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OCR A BIOLOGY > 4.1 communicable diseases > Flashcards

4.1 communicable diseases Flashcards

1
Q

what is callose?

A

a large polysaccharide with beta 1-3 and 1-6 linkages between glucose molecules

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2
Q

How does callose defend against pathogens in plants?

A

it is deposited into sieve tubes at the end of the growing season so pathogens cant enter. Extra callose is deposited between the cell wall and membrane when the plant is stretched

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3
Q

what are some passive chemical plant defences?

A
  • phytoanticipins
  • toxins
  • enzyme inhibitors
  • receptor molecules
  • sticky resins
  • repenes
  • tannins
  • tylose
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4
Q

what are some active chemical plant defences?

A
  • phytoalexins
  • signal molecules
  • oxidative bursts
  • DAPHT chemical
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5
Q

what are phytoalexins?

A
  • chemicals produced in response to the pathogen
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6
Q

how do phytoalexins defend against pathogens?

A
  • disrupt the cell surface membrane of bacteria
  • disrupt the pathogens metabolism
  • delay pathogen reproduction.
  • stimulate the production of chitinases
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7
Q

what are examples of signal molecules?

A
  • ethylene
  • salicylic acid
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8
Q

how to signal molecules defend plants against pathogens?

A

they travel through the plant to activate defenses in uninfected areas

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9
Q

what are defensins?

A

small cysteine rich proteins with broad microbial action

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10
Q

how do defensins defend plants against pathogens?

A

they act on molecules in the plasma membrane of pathogens

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11
Q

why do plants need defenses against pathogens?

A

they dont have an immune system so they have structural, chemical and physical defences against pathogens

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12
Q

what are some passive physical plant defences?

A
  • waxy cuticle
  • cellulose cell walls
  • casparian strip
  • stomata
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13
Q

what are phenols?

A

antibiotic/antifungal chemicals

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14
Q

how do tannins defend plants against pathogens?

A

they bind to the salivary proteins andd digestive enzymes in insects to deactivate them. This means insects die from ingesting too many tannins

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15
Q

what are some active physical plant defences?

A
  • lignin
  • extra cellulose
  • necrosis
  • canker
  • callose
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16
Q

what is necrosis?

A

cell suicide

sacrificing a few cells could save the rest of the plant

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17
Q

what is a canker?

A

the death of cambium tissue in bark

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18
Q

what are examples of fungal diseases?

A
  • athletes foot
  • black sigatoka
  • ringworm
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19
Q

what are examples of bacterial diseases?

A
  • meningitis
  • tuberculosis
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20
Q

what are examples of viral dieases?

A
  • HIV
  • influenza
  • tobacco mosaic virus
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21
Q

what are examples of protoctistan diseases?

A
  • late tomato/potato blight
  • malaria
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22
Q

what are the characteristics of ring rot?

A
  • ring of decay in the vascular tissue of tomatoes or potato tubers
  • leaf wilting
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23
Q

what characteristics of HIV/AIDS?

A
  • flu-like symptoms
  • compromised immune system
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24
Q

what are the characteristics of influenza?

A

flu
- muscle pains
- headache
- fever

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25
Q

what are the characteristics of tobacco mosaic virus?

A

mottling and leaf discolouration

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26
Q

what are the characteristics of black sigatoka?

A

black leaf spots on banana plants

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27
Q

what are the characteristics of blight?

A

affects the leaves and potato tubers

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28
Q

what are the characteristics of ringworm?

A

growth of fungus in the skin, causing a rash in cattle and humans

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29
Q

what are the charcateristics of athletes foot?

A

growth under the skin of the foot and toes
cracking, red skin

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30
Q

what are the characterisitcs of malaria?

A

parasite in blood causing headaches and fever, sometimes death or a coma

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31
Q

what are the characteristics of tb?

A

killing of the cells and tissues, frequently the lungs

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32
Q

what is indirect transmission?

A

passing a pathogen from host to a new host via an intermediate

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33
Q

what are spores?

A

a unit of asexual reproduction adapted to spending time in unfavourable conditions before developing into offspring

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34
Q

what are examples of intermediates?

A
  • fomites
  • vectors
  • droplets
  • soil contamination
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35
Q

what are fomites?

A

inanimate objects that transmit disease
e.g.
- bedding
- socks
- cosmetics

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36
Q

what are vectors?

A

animals or objects that transmit disease without being infected themselves
e.g.
- mosquitoes
- dogs
- water

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37
Q

what are examples of indirect transmission in plants?

