drugs for travellers	Kill parasites before an infection becomes established

is treated with antimalarial drugs, not . The first was quinine, from the bark of a tree. Today the main treatment is artemisinin given together with a second drug, so that the parasite is unlikely to become to both. Drugs work best while the parasite is in the blood plasma, and less well while it is hidden inside liver and red blood cells. Two are now given to young children in parts of Africa, but they give only partial protection. A fully effective is hard to make because Plasmodium has many , changes its between stages of its life cycle, and spends much of its time inside human cells.

Lesson 8 of 24

How do the five named diseases compare?

Exam questions often give a new disease and ask you to apply what you know. The table below brings the five named diseases together so you can compare the type of organism, how each is spread and how it is controlled.

The five diseases named in the specification compared
Disease	Organism	Tissue affected	Spread by	Prevention and control	Treatment
	Bacterium	Small intestine	Contaminated water and food	Clean water, sewage treatment, hygiene, oral	Rehydration;
Tuberculosis	Bacterium	Lungs	Airborne droplets	, contact tracing, better housing	Several for at least six months
	Virus (DNA)	Respiratory tract, then skin	Droplets and close contact	and isolation; now eradicated	No cure; supportive care
	Virus (RNA)	Epithelium of the airways	Droplets and contaminated surfaces	Annual , hygiene, staying at home when ill	Rest; antivirals; only for secondary infections
	Protoctist	Liver cells, then red blood cells	Female Anopheles mosquito ()	Nets, insecticides, draining water, partial	Antimalarial drugs such as artemisinin combinations

Lesson 9 of 24

How do viruses reproduce and cause disease?

A virus is a particle of nucleic acid (DNA or RNA) inside a protein coat called a . Some also have an envelope taken from the membrane of the cell. Viruses have no metabolism of their own, so outside a living cell they do nothing at all. Inside a cell, they take over the cell's and to make copies of themselves.

The diagram below shows the two ways in which a virus can reproduce.

Diagram with two rows. The top row, headed lytic cycle, shows five rounded cream host cells, each with a purple loop of host DNA, joined by arrows. In the first a grey hexagonal virus containing a red squiggle sits on a green receptor on the cell surface. In the second an empty hexagon is outside and a red squiggle is inside. In the third there are several red squiggles and small grey squares for capsid proteins. In the fourth there are six small hexagons with red squiggles inside. In the fifth the cell outline is broken and hexagons are leaving through the gaps. Captions under each give the step. An arrow from the second cell leads down to the bottom row, headed lysogenic cycle, where a cell has a short red section joined into its purple DNA loop, labelled viral DNA is inserted into a host chromosome and stays there with no symptoms. An arrow labelled cell divides leads to two smaller cells, each with the red section in its DNA. A dashed arrow from them curves back up to the third lytic step, labelled later a trigger starts the lytic cycle: symptoms. A key explains the symbols. — The lytic and lysogenic cycles of a virus. Original BioWelsh diagram.

The virus attaches to molecules on the surface of the cell, and its nucleic acid enters the cell.
In the , the 's copy the viral nucleic acid straight away and its make proteins.
New virus particles are assembled from these parts and released, either by bursting the cell () or by budding off wrapped in the 's membrane, which becomes their envelope.
In the , the viral DNA is inserted into a chromosome instead. It is copied every time the cell divides and causes no symptoms.
Later, a trigger such as stress switches the virus into the , and symptoms appear. Herpes viruses and HIV behave like this.

Cell : new particles burst out of the cell and kill it, as when the common cold virus destroys cells of the nasal lining.
Toxic effects: viral proteins can stop the making its own DNA, RNA and proteins, or make neighbouring cells fuse together.
Cell : some viruses cause cancer. Human papillomavirus (HPV) makes proteins that switch off suppressor proteins, so infected cervical cells can divide uncontrollably.
Immune suppression: HIV destroys , so B cells cannot be activated to make and the person becomes vulnerable to other infections.

Lesson 10 of 24

What are antibiotics, and how are they classified?

Chemicals that kill or stop them growing are called antimicrobials. Antiseptics are used on living tissue, such as skin, and disinfectants on non-living surfaces, such as floors. are different: they were first discovered as substances made by fungi and bacteria, and they can be taken into the body because they affect bacteria but not human cells.

Two ways of classifying antibiotics
Term	Meaning	Example
	Kills bacteria	, which makes cell walls burst
	Stops bacteria growing and dividing, without killing them; the immune system then removes them	Tetracycline, which stops protein synthesis
	Works against many kinds of bacteria, both and	Tetracycline, ampicillin
	Works against a small of bacteria	G, which mainly affects bacteria

The graph below shows what happens to a of bacteria when each type of is added.

Line graph. The horizontal axis is time from 0 to 10 hours and the vertical axis is log to base 10 of the number of living bacteria per cubic centimetre from 0 to 10. All three lines start at 6 and rise together to about 7.3 at 3 hours, where a dashed vertical line is labelled antibiotic added. After this the green line, no antibiotic, keeps rising and levels off at about 9. The blue line, bacteriostatic antibiotic, stays flat at about 7.3. The red line, bactericidal antibiotic, falls steadily to about 2.4 at 10 hours. — Number of living bacteria after adding a bactericidal or a bacteriostatic antibiotic. Original BioWelsh graph with illustrative data.

