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My AS level biology - OCR A > 4.1 - Commuicable Diseases > Flashcards

4.1 - Commuicable Diseases Flashcards

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1
Q

Def of a pathogen

A

A microorganism that causes diseases

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2
Q

Different types of microorganism

A

Bacteria
Fungi
Virus
Protoctista

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3
Q

What do pathogens infect and why?

A

They live in the host

Host body creates a good habitat in which microorganisms can live

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4
Q

How do pathogens survive in the host?

A

They take nutrition form their host

But also cause damage in the process

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5
Q

Features of bacteria

A

Are prokaryotic cells
Can reproduce rapidly once in the host
Their presence can cause disease by damaging cells or by releasing waste products and/or toxins that are toxic to the host
In plants bacteria often live in vascular tissue and cause blackening and death of tissues

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6
Q

Fungi in animals

A

They live in the skin of an animal
It’s hyphae forms a mycelium underneaths the skin surface
Can send out specialised reproductive hyphae
These grow to surface of skin to release spores
This can cause redness and irritation

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7
Q

Fungi in plants

A

Often lives in vascular tissue of plants where it can gain nutrients
Hyphae release extracellular enzymes to digest surrounding tissue - causes decay
Leaves often become mottled in colour, curl up and shrivel, before dying.
Fruit and storage organs, like tubers in potatoes will turn black and decay

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8
Q

Features and effects of viruses

A

They invade cells and take over the genetic machinery and other organelles of the cell
They cause the cell to manufacture more copies of the virus
Host cell eventually burst, releasing many new viruses which infect healthy cells

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9
Q

Features and effects of protoctista

A

Enter host cell and feed on contents as they grow.

Malarial parasite “Plasmodium” has immature forms that feed on haemoglobin inside RBCs

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10
Q

Info about TB

A

Tuberculosis
Bacteria
Affects and kills may cells and tissues in the body, most often lungs

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11
Q

Info about bacterial meningitis

A

Bacteria
Infection of the meninges - membranes surrounding nerves and spinal cord
Causes damage to these areas

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12
Q

Info for ring rot

A

Bacteria
Affects plants
Causes ring of decay in vascular tissue of potato tuber or tomato, accompanied by leaf wilting

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13
Q

Info about HIV/AIDS

A

Virus

Attacks cells in the immune system and compromises the immune response

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14
Q

Info about influenza

A

Virus

Attacks respiratory systems and causes muscle pains and headaches

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15
Q

Tobacco mosaic virus info

A

Virus
Affects plants
Causes mottling and discolouration of leaves

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16
Q

Blight info(tomatoes and potatoes)

A

Protoctista
Affects plants
Affects both leaves and potato tubers

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17
Q

Ringworm(cattle)

A

Fungus

Growth of fungus in skin with spore cases erupting through skin to cause a rash

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18
Q

Athlete’s foot(humans)

A

Fungus

Growth under skin of feet - particularly between toes

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19
Q

Malaria info

A

Protoctistan

Parasite in blood that causes headaches and fever and may progress to coma and death

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20
Q

Def of direct transmission

A

Passing a pathogen form host to new host, with no intermediary

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21
Q

Def of indirect transmission

A

Passing a pathogen from host to new host, via a vector

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22
Q

Def of transmission

A

Passing a pathogen from an infected individual to an uninfected individual

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23
Q

Def of vector

A

An organism that carries a pathogen from one host to another

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24
Q

Short life cycle of a pathogen

A

Transmission from one host to another
Entering the host’s tissues
Reproducing
Leaving the host’s tissues

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25
Q

Different means of direct transmission

A

Direct physical contact - e.g touching
Faecal - oral transmission - eating contaminated food or water
Droplet infection - pathogen carried by tint water droplets in air
Transmission by spores -

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26
Q

How to prevent transmission by direct physical contact

A 
Hygiene 
Keeping surfaces clean
Cleaning and disinfecting cuts and abrasions 
Sterilising surgical equipment
Using condoms during sex
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27
Q

How to prevent faecal-oral transmission

A

Treating waste and water
Thorough washing of all fresh food(using treated water)
Careful preparation and thorough cooking of all food(kill pathogens in food)

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28
Q

How to prevent transmission by droplet infection

A

Catch it - bin it - kill it
Cover mouth when sneezing
Ensure tissues are disposed of correctly after using

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29
Q

Preventing transmission by spores

A

Use of a mask

Washing skin after contact with soil

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30
Q

Social factors affecting transmission

A 
Overcrowding in accommodation 
Poor ventilation in living space
Poor health(especially HIV/AIDS)
Poor diet
Homelessness(bad hygiene)
Living or working with people who have migrated from areas where disease is more common
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31
Q

What is an example of vectors in indirect transmission?

