OCR A Level Biology A: Pathogens, transmission and the first lines of defence (H420)

This study guide covers OCR A Level Biology A (H420) specification statements 4.1.1(a) to 4.1.1(e) in Module 4, Biodiversity, evolution and disease. It is aligned to the OCR specification Version 4.1 (April 2026), for first assessment in 2025. Module 4 content is assessed in the Biological diversity component and in the Unified biology component. Use it with the revision notes and the practice questions. The course hub is OCR A Level Biology and the printable list is the OCR A Level Biology checklist.

What this unit covers

Statement	What you must be able to do
4.1.1(a)	Name the types of pathogen and link each listed disease to its type
4.1.1(b)	Explain how animal and plant pathogens are transmitted: vectors, spores, living conditions, climate and social factors
4.1.1(c)	Describe plant defences: chemicals and responses that limit spread, such as callose deposition
4.1.1(d)	Describe the primary non-specific defences of animals
4.1.1(e)(i)	Describe the structure and action of phagocytes
4.1.1(e)(ii)	Examine and draw cells seen in blood smears

If you want a refresher on magnification first, see Foundations in Biology. Practical drawing skills are developed in Development of practical skills. To test yourself on this unit before you start, try the free diagnostics.

4.1.1(a) Types of pathogen

A pathogen is an organism or virus that causes disease. The specification asks for four types and gives these examples. You do not need the binomial names.

Type	Examples to know	Key features
Bacteria	Tuberculosis (TB) in humans; ring rot in potatoes	Prokaryotic cells with no nucleus; many damage tissue or release toxins
Viruses	HIV/AIDS (humans); influenza (animals); Tobacco Mosaic Virus (plants)	Not cells; they can reproduce only inside host cells
Protoctista	Malaria (animals); potato and tomato late blight (plants)	Eukaryotes; some are single-celled parasites, some are fungus-like
Fungi	Black sigatoka (bananas); athlete’s foot (humans)	Eukaryotes that grow as threads called hyphae and make spores

The question will often give a disease and ask for its type, so learn the table as pairs. The specification says no detail of the symptoms of specific diseases is required.

4.1.1(b) Transmission

Transmission is the passage of a pathogen from an infected host, or from a source in the environment, to a new host. The specification asks you to consider vectors, spores and living conditions. You are not asked to sort pathogens into direct and indirect transmission.

Vectors. A vector is an organism that carries a pathogen from one host to another without usually being harmed. The female Anopheles mosquito picks up the malaria pathogen when it feeds on infected blood and passes it on when it feeds on someone else. Many plant viruses are carried by sap-feeding insects such as aphids.

Spores. Fungal and fungus-like pathogens make spores that are light and easily carried. Late blight spores are carried by wind and splashed by rain from leaf to leaf, and black sigatoka spores spread in the same way on banana plantations. Athlete’s foot spores survive on damp floors, socks and towels.

Contact, droplets and body fluids. TB and influenza are passed on in droplets from coughs and sneezes. HIV passes in body fluids such as blood and semen, and from mother to child. Tobacco Mosaic Virus passes in sap on hands, tools and leaves that touch. Ring rot bacteria are spread in infected seed potatoes and on cutting tools and machinery.

Living conditions and climate. Warm, wet climates give mosquitoes standing water to breed in. Cool, damp weather suits late blight. Overcrowded housing and poorly ventilated rooms raise the chance that droplets are inhaled. Social factors include poor sanitation, shared needles, limited healthcare, travel and trade that move infected people, animals or plant material, and crops grown close together in monoculture.

Worked example: linking transmission to conditions

A farmer notices late blight spreading across a potato field after three days of rain. Explain why.

1. Rain splashes spores from infected leaves onto healthy leaves nearby.
2. Wind carries spores further across the field.
3. Wet leaves and humid air help spores germinate and infect.
4. Plants grown close together touch, so spread between neighbours is easy.

A good answer ties each point to the pathogen’s spores and the weather, not to “bad conditions” in general.

4.1.1(c) Plant defences

Plants have no immune system with antibodies. They use chemicals and responses that limit the spread of a pathogen.

Chemical defences. Plants make substances that kill or inhibit pathogens, and often pests as well. Examples include terpenoids, phenols, alkaloids, defensins (small antimicrobial proteins) and enzymes such as chitinase, which digests the chitin in fungal cell walls. Some are made all the time and some only after infection.

Responses that limit spread. Once a pathogen is detected, the plant can:

• Deposit callose. Callose is a polysaccharide laid down between the cell wall and the cell surface membrane, in plasmodesmata and in sieve plates. Blocking plasmodesmata stops the pathogen passing from cell to cell, and blocking sieve plates stops it moving in the phloem.
• Thicken and strengthen cell walls, for example by adding lignin around the site of attack.
• Kill cells around the infection (a hypersensitive response), leaving the pathogen with no living cells to feed on.
• Close stomata, so fewer bacteria can enter through the pores.
• Send chemical signals, such as salicylic acid, so that cells further away switch on their own defences.

Worked example: interpreting lesion data

A leaf infected with late blight has a lesion 4 mm across on day 0 and 14 mm across on day 3.

Increase in diameter = 14 - 4 = 10 mm
Mean rate = 10 / 3 = 3.3 mm per day (2 s.f.)
Area ratio (circular lesion) = (14 / 4)² = 12.25

The diameter grows 3.5 times but the area grows about 12 times. If a second variety showed a slower rate, one explanation is stronger callose deposition or an earlier hypersensitive response.