Without (green), the number of living bacteria keeps rising until it levels off.
After a is added at 3 hours (blue), the line goes flat: the bacteria stay alive but stop dividing.
After a is added (red), the line falls, because bacteria are being killed.
The vertical axis is a , so a fall of one unit the number of living bacteria has dropped to a tenth.

do not work against viruses. They act on structures and processes that viruses do not have, such as a cell wall, 70S and the cell's own metabolism. Giving for a cold or does nothing to the virus and helps to spread.

Lesson 11 of 24

How does the cell wall of Gram-negative bacteria protect them?

All bacteria have a cell wall made of , also called : long chains of sugars joined by short chains of amino acids. The way the wall is built splits bacteria into two groups, named after the . (If the is unfamiliar, read the microbiology lesson on the Gram stain.)

The diagram below compares the cell walls of the two groups.

Two cross sections side by side, each with outside the cell at the top and a pale purple band labelled cytoplasm at the bottom. On the left, Gram-positive, ten stacked gold bars joined by short orange lines form a thick peptidoglycan layer, labelled up to 90% of the wall, above a blue phospholipid bilayer labelled cell surface membrane. On the right, Gram-negative, from the top down there are green wavy lipopolysaccharide chains, a brown phospholipid bilayer labelled outer membrane with a blue barrel-shaped porin channel at its right end, a gap, just two gold bars labelled thin peptidoglycan layer, about 10% of the wall, and a blue bilayer labelled cell surface membrane. Text below the left side says the cells keep the crystal violet stain and look purple, and that penicillin and lysozyme reach the thick peptidoglycan easily. Text below the right side says the outer membrane breaks up in the stain so safranin makes the cells red, and that the outer membrane protects the thin murein from many antibiotics, lysozyme and other immune defences. — The cell walls of Gram-positive and Gram-negative bacteria compared. Original BioWelsh diagram.

bacteria have a thick layer of outside the cell surface membrane. It holds on to the stain, so the cells look purple.
bacteria have only a thin layer of , with an outer membrane outside it.
The outer membrane is a lipid layer covered with chains. Alcohol in the breaks it up, the washes out, and the red counterstain, , makes the cells look red.
Many , including , and the cannot easily get through the outer membrane to the . Some molecules only get in through protein channels called .

So bacteria, such as cholerae and E. coli, are protected from many and from some immune defences. Infections with them often need broad-spectrum or drugs that can pass through .

Lesson 12 of 24

How do penicillin and tetracycline work?

is made by the mould Penicillium. Today it is produced in huge fermenters using high-yielding strains of Penicillium chrysogenum, and chemists have modified it to make related drugs such as ampicillin and amoxicillin. It works by attacking the wall while bacteria are growing.

The diagram below shows how kills a growing bacterium.

Three panels. Panel 1, normal growth, shows four rows of alternating green and blue rounded rectangles for glycan chains, joined between rows by solid orange vertical lines for peptide cross-links, with a purple enzyme shaped like a circle with a notch below the mesh and an arrow pointing up, labelled transpeptidase forms peptide cross-links. Panel 2, penicillin added, shows the same mesh but with four of the cross-links drawn as dotted lines, and the purple enzyme below with a small red block labelled penicillin filling its notch. The caption says new cross-links cannot form and the wall becomes weak. Panel 3, the cell bursts, shows a rod-shaped cell with a double outline and a gap at the top right with small blue dots escaping, labelled contents escape. Blue arrows labelled water point into the cell from the left and from below. A key at the bottom explains the symbols. — How penicillin kills a growing bacterium. Original BioWelsh diagram.

As a bacterium grows, parts of its wall are broken down and rebuilt all the time. The forms the peptide cross-links that join the glycan chains and make the wall strong.
binds to the of , so the cannot form new cross-links. It binds permanently, so the is inhibited for good.
The wall is still being broken down as normal, so it becomes thinner and weaker.
Water enters the cell by . The weak wall cannot resist the pressure, so the cell swells and bursts. This is why is .

Tetracycline, made by Streptomyces bacteria, works in a completely different way. The diagram below shows it at a bacterial .

A large lilac oval labelled 50S sits above a smaller pale blue oval labelled 30S, with a yellow strip labelled mRNA running between them. Inside the large oval are two white boxes labelled P site and A site. A green tRNA shape stands in the P site on the mRNA, with a chain of pink beads rising from its top to the upper left, labelled growing polypeptide chain. The A site is empty. Four joined red hexagons lie in the small subunit just below the A site, labelled tetracycline binds to the 30S subunit and blocks the A site. At the top right a yellow tRNA carrying a green bead has a dashed arrow curving towards the A site, crossed through with a red X, labelled tRNA carrying the next amino acid cannot enter the A site. Text below says no new amino acids are added, protein synthesis stops, and tetracycline binds reversibly so it is bacteriostatic. — Tetracycline blocks the A site of a bacterial ribosome. Original BioWelsh diagram.

