OCR GCSE Biology A: Gateway Science (J247)

B6.3 Monitoring and maintaining health

OCR Gateway B6.3 'Monitoring and maintaining health' is the OCR J247 equivalent of communicable diseases. It pulls together pathogens (bacteria, viruses, fungi, protists), the body's physical and immune defences, and the three big drug classes — antibiotics, antivirals and antifungals — plus drug resistance and HIV/AIDS. This page works through each piece with the exact phrasing OCR examiners reward. By the end you'll be able to write a 6-mark answer on why incomplete antibiotic courses drive resistance, explain why antibiotics don't touch influenza, and describe how HIV leads to AIDS and death by secondary infection.

From the J247 specification

Health is the state of physical and mental wellbeing. Communicable diseases are caused by pathogens — bacteria, viruses, fungi, protists — and spread between people or organisms. Non-communicable diseases (cardiovascular disease, cancer, etc.) are not spread between people. The body has physical defences (skin, mucus, cilia, stomach acid) and an immune system (phagocytes + lymphocytes + antibodies + memory cells). Antibiotics target bacteria only and have NO effect on viruses or fungi — using antibiotics inappropriately drives the evolution of antibiotic resistance through natural selection. Antivirals treat viral infections; antifungals treat fungal infections. HIV is a virus that infects T-helper lymphocytes; over time it weakens the immune system, leading to AIDS where the patient becomes susceptible to secondary infections. Drug development: preclinical + 3-phase clinical trials before approval.

Why this matters

Throughout history the biggest killers have been infectious diseases — plague, smallpox, cholera, tuberculosis, malaria. Today we control most of them in wealthy countries, but globally pathogens still kill millions every year (HIV, TB, malaria, plus emerging diseases like COVID-19). Understanding how pathogens infect, how the body fights back, and how vaccines and antimicrobial drugs work is some of the most important biology you learn at school. The four types of pathogen (bacteria, viruses, fungi, protists) all have different structures and life cycles, which is why no single drug treats all of them. OCR Gateway frames this topic around maintaining health — so the focus is not only on the pathogens themselves but on how clinicians decide which drug to prescribe, and how poor prescribing (incomplete courses, antibiotics for viral colds) drives antimicrobial resistance. HIV/AIDS is the showcase example of how a virus can disable the immune system itself, leading to death by secondary infection rather than the original pathogen.

How to learn this topic

Build on what you already know

OCR B1 / B2: bacteria are prokaryotic; viruses are not cells; cell ultrastructure.
OCR B2: blood contains white blood cells; the digestive system contains hydrochloric acid.
OCR B6 earlier sections: non-communicable diseases (cardiovascular, cancer) and lifestyle risk factors — health is more than absence of disease.
KS3: pathogens spread between people; vaccines protect against disease.

Define health and distinguish communicable vs non-communicable diseases.
Pathogens — four types (bacteria, viruses, fungi, protists) with named examples.
Transmission routes (air, water, direct contact, vectors).
Physical defences — skin, mucus, cilia, stomach acid (OCR mark-scheme bundle).
Immune system — phagocytes, lymphocytes, antibodies, memory cells.
Antibiotics target bacteria only — why they fail on viruses and fungi.
Antivirals, antifungals — class of drug and what they target.
Antibiotic resistance — including incomplete courses + natural selection.
HIV → AIDS → secondary infection pathway.
Drug development: preclinical + 3-phase clinical trials before approval.