A

Mosquitoes in spreading malaria

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32
Q

Cycle of malaria transmission

A 
A person with malaria contains gametes of “Plasmodium” in their blood 
Female anopheles mosquito sucks blood
Plasmodium develops and migrates to mosquito’s salivary gland
Uninfected person is bitten
Plasmodium migrates to liver
Plasmodium then migrates to blood
Person then has malaria 
Cycle goes on
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33
Q

How can plants be affected by direct transmission?

A

Some pathogens present in soil and enter roots of the plant

Some fungi produce spores to reproduce, these can be carried in the wind

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34
Q

What do pathogens usually attack in a plant?

A

Vascular tissue

Can infect seeds so that offspring are infected

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35
Q

Indirect transmission into plants

A

Often occurs as a result of insect attack
Spores or bacteria attach to insect, e.g beetle
They act as vectors
Pathogen is transmitted to plant when insect attacks or eats it
E.g. Dutch Elm disease caused by Dutch elm beetle

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36
Q

What climates do pathogens thrive in most?

A

Most bacteria, fungi and protoctists reproduce more rapidly in warm and moist conditions
So are more common in these climates
So more infections in these areas

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37
Q

What happens to pathogens in cooler climates?

A

They can be damaged or even killed

Reduces their ability to grow and reproduce

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38
Q

Callose def

A

Large polysaccharide deposit that blocks old phloem sieve tubes

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39
Q

Why do plants need defences?

A

They don’t have an immune system

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40
Q

What are passive defences

A

Defences present before infection
Prevent entry and spread of pathogen
These include physical barriers and chemicals

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41
Q

Physical defences of a plant

A 
Cellulose cell wall
Lignin thickening of cell walls
Waxy cuticle 
Bark
Stomatal closure
Callose
Tulles Formation
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42
Q

Function of cellulose cell wall

A

Acts as a physical barrier

Contains variety of chemical defences activated once a pathogen is detected

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43
Q

Effect of lignin thickening of cell walls

A

Lignin is waterproof and completely indigestible

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44
Q

Effect of waxy cuticles

A

Prevent water collecting on cell surfaces

Since pathogens collect in water and need water to survive, the absence of water is a passive defence

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45
Q

Effect of bark in defence of plants

A

Contains a variety of chemicals that work against pathogenic organisms

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46
Q

Effect of stomatal closure

A

Stomata are possible points of entry for pathogens
Stomatal aperture is controlled by guard cells
When pathogens are detected, guard cells close stomata in that part of the plant

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47
Q

Effect of callose in plant defence

A

A large polysaccharide that is deposited in sieve tubes at end of growing season
Deposited around the sieve plates and blocks the flow of sieve tubes
Prevents a pathogen spreading around the plant

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48
Q

Tylose effect in plant

A

A balloon-like swelling/projection that fills the xylem vessel
When fully formed it plugs the vessel, so it cannot carry water.
Blocking xylem prevents spread of pathogens through heartwood
Tylose contains high concentration of chemicals, e.g terpenes are toxic to pathogens

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49
Q

Info about plant chemical defences

A

Plants contain chemicals that have variety of anti-pathogenic properties
Some are present before infection, e.g tannins in bark
Most chemical produced when pathogen is detected, as lots of energy required to make them.