Bacteria have 70S , made of a small 30S subunit and a large 50S subunit.
During translation, the tRNA carrying the growing polypeptide sits in the P site, and the tRNA bringing the next amino acid must bind in the A site.
Tetracycline binds to the 30S subunit and blocks the A site, so no new tRNA can attach and no more amino acids are added.
The bacteria cannot make proteins, so they stop growing and dividing. Tetracycline binds reversibly, so it is .
Bacteria actively take tetracycline in, but human cells take up very little, so human protein synthesis is hardly affected.

Penicillin and tetracycline compared
Feature	Penicillin	Tetracycline
Made by	The fungus Penicillium	The bacterium Streptomyces
Target	, the that cross-links	The 30S subunit of the
Effect	The wall weakens and the cell bursts by	Protein synthesis stops
of action
Spectrum	Narrow ( G): mainly	Broad: and

Lesson 13 of 24

How do you find out which antibiotic works best?

Before treating a serious infection, a laboratory often tests which the bacteria are sensitive to. The same method is used in school with harmless bacteria. It relies on , so that only the bacteria being tested grow and nobody is exposed to them. (For the details of , read the microbiology lesson on aseptic technique.)

Spread a thin, even layer (a lawn) of the bacteria over sterile in a Petri dish, using a sterile spreader.
Use sterile forceps to place paper discs soaked in different on the , spaced well apart. Include a disc soaked in sterile water as a .
Tape the lid on in two places, label the base, and upside down. In school, at about 25 °C so that human are not encouraged. In a hospital laboratory, cultures from patients are at about 35 to 37 °C, close to body temperature, because the bacteria are human .
After a day or two, measure the diameter of the () around each disc.

The diagram below shows two ways of reading such a test.

Two Petri dishes seen from above, each covered with a dense stippled lawn of brown dots representing bacteria. Dish A has five white discs numbered 1 to 5. Disc 1 has no clear area around it. Discs 2, 3, 4 and 5 are each surrounded by a clear circle of different size, disc 3 in the centre having the largest, with a double-headed arrow across it labelled diameter. Text below says the clear zone is where bacteria are killed or stopped from growing, disc 1 shows resistance and disc 3 is most effective. Dish B has a long white strip down the middle marked with concentrations 32, 16, 8, 4, 2, 1, 0.5, 0.25 and 0.12 from top to bottom. A clear teardrop-shaped zone is widest at the top and narrows to meet the strip at the mark 2. A red line from this point is labelled MIC: where the edge of the clear zone meets the strip. Text says the antibiotic diffuses out forming a gradient and the numbers are micrograms per cubic centimetre. — Two ways to test the sensitivity of bacteria to antibiotics: discs and a gradient strip. Original BioWelsh diagram.

In A, each diffuses out of its disc into the , so its concentration is highest near the disc and falls further away.
Where the concentration is high enough, the bacteria are killed or cannot grow, leaving a . The larger the zone, the more effective the is against these bacteria, provided the discs held the same amount of .
No zone at all, as around disc 1, the bacteria are to that .
In B, a strip holds a gradient of one , from high concentration at the top to low at the bottom. The is teardrop-shaped, widest at the high end.
The () is the lowest concentration that stops growth. It is read where the edge of the meets the strip.

The photograph below shows a real test on one of bacteria.

Photograph from above of a round Petri dish containing dark red-brown agar. Six small paper discs printed with letters and numbers sit on the agar, one in the centre and five around it. Each disc is surrounded by a darker, clear-looking circular zone, and the zones differ greatly in size; some overlap their neighbours. — An antibiotic sensitivity test with six antibiotic discs on a lawn of bacteria. Photo: Ajay Kumar Chaurasiya, CC0.

Six discs, each carrying a different , sit on a lawn of bacteria growing on a dark .
Each disc has a around it, but the are very different in size.
The with the largest zone would be the best choice to treat an infection with these bacteria.

Lesson 14 of 24

How has the overuse of antibiotics spread resistance?

is not something a bacterium learns. It comes from random changes in its DNA. then act as a : they kill the bacteria that are susceptible and leave the ones to multiply.

The diagram below shows how a is selected.

Four panels joined by arrows. Panel 1, a mutation, shows about eighteen oval bacteria, all blue except one orange. Panel 2, antibiotic used, has a pink background; every blue bacterium is grey and crossed out with a red X, and only the orange one is unmarked. Panel 3, survivor divides, shows six orange bacteria. Panel 4, resistant population, shows about eighteen bacteria, all orange except one blue. Captions explain each step. A line of text below says resistance alleles can also be passed between bacteria, even of different species, on plasmids, and a key shows blue as susceptible and orange as resistant. — Selection for antibiotic resistance in a population of bacteria. Original BioWelsh diagram.

Bacteria divide very quickly, so arise often. By chance, one may give , for example by coding for an that breaks down the .
When the is used, the susceptible bacteria are killed but the one survives.
It has a , so it reproduces and passes the to its offspring.
Soon most of the is , and the no longer works.
are often carried on , which can be passed from one bacterium to another, even to a different .