Key terms

pathogen: A microorganism that causes a communicable (infectious) disease. Four types: bacteria, viruses, fungi, protists. (OCR rewards 'microorganism that causes disease'. Don't just say 'germ'.)
communicable disease: A disease that can be transmitted between organisms — caused by a pathogen.
non-communicable disease: A disease that is not spread between people — e.g. cardiovascular disease, most cancers, type 2 diabetes. Usually linked to lifestyle or genetic risk factors.
antigen: A molecule on the surface of a pathogen that the immune system recognises as foreign. (Antigens are on the PATHOGEN; antibodies are made by the BODY in response.)
antibody: A Y-shaped protein made by lymphocytes that binds specifically to one type of antigen and marks the pathogen for destruction. (Specific = one antibody binds one antigen. Antibodies tag pathogens — they do not 'eat' them.)
phagocyte: A type of white blood cell that engulfs and digests pathogens (phagocytosis). Non-specific — works on any pathogen. (Phagocytes engulf. Lymphocytes produce antibodies. Different jobs.)
lymphocyte: A type of white blood cell that produces antibodies (specific to a particular antigen) and antitoxins, and forms memory cells after an infection.
T-helper lymphocyte: A lymphocyte that coordinates the immune response by activating other white blood cells. The cell type that HIV specifically infects and destroys. (Naming the T-helper lymphocyte explicitly is the OCR mark for explaining how HIV weakens the immune system.)
memory cell: A long-lived lymphocyte that remains in the body after an infection or vaccination. Responds rapidly to the same pathogen if it appears again.
antibiotic: A medicine, such as penicillin, that kills bacteria or stops them growing. Targets bacterial features (cell wall, 70S ribosomes). Does NOT work on viruses or fungi. (OCR always tests 'antibiotics kill bacteria; antivirals treat viruses' — keep them paired.)
antiviral: A medicine used to treat a viral infection. Targets viral replication inside host cells (e.g. by blocking viral enzymes such as reverse transcriptase or neuraminidase). (OCR phrase: 'antivirals are used to treat viral infections'. Influenza needs antivirals, not antibiotics.)
antifungal: A medicine used to treat a fungal infection. Targets fungal-specific features such as the chitin cell wall or ergosterol in the fungal membrane. (OCR phrase: 'antifungal medication should be prescribed' for fungal infections like athlete's foot — not antibiotics.)
antibiotic resistance: When bacteria evolve so antibiotics no longer kill them. Driven by mutation + natural selection — antibiotic overuse and incomplete courses select for resistant strains. (Linking phrase: 'naturally resistant bacteria survive, multiply, and spread resistance genes'.)
HIV: Human immunodeficiency virus — a virus spread through body fluids that infects and destroys T-helper lymphocytes, weakening the immune system.
AIDS: Acquired immune deficiency syndrome — the late stage of HIV infection, when the immune system is so weakened that the patient becomes susceptible to secondary (opportunistic) infections. (Death in AIDS patients is usually caused by a DIFFERENT pathogen (secondary infection), not by HIV itself.)
secondary infection: An infection that occurs when the immune system has already been weakened by something else (e.g. HIV/AIDS). Sometimes called an opportunistic infection.

Notes

Health and disease

OCR Gateway defines health as the state of physical and mental wellbeing — not just the absence of disease. Diseases come in two big categories:

Communicable diseases are caused by a pathogen and spread between organisms (influenza, HIV, tuberculosis, athlete's foot, malaria).
Non-communicable diseases (cardiovascular disease, most cancers, type 2 diabetes) are not spread between people — they have lifestyle or genetic causes.

This topic focuses on communicable diseases — how pathogens cause illness, how the body defends itself, and which drugs work against which class of pathogen.

Pathogens — four types

A pathogen is a microorganism that causes a communicable disease. Four kinds you must know for OCR Gateway:

| Type | Structure | Example disease |

|---|---|---|

| Bacteria | prokaryotic cells (no nucleus, plasmids, cell wall) | tuberculosis; salmonella food poisoning; gonorrhoea |

| Viruses | not cells — genetic material in a protein coat | influenza; HIV; measles; common cold; COVID-19 |

| Fungi | eukaryotic, often multicellular | athlete's foot (humans); rose black spot (plants) |

| Protists | eukaryotic, single-celled | malaria (caused by Plasmodium, spread by mosquitoes) |

How pathogens spread

Through the air — droplets from coughs and sneezes (influenza, measles, COVID).
Through water — drinking contaminated water (cholera).
Direct contact — touching infected skin, fluids or blood (athlete's foot, HIV, STIs).
Vectors — animals that carry pathogens (mosquitoes spread malaria).
Food — eating contaminated food (salmonella from undercooked meat).

Reducing spread: hygiene (handwashing, food safety), isolating infected people, vaccination, destroying vectors, treating water supplies.

Physical defences

Before the immune system gets involved, the body keeps pathogens out with a layered set of physical and chemical barriers — the OCR mark scheme wants all four phrases:

Skin acts as a barrier — tough, dry, mostly impenetrable; also produces antimicrobial secretions.
Mucus traps pathogens — lining the nose and airways.
Cilia beat to move mucus away — ciliated epithelial cells in the trachea and bronchi sweep trapped pathogens up to the throat to be swallowed.
Stomach acid kills pathogens — hydrochloric acid (~pH 2) destroys pathogens swallowed in food or mucus.

Tears and saliva also contain the enzyme lysozyme, which breaks down bacterial cell walls.