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50
Q

Active defences in plants

A

Cell walls become thicker and strengthened with additional cellulose
Callose deposited between plant cell wall and cell membrane near invading pathogen - strengthens cell wall and blocks plasmodesmata
Oxidative bursts produce highly reactive oxygen molecules capable of damaging cells of invading organisms
Increase in chemical production
Necrosis - deliberate cell suicide. Sacrifice a few infected cells to save rest of plant

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51
Q

Different chemicals produced in plants

A 
Terpenoids
Phenols
Alkaloids
Defensive proteins(defensins)
Hydrolytic enzymes
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52
Q

Description of terpenoids in plant

A

A range of essential oils that have antibacterial and anti fungal properties
May also have scent, e.g. menthols made by plants

53
Q

Description of phenols in plant

A

Have antibiotic and anti fungal properties
Tannins found in bark inhibit attack by insects as bind to salivary proteins and digestive enzymes such as trypsin, deactivating the enzymes
Tannins can also cause of death of insects that ingest too much of it

54
Q

Description of alkaloids in plants

A

Nitrogen-containing compounds such as caffeine, nicotine, cocaine, morphine.
Give bitter taste to inhibit herbivores feeding
Also act on a variety of metabolic reactions via inhibiting or activating enzyme action
Can also inhibit protein synthesis if ingested

55
Q

Description of defensive proteins(defensins) in plants

A

Small cysteine-rich proteins that have broad anti-microbial activity.
Act upon molecules of the plasma membrane of pathogens
Possibly inhibit action of ion transport channels

56
Q

Effect of hydrolytic enzymes in plants

A 
Found in spaces between cells
Include chitinases(break down chitin in fungal cell walls)
Include lysosomes(capable of degrading bacterial cell walls
57
Q

Def of inflammation

A

Swelling and redness of tissue caused by infection

58
Q

Def of mucous membrane

A

Specialised epithelial tissue that is covered by mucus

59
Q

Def of primary defences

A

Defences that prevent pathogens entering the body

60
Q

Process of inflammation

A

Microbes detected by mast cells which release histamines
Histamines cause vasodilation - makes capillaries more permeable so more WBCs can leave
More tissue fluid forms as more plasma leaves
This causes swelling(odoema)
Tissue fluid can drain into the lymph vessels so pathogens may come into contact with lymphocytes (WBCs) and cause a specific immune response

61
Q

Why we cough and sneeze

A

They are explosive reflexes

Irritation caused by microbes or their toxins causes expulsion which will carry microbes with it.

62
Q

Process of blood clot

A

Blood vessel is damaged
Platelets bind to exposed collagen to form temporary plug
Platelets also release clothing factors which activate an enzyme cascade
Enzymes cause fibrinogen to form insoluble fibres which attach to the plug
Red blood cells are also trapped, this forms a clot

63
Q

Process of skin repair after clot

A

Clot dries and forms a scab which pulls skin closer together
Under skin collagen is deposited
Stem cells in epidermis divide by mitosis and differentiate to form new skin cells at the edge of the cut
New blood vessels form
When edges of cut are drawn together the repair is complete

64
Q

Other primary defences

A

Eyes are protected by antibodies and enzymes in the tear fluid
Ear canal is lined by ear wax, which traps pathogens
Female reproductive system protected by a mucus plug in the cervix and by maintaining relatively acidic conditions in the vagina

65
Q

Def of antigen-presenting cell

A

A cell that isolates the antigen from a pathogen an places it on the plasma membrane so that it can be recognised by other cells in the immune system

66
Q

Def of clonal selection

A

Selection of specific B or T cell that is specific to the antigen

67
Q

Def of cytokines

A

Hormone-like molecules used in cell signalling to stimulate the immune response

68
Q

Def of neutrophil

A

A type of WBC that engulfs foreign matter and traps it in a large vacuole(pagosome), which fuses with lysosomes to digest the foreign matter

69
Q

Def of opsonins

A

Proteins that bind to the antigen on a pathogen and allow phagocytes to bind

70
Q

What are secondary defences used to combat?

A

Combat pathogens that have entered the body

71
Q

What do opsonins do?

A

Enhance the ability of phagocytise cells to bind and engulf the pathogen

72
Q

3 types of phagocytes

A

Neutrophils
Macrophages
Antigen-presenting cells

73
Q

2 types of lymphocytes

A

B cells

T cells

74
Q

What is clonal selection?

