Year 13 Biology

Unit 4 – Option A Immunology and disease

Objectives

Name:

By the end of this unit, you should be familiar with: Can do Need to
this improve

The body is host to many other organisms.

The characteristics and treatment of cholera, tuberculosis, smallpox,

influenza, and malaria.
The relationship between the pathogenic action of viruses and their mode
of reproduction.
The features of antibiotics, including the mechanism of action of penicillin
and tetracycline.
How the overuse of antibiotics has resulted in the spread of antibiotic
resistant strains of bacteria.
How natural barriers reduce the risk of infection.

Innate and adaptive immunity.

Active and passive immunity.

The differential effectiveness of vaccines.

The ethical and moral implication of vaccination programmes.

Work through the WJEC Blended Learning activities:

Immunology and disease - Blended Learning (d3kp6tphcrvm0s.cloudfront.net)

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Disease
Our body is made up of 10 13 cells, but we carry at least that many microorganisms either within or
on our body. This is termed the microflora of the body. Some of these are as a result of a
mutualistic relationship developed through evolution and provide a valuable contribution to our
general health and wellbeing. Many are parasitic and have the potential to cause disease.
Whether these organisms are mutualistic or pathogenic depends upon their population density
and their position within the body. An organism that is beneficial in one part can be parasitic if
present in another.
Task: Use pg. 265 to research four examples.

Task: Research the terms for the following definitions that will be used throughout this unit.
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 Term Definition
Where a pathogen is normally found; this may be in humans or in
another animal and may be a source of infection.
A living organism which transfers a disease from one individual to
another.
Substances produced by microorganisms which affect the growth of
other microorganisms.
A chemical which is produced by a micro-organism which causes damage
to its host.
An organism that causes damage to its host.

Uses non-pathogenic forms, products, or antigens of micro-organisms to

stimulate an immune response which confers protection against
subsequent infection.
An epidemic occurring worldwide, or over a very wide area, crossing
international boundaries and usually affecting a large number of people.

A disease that may be passed or transmitted from one individual to

another.
A cell surface marker (protein/carbohydrate) that causes your immune
system to produce antibodies against it.
Where there is significant increase in the usual number of cases of a
disease often associated with rapid spread.
Organisms with the same or very similar antigens on the surface. Such
types are subgroups or strains of a microbial species which can be used
to trace infections. They are usually identified by using antibodies from
serum.
Where a micro-organism, which should be affected by an antibiotic, is no
longer susceptible to it.
An organism that causes damage to its host.

A person who shows no symptoms when infected by a disease organism

but can pass the disease on to another individual.

A disease which is always present at low levels in an area.

An immunoglobulin protein produced by the body’s immune system in

response to an antigen.

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Infectious disease
Infectious disease is one that may be passed or transmitted from one individual to another.
Consider the causes, symptoms, prevention, and treatment of the following diseases: cholera,
tuberculosis, smallpox, influenza, and malaria.

1. Cholera (bacterial)
https://www.youtube.com/watch?v=jG1VNSCsP5Q

Cause:

• Gram negative, comma-shaped bacterium, Vibrio cholera

• Can only replicate when inside human host
• Endemic in certain parts of the world

Mode of transmission:

• Contaminated food or water (faecal-oral route)

• Once contaminated, people act as a disease reservoir or carrier. They do not suffer the
symptoms but can contaminate other water supplies in which the organism is transmitted,
and this spreads the disease (although it only multiplies in the human host).

Symptoms:

• After 2/3 days of incubation, the bacterium releases a potent toxin in the small intestine
that affects the chloride channel protein, CFTR, in the gut lining. Water and many ions
including Cl-, Na+, K+, HCO3- and water are not absorbed into the blood, causing severe
watery diarrhoea. This causes severe dehydration so the blood pressure drops which can
cause death within hours (poor nerve conduction and heart problems).

Prevention:
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 • Treatment of water, good hygiene, and the provision of clean drinking water. Good
sanitation, better sewage treatment, safe food handling, regular hand washing with soap
are all required.
• A vaccine (killed organism or genetically engineered) is available but only provides
temporary protection.

Treatment:

 Oral rehydration therapy (ORT) - water and ions are replaced by giving the patient
electrolytes either orally or in severe cases, intravenously.
 Antibiotics

Task: How would you treat an outbreak of cholera in the developing world? Produce a poster to
educate the population and prevent another outbreak.

