Defence against infectious disease

An **organism or particle that causes disease** — a bacterium, virus, fungus or protist.

**Bacteria, viruses, fungi and protists.**

By **damaging the cells** it infects, and by releasing **toxins** that disrupt how cells work.

A barrier that **stops pathogens entering** the body in the first place — the skin, mucous membranes and stomach acid.

The **skin**, the **mucous membranes** (mucus + cilia) and **stomach acid**.

It is a tough, dry **physical barrier** of dead cells that pathogens cannot easily cross while it is unbroken.

They make sticky **mucus** that **traps** pathogens; in the airways, **cilia** then sweep the mucus away.

Its strong acid (very **low pH**) **kills most pathogens** that are swallowed in food or mucus — a **chemical** barrier.

**Stomach acid** — it chemically kills pathogens. Skin and mucus are physical barriers.

They work against **any pathogen**, not just one particular kind.

It **breaks the skin barrier**, giving pathogens a direct way into the body.

Less acid **kills fewer swallowed pathogens**, so more survive, reach the gut and cause infection.

Through **dehydration** — a large loss of water (and salts) from the body, which can be fatal.

A plug of trapped blood cells held together by a mesh of **fibrin** fibres, which seals a damaged blood vessel.

It **stops blood loss** AND acts as a **barrier that keeps pathogens out** of the wound.

A **cut / damaged blood vessel** — its exposed surface activates platelets, which start the cascade.

They **stick** to the wound, **clump** together and **release clotting factors** that start the cascade.

Chemicals released at a wound that **switch on** the cascade of reactions leading to a clot.

**Thrombin** — it turns soluble fibrinogen into insoluble fibrin.

**Fibrinogen** is **soluble** (dissolved in plasma); **fibrin** is **insoluble** and forms the fibre mesh of the clot.

Clotting factors convert inactive **prothrombin** into the active enzyme **thrombin**.

It **traps platelets and red blood cells**, forming the clot that dries into a **scab**.

Cut vessel → platelets stick / release clotting factors → thrombin formed → fibrinogen → fibrin mesh → clot / scab.

It is triggered by a **damaged vessel surface**; clots in healthy vessels could block blood flow, so 'no damage → no clot'.

The clot / scab **seals the cut**, forming a **physical barrier** so pathogens cannot enter the tissues.

It is **fast**, **non-specific**, and has **no memory**.

**Phagocytes** — for example **macrophages** and **neutrophils**.

A type of white blood cell (leucocyte) that **engulfs and digests pathogens** by phagocytosis.

The process in which a phagocyte **engulfs a pathogen, encloses it in a vacuole, and digests it with enzymes**.

**Recognise** the pathogen → **engulf** it → **enclose** it in a vacuole → **digest** it with enzymes.

It acts against **any pathogen** in the same way, rather than targeting just one type.

It is the **membrane-bound 'bubble'** that holds the engulfed pathogen while enzymes break it down.

**Enzymes** released into the vacuole, which break the pathogen down.

Innate = **fast, non-specific, no memory** (phagocytes). Adaptive = **slow, specific, has memory** (lymphocytes).

**No** — they are part of the **adaptive** system. The innate cells are the phagocytes.

The **phagocyte** count rises first, because the innate response is the **fast** one; lymphocytes rise later.

Because they are **non-specific** — they do not need to 'learn' the pathogen first, so they act straight away.

Immunity that targets **one particular pathogen**, recognised by its **antigen** — unlike the non-specific skin and phagocytes.

A molecule (usually on a pathogen's surface) that the immune system **recognises as foreign** and responds to.

**Lymphocytes** — mainly **B-cells** and **T-cells**.

To **activate other immune cells**, especially the **B-cells** — it does **not** make antibodies itself.

**B-cells** (which become **plasma cells**) once they have been activated.

A **lymphocyte detecting the antigen** of an invading pathogen.

An antibody is a **Y-shaped protein**; the **tips of its arms** are **antigen-binding sites** (the variable region) that fit one antigen.

Its binding sites are a **specific shape, complementary to one antigen** — like a key that fits only one lock.

A **long-lived lymphocyte** kept after an infection, giving a **faster, stronger** response if the same pathogen returns.

**Memory cells** from the first exposure recognise the antigen **immediately**, so antibodies are made **faster and in greater amounts**.

Primary: a **slow, late, low** curve. Secondary: a **fast, early, much higher** curve.

They have had **no prior exposure** to that antigen — no previous infection or vaccination against it.

The **skin** barrier and **phagocytes** (phagocytosis) — they attack any pathogen the same way, with no memory.

**Human Immunodeficiency Virus** — it infects and destroys **helper T-cells**.

**HIV** is the virus; **AIDS** is the late stage of infection, when helper T-cell numbers are so low the immune system collapses.

Helper T-cells **activate other immune cells** (including B-cells that make antibodies), so losing them cripples the whole immune response.

Infections that take hold because the immune system is too weak to stop them — a hallmark of **AIDS**.

**Opportunistic infections and cancers** that a healthy immune system would normally prevent — not the virus directly.

A molecule (often on a pathogen's surface) that the immune system **recognises as foreign** and responds to.

A **Y-shaped protein** that binds to **one specific antigen**, marking the pathogen for destruction.

A **harmless** preparation of a pathogen's antigens that triggers **immunity (memory)** without causing the disease.

Harmless **antigen** → **primary response** (antibodies) → **memory cells** form → faster, larger **secondary response** on real infection.

The ability of the immune system to respond **faster and more strongly** the second time it meets the same antigen, thanks to **memory cells**.

**Memory cells** from the first exposure are already present, so antibodies are made **quickly and in greater numbers**.

As the **count drops** over years, the immune response weakens, so the patient suffers more **opportunistic infections** — progressing to **AIDS**.

HIV destroys the very **helper T-cells** a vaccine relies on to build immune memory.

A medicine that **kills bacteria** (or stops them growing) by attacking a structure or process **only bacteria have**.

The **cell wall** (its building), or bacterial **ribosomes** / **enzymes** — structures unique to bacterial cells.

A **virus is not a cell** — it has no cell wall, no ribosomes and no metabolism of its own, so there is **no bacterial target** for the antibiotic to attack.

They attack targets **unique to bacteria** (e.g. cell-wall building, bacterial ribosomes) that human cells do not have.

The ability of some **bacteria to survive** an antibiotic that would normally kill them.

By **natural selection**: a few bacteria are already resistant → the antibiotic kills the non-resistant ones → the **resistant survivors reproduce** → the strain becomes common.

**No** — resistance comes from existing **variation** (often a mutation) and is **selected** by the antibiotic; it is not learned during a bacterium's life.

A **resistant strain** has been selected — the resistant bacteria survived the first time and reproduced, so the drug no longer kills them.

Those colonies are a **resistant strain** that can survive the antibiotic.

An infectious disease that can be transmitted **directly from an animal to a human**.

**Rabies** (from a bite), some forms of **tuberculosis** (from cattle) and **Japanese encephalitis** (animal reservoir in pigs/birds).

They are all **zoonoses** — they can pass from an **animal to a human**.