How bacteria resist penicillin and tetracycline
Antibiotic	Ways bacteria resist it
	Secreting an , (), that breaks down ; a changed that cannot bind to; fewer or smaller , so less gets in
Tetracycline	Pumping tetracycline out of the cell; proteins that remove it from the ; changed that it cannot bind to

Prescribing for viral infections, such as colds, where they cannot help.
Not taking as prescribed, which can leave partly bacteria alive.
Using in farm animals to prevent disease in crowded conditions or to make them grow faster. Using them as growth promoters has been banned in the EU since 2006.
getting into the environment, for example in sewage and farm waste, where they select bacteria.

Examples include (methicillin- aureus), which resists and related drugs and spreads in hospitals, and Clostridioides difficile, which causes severe diarrhoea when broad-spectrum kill the normal gut bacteria. Some strains of and gonorrhoea now resist several drugs. Vancomycin is kept as a last resort for such infections, and new are urgently needed, because without them ordinary surgery would become dangerous again.

Lesson 15 of 24

How does the body keep pathogens out?

The body's first defences work against any , so they are called non-specific. They are always ready and act within minutes, before the specific immune response has had time to start.

The body's natural barriers to infection
Barrier	How it reduces the risk of infection
Skin	A tough outer layer of dead, keratin-filled cells that cannot get through; the beneath is strengthened by
Skin flora	Harmless bacteria and fungi that use up space and nutrients, so cannot settle
Mucus and ciliated epithelium	Sticky mucus in the airways traps , and cilia sweep it up to the throat to be swallowed
Tears and saliva	Contain , an that breaks down the in bacterial cell walls
Stomach acid	Hydrochloric acid kills most swallowed with food and drink
Blood clotting	Seals a wound quickly, so cannot enter through the break
	Brings extra blood and to an infected or damaged area
	White blood cells engulf and digest

starts when damaged cells release chemicals such as . Arterioles widen, so more blood flows to the area, making it red and warm, and capillaries become leakier, so fluid and white blood cells move into the tissue, which swells. The raised temperature is also unfavourable to many .

The main are and . The diagram below shows .

Five stages joined by arrows, each showing a round lilac phagocyte with a two-lobed purple nucleus. In stage 1 a green oval bacterium with small orange triangles on it touches the top of the cell. In stage 2 the phagocyte has two arms curving up round the bacterium. In stage 3 the bacterium is inside a white circular vesicle in the cell, with three dark purple circles, the lysosomes, nearby. In stage 4 the vesicle is pale purple and filled with small purple dots around a smaller bacterium. In stage 5 only a few green dots remain inside the cell and orange triangles sit on its outer surface. Captions explain each stage and a line of text explains that orange triangles are antigens and dark purple circles are lysosomes. — Phagocytosis of a bacterium. Original BioWelsh diagram.

on the recognise on the surface of the bacterium, marking it as foreign.
The 's membrane flows round the bacterium and engulfs it.
The bacterium ends up in a vesicle called a phagosome, and lysosomes move towards it.
Lysosomes fuse with the phagosome and release , including , which digest the bacterium.
Useful products are absorbed. A then puts the bacterium's on its own surface, which starts the specific immune response.

Lesson 16 of 24

How does the body recognise a foreign antigen?

Every cell carries molecules on its surface, many of them proteins. The immune system learns to ignore the body's own molecules, called self, and to respond to anything else, called non-self or foreign. A foreign molecule that triggers a response is an . Because each response is aimed at one , it is called a specific immune response.

Where the cells of the immune system come from

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in the bone marrow
- : and
- B : mature in the bone marrow
  - : secrete
  - Memory B cells
- T : mature in the thymus
  - : release
  - T killer () cells: destroy infected cells
  - Memory T cells

are made in huge variety. Each one has of just one shape, so only a few fit any particular . The response starts when a engulfs a and displays its on its own membrane. This is , and it lets the right find the .

The cells of the specific immune response
Cell	Role
	Engulfs and presents their on its surface
	Binds a presented and releases that activate B cells, and
	Binds to and destroys body cells that display a foreign , such as infected or cancerous cells
B cell	Divides when activated to form and memory B cells
	Secretes large amounts of one
(B or T)	Stays in the blood for years and divides quickly if the same returns

Lesson 17 of 24

How do B cells and antibodies fight infection?

The is the part of the specific response that works through dissolved in the blood and tissue fluid. It is carried out by B , each of which has molecules on its membrane acting as .

The diagram below shows the .

Flow diagram from left to right. First, a large lilac macrophage with orange triangles on its surface. An arrow leads to a blue round T helper cell labelled Th, with a small receptor on its left edge holding an orange triangle, and yellow dots labelled cytokines on its right. An arrow leads to three green B cells, each with small Y-shaped receptors round its edge; the two upper cells have blue or grey receptor tips, and the lower one has orange tips and an orange triangle bound to its top receptor. An arrow leads to a cluster of seven identical small green cells. Two arrows lead from the cluster: up to a larger green plasma cell with wavy lines inside and small purple Y-shaped antibodies drifting away from it, and down to a green cell marked M, labelled memory B cell. Numbered captions below explain each step. — The humoral response: from antigen presentation to plasma cells and memory cells. Original BioWelsh diagram.