2. Tuberculosis/TB (bacterial)
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https://www.youtube.com/watch?v=IGZLkRN76Dc

Cause:

• Bacillus bacterium, Mycobacterium tuberculosis.

• Named as a result of the tubercles or nodules of dead or damaged cells in the lungs of
infected individuals. Tubercles may contain gas filled cavities that can be seen in x-rays.

Mode of transmission:

• Droplet infection – the inhalation of contaminated airborne droplets when infected

individuals cough or sneeze. It can spread very rapidly in crowded conditions or in densely
populated areas. It has remerged in recent years due to increased population and the
global spread of HIV-AIDS (compromised immune systems).

Symptoms:

• It primarily infects the lungs. Patients develop chest pains and cough up phlegm (sputum)
that often contains blood.
• The bacteria may infect lymph nodes in the neck which swell. People lose their appetite
and develop a fever.

Prevention:

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  The BCG vaccine is given to babies if recommended by a doctor and can be given up to the
age of 16 years.

Treatment:
 A long course of antibiotics but the bacterium does show some resistance. This is a huge
global issue.

Task: What does BCG stand for? Find out about the Heaf Test and Mantoux Test. Under
what circumstances would a doctor suggest a young person has a BCG vaccination in the
UK?

3. Smallpox (viral)
https://www.youtube.com/watch?v=yqUFy-t4MlQ
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Cause:

• DNA containing virus – Variola major

Mode of transmission:

• It is highly contagious. It is inhaled or transmitted in infected saliva droplets and other

bodily fluids.

Symptoms:

• It enters small blood vessels in the skin, mouth and throat and is dispersed around the
body. It causes a rash and then fluid-filled blisters. These leave scars in survivors. Smallpox
can also cause blindness and limb deformities. 30-60% fatality rate.

Prevention:

 The vaccine is very effective produces a strong immune response (the antigens are highly
immunogenic). It is made from live Vaccinia virus, a close relative of smallpox. It also has
very few antigenic types due to its low rate of antigenic variation/mutation. Before it
became available, people were isolated to prevent the virus spreading. There is no animal
reservoir. Up to 500 million people died of smallpox between 1900 and 1979, when it was
declared eradicated due to the effectiveness of the vaccination programs. It is the only
species that humans have deliberately made extinct. Some remaining virus is kept in
research labs with very high biosecurity.

Treatment:
 Fluids, drugs to control the fever and pain and antibiotics to control bacterial infections.
However, 60% of those infected die.

4. Influenza (viral)
https://www.youtube.com/watch?v=yhhJfT86Bgg

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Cause:
• There are three sub-groups of the influenza virus, A, B and C, with each group containing
many antigenic types. ‘Flu A is the most common and is described.
• there are many different antigenic types (serotypes). When a new strain appears, there is
no immunity in the population and epidemics and, sometimes, pandemics occur. E.g., the
Spanish ‘flu infected over 500 million people worldwide and killed 50 million in 1918-1920.
• Influenza can attack many species e.g., avian ‘flu and swine ‘flu, and they are a source of
new antigenic types that can infect humans.
• Influenza is an RNA virus. Unusually, it has 8 separate strands (gene segments) rather than
one. A phospholipid envelope, derived from the host’s cell surface membrane, surrounds
the virion. The envelope contains 2 important proteins which are antigens and form spikes
on the surface of the virus particle:

 Haemagglutinin (H) has a role in the virus entering a host cell. Needed for virus to
bind to the host cell.
 Neuraminidase (N) has a role in the virus leaving the host cell. Needed to release
from host cell.

Mode of transmission:

• Droplet infection - Inhalation of infected aerosol droplets from coughs and sneezes. It
survives winter better than summer (lower UV light), hence the term seasonal ‘flu. Mucus
protects the virus.

Symptoms:

• The virus infects cells lining the upper respiratory tract causing sore throat, mucous
production, cough, and fever.
Prevention:

 Regular hand washing

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  Hygiene - discarding used tissues, sneezing into an arm, cleaning surfaces
 Quarantine
 Vaccines can be effective but are variable in their success. As the surface antigens change,
a new vaccine is required every year.

