DP Biology SL C3.2 Defence Against Disease

DP Biology SL C3.2 Defence Against Disease - Full notes

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DP Biology SL | C3.2 Defence Against Disease

DP BIOLOGY · THEME C: INTERACTION AND INTERDEPENDENCE

C3.2

Defence Against Disease

Full notes for SL · IB-style

Contents

1	Pathogens and infectious disease
2	Primary defences: skin, mucous membranes and blood clotting
3	The innate immune system: phagocytes
4	The adaptive immune system: lymphocytes and antibodies
5	Immunological memory and vaccination
6	Antibiotics and antibiotic resistance
7	HIV, AIDS and zoonoses
8	Pathogens
9	Skin and mucous membranes
10	Blood clotting
11	Innate immunity: phagocytes
12	Adaptive immunity: lymphocytes
13	Antigens and antibodies
14	Primary and secondary immune responses
15	Vaccination
16	Herd immunity
17	Antibiotics and resistance
18	HIV and AIDS
19	Zoonoses
20	Mixed review: worked problems
21	Additional exam-style practice
22	Evaluating data on vaccines and disease
23	Common misconceptions and links
24	Exam-style question with markscheme
25	Check your understanding
26	Summary and topic map

These are full teaching notes. Read each section in order, try the Think about it question before you read on, and do every Quick check before moving to the next section.

Before you start

Rate yourself on each statement now, and again after you've worked through the notes. Shade R (not yet), A (getting there) or G (confident).

I can…	R	A	G
define pathogen and give examples of different types
explain the skin and mucous membranes as primary defences
explain blood clotting
explain phagocytosis as part of innate immunity
explain the roles of B and T lymphocytes, antigens and antibodies
explain immunological memory and how vaccines work
explain herd immunity
explain why antibiotics work on bacteria but not viruses, and how resistance evolves
explain how HIV affects the immune system and outline zoonoses

There is no additional HL content in this subtopic. SL and HL students study the same material.

Guiding questions

How do organisms protect themselves against pathogens? How do vaccines and antibiotics help, and why is antibiotic resistance a growing threat?

How this topic is examined

C3.2 is examined through descriptions of immune responses, antibody concentration graphs (primary and secondary responses), vaccination data and antibiotic resistance.

Use precise terms: antigen, antibody, B lymphocyte, plasma cell, memory cell, helper T cell, herd immunity.

Command term	What the examiner wants
State / Identify	a brief answer with no explanation needed
Outline	a brief account or summary
Describe	a detailed account, including trends or features, without reasons
Explain	a detailed account including causes, reasons or mechanisms
Distinguish / Compare and contrast	give the differences (and similarities), point by point
Calculate	a numerical answer with working and units
Deduce / Suggest	reach a conclusion from data; propose a reasonable explanation
Evaluate / Discuss	weigh strengths and limitations and reach a judgement

How to use these notes

Each section teaches one part of the syllabus in full. You'll see these boxes throughout; each has one job:

Box	What it's for
Think about it	a question to get you thinking before a section; the answer comes in the section
Key point	the one idea you must not forget
Common mistake	an error examiners see every year, and how to avoid it
In the real world	where the biology shows up outside the classroom
Try this	something quick you can do yourself to test the idea
Worked example	full solutions with IB-style marks (M1 method, A1 answer, R1 reasoning)
Quick check	short questions to test yourself at the end of each section

1 Pathogens and infectious disease

Disease-causing organisms and particles.

Think about it

Why do we usually get chickenpox only once, but can catch a cold many times?

A pathogen is an organism or virus that causes disease. Pathogens include viruses (influenza, measles, HIV, SARS-CoV-2), bacteria (Mycobacterium tuberculosis, Salmonella), fungi (athlete's foot), protists (Plasmodium, which causes malaria) and parasitic worms. Prions, misfolded proteins, cause diseases such as Creutzfeldt-Jakob disease.