A engulfs the and presents its on its surface.
A with a complementary binds to the and releases .
The activate the one B cell whose are complementary to the . This is .
The selected B cell divides by mitosis many times, making a clone of identical cells. This is .
Most of the clone become , which secrete thousands of every second. The rest become memory B cells, which stay in the blood for years.

are proteins called . The diagram below shows the structure of one molecule.

A large Y shape made of four coloured bars. Two long purple heavy chains run side by side up the stem, joined by two short black bars labelled disulphide bridges hold the two heavy chains together, then separate to form the two arms. Each arm has a shorter blue light chain alongside it on the outside, joined to the heavy chain by a short black bar labelled disulphide bridge between light and heavy chain. The outer parts of both chains at the tips of the arms are paler, labelled variable region of heavy chain and variable region of light chain. The darker lower parts are labelled constant region of light chain and constant region of heavy chain, the same in all antibodies of this class. An orange antigen shaped like a block with a wedge sits in the cleft at the tip of each arm, labelled antigen and antigen binding site, its shape complementary to one antigen. A colour key is at the bottom right. — The structure of an antibody molecule. Original BioWelsh diagram.

An is made of four polypeptide chains, two long heavy chains and two short light chains, so it has quaternary structure.
The chains are held together by disulphide bridges, giving a Y shape.
The tips of the arms are the . Their amino acid sequence differs from one to the next, so each has its own binding sites.
The shape of an binding site is complementary to one , so the binds only to that , forming an - complex.
The rest of the molecule is the constant region, which is the same in all of one class. It lets recognise the .

Each has two binding sites, so it can bind to two at once. The diagram below shows the result.

On the left, six green oval bacteria arranged in two rows of three. Purple Y-shaped antibodies link them: along each row an antibody touches the end of one bacterium with one arm and the next bacterium with the other, and between the rows three antibodies each touch a bacterium above and below. Text below says each antibody has two binding sites, so it links two bacteria and they clump together. An arrow leads right to a large lilac phagocyte with a nucleus, containing a large white vesicle holding four green bacteria. Text below says a phagocyte engulfs a whole clump at once, so the bacteria are destroyed more quickly. A small key at the top right shows the antibody symbol. — Agglutination: antibodies clump bacteria so phagocytes can engulf them. Original BioWelsh diagram.

link bacteria together into clumps. This is .
A can engulf a whole clump at once, so the bacteria are destroyed more quickly.
also cover and the parts of viruses that attach to cells, so they can no longer do harm.

Because are so specific, they are used in tests. In an test, bacteria from a patient are mixed with against one strain: shows that strain is present, and no shows it is a different strain with different . In an , an is to a well, and a patient's blood is added. If the patient has made against that , they bind, and a second carrying an produces a colour change. A negative result early in an infection may be false, because have not yet been made.

Lesson 18 of 24

How do T cells destroy infected cells?

cannot reach a virus once it is inside a cell. The deals with this by destroying the infected cell itself, by direct cell contact. It also destroys cancer cells and the cells of transplanted organs, which carry non-self .

The diagram below shows the .

Three stages joined by arrows. Stage 1 is a rounded cream body cell with a brown nucleus and three small grey hexagonal viruses inside, and three red triangles on its top surface, labelled a body cell infected by a virus displays viral antigens on its surface. In stage 2 the same cell has a blue round T killer cell, labelled Tk, sitting on top, with a notch in its underside fitting over one red triangle; a yellow cell labelled Th with small yellow dots is at the top right. The caption says a T killer cell with a complementary receptor binds the antigen and cytokines from T helper cells make it divide. In stage 3 the infected cell has a dashed outline, the T killer cell is on top, and small red dots labelled perforin lie between them. The caption says perforin makes holes in the membrane so the cell dies, and cancer cells are killed the same way. A key line explains the symbols and notes that some T cells become memory T cells. — The cell-mediated response: a T killer cell destroys an infected body cell. Original BioWelsh diagram.

A body cell infected by a virus displays pieces of viral protein on its surface, so it now carries a foreign .
A with a complementary to that binds to the infected cell.
from make the matching divide by mitosis (), and also stimulate .
The releases a protein called , which makes holes in the infected cell's membrane, so the cell dies before the virus can be copied.
Some of the clone become memory T cells, ready for another infection.

The humoral and cell-mediated responses compared
Feature	Humoral response	Cell-mediated response
Main cells	B and	T (T helper and )
How it works	in the blood and tissue fluid	Direct contact between cells
Main targets	and outside cells	Infected body cells and cancer cells
	Memory B cells	Memory T cells

Lesson 19 of 24

Why is the second response to an antigen faster and bigger?

The first time the body meets an , there are only a few that fit it, and they must be found, activated and multiplied before any appear. This is the . If the same returns, are already waiting, and the is much faster and stronger.

The graph below shows the concentration of in the blood after two exposures to the same .