A

Activation of the specific B and T cells
This leads to the production of antibodies that can combat the specific pathogen
Also leads to production of memory cells that provide long-term immunity

75
Q

Def of antibodies

A

Specific proteins released by plasma cells that can attach to pathogenic antigens

76
Q

Def of B memory cells

A

Cells that remain in the blood for a long time, providing long-term immunity

77
Q

Def of clonal expansion

A

An increase in the number of cells by mitotic cell division

78
Q

Def of interleukins

A

Signalling molecules that are used to communicate between different white blood cells

79
Q

Def of plasma cells

A

Derived from B lymphocytes, these are cells that manufacture antibodies

80
Q

Def of T helper cells

A

Cells that release signalling molecules to stimulate the immune response

81
Q

T killer cells def

A

Cells that attack and destroy our own body cells that are infected by a pathogen

82
Q

Def of T memory cells

A

Cells that remain in the blood for a long time, providing long-term immunity

83
Q

Def of T regulator cells

A

Cells that are involved with inhibiting or ending the immune response

84
Q

Four types of T lymphocytes

A

T helper cells
T killer cells
T memory cells
T regulator cells

85
Q

Function of t helper cells

A

Release cytokines that stimulate the B cells to develop and stimulate phagocytosis by the phagocytes

86
Q

Function of T killer cells

A

They attack and kill host-body cells that display the foreign antigen

87
Q

Function of T memory cells

A

These provide long term immunity

88
Q

Function of T regulator cells

A

These shit down immune response after pathogen has been successfully removed.
Also involved in preventing autoimmunity

89
Q

2 types of B lymphocytes

A

Plasma cells

B memory cells

90
Q

Function of plasma cells

A

Type of B lymphocyte

Circulate in the blood, manufacturing and releasing antibodies

91
Q

Function of B memory cells

A

Remain in body for a number of years and act as immunological memory

92
Q

Examples of communication using cytokines

A
  • Macrophages release monokines
    Some of these attract neutrophils(by chemotaxis)and others stimulate B cells to differentiate and release antibodies
  • T cells and macrophages release interleukins, which can stimulate clonal expansion(proliferation) and differentiation of B and T cells
  • Many cells can release interferon, which inhibits virus replication and stimulates activity of T killer cells
93
Q

What are autoimmune diseases?

A

Occurs when immune system attacks a part of the body.
Arises when antibodies start to attack our own antigens - possibly because antigens that are not normally exposed become exposed to attack

94
Q

Process of phagocytosis

A
  • Receptor on phagocyte’s cell surface membrane binds to antigen on pathogen’s cell surface membrane
  • Pathogen engulfed by endocytosis
  • This produces a phagosome
  • Lysosomes fuse with phagosome, releasing enzymes(lysins) into it
  • The pathogen is digested into amino acids and fatty acids
  • Products are absorbed into cytoplasm by diffusion
  • Phagocyte can incorporate antigens into cell membrane to become an antigen-presenting cell
95
Q

Where are each lymphocyte produced and found?

A

B lymphocytes - mature in the bone marrow
T lymphocytes - mature in thymus
Both cells have large nuclei and specialised receptors on their cells surface membranes
Mature B and T lymphocytes circulate around blood and lymph

96
Q

Three ways to trigger an immune response

A

Pathogen detected in blood stream
Antigens presenting cells
Antigens on infected host cells detected

97
Q

Process of triggering an immune response

A
  • Antigens on pathogen’s surface communicate to body cells is foreign
  • To initiate immune response, pathogens have to be detected by B and T lymphocytes with complementary receptors on pathogen’s antigens
  • Infected cells sometimes get pathogen’s antigens on their surface - helps to select right B and T lymphocytes
  • Macrophages in the lymph nodes engulf and digest pathogens. They separate the pathogen’s antigens and incorporate them into their own cell surface membrane. They are now antigen presenting cells ‐ they increase the chances of the correct T lymphocytes locating the foreign antigens.
    • The selection of the correct lymphocytes with receptors complementary in shape to the antigens is call clonal selection.
    • More of these lymphocytes are needed to fight the pathogens so they divide by mitosis in clonal expansion.
98
Q

Another name for immune response

A

Humoral immunity

99
Q

Examples of cell signalling in immune response

A
  • Pathogen’s antigens communicate to body cells that they are foreign
  • Cells infected with foreign antigens on surface communicate to lymphocytes to be selected in clonal selection and to T killer cells that they need to be killed
  • Macrophages engulf and digest pathogens and incorporate pathogen’s antigens on their cell surface membrane
    This communicates to lymphocytes to be selected in clonal selection
  • T helper cells release cytokines
    These bind to receptors on B cells and stimulate them to divide by mitosis and differentiate
100
Q

Primary Immune Response info

A
  • there is a time delay to trigger immune response after first infection
  • takes time for clonal selection and clonal expansion to happen
  • no memory cells ‐ slow antibody production and few produced
101
Q

Secondary Immune Response Info

A
  • T memory cells & B memory cells are already present in the blood ‐ antibody production is immediate (clonal selection and clonal expansion happen faster)
  • higher level of antibody production and antibodies produced more quickly
102
Q

Diff between secondary and primary immune response

A

Secondary:
Produces antibodies immediately after exposure
Produces more antibodies
Antibodies produced more quickly

103
Q

What are autoimmune diseases?