Pathogens enter the body through the skin (cuts, insect bites), the respiratory system (droplets), the digestive system (contaminated food and water), and sexual contact. The body defends itself in layers: primary defences keep pathogens out; the innate immune system responds rapidly but non-specifically; and the adaptive immune system responds specifically and remembers.

2 Primary defences: skin, mucous membranes and blood clotting

The first line keeps pathogens out.

Skin is a tough physical barrier. Its outer layer consists of dead, keratin-filled cells that pathogens cannot easily penetrate. Sebaceous glands secrete sebum, containing fatty acids that keep the skin slightly acidic and inhibit bacterial growth.

Mucous membranes line the airways, digestive tract and urogenital tract. They secrete mucus, which traps pathogens; in the airways, cilia sweep mucus up to the throat to be swallowed. Tears and saliva contain lysozyme, an enzyme that digests bacterial cell walls. Stomach acid kills many pathogens in food.

Blood clotting seals cuts quickly, preventing blood loss and pathogen entry. Damaged tissues and platelets release clotting factors, triggering a cascade that converts the inactive protein prothrombin to the enzyme thrombin. Thrombin converts soluble fibrinogen into insoluble fibrin, which forms a mesh of fibres trapping blood cells to form a clot.

Figure 1. The blood clotting cascade.

Quick check

1. How does the skin prevent infection?

2. What converts fibrinogen to fibrin?

Answers: 1. tough keratinized barrier; acidic sebum 2. thrombin

3 The innate immune system: phagocytes

Fast, non-specific responses.

If pathogens get past the primary defences, the innate immune system responds. It is present from birth and responds in the same way to any pathogen. Damaged cells release chemicals that cause inflammation: blood vessels widen and become more permeable, bringing more white blood cells to the site.

Phagocytes (white blood cells such as neutrophils and macrophages) leave the blood and engulf pathogens by phagocytosis: the phagocyte recognizes the pathogen as foreign, extends its membrane around it, and encloses it in a vesicle (phagosome). Lysosomes fuse with the vesicle and their enzymes digest the pathogen. Macrophages then display fragments of the pathogen's antigens on their surface, which helps activate the adaptive immune system.

Figure 2. Phagocytosis.

Quick check

1. What does non-specific mean?

2. Describe phagocytosis.

Answers: 1. responds the same way to all pathogens 2. engulfing pathogen into a vesicle, digested by lysosomal enzymes

4 The adaptive immune system: lymphocytes and antibodies

Specific responses to specific antigens.

An antigen is a molecule, usually a protein or glycoprotein on the surface of a pathogen, that triggers an immune response. An antibody is a Y-shaped protein (immunoglobulin) produced by lymphocytes, with binding sites whose shape is complementary to a specific antigen.

Lymphocytes are white blood cells. Each B lymphocyte carries antibodies of one specificity on its surface. There are millions of different B cells, each able to recognize a different antigen.

The immune response: (1) a macrophage engulfs the pathogen and displays its antigens; (2) a helper T lymphocyte with a receptor matching the antigen binds and is activated; (3) a B lymphocyte with antibodies matching the same antigen binds the antigen; (4) the activated helper T cell binds the B cell and releases cytokines, activating it; (5) the activated B cell divides by mitosis to form a clone of cells (clonal selection and expansion); (6) most become plasma cells, which secrete large amounts of antibodies; some become memory cells.

Antibodies help destroy pathogens by agglutination (sticking pathogens together, so they are easier to engulf), neutralization of toxins and viruses (blocking their binding sites), opsonization (marking pathogens for phagocytes) and activating complement proteins that burst bacteria.

Figure 3. The adaptive immune response.

Cell	Role
Macrophage	engulfs pathogens; presents antigens
Helper T lymphocyte	recognizes antigen; activates specific B cells
B lymphocyte	recognizes antigen; divides to form clones
Plasma cell	secretes antibodies
Memory cell	long-lived; rapid response to reinfection

Common mistake

Saying antibodies kill pathogens directly. They bind to antigens, marking or immobilizing pathogens for destruction by phagocytes or complement.