Line graph. The horizontal axis is time from 0 to 80 days and the vertical axis is antibody concentration in arbitrary units from 0 to 110. Dashed vertical lines mark the first exposure at day 0 and the second exposure at day 40. After the first exposure the line stays at zero for about 6 days, then rises to a small peak of about 10 at day 14, labelled primary response, and falls slowly to almost zero by day 40. After the second exposure the line rises steeply from about day 42, reaching about 99 at day 52, labelled secondary response, then falls slowly to about 62 at day 80. — Antibody concentration in the blood after two exposures to the same antigen. Original BioWelsh graph with illustrative data.

After the first exposure there is a of several days with no . During this time present the , release , and the right B cells are selected and divide.
then rises as secrete it, reaching only a small peak, and falls again as the are broken down. Symptoms usually appear during a .
After the second exposure the is much shorter, because recognise the at once and divide rapidly.
rises faster, to a much higher concentration (here about ten times higher), and stays high for longer, so the is destroyed before symptoms develop.

The primary and secondary responses compared
Feature	Primary response	Secondary response
	Long, several days	Short, one or two days
Cells that respond first	A few naive B and T cells	Many
Peak concentration	Low	Much higher
How long stays high	A short time	Much longer
Symptoms	Usually	Usually none: the person is immune

Two classes of are often measured. IgM is made first, early in a , and soon falls. IgG is made later and in larger amounts, and it dominates the . So a high level of IgM suggests a recent, first infection.

Lesson 20 of 24

What is the difference between active and passive immunity?

In your own immune system makes the , after meeting the , and are formed, so protection lasts. In you are given made by someone else. Protection starts at once, but no are made and the are soon broken down, so it lasts only weeks.

The four kinds of immunity
How it is gained	Active: you make the antibodies	Passive: you receive antibodies
Natural	Catching the disease	crossing the , or in breast milk
Artificial		An injection of , for example after a exposure

is a viral disease of the nervous system, usually passed on by the bite of an infected animal. Once symptoms start it is almost always fatal, but the virus travels slowly along to the brain, which gives time to act. After a bite, the wound is washed thoroughly, (ready-made ) is injected, and a course of is started.

The graph below shows why both are given.

Line graph. The horizontal axis is time after the bite from 0 to 60 days and the vertical axis is antibody concentration in arbitrary units from 0 to 50. The orange line, injected antibodies (passive), starts at 8 on day 0 and falls gradually to about 2 by day 30 and under 1 by day 60. The purple line, antibodies made after vaccination (active), is zero until about day 7, then rises steeply to about 40 by day 25 and levels off at about 42. — Antibody concentration after a bite from a rabid animal: injected antibodies and a course of vaccine. Original BioWelsh graph with illustrative data.

The injected (orange) are present from the start, so they attack the virus at once, while the person's own response is still in its .
They are foreign proteins, so they are gradually broken down, and after a few weeks few are left.
The (purple) produces no for about a week, then the person's own rise to a much higher level and stay high, because have been made.
Together they give immediate protection and long-lasting immunity.

Lesson 21 of 24

How does vaccination protect against disease?

A uses the principles of the active immune response. It gives the body the of a without causing the disease. The body makes a , including , so that if the real arrives it meets a fast and is destroyed before it can cause illness.

Kinds of vaccine
What the vaccine contains	Example
Live, weakened ()	MMR (measles, mumps and ),
Killed or inactivated	Whooping cough, the injected polio
Inactivated (toxoids)	Tetanus, diphtheria
Isolated	HPV
mRNA that the body's cells use to make the	Some COVID-19

(German measles) is a mild disease in children, but if a woman catches it in early pregnancy the virus can damage the developing foetus, causing deafness, blindness and heart defects. Vaccinating all children with MMR that almost everyone is immune before they are old enough to become pregnant, and the virus has little chance to circulate. has only one , so one protects against all of it.

The number of slowly falls after , so some are followed by a : a second dose that causes a , raising levels and making more . Some need two doses for this reason, and some, such as the , are given every year because the change.

Lesson 22 of 24

Why do some vaccination programmes work better than others?

Some give lifelong protection after one or two doses; others need boosters, protect only partly, or have never been made at all. The difference depends on the and on how many people are vaccinated.

The must be highly , producing a strong response and many .
The should have only one . If there are many, a must contain from all of them.
The should not change. A high rate, as in and HIV, stop fitting.
The should not hide from the immune system inside cells or in the gut, as Plasmodium and cholerae partly do.
There should be no animal , or the can return from animals.
Enough people must be vaccinated for .

How well vaccination works against different diseases
Disease	How well vaccination works	Main reason
	Eradicated	One stable , highly , no animal
Measles and	Very well, if uptake is high	One ; live gives long-lasting memory
	Partly; new every year	and shift; animal
	Partly; protection lasts a few years	Bacteria live in the gut, out of reach of much of the immune system
Tuberculosis	Good in children, poor in adults	Bacteria hide inside
	Only partial so far	Many , change between life stages, parasite inside cells

When most people are immune, a struggles to find anyone to infect. The diagram below shows this idea, called .