Treatment:

 No real treatment. Keep hydrated and take medication for symptoms. Anti-viral
medication if hospitalisation occurs. Antibiotics are ineffective – only used to treat the
symptoms of a secondary bacterial infection.

Antigenic types
There are many antigenic types of influenza that have 2 main origins:

1. Antigenic drift (slow change):

Due to the lack of an RNA proofreading enzyme, any mutations that occur during replication
remain. Therefore, after every replication, a new virion is formed. This produces a gradual change
in the surface proteins, known as antigenic drift. This explains why new vaccines are required
annually.

2. Antigenic shift (rapid change):

‘Flu A has 16 types of haemagglutinin, of which H1, H2 and H3 are the most common in humans. It
has 9 types of neuraminidases, of which N1 and N2 are the most common in humans. If viruses
that have different combinations of H and N antigens infect a cell, the separate strands of RNA can
recombine, giving rise to new virus types
e.g., H1N2 and H2N1 can rearrange to form H1N1 and H2N2. This change is antigenic shift and the
new types of virus can cause epidemics.
In areas of the world where humans live in close contact with animals, chickens, and pigs in
particular, the animals act as a reservoir for new viral infections in humans. This occurs when an
animal virus mutates and gains the ability to infect human cells. Epidemiologists (scientists who
study the spread of infections) continuously monitor influenza strains. H7N9 has been of particular
concern since 2013.

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5. Malaria (protoctistan)
https://youtu.be/UUq0byqxluk

Cause:

• A protoctistan parasite – Plasmodium spp. Malaria is endemic in some sub-tropical regions,

epidemic during wet seasons but could also be regarded as pandemic as it kills more
individuals than any other disease despite years of research and drug development.
• Two main species – P.vivax and P.falciparum. Within these two species are many antigenic
types. The organism initially invades liver cells (hepatocytes). It then multiplies in red blood
cells that burst, releasing more parasites (Plasmodium) into the blood, and causing severe
bouts of fever.

Mode of transmission:
Transmission occurs by female Anopheles mosquitoes. The female pierces
the human skin to take a protein rich blood meal before laying eggs. Only
the females are vectors, the males feed on plant nectar.
Task: Define the term vector:

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Task: Use the diagram above to write an account of the life cycle of the protoctist. Start with:

Mosquito bites an infected human

Prevention:

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Task: Prevention of malaria relies on knowledge of the life cycle of both the vector and the parasite
to exploit their weak points. Use pg. 270 of your textbook to complete the following table. What
are the advantages/disadvantages of these various prevention measures?

Prevention measure Explanation

Sleep under mosquito nets

Wear long sleeved clothing at night

Use insect repellent

Drain or cover stagnant water

Pour a thin film of oil on stagnant

water

Spray walls with insecticide

Introduce fish to ponds/lakes

Infect mosquito with Wolbachia

bacterium

Sterilise female mosquitoes with X rays

Task: Shade in those rows that prevent the mosquito biting in one colour, those rows that prevent
mosquitos breeding in another colour and those rows that kill the vector in another colour.

Treatment:

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  Drugs cannot attack the Plasmodium when it is inside human cells, so their effectiveness is
limited to when it is free in the blood. Quinine was developed as a treatment for malaria in
the 17th century but has lost its effectiveness due to resistance. Artemisinin is a newer
drug, but the Plasmodium has evolved some resistance against it. The most recent
treatment is artemisinin in combination with other drugs as development of resistance to
more than one drug simultaneously is unlikely.
 P.falciprum has a high mutation rate, resulting in many antigenic types, therefore vaccine
development is only just being developed.

Sporozoites

Reproduction in the red blood cells

Gametocytes

Virus lifecycles
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https://youtu.be/8FqlTslU22s
Viruses are inert and show no characteristics associated with life unless they are within a host cell,
where they replicate. As a result, they have been described as the ‘ultimate intracellular parasite.’
The first step in a virus life cycle is to gain entry to a host cell. The virus attaches to receptors on
the host cell membrane and enters the cell often by phagocytosis. One of two life cycles follows:

1.The Lytic Cycle

The viruses immediately reproduce using the host cell’s metabolic pathways to copy their own
nucleic acid and to synthesise a new protein coat. Their release may be by:
- Lysis of the host cell e.g., common cold virus, or by
- Budding, in which case they acquire an envelope from the host’s cell membrane e.g.,
the influenza virus.