Quick check

1. Define antigen.

2. What is clonal selection?

3. Give two ways antibodies help destroy pathogens.

Answers: 1. a molecule that triggers an immune response 2. activation and division of the specific B cell matching the antigen 3. agglutination, neutralization, opsonization

5 Immunological memory and vaccination

Remembering pathogens gives immunity.

After the first infection (the primary response), memory cells remain in the body for years. If the same pathogen infects again, memory cells recognize it immediately and produce a secondary response that is faster, stronger (much higher antibody concentration) and longer-lasting, usually destroying the pathogen before symptoms appear. The person is immune.

Vaccines contain antigens from a pathogen, in a form that cannot cause disease: weakened (attenuated) or killed pathogens, fragments such as proteins, or mRNA coding for an antigen (as in some COVID-19 vaccines). The vaccine triggers a primary response and the formation of memory cells, without the person having the disease. Booster doses may be given to strengthen memory.

Herd immunity occurs when a high proportion of a population is immune. The pathogen cannot spread easily, so non-immune individuals (such as babies or people who cannot be vaccinated) are protected indirectly. The proportion needed depends on how contagious the disease is: about 95% for measles.

Figure 4. Primary and secondary antibody responses.

WORKED EXAMPLE 1 Interpreting antibody data

Using the graph, compare the primary and secondary responses.

Solution

Secondary response is faster: antibodies rise within days of the second exposureA1

Secondary peak (160) is about ten times higher than the primary peak (15)A1

Due to memory cells that rapidly divide into plasma cellsR1

In the real world

Smallpox was declared eradicated in 1980 after a worldwide vaccination campaign, the only human disease eradicated so far. Polio has been eliminated from most of the world.

Quick check

1. Why is the secondary response faster?

2. How do vaccines work?

3. Define herd immunity.

Answers: 1. memory cells recognize the antigen immediately 2. introduce antigens to trigger a primary response and memory cells 3. protection of non-immune individuals when most of the population is immune

6 Antibiotics and antibiotic resistance

Drugs that target bacteria, and the bacteria that evolve to survive them.

Antibiotics are chemicals that kill bacteria or inhibit their growth, by targeting structures or processes found in bacteria but not in human cells: for example, penicillin blocks cell wall synthesis; tetracycline blocks bacterial (70S) ribosomes. Because they target bacterial features, antibiotics do not harm human cells.

Antibiotics do not work against viruses, because viruses have no cell walls, ribosomes or metabolism of their own; they use the host cell's machinery. Treating viral infections with antibiotics is useless and contributes to resistance.

Antibiotic resistance evolves by natural selection. In a large bacterial population, random mutations may produce a few resistant bacteria. When an antibiotic is used, susceptible bacteria die and resistant ones survive and reproduce, passing on the resistance gene. Resistance genes can also spread between bacteria on plasmids (horizontal gene transfer). Overuse and misuse of antibiotics, incomplete courses, and use in livestock speed this up. MRSA (methicillin-resistant Staphylococcus aureus) is a well-known example.

Reducing resistance requires using antibiotics only when necessary, completing courses, reducing agricultural use, good hygiene, and developing new antibiotics.

Quick check

1. Why don't antibiotics work against viruses?

2. Explain how resistance evolves.

Answers: 1. viruses lack the bacterial structures antibiotics target 2. mutation gives resistance; antibiotic selects resistant bacteria; they reproduce

7 HIV, AIDS and zoonoses

When a virus attacks the immune system itself.

The human immunodeficiency virus (HIV) infects and destroys helper T lymphocytes. Without helper T cells, B cells cannot be activated, so antibody production falls. Over years, the immune system is weakened until the person develops acquired immunodeficiency syndrome (AIDS), and suffers opportunistic infections and cancers that a healthy immune system would control.

HIV is transmitted through blood, sexual contact, shared needles, and from mother to baby. Antiretroviral drugs can control the virus and allow people with HIV to live long lives.