4.1.1(d) Primary non-specific defences in animals

Non-specific defences act against any pathogen in the same way. You need these six.

Skin. Intact skin is a barrier that pathogens cannot easily cross. It also makes sebum and carries harmless microorganisms that compete with pathogens. You do not need the details of skin structure.

Mucous membranes. Goblet cells secrete mucus, which traps microorganisms. Ciliated cells beat their cilia to sweep the mucus along the airway towards the pharynx, so it is swallowed and meets stomach acid. Mucus and tears contain lysozyme, an enzyme that breaks down bacterial cell walls.

Expulsive reflexes. Coughing and sneezing force mucus and trapped pathogens out of the airways. Vomiting and diarrhoea remove pathogens from the gut.

Blood clotting. The specification limits this to the main sequence. Damaged blood vessels expose platelets, which release substances. Through a cascade of events these cause soluble fibrinogen to be converted into insoluble fibrin. Fibrin forms a network that traps platelets and red cells and makes a clot. The clot stops blood loss and seals the wound against entry of pathogens. You do not need the names of clotting factors.

Wound repair. The clot dries to form a scab. Cells at the edge of the wound divide to replace lost tissue, and new connective tissue and blood vessels grow beneath the scab. The scab is shed when the skin is restored.

Inflammation. Damaged cells and mast cells release histamine and cytokines. Histamine makes arterioles dilate and capillary walls more permeable. More blood flows to the area and more fluid leaves the capillaries, so the area becomes red, warm and swollen. Phagocytes arrive in the tissue fluid and attack pathogens.

4.1.1(e)(i) Phagocytes

Phagocytes are white blood cells that engulf and digest pathogens.

Feature	Neutrophil	Macrophage (an antigen-presenting cell)
Nucleus	Lobed, usually 2 to 5 lobes	Large and often kidney-shaped
Cytoplasm	Pale and granular, many lysosomes	Abundant, many lysosomes
Origin	Made in bone marrow and released into blood	Develops from monocytes that leave the blood
Lifespan	Short, a few days	Long, weeks or months
Special role	First to arrive at infection	Displays antigens to activate the specific immune response

Mode of action.

1. Infected or damaged cells release cytokines. These signalling molecules attract phagocytes, which move towards the source (chemotaxis), and activate them.
2. Neutrophils squeeze between the cells of the capillary wall to reach the tissue.
3. Receptors on the phagocyte bind to molecules on the pathogen. Opsonins are proteins that coat the pathogen and make this binding easier, so the pathogen is engulfed more efficiently.
4. The cell surface membrane folds round the pathogen and the pathogen is taken in by endocytosis, inside a vesicle called a phagosome.
5. Lysosomes fuse with the phagosome and release hydrolytic enzymes that digest the pathogen.
6. A neutrophil usually dies after a few rounds of killing. An antigen-presenting cell instead places pieces of the pathogen’s antigens on its surface membrane, so that other cells of the immune system can recognise them.

4.1.1(e)(ii) Blood smears and drawing

A blood smear is a thin film of blood spread across a slide, stained (for example with Leishman’s or Giemsa stain) so that the nuclei and granules show. Find the cells under low power, then change to high power.

Cell	What you see
Red blood cell	Small, pink, round, no nucleus, pale centre; the most numerous
Neutrophil	About 10 to 12 µm; lobed nucleus; pale granular cytoplasm
Lymphocyte	Round, very large nucleus filling most of the cell, thin rim of cytoplasm
Monocyte	Largest white cell; kidney-shaped nucleus
Platelet	Tiny fragment, no nucleus

Drawing rules. Use a sharp pencil and single, continuous lines. Do not shade. Draw what you see, at a size that fills the space, in correct proportion. Draw only a few cells, label with ruled lines that do not cross, and give a title, the magnification and a scale bar.

Worked example: magnification

A neutrophil is drawn 60 mm across. Its actual diameter is 12 µm.

Convert: 60 mm = 60 000 µm
Magnification = image size / actual size = 60 000 / 12 = ×5000

If a scale bar 25 mm long represents 5 µm, the magnification is 25 000 / 5 = ×5000, which agrees. To find actual size, rearrange: actual size = image size / magnification.

Worked example: a differential count

A student counts 200 white cells in a stained smear.

Cell	Number	Percentage
Neutrophils	124	62
Lymphocytes	56	28
Monocytes	12	6
Eosinophils	6	3
Basophils	2	1

The percentage is number / 200 × 100. Suppose a patient’s neutrophil count rises from 4.2 to 9.8 (×10⁹ per dm³):

Percentage change = (9.8 - 4.2) / 4.2 × 100 = +133 % (3 s.f.)

A rise in neutrophils fits a bacterial infection, because neutrophils are the first phagocytes called to infected tissue.

Common errors

• Writing that viruses are “cells” or that they “divide”. They are made inside host cells.
• Saying a vector “causes” the disease. The pathogen causes it; the vector carries it.
• Describing callose as a chemical that kills the pathogen. It blocks movement and strengthens walls.
• Saying fibrin is converted into fibrinogen. It is the other way round.
• Forgetting the unit conversion between mm and µm in magnification questions.
• Writing “the lysosome eats the bacterium”. The phagosome holds the pathogen and lysosome enzymes digest it.

Official syllabus

OCR A Level in Biology A (H420), specification Version 4.1 (April 2026), for first assessment in 2025, published by OCR. This page covers statements 4.1.1(a) to 4.1.1(e) in Module 4.