2.The Lysogenic Cycle

The viruses integrate their nucleic acid into the host cell genome and may lie dormant for several
generations. At a later time, there may be a trigger and the virus may enter the lytic cycle which is
when they produce symptoms e.g., herpes or HIV.

Virus pathogenicity

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Viruses can cause harm in several ways:

 Cell lysis: the host cell bursts. In addition, virus particles escape from cells to infect other
cells (shedding).

 Toxins: many viral components and their by-products are toxic. The mechanisms are not
well understood, but the following have been observed in cells local to the infection:

- Measles viruses can cause chromosome fusion.

- Herpes virus can cause cell fusion.
- Viral proteins can inhibit RNA, DNA, and protein synthesis.

 Cell transformation: when viruses trigger cells to become cancerous. Viral DNA can
integrate into the host chromosome. If this occurs in a proto-oncogene or tumour
suppressor gene, it can result in the uncontrolled mitotic division of the cell resulting in a
tumour. An example is HPV, which can cause cervical cancer by inserting into the tumour
suppressor gene TP53.

 Immune suppression: if the virus is specific to an immune cell, then the immune system
may become supressed.
e.g., HIV destroys a group of T helper cells so that B lymphocytes can no longer make
antibodies, making the patient immuno-compromised and susceptible to infection.

 Difficult to treat because the virus is inside the host cells. Any treatment would damage
host cells as well as the virus.

Antibiotics
Compounds that inhibit the growth of bacteria are called antimicrobials.
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There are 3 groups:

 Antiseptics used on living tissue, e.g., Dettol.

 Disinfectants used on non-living surfaces, e.g., bleach.
 Antibiotics – human use in or on body e.g., penicillin

Antibiotics are natural products of fungal cells that are produced to kill bacteria to reduce
competition in the environment for food. They do not act on viruses or eukaryotic cells. They can
therefore treat bacterial infection without causing harm to the patient.
https://www.youtube.com/watch?v=X1GT2bKgci8

Broad-spectrum antibiotics e.g., ampicillin and tetracycline, affect metabolic processes common
to most bacteria i.e., Gram +ve and Gram –ve bacteria.
Narrow-spectrum antibiotics are much more selective, e.g., penicillin G kills Gram-positive
bacteria only.

Different antibiotics affect different aspects of bacterial metabolism. Their use in medicine has
allowed them to be classified:

 Bactericidal antibiotics kill bacteria, e.g., penicillin, which destroys bacterial cells walls.

 Bacteriostatic antibiotics prevent bacterial growth/multiplication, but do not cause death,

e.g., sulphonamides, which are competitive inhibitors of enzymes and tetracycline, which
inhibits protein synthesis. The bacteria resume their normal metabolism when the
antibiotic is no longer present. These enable the host’s immune system to then destroy the
pathogen.

Bacterial cell walls

Peptidoglycan (murein) forms part of the bacterial cell wall. It contains polysaccharide cross-linked
by amino acid side chains. Transpeptidase enzymes cross-link the polysaccharide molecules by

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attaching them to the side chains of the amino acids. The cross-linking makes the cell wall strong,
gives the cell its shape and allows it to resist bursting (lysis) due to the osmotic uptake of water.

Gram-positive bacteria have a cell wall with a thick peptidoglycan (murein) layer, which retains a
crystal violet stain. After Gram staining, they appear purple down the microscope. The
peptidoglycan is accessible to molecules outside the cell, making it susceptible to attack by
lysozyme enzyme and penicillin.

Gram-negative bacteria have a cell wall with a thin layer of peptidoglycan, surrounded by a layer
of lipopolysaccharide. Alcohol used in the Gram’s stain procedure washes the crystal violet out.
The counterstaining with safranin stains the cells red. The extra layer of lipopolysaccharide
protects the cells from lysozyme and the action of penicillin

Antibiotic mechanisms
Penicillin

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The fungus Penicillium releases penicillin when its growth is inhibited, and it is under stress.
Penicillin is a narrow spectrum antibiotic that was mass-produced from P. notatum initially, but
now, high-yielding strains of P. chrysogenum are used. The fungus is grown aerobically in
industrial fermenters and the penicillin is purified for use. The first available penicillin was
penicillin G. This had to be injected, rather than ingested, because the stomach acid broke it
down. Penicillin V (5) and other derivatives, such as ampicillin, can be taken orally. They work by
disrupting the bacterial cell wall:

 Penicillin readily diffuses through the cell wall of Gram-positive bacteria, and it enters
some Gram-negative bacteria (less active against G-).