A zoonosis is an infectious disease that spreads from animals to humans. Examples include tuberculosis (from cattle), rabies, Ebola, avian influenza and probably COVID-19. Many new diseases are zoonoses, and their emergence is linked to human contact with wildlife, intensive livestock farming and habitat destruction.

Quick check

1. Which cells does HIV destroy?

2. Define zoonosis.

Answers: 1. helper T lymphocytes 2. a disease transmitted from animals to humans

8 Pathogens

Agents of infectious disease.

Type	Example	Disease
virus	influenza virus, HIV	influenza, AIDS
bacterium	Mycobacterium tuberculosis	tuberculosis
fungus	Candida albicans	thrush
protist	Plasmodium	malaria

WORKED EXAMPLE 2 Pathogen (basic)

Define pathogen.

Solution

An organism or virus that causes diseaseA1

9 Skin and mucous membranes

First line of defence.

The skin is a tough physical barrier: the outer layer of dead keratinized cells is hard to penetrate, and sebum and sweat make it slightly acidic. Mucous membranes in the airways, gut and genital tract secrete mucus that traps pathogens; cilia sweep it away; lysozyme in tears and saliva digests bacterial walls.

WORKED EXAMPLE 3 Barriers (standard)

Outline two features of skin that prevent infection.

Solution

Tough outer layer of dead cellsR1

Acidic secretions (sebum) inhibit bacterial growthR1

10 Blood clotting

Sealing wounds.

When a blood vessel is damaged, platelets and damaged tissue release clotting factors. A cascade converts prothrombin to thrombin, which converts soluble fibrinogen into insoluble fibrin. Fibrin forms a mesh that traps blood cells, forming a clot that seals the wound and prevents entry of pathogens.

WORKED EXAMPLE 4 Cascade (exam level)

Outline the role of thrombin in clotting.

Solution

Thrombin is an enzyme that converts fibrinogen into fibrinR1

Fibrin fibres form a mesh trapping cellsR1

Quick check

1. Why must clotting be tightly controlled?

Answers: 1. clots in vessels (thrombosis) can cause heart attacks and strokes

11 Innate immunity: phagocytes

Non-specific defence.

Phagocytes (neutrophils, macrophages) recognize pathogens, engulf them by endocytosis into a phagosome, and fuse it with lysosomes, whose enzymes digest the pathogen. Inflammation brings more phagocytes to infected sites.

WORKED EXAMPLE 5 Phagocytosis (standard)

Describe the process of phagocytosis.

Solution

Pathogen engulfed by endocytosis into a vesicleR1

Lysosomes fuse and enzymes digest the pathogenR1

12 Adaptive immunity: lymphocytes

Specific defence.

Lymphocytes recognize specific antigens. B lymphocytes produce antibodies; helper T cells activate B cells; cytotoxic T cells kill infected cells. Each lymphocyte has receptors for one antigen.

WORKED EXAMPLE 6 Activation (exam level)

Outline how B cells are activated.

Solution

B cell binds a specific antigenR1

Activated by a helper T cell with the same antigen specificityR1

Divides to form plasma cells and memory cells (clonal selection)R1

13 Antigens and antibodies

Lock and key of immunity.

Antigens are molecules (usually proteins or glycoproteins) that trigger an immune response. Antibodies are Y-shaped proteins with two antigen-binding sites (variable regions) and a constant region. Antibodies neutralize toxins, agglutinate pathogens and mark them for phagocytosis.

WORKED EXAMPLE 7 Antibody action (standard)

State two ways antibodies help destroy pathogens.

Solution

Agglutination (clumping)A1

Opsonization (marking for phagocytes); neutralizing toxinsA1

14 Primary and secondary immune responses

Memory cells.

The first exposure produces a slow, small primary response. Memory cells remain, so a second exposure produces a faster, larger and longer secondary response, often preventing illness: this is immunity.