Two grids of 70 circles in 7 rows of 10, separated by a dashed line. Green circles are vaccinated, white circles are not vaccinated and not infected, and red circles are infected. In the centre of each grid one circle is ringed as the first case. The left grid, headed 30% vaccinated, has 41 red circles spread across most of the grid, with green circles scattered among them and a few white circles at the right. The caption says the first case passes the infection on to 40 unvaccinated people. The right grid, headed 85% vaccinated, is mostly green, with the ringed red first case, two more red circles next to it and about eight white circles scattered around the edges. The caption says the infection reaches only 2 more people, then has nowhere to go, so the outbreak dies out. — Herd immunity: how the proportion vaccinated affects the spread of an infection. Original BioWelsh diagram.

On the left, only 30% of people are vaccinated, so the infection passes from person to person through the many who are not.
On the right, 85% are vaccinated, so the infection meets a vaccinated person on almost every side and soon dies out.
This protects people who cannot be vaccinated, such as babies and people having chemotherapy.
The proportion needed depends on how the disease is. For measles, about 95% of people must be immune.

Lesson 23 of 24

What ethical issues must vaccination programmes consider?

saves millions of lives a year, and a high uptake protects the whole . But deciding who is vaccinated, when, and whether it should be compulsory raises difficult ethical questions.

Issues to weigh when designing a vaccination programme
Issue	What must be considered
Safety and side effects	Mild effects such as a sore arm and fever are common; serious effects are very rare but must be weighed against the risk of the disease
Testing	New must be tested on animals and then on volunteers in trials before use
Individual rights	In the UK is voluntary, respecting a person's right to choose treatment
The	People who refuse put others at risk, including those who cannot be vaccinated
Cost-effectiveness	Whether the cost of vaccinating everyone is justified by the illness prevented, or whether only groups at risk should be offered it
Fairness	Who gets a first when supplies are short, and whether poorer countries can afford it or store it cold

Medical reasons: people with weakened immune systems, for example those with HIV or having chemotherapy, cannot safely have live .
Religious or personal beliefs.
Mistrust of drug companies or of government.
Fear of side effects, often from misinformation.

The MMR shows how fear can spread. In 1998 a small, flawed study claimed a link between MMR and autism. The claim was investigated, found to be false, and the paper was retracted, but MMR uptake in the UK fell from over 90% to around 80%. Measles returned: in 2012 and 2013 an outbreak centred on Swansea caused over a thousand cases. Science corrects its mistakes through peer review and repeated studies, but misinformation can move faster.

Related learning

Microbiology
The , bacterial cell walls, culturing and are the basis of action and testing.
Human reproduction
cross the , giving natural to the foetus.
Variation & evolution
is an example of .
Applied genetics
projects on Anopheles and Plasmodium aim to improve .

Specification & sources

https://www.wjec.co.uk/media/mxbh1zaf/wjec-gce-biology-spec-from-2015-e-101025.pdf
https://openstax.org/books/biology-2e/pages/42-1-innate-immune-response
https://openstax.org/books/biology-2e/pages/42-2-adaptive-immune-response
https://openstax.org/books/biology-2e/pages/42-3-antibodies
https://openstax.org/books/biology-2e/pages/21-2-virus-infections-and-hosts
https://openstax.org/books/microbiology/pages/14-2-fundamentals-of-antimicrobial-chemotherapy
https://openstax.org/books/microbiology/pages/14-3-mechanisms-of-antibacterial-drugs
https://openstax.org/books/microbiology/pages/14-5-drug-resistance
https://openstax.org/books/microbiology/pages/14-6-testing-the-effectiveness-of-antimicrobials
https://openstax.org/books/microbiology/pages/16-1-the-language-of-epidemiologists
https://openstax.org/books/microbiology/pages/18-5-vaccines
https://openstax.org/books/microbiology/pages/22-2-bacterial-infections-of-the-respiratory-tract
https://openstax.org/books/microbiology/pages/24-3-bacterial-infections-of-the-gastrointestinal-tract
https://openstax.org/books/microbiology/pages/25-4-parasitic-infections-of-the-circulatory-and-lymphatic-systems
https://openstax.org/books/microbiology/pages/22-3-viral-infections-of-the-respiratory-tract
https://openstax.org/books/microbiology/pages/21-3-viral-infections-of-the-skin-and-eyes
https://openstax.org/books/microbiology/pages/3-3-unique-characteristics-of-prokaryotic-cells
https://openstax.org/books/microbiology/pages/18-1-overview-of-specific-adaptive-immunity
WJEC GCE A Level Biology Unit 4 mark schemes and examiner reports, Option A: Summer 2017 (Q7), 2018 (Q6), 2019 (Q8), 2023 (Q7), 2024 (Q7) and 2025 (Q7): depth, exam wording and rejected answers
images/u4.immunology__photo-vibrio.jpg · Ronald Taylor, Tom Kirn and Louisa Howard, Dartmouth Electron Microscope Facility · Copyrighted free use · https://commons.wikimedia.org/wiki/File:Cholera_bacteria_SEM.jpg
images/u4.immunology__photo-tb.jpg · CDC/Dr. George P. Kubica · Public domain · https://commons.wikimedia.org/wiki/File:Mycobacterium_tuberculosis_Ziehl-Neelsen_stain_02.jpg
images/u4.immunology__photo-smallpox.jpg · CDC/Dr. Fred Murphy and Sylvia Whitfield · Public domain · https://commons.wikimedia.org/wiki/File:Smallpox_virus_virions_TEM_PHIL_1849.JPG
images/u4.immunology__photo-flu.jpg · CDC/F. A. Murphy · Public domain · https://commons.wikimedia.org/wiki/File:Influenza_A_virus_-_negative_stain_image_TEM.JPG
images/u4.immunology__photo-anopheles.jpg · Edward McClellan, CDC · CC0 · https://commons.wikimedia.org/wiki/File:A._quadrimaculatus.jpg
images/u4.immunology__photo-malaria-rings.jpg · CDC/Dr. Greene · Public domain · https://commons.wikimedia.org/wiki/File:Plasmodium_falciparum_rings_form_parasites4885_lores.jpg
images/u4.immunology__photo-gametocytes.jpg · CDC/Dr. Mae Melvin · Public domain · https://commons.wikimedia.org/wiki/File:Plasmodium_falciparum_01.png
images/u4.immunology__photo-antibiogram.jpg · Ajay Kumar Chaurasiya · CC0 · https://commons.wikimedia.org/wiki/File:Lactococcus_garvieae_antibiogram_pattern_on_blood_agar.jpg
https://creativecommons.org/publicdomain/zero/1.0/
https://creativecommons.org/publicdomain/mark/1.0/