 Bacteria continually make and break down parts of their cell wall as they grow/divide.

 Penicillin inhibits the formation of crosslinks between molecules of peptidoglycan in the

cell wall during the growth and division of bacterial cells. It binds to and inhibits the
enzyme responsible for the formation of cross-links between the molecules of
peptidoglycan (DD-transpeptidase or PBP penicillin binding protein)

 The cell wall is weakened so that as water enters the cell by osmosis the cell lyses. In this
way penicillin is bactericidal and effective against G+ bacteria.

Tetracycline

The fungus Streptomyces produces tetracycline, a broad-spectrum antibiotic. It affects metabolic

processes common to most bacteria. It acts against Gram-positive and Gram-negative bacteria
and so it has wide medical use against bacteria that causes acne, Chlamydia, anthrax etc. It even
has some activity against some eukaryote parasites, including Plasmodium. Many bacteria,
however, now show some resistance to tetracycline.

 Tetracycline inhibits protein synthesis in bacteria.

 It acts as a competitive inhibitor of the second anticodon-binding site on the 30S subunit of
bacterial ribosomes and prevents the binding of a tRNA molecule to its complementary
codon. In this way, tetracycline inhibits the translation stage of protein synthesis. As the
binding of tetracycline is reversible, it is a bacteriostatic antibiotic.

 Mammalian cells cannot pump tetracycline into their cells, it may diffuse in but then has a
negligible effect.

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n.b. Viruses are not affected by antibiotics due to the absence of peptidoglycan cell walls and
metabolic pathways.

Experiments demonstrating the effectiveness of antibiotics:

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The effectiveness of different strengths/types of antibiotic against a species of bacteria can be
assessed by:

 making a lawn plate of the bacteria

 placing discs of different strengths of one antibiotic or different antibiotics on the surface

 measuring the clear zone where the bacteria have not grown or have been killed. The
larger the area of the clear zone, the more bacteria have been killed, so the more effective
the antibiotic is.

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Antibiotic resistance
The overuse of antibiotics has resulted in the spread of antibiotic resistant strains of bacteria.
These strains of bacteria should be affected by an antibiotic but are no longer susceptible.
Bacteria divide rapidly under optimum conditions and have a high mutation rate.

 Naturally occurring mutations that confer resistance to antibiotics have given these
bacteria a selective advantage in the presence of antibiotics. When antibiotics are used,
the resistant bacteria survive and replicate, so the resistance passes to the next
generation. This is vertical transmission.
 Horizontal transmission of resistance happens when bacteria transfer plasmids between
each other. This can happen between bacteria of the same or different species.
Overuse of antibiotics by doctors and in agriculture, has resulted in the accidental selection of
bacterial strains that are completely unaffected by some antibiotics. In agriculture, antibiotics are
used as a preventative to keep livestock healthy.
In the absence of antibiotics, resistant strains no longer have an advantage over non-mutated
forms, but if they cause an infection the bacteria are becoming increasingly difficult to control
with antibiotics.
Through mutation and natural selection, bacteria can be resistant to many different antibiotics.
This is called multidrug resistance. E.g., multidrug resistant TB. The concern is that in the future,
antibiotics will be unable to treat infections.
• MRSA – methicillin resistant Staphylococcus aureus is resistant to penicillin and all its
derivatives and is now treated with vancomycin, an antibiotic of last resort.

• Clostridium difficile is also treated with vancomycin.

Development of new antibiotics must be a priority to prevent basic bacterial infections becoming
life threatening once again.

https://www.youtube.com/watch?v=oMnU6g2djm4
https://www.youtube.com/watch?v=znnp-Ivj2ek

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The immune response

https://youtu.be/GIJK3dwCWCw
https://www.youtube.com/watch?v=CeVtPDjJBPU

The immune system enables the body to resist disease. There are physical barriers to prevent the
entry of pathogens. If they fail, there are cellular and chemical responses.