A
  • wind
  • water
  • animals
  • humans
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38
Q

how do living conditions affect transmission?

A

overcrowed living or work conditions may increase the rate of transmission

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39
Q

what social factors affect transmission?

A
  • poor healthcare
  • poor nutrition
  • homelessness
  • poor disposal of waste
  • culture
  • infrastructure
  • socio-economic
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40
Q

how does climate affect transmission?

A
  • pathogens spread faster in warmer, damp conditions
  • increased rain and wind increases spread
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41
Q

what are contributing factors to the transmission of diease?

A
  • human demographics + behaviour
  • economic development + land use
  • microbial adaptation + change
  • climate change
  • international travel
  • breakdown of public health measures
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42
Q

what are protoctista?

A

a group of eukaryotic organisms with a wide variety of feeding methods. They require a vector to transfer to their host

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43
Q

what are fungi?

A

eukaryotic organisms with a structure similar to plant cells

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44
Q

where is fungi found in plants?

A

the vascular system

the hyphae release extracellular enzymes to digest the surrounding tissues causing decay

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45
Q

where is fungi found in animals?

A

found in the skin

the fungus sends out reproductive hyphae that grow to the surface and release spores, causing redness and irritation

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46
Q

what is a parasite?

A

an organism that lives on or inside another organism

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47
Q

what is direct transmission?

A

passing a pathogen from a host to a new host with no intermediary

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48
Q

what are 2 modes of action for pathogens?

A

DIRECT- damage to the tissues

INDIRECT- producing toxins that damage host tissues

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49
Q

how can direct transmission be reduced?

A
  • basic hygiene
  • keeping surfaces clean
  • using condoms
  • waste water treatment
  • using a tissue
  • using a mask
  • wash skin after touching soil
  • washing fresh food
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50
Q

what are examples of direct transmission?

A
  • physical contact
  • faecal-oral transmission
  • droplet infection
  • transmission by spores
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51
Q

describe the virus cycle

A
  1. virus invades cells and takes over genetic machinery
  2. the host cell manufactures more copies of the virus
  3. host cell bursts, releasing more viruses that will infect neighbouring cells
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52
Q

what are viruses?

A
  • nonliving infectious agents
  • 0.02-0.3 micrometers
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53
Q

how can bacteria be classified?

A
  1. by their basic shape
    e.g rod shaped= bacilli
  2. by their cell walls
    gram positive bacteria
    gram negative bacteria
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54
Q

how do bacteria cause disease?

A
  • damaging host cells
  • releasing waste products/toxins
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55
Q

what are bacteria?

A

prokaryotic organisms that are smaller than eukaryotic cells, they can reproduce rapidly

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56
Q

what is a pathogen?

A

a microorganism that causes disease

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57
Q

what is disease?

A

abnormal conditions that affect an organisms body, organs, tissues, or cells

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58
Q

what is inflammation?

A

the swelling and redness of tissues caused by infection

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59
Q

what is a mucous membrane?

A

specialised epithelial tissue that is covered by mucus

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60
Q

what are primary defences?

A

defences that prevent the pathogen from entering the body

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61
Q

what are examples of primary defences in animals?

A
  • skin
  • blood clotting
  • skin repair
  • mucous membranes
  • coughing
  • sneezing
  • inflammation
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62
Q

what are specific defences?

A
  • ACQUIRED IMMUNITY
  • responses to a particular pathogen, the immune system has a built up defence
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63
Q

what are some features of specific defences?

A
  • antigen-dependant
  • antigen specific
  • exposure results in immunological memory
  • lag time between exposure and maximum response
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64
Q

what are non-specific defences?

A
  • INNATE IMMUNITY
  • present from birth, cant distinguish between specific pathogens
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65
Q

what are some features of non-specific defences?

A
  • antigen-independant
  • immediate max response
  • not antigen specific
  • no immunological memmory
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66
Q

what are the 4 main ways animals defend themselves against infectious diseases?

A
  • physical
  • cellular
  • chemical
  • commensal organisms
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67
Q

what are physical defences?

A

where body tissue acts as a barrier

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68
Q

what are cellular defences?

A

cells can detect the pathogen and produce a substance in response

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69
Q

what are chemical defences?

A

substances secreted by the body to provide an unsuitable environment for the pathogen

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70
Q

what are commensal organism defences?