Why is the human body described as a host?

What do the key terms about disease mean?

How is cholera caught, prevented and treated?

How does tuberculosis spread and how is it controlled?

How was smallpox wiped out?

Why does influenza keep coming back?

How is malaria transmitted and controlled?

How do the five named diseases compare?

How do viruses reproduce and cause disease?

What are antibiotics, and how are they classified?

How does the cell wall of Gram-negative bacteria protect them?

How do penicillin and tetracycline work?

How do you find out which antibiotic works best?

How has the overuse of antibiotics spread resistance?

How does the body keep pathogens out?

How does the body recognise a foreign antigen?

How do B cells and antibodies fight infection?

How do T cells destroy infected cells?

Why is the second response to an antigen faster and bigger?

What is the difference between active and passive immunity?

How does vaccination protect against disease?

Why do some vaccination programmes work better than others?

What ethical issues must vaccination programmes consider?

Putting Option A together

Worksheets

Worksheet 1: Option A Immunology and disease (160 marks)

Check your understanding.

Tick-borne encephalitis is always present at low levels in some forested parts of Europe. Which term describes the disease in these areas?

Immunology and disease

Why is the human body described as a host?

What do the key terms about disease mean?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 5 of 7 WJEC exam series (2017 to 2025), 8 marks in total. This is a revision priority, not a prediction of your exam.

How is cholera caught, prevented and treated?

How does tuberculosis spread and how is it controlled?

How was smallpox wiped out?

Why does influenza keep coming back?

How is malaria transmitted and controlled?

How do the five named diseases compare?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 3 of 7 WJEC exam series (2017 to 2025), 8 marks in total. This is a revision priority, not a prediction of your exam.

How do viruses reproduce and cause disease?

What are antibiotics, and how are they classified?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 3 of 7 WJEC exam series (2017 to 2025), 13 marks in total. This is a revision priority, not a prediction of your exam.

How does the cell wall of Gram-negative bacteria protect them?

How do penicillin and tetracycline work?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 3 of 7 WJEC exam series (2017 to 2025), 13 marks in total. This is a revision priority, not a prediction of your exam.

How do you find out which antibiotic works best?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 3 of 7 WJEC exam series (2017 to 2025), 10 marks in total. This is a revision priority, not a prediction of your exam.

How has the overuse of antibiotics spread resistance?

How does the body keep pathogens out?

How does the body recognise a foreign antigen?

How do B cells and antibodies fight infection?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 4 of 7 WJEC exam series (2017 to 2025), 13 marks in total. This is a revision priority, not a prediction of your exam.

How do T cells destroy infected cells?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 4 of 7 WJEC exam series (2017 to 2025), 13 marks in total. This is a revision priority, not a prediction of your exam.

Why is the second response to an antigen faster and bigger?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 5 of 7 WJEC exam series (2017 to 2025), 15 marks in total. This is a revision priority, not a prediction of your exam.

What is the difference between active and passive immunity?

How does vaccination protect against disease?

Why do some vaccination programmes work better than others?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 4 of 7 WJEC exam series (2017 to 2025), 9 marks in total. This is a revision priority, not a prediction of your exam.

What ethical issues must vaccination programmes consider?BWRBioWelsh recommendedWe recommend revising this because it has appeared regularly in past papers. Asked in 3 of 7 WJEC exam series (2017 to 2025), 7 marks in total. This is a revision priority, not a prediction of your exam.

Putting Option A together

Worksheets

Worksheet 1: Option A Immunology and disease (160 marks)

Check your understanding.

What do the key terms about disease mean?

How do the five named diseases compare?

What are antibiotics, and how are they classified?

How do penicillin and tetracycline work?

How do you find out which antibiotic works best?

How do B cells and antibodies fight infection?

How do T cells destroy infected cells?

Why is the second response to an antigen faster and bigger?

Why do some vaccination programmes work better than others?

What ethical issues must vaccination programmes consider?