The innate immune system – non-specific

These barriers respond to all pathogens in the same way.
Task: Complete the table on the group of natural barriers that resist infection in the body. Use pg.
275 in your textbook.

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 Skin

When skin breached

If microbes enter

Inhaled air

Tears, mucus, and saliva

Stomach acid

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The adaptive immune system - specific
‘Adaptive’ means that the body produces a specific response to each different antigen that enters
it, so the body is adapting. An antigen is defined as a cell surface marker (protein/carbohydrate)
that initiates an immune response. Lymphocytes provide this response. They are derived from
stem cells in the bone marrow and their precise role depends on their subsequent location.
https://resource.download.wjec.co.uk/vtc/2015-16/14-15_15/eng/unit1-animation.mp4

The adaptive response

There are 2 components of an adaptive response are:

 The humoral response

 The cell-mediated response

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1. The humoral response

This results in the production of specific antibodies (immunoglobulins, specific proteins not cells)
against specific antigens by B lymphocytes cells.
B lymphocytes originate from stem cells in the bone marrow and mature in the spleen and lymph
nodes. There are many different types, and each B lymphocyte has receptors on its cell membrane
for the detection of its specific antigen. When a B lymphocyte with a specific receptor binds to the
specific antigen, it is activated. This is called clonal selection. Activation stimulates the
proliferation of B lymphocytes by repeated mitotic divisions, this is called clonal expansion. These
B lymphocytes differentiate to form antibody-secreting cells called plasma cells and memory
cells.

1. Plasma cells - which produce specific antibodies to the antigen and release them into the
plasma. They bind to the antigen and form antigen-antibody complexes. Antibodies are
short-lived.

2. Memory cells - these remain dormant in the circulatory system ready to recognise the
same antigen again. If the same antigen is encountered, they divide rapidly to form more B
lymphocytes and antibodies. They are long-lived.

Antibodies are Y-shaped, formed from four polypeptide chains and have two binding sites. There
are two heavy and two light polypeptide chains in antibodies; these chains are held together by
disulphide bonds. The binding sites are variable regions that have specific complementary shapes
to the antigen. As there are two binding sites, two different antigens can be joined by one
antibody molecule. If the antigens are on separate organisms this is called clumping or
agglutination. The hinge region is flexible, allowing the antibody to flex and bind to two antigens.

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An antigen-antibody complex renders the antigen inactive in some way, such as by agglutination,
which increases the rate of engulfment by phagocytes. If viruses or toxins are joined together
by agglutination, it can also mean that they are too large to enter other cells and infect them.

Task: Fully label the antibody below

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2. The cell mediated response

Cell-mediated immune response involves T lymphocytes, which also originate from stem cells in
the bone marrow, are activated in the thymus gland.
The first step in this response is when macrophages (phagocytes), which have engulfed the
microbes in the innate response, display the antigens of the microbe on their cell surface; they are
antigen presenting cells.
Specific T lymphocytes with complementary receptors, detect the corresponding specific antigen
(clonal selection), which causes the proliferation of the specific T lymphocytes (clonal expansion).
The T lymphocytes differentiate into effector cells, helper T cells and memory cells.

 Effector cells (T killer or cytotoxic T lymphocytes) cause lysis of the target cells.

 Helper T cells release cytokines, which stimulate B lymphocytes to initiate an antibody

response. Cytokines also stimulate phagocytosis by macrophages. Cytokines stimulate
clonal expansion of B and T lymphocytes – mitosis results in a large population of cells
specific to that particular antigen.

 Memory cells, which remain dormant in the circulation until the host is next exposed to
the same antigen.

https://www.youtube.com/watch?v=1LXlpZP7M1c&list=PLHciJmRHa4B -vHIsKCcCuRF7I99ePhG16

Task: Find out what happens to helper T cells in AIDS?

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Task: Further annotate this diagram to explain the full adaptive response of the immune system.

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Fighting infection
The primary immune response (first exposure)

• There is a short latent period in which macrophages, a type of white blood cell, which
detects and engulfs (phagocytosis) foreign antigens or the cell or virus to which it is
attached. It then incorporates the antigenic molecules into its own cell membrane. This is
called antigen presentation and macrophages are therefore a type of antigen-presenting
cell.