Figure 5. Primary response (days 0–20) and secondary response after second exposure (day 25).

WORKED EXAMPLE 8 Secondary response (exam level)

Explain why the secondary response is faster.

Solution

Memory cells specific to the antigen remainR1

They divide rapidly into plasma cells on re-exposureR1

15 Vaccination

Artificial active immunity.

Vaccines contain antigens (weakened or inactivated pathogens, proteins, or mRNA coding for antigens) that stimulate a primary response and memory cells without causing disease. Vaccination programmes have eradicated smallpox and nearly eradicated polio.

WORKED EXAMPLE 9 mRNA vaccines (standard)

Explain how an mRNA vaccine produces immunity.

Solution

Cells translate the mRNA into the antigen proteinR1

Immune system responds, forming memory cellsR1

In the real world

Smallpox was declared eradicated in 1980 after a global vaccination campaign; it is the only human disease eradicated so far.

16 Herd immunity

Protecting the unvaccinated.

When a high enough proportion of a population is immune, transmission chains are broken, protecting those who cannot be vaccinated. The threshold depends on how infectious the disease is: about 95% for measles.

WORKED EXAMPLE 10 Threshold (standard)

The herd immunity threshold is 1 − 1/R0. Calculate it for measles (R0 = 15).

Solution

1 − 1/15M1

= 0.93 (93%)A1

17 Antibiotics and resistance

Treating bacterial infections.

Antibiotics kill or inhibit bacteria by targeting structures absent in human cells (cell walls, 70S ribosomes). They are ineffective against viruses. Overuse selects for resistant bacteria (such as MRSA); resistance spreads by natural selection and horizontal gene transfer.

WORKED EXAMPLE 11 Resistance (exam level)

Explain how antibiotic resistance spreads in a bacterial population.

Solution

Random mutation produces a resistant bacteriumR1

Antibiotic kills susceptible bacteria; resistant ones survive and reproduceR1

Resistance genes spread on plasmidsR1

18 HIV and AIDS

Attacking the immune system.

HIV infects helper T cells, reducing their number. Without helper T cells, B cells cannot be activated, so the immune system fails (AIDS), leaving the body open to opportunistic infections. HIV spreads through blood, sexual contact and from mother to child.

Quick check

1. Why do people with AIDS often die from infections such as tuberculosis?

Answers: 1. loss of helper T cells weakens the immune response

19 Zoonoses

Diseases from animals.

Zoonotic diseases pass from animals to humans: COVID-19 (probably from bats), rabies, bird flu, Ebola, tuberculosis (from cattle). Habitat loss and close contact with wildlife and livestock increase risk.

Quick check

1. Give two examples of zoonoses.

Answers: 1. rabies, avian influenza (or COVID-19, Ebola)

20 Mixed review: worked problems

Bringing the ideas together.

WORKED EXAMPLE 12 Mixed problem (exam level)

Distinguish between innate and adaptive immunity.

Solution

Innate: non-specific, immediate, no memory (barriers, phagocytes)R1

Adaptive: specific, slower first time, memory (lymphocytes, antibodies)R1

21 Additional exam-style practice

Paper 1 and Paper 2.

WORKED EXAMPLE 13 Paper 1 question (standard)

Which cells produce antibodies? A. macrophages B. plasma cells C. helper T cells D. platelets

Solution

BA1

WORKED EXAMPLE 14 Paper 2 question (exam level)

Explain why antibiotics are ineffective against viruses.

Solution

Viruses lack cell walls, ribosomes and metabolismR1

Antibiotics target bacterial structuresR1

22 Evaluating data on vaccines and disease

Epidemiology.

Epidemiologists use incidence (new cases per population per time) and prevalence data to assess vaccines. A sharp fall in cases after a vaccine is introduced, compared with control populations, supports its effectiveness; correlation must be interpreted carefully.

WORKED EXAMPLE 15 Incidence (standard)

A town of 50 000 has 120 new measles cases in a year. Calculate the incidence per 100 000.