A

When the immune system attacks the body

Occurs when antibodies start to attack our own antigens

104
Q

Examples of autoimmune diseases

A

Arthritis - antibodies attack the membranes around joints

Lupus - antibodies attack proteins in the nucleus

105
Q

Why we need to find new drugs

A

New drugs needed to combat new diseases

New antibiotics needed as some strains of bacteria have evolved antibiotic resistance

106
Q

How are new drugs found?

A
  • Produced naturally by microbes
    E.g. penicillin
  • Some plants produce compounds with medicinal properties
    Isolate active ingredients on plant medicines
  • Maintain Biodiversity
    To find new sources of drugs
107
Q

What is personalised medicine?

A

Where the genomes of plants or microorganisms are screened to identify medicinal compounds
Idea is that scientists will eventually be able to sequence genes from individuals and develop specific drugs for the condition

108
Q

What is synthetic biology?

A

The development of new molecules that mimic biological molecules
E.g. enzymes

109
Q

Use of antibiotics

A

Used to treat/avoid bacterial infection

110
Q

Benefits of antibiotics

A

Prevent infection after surgery - reduces complications/death rate
Treat infections that the body can’t ‘fight off’

111
Q

Risks of antibiotics

A

Overuse and misuse of antibiotics allow bacterial strains to become resistant to antibiotics
- antibiotic resistance
This means certain antibiotics will be less effective/won’t have an effect of the bacteria

112
Q

Why is the term ‘immune’ incorrect when referring to bacteria and antibiotics?

A
  • Because the term is “resistant”
    Immune implies they have an immune system
    They don’t as they are single called organisms
113
Q

Def of active immunity

A

Where the immune system is activated and manufactures its own antibodies

114
Q

Def of artificial immunity

A

Immunity achieved as a result of medical intervention

115
Q

Def of epidemic

A

A rapid spread of diseases through a high proportion of the population(national)

116
Q

Def of vaccination

A

A way of stimulating an immune response so that immunity is achieved

117
Q

Def of natural immunity

A

Immunity achieved through normal life processes

118
Q

Def of passive immunity

A

Immunity achieved when antibodies are passed to the individual through breast feeding or injection

119
Q

What in the blood provides immunity to a disease

A

The memory lymphocytes

120
Q

What is antigenic material

A

A source of antigens

121
Q

Different sources of antigens

A

Whole, live microorganism
A harmless or weakened version of the pathogen
A dead pathogen
A preparation of the antigens from a pathogen
A toxoid, a harmless version of a toxin

122
Q

Two applications of vaccinations

A

Herd Immunity

Ring Vaccination

123
Q

Description of herd immunity

A

Vaccinate all people that are at risk from the disease
Vaccinate enough of the population(85-95%) and it stops the infection spreading, as there won’t be enough people to infect

124
Q

Description of ring vaccination

A

Vaccinate all people with or near victim
Contain the spread of disease within ring/certain area
Requires people to report victims of disease or infected

125
Q

How to identify Neutrophils

A

They have a multi-lobed nucleus

126
Q

Facts about neutrophils

A

Have a multi-lobed nucleus
Manufactured in bone marrow
Travel in blood - often squeeze out of blood trough capillaries into tissue fluid
Released in large numbers on response to infection

127
Q

Macrophages facts

A

H

128
Q

Antigen presentation

A

Antigen presenting cells move around body where can come into contact with specific cells and activate the immune response
These are B and T lymphocytes
The antigen-presenting cells increase chances that the lymphocytes will come into contact with pathogen

129
Q

What is clonal expansion?

A

When the chosen lymphocytes divide by mitosis and differentiate

My AS level biology - OCR A (19 decks)

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