• T helper cells detect these antigens and respond by secreting cytokines. Cytokines
stimulate B lymphocyte cells, T lymphocyte cells and macrophages.

• B cells are activated and undergo clonal selection and expansion – some differentiate to
become antibody secreting plasma cells with short lives. Others become long-lived memory
cells that retain the ability to undergo mitosis. A low level of antibody is secreted over a 2–
3-week period. This clears the infection and the symptoms of infection subside.

The secondary immune response (re-exposure)

This relies on memory cells and may protect against an identical antigen, even many decades
after the primary infection.

• On re-exposure even to a very small amount of an antigen, there is a very short latent
period due to the presence of memory cells that undergo clonal expansion even faster
than in the primary response.

• Antibodies are made more quickly and are up to 100 times more concentrated than in the
primary response.

• Antibodies remain at a high concentration in the circulation for longer and no symptoms
develop.

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Active and passive immunity
Active immunity
The body makes its own antibodies in active immunity, stimulated either naturally during
infection or artificially during vaccination. It is long lasting because the response produces
memory cells.
Vaccination https://www.youtube.com/watch?v=rb7TVW77ZCs
When you are vaccinated, the cell-mediated and humoral responses are initiated, even though
there is no harmful pathogen present. Vaccines can be:

The antigen is recognised by the immune system as non-self and responds as if the pathogen was
present. This is ‘active’ immunity as the body is making its own antibodies. Over time, the number
of memory cells decreases if the body is not exposed to the antigen again. So, in some cases, one
or more boosters are given e.g., a tetanus booster every 10 years is recommended. A booster is a

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further exposure to the vaccine and the responses is faster, bigger, and longer lasting than the
first. More memory cells are made and so the body is protected for longer.

Passive immunity
The body receives antibodies produced by another individual in passive immunity. This happens
naturally when they are transferred:

• From mother to foetus across the placenta

• To the baby in breast milk

Or artificially when antibody injections, sometimes called Ig (immunoglobulin) replacement

therapy, are given in various situations including:

• When rapid protection is needed and there is no time for an active immunity response to
develop e.g., when someone is bitten by an animal infected with rabies; some people who
recovered from COVID donated blood to treat those still in intensive care. Immunity is
immediate but short-lived protection - no memory cells are made.

Natural immunity: This is where there is no medical stimulation of immunity. It can involve
catching the disease or when antibodies are passed from mother to child.

Artificial immunity: This is where medical intervention is used in vaccination programmes or in

transfusion of antibodies.

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Task: Complete the table below comparing active and passive immunity

Feature Passive immunity Active immunity

Who produces antibodies?

In response to what?

How long does the immunity last?

Features of vaccinations
Successful vaccines have the following features:
 They provoke a strong immune response, are highly immunogenic and protect the
individual from developing the disease.
 They have no or few side-effects which are mild in nature.
 They lead to long-lasting immunity from the disease.

If the pathogen has little antigenic change a single round of immunization is needed to provide
long-term immunity. Rubella is a good example; children are immunized as babies, and a booster
vaccine given in their teens providing life-long protection. Organisms with many antigenic types
like influenza require annual vaccination programmes against the most common antigen types for
that year. Even so, it is not 100% effective.
To be successful, a vaccination programme should be taken up by enough of the population to
provide “herd immunity.” This is the idea that if enough people are immune to the disease
through vaccination, there is a reduced reservoir of the pathogen in the population. This provides
protection to people who are unable to be vaccinated because of compromised immune systems
or illness.
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There are various ethical issues connected to vaccination programmes:
 The cost and effectiveness of the vaccine.
 The protection of individuals and the community and whether vaccination should be
compulsory e.g., for health care workers.
 The rights of individuals to refuse vaccinations; this may particularly apply to parents
choosing not to vaccinate their children.
 Real and perceived side effects.

Task: Why might some individuals chose not to be vaccinated against particular pathogens.

Task: Find out how the decrease in uptake of the MMR in Swansea has affected the population.

Examiners’ Foibles

Best to use ‘specific antibodies’ not just antibodies

Killer T cells lyse or destroy target cells not kill

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Task: Summarise this topic with a mind map.

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