Solution

120/50 000 × 100 000M1

= 240 per 100 000 per yearA1

23 Common misconceptions and links

Students often think…	Actually…
antibodies kill pathogens directly	they bind antigens and help other mechanisms destroy pathogens
antibiotics treat viral infections	they only work on bacteria
bacteria become resistant because they 'get used to' antibiotics	resistant mutants are selected
vaccines contain antibodies	vaccines contain antigens

How C3.2 connects to the rest of the course

Topic	Connection
A2.3 Viruses (HL)	viral structure and evolution
C1.1 Enzymes (HL: penicillin)	mechanism of antibiotic action
D4.1 Natural selection	evolution of resistance
B2.1 Membranes (HL)	phagocytosis
C2.1 Signalling (HL)	cytokines

24 Exam-style question with markscheme

Try this under exam conditions (about 18 minutes) before reading the markscheme.

Figure 6. Antibody concentration after two exposures to an antigen.

(a) Compare the primary and secondary responses. [2]

(b) Explain why the secondary response differs. [3]

(d) Explain why antibiotics are ineffective against viral infections. [2]

(e) Explain how antibiotic resistance evolves. [3]

Markscheme

Part	Answer	Marks
(a)	secondary faster	A1
	secondary much higher concentration	A1
(b)	memory cells from primary response	R1
	recognize antigen quickly	R1
	rapidly divide into plasma cells	R1
(c)	vaccine contains antigen	R1
	primary response; memory cells formed	R1
	secondary response on infection	R1
(d)	viruses lack bacterial structures (walls, 70S ribosomes)	R1
	use host cell machinery	R1
(e)	mutation gives resistance	R1
	antibiotic kills non-resistant bacteria	R1
	resistant survive and reproduce; plasmid transfer	R1

Examiner's comments. In (c), weaker answers said vaccines contain antibodies. Vaccines contain antigens.

25 Check your understanding

Section A: multiple choice

1. Fibrin is formed from

A. fibrinogen B. prothrombin C. platelets D. thrombin

2. Plasma cells

A. engulf pathogens B. present antigens C. secrete antibodies D. destroy helper T cells

3. HIV destroys

A. red blood cells B. helper T lymphocytes C. platelets D. B cells only

4. Vaccines contain

A. antibodies B. antibiotics C. memory cells D. antigens

5. Herd immunity

A. requires 100% vaccination B. protects non-immune individuals indirectly C. only protects the vaccinated D. replaces antibodies

6. Antibiotic resistance spreads between bacteria on

A. plasmids B. ribosomes C. mitochondria D. capsids

Section B: structured

7. Outline the primary defences of the body. [4]

8. Explain the roles of B and T lymphocytes. [4]

9. Discuss the importance of herd immunity. [3]

Answers

1. A 2. C 3. B 4. D 5. B 6. A

7. Skin (keratin, sebum), mucous membranes (mucus, cilia), lysozyme, stomach acid, clotting.

8. Helper T cells recognize antigen and activate specific B cells; B cells divide into plasma cells and memory cells.

9. Protects those who cannot be vaccinated; threshold depends on contagiousness; outbreaks when coverage falls.

26 Summary and topic map

Idea	Remember
Pathogens	viruses, bacteria, fungi, protists, prions
Primary defences	skin, mucous membranes, clotting
Innate	inflammation, phagocytosis
Adaptive	antigens, helper T, B cells, plasma cells, antibodies
Memory	secondary response; vaccines; herd immunity
Antibiotics	target bacteria; resistance by selection
HIV / zoonoses	helper T cells destroyed; animal-to-human diseases

Before the exam, make sure you…

•say antibodies bind antigens, not kill directly
•say vaccines contain antigens
•explain resistance as natural selection
•compare primary and secondary responses with data

Defence Against Disease on one page

Cover this page with a sheet of paper and try to rebuild it from memory. Whatever you can't recall is what to revise next.

Figure 7. Topic map for Defence Against Disease.

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