The immune system — white blood cells

If a pathogen breaches the physical and chemical barriers, white blood cells take over:

Phagocytes engulf and digest pathogens (phagocytosis) — non-specific.
Lymphocytes detect the unique antigens on a pathogen's surface and produce specific antibodies that bind to those antigens, causing agglutination (clumping) and marking the pathogens for destruction.
Some lymphocytes produce antitoxins that neutralise bacterial toxins.
After infection, some lymphocytes become memory cells that stay in the body and respond rapidly if the same pathogen returns — this gives long-term immunity.

Antibiotics — bacteria only

Antibiotics (e.g. penicillin) kill bacteria or stop them growing. They work by attacking features unique to bacterial cells — the peptidoglycan cell wall, the bacterial 70S ribosome, bacterial DNA gyrase — without harming our own cells.

Antibiotics do not work on viruses or fungi:

Viruses are not cells. They are genetic material inside a protein coat, and they replicate inside our own body cells using OUR cellular machinery. They don't have the bacterial cell wall, bacterial ribosomes or bacterial enzymes that antibiotics target. Influenza is a viral disease, so antibiotics do not treat it — antivirals are used to treat viral infections.
Fungi are not bacteria. Fungal cells are eukaryotic and have a chitin cell wall plus 80S ribosomes — very different from bacteria. Antibiotics designed for bacterial machinery don't touch them. Antifungal medication should be prescribed for fungal infections. Using antibiotics for a fungal infection is useless AND it raises the bacterial population's exposure to antibiotics, so unnecessary antibiotic use increases resistance.

Antibiotic, antiviral, antifungal — three different classes

|---|---|---|---|

| Antiviral | viral replication inside host cells (viral enzymes, e.g. reverse transcriptase, neuraminidase) | aciclovir, oseltamivir, antiretrovirals | viral infections (influenza, HIV, herpes) |

A doctor must match the drug class to the pathogen class. Prescribing an antibiotic for a viral or fungal infection wastes the drug, does not help the patient, and drives resistance.

Antibiotic resistance

Antibiotic resistance is the textbook example of natural selection in action:

Random mutations in bacterial DNA sometimes give a few bacteria resistance to a particular antibiotic.
When the antibiotic is used, non-resistant bacteria are killed but naturally resistant bacteria survive.
The resistant bacteria multiply and spread resistance genes — often via plasmids that can pass between species.
Over generations the whole population becomes resistant — the antibiotic becomes ineffective. MRSA is the classic example.

### Why finishing the course matters

If a patient stops taking an antibiotic course early, not all bacteria are killed if the course is stopped early. The surviving bacteria are the ones with most resistance. They multiply and spread resistance genes. So incomplete courses directly accelerate the evolution of resistance.

### Slowing resistance

Doctors should only prescribe antibiotics when truly needed (not for viral colds).
Patients must finish the full course.
Restricting agricultural antibiotic use in livestock.
Developing new antibiotics — but the pipeline is slow.

HIV and AIDS

HIV is the key OCR Gateway viral-disease example.

HIV (human immunodeficiency virus) is a virus transmitted through body fluids — unprotected sex, sharing needles, mother-to-baby during birth or breastfeeding.
HIV specifically infects and destroys T-helper lymphocytes — the white blood cells that coordinate the immune response by activating other lymphocytes and phagocytes.
Without enough T-helper lymphocytes, the immune system can no longer mount an effective response. HIV weakens the immune system.
After months or years (often slowed by antiretroviral drugs), the patient's T-helper count falls so low that AIDS develops (acquired immune deficiency syndrome).
An AIDS patient is susceptible to other infections that a healthy immune system would normally fight off — these are called secondary infections (or opportunistic infections). Common ones include tuberculosis, pneumonia, and certain cancers.
Patients with AIDS often die from a different pathogen / secondary infection — not from HIV directly. HIV disables the defences; another pathogen finishes the job.

Antiretroviral drugs (a class of antivirals) slow HIV replication and can keep patients alive for decades, but there is no cure.

Drug development pipeline

New drugs go through testing:

Preclinical testing — tested on cells, then on animals. Checks safety, efficacy, and dose.
Clinical trials phase 1 — healthy human volunteers, very low doses. Checks safety in humans.
Clinical trials phase 2 — small group of patients with the disease. Checks the drug works.
Clinical trials phase 3 — large group of patients, often double-blind placebo-controlled (neither doctor nor patient knows who's getting the real drug). Checks effectiveness vs control.
Approval and monitoring — drug licensed; long-term effects tracked after release.

The whole process typically takes 10+ years and costs hundreds of millions.

Exam tips

Name all FOUR pathogen types: bacteria, viruses, fungi, protists — with one named disease each (tuberculosis, influenza/HIV, athlete's foot, malaria).
Match the drug class to the pathogen class: antibiotic → bacteria; antiviral → virus; antifungal → fungus. Never write 'antibiotics for influenza'.
For HIV/AIDS questions, include the full chain: HIV infects T-helper lymphocytes → immune system weakens → AIDS develops → secondary infections → death from a different pathogen.
For incomplete-antibiotic-course questions, say 'not all bacteria are killed; naturally resistant ones survive and multiply, spreading resistance genes'.
For 'physical defences' questions, list the four-phrase bundle: skin barrier, mucus traps, cilia beat mucus away, stomach acid kills pathogens.
Antibiotic resistance = natural selection. Mutations are RANDOM; the antibiotic selects for already-resistant bacteria — it doesn't cause the resistance.
Phagocytes ENGULF; lymphocytes PRODUCE ANTIBODIES. Don't muddle the two white blood cell types.

Mark-scheme phrasing

Common misconceptions

Worked example

Question:

Answer:

Frequently asked questions

Why doesn't an antibiotic work on influenza?

Antibiotics kill bacteria — they attack features unique to bacterial cells like the peptidoglycan cell wall and the bacterial 70S ribosome. Influenza is a viral disease. Viruses are not cells at all; they are packets of genetic material in a protein coat that replicate inside YOUR own body cells. They don't have the bacterial cell wall or bacterial ribosomes that antibiotics target. Antivirals are used to treat viral infections — they target viral enzymes (like neuraminidase for flu, or reverse transcriptase for HIV) instead.

How does HIV lead to death from a different pathogen?

HIV is a virus that specifically infects and destroys T-helper lymphocytes — the white blood cells that coordinate the immune response. As T-helper numbers fall, HIV weakens the immune system. After months or years, the patient's T-helper count gets so low that AIDS develops. With a crippled immune system, the patient becomes susceptible to other infections — tuberculosis, pneumonia, certain cancers. These secondary infections are what usually cause death. So death is caused by a different pathogen / secondary infection — HIV disabled the defences but didn't kill the patient directly.

Why does finishing the full antibiotic course matter?

If you stop early because you feel better, not all the bacteria have been killed. The ones still alive are the toughest — often the ones with mutations giving them most resistance. These naturally resistant bacteria survive, multiply, and spread their resistance genes (sometimes via plasmids that can pass between species). Over time the antibiotic becomes ineffective. Finishing the full course gives the immune system + drug the best chance of wiping out the infection completely before any resistant bacteria can establish themselves.

Antibiotic, antiviral, antifungal — what's the difference?

Three different drug classes for three different pathogen types. ANTIBIOTICS (e.g. penicillin) kill bacteria by attacking the bacterial cell wall or 70S ribosomes — they treat bacterial infections like TB or strep throat. ANTIVIRALS (e.g. oseltamivir for flu, antiretrovirals for HIV) block viral replication inside host cells — they treat viral infections. ANTIFUNGALS (e.g. clotrimazole for athlete's foot) attack fungal-specific features like the chitin cell wall or ergosterol in the fungal membrane — they treat fungal infections. The doctor must match drug class to pathogen class. An antibiotic for athlete's foot or flu does nothing useful and contributes to resistance.

What is antibiotic resistance and why is it a problem?

Antibiotic resistance is when bacteria evolve so antibiotics no longer kill them. Random mutations in bacterial DNA sometimes confer resistance. When antibiotics are used (especially overused or in incomplete courses), the non-resistant bacteria die but naturally resistant bacteria survive and multiply. They spread resistance genes — sometimes between species via plasmids. As more and more bacteria become resistant, our antibiotics stop working. MRSA is a famous example. Developing new antibiotics is slow and expensive, so global health authorities now treat antibiotic stewardship as a major priority.

What's the difference between an antigen and an antibody?

Easy to muddle. ANTIGEN: a molecule on the SURFACE of a pathogen that the immune system recognises as foreign. ANTIBODY: a Y-shaped protein the BODY (lymphocytes) makes in response to a particular antigen — antibodies bind to that antigen and mark the pathogen for destruction. Memory aid: anti-GEN = on the GERM; anti-BODY = made by the BODY.