A

there are harmless bacteria and fungi living on/inside the body, which compete with pathogens

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71
Q

what are the 3 lines of defence?

A

1- physical+chemical barriers
2- response against pathogens that have past the 1st line of defence
3- specific response against specific pathogens

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72
Q

what are examples of the 1st line of defence?

A
  • the skin
  • mucous membranes
  • blood clotting
  • inflammation
  • wound repar
  • expulsive reflexes
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73
Q

what are examples of the 2nd line of defence?

A
  • phagocytes
  • neutrophils
  • macrophages
  • antigen-presenting cells
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74
Q

what are examples of the 3rd line of defence?

A

T cells
B cells

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75
Q

what are primary defences?

A

the defences that prevent pathogens entering the body

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76
Q

what are 6 examples of primary defences?

A
  • skin
  • mucous membranes
  • blood clotting
  • inflammation
  • wound repair
  • expulsive reflexes
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77
Q

how does the skin act as a chemical barrier?

A

it produces antimicrobial chemicals
- fatty acids
- lysozyme

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78
Q

how do fatty acids defend against pathogens?

A

they lower the skin pH to inhibit patjogen growth

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79
Q

how do lysozymes defend against pathogens?

A

they are enzymes that break down the carbohydrates in the cell walls of some bacteria

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80
Q

how does the skin act as a physical barrier?

A

it prevents pathogens fromentering the body

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81
Q

what is the skin epidermis made from?

A

keratinocytes

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82
Q

how long does keratinisation take?

A

about 30 days

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83
Q

what is keratinisation?

A
  • keratinocytes are made by mitosis at the base of the epidermis
  • the keratinocytes move of the epidermis, as they do this the cytoplasm dries out and is replaced by keratin
  • by the time the cells reach the outer epidermis they are dead
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84
Q

where are mucous membranes found?

A
  • at body openings exposed to the external environment
    e.g.
  • eyes
  • mouth
  • nostrils
  • ears
  • genitals
  • anus
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85
Q

what do mucous membranes secrete?

A

sticky substance such as mucus, tears or wax which trap the pathogen

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86
Q

what are the components of mucous membranes?

A
  • goblet cells
  • cilia
  • mucus secreting glands
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87
Q

what are charcateristics of inflammation?

A

pain, redness, heat and swelling of the tissue

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88
Q

what do mast cells release?

A
  • histamines
  • cytokines
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89
Q

when are mast cells activated?

A

during inflammation

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90
Q

how do histamines cause inflammation?

A
  • vasodilation causes localised heat and redness, preventing pathogens reproducing
  • increased permeability of blood vessel walls, creates more tissue fluid, causing swelling
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91
Q

what do cytokines do to defend against pathogens?

A

they are signalling molecules that attract phagocytes to them, so they can dispose of the pathogens by phagocytosis

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92
Q

what is a blood clot?

A
  • a temporary seal made of a mesh of fibrin fibres to prevent infection until the skin is repaired
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93
Q

what is required for the blood to clot?

A
  • calcium ions
  • at least 12 clotting factors
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94
Q

where are clotting factors released from?

A

platelets from the damaged tissues

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95
Q

what to clotting factors activate?

A

an enzyme cascade which produces a large amount of fibrin to quickly seal the wound

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96
Q

how does a blood clot form?

A

1) platelets encounter the collagen in the damage blood vessel
2) platelets adhere to the wall and begin secreting thromboplastin and serotonin
3) once the clot had formd it dries out, forming a scab, which pulls the sides of the cut together

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97
Q

how does thromboplastin help the blood to clot?

A
  • triggers a cascade of reactions needed to form a blood clot
98
Q

how does serotonin help the blood to clot?

A
  • makes the smooth muscle in the blood vessels contract, so they narrow, reducing blood flow
99
Q

what is the active form of prothrombin called?

100
Q

what does thrombin catalyse?

A

fibrinogen —-> fibrin

101
Q

what are expulsive reflexes?

A

coughing and sneezing

102
Q

what do expulsive reflexes do?

A

they force the pathogen out of the nose or airways when they are irritated

103
Q

what is the process of skin repair?

A

1) new blood vessels grow to supply o2 and nutrients to new tissues
2) fibrous collagen is deposited under the scab
3) granulation tissues fill the gaps
4) stem cells divide by mitosis in the epidermis to form new skin cells that migrate towards the edge of the cut
5) the tissue contracts bringing the edges togther
6) collagen fibres form the repair

104
Q

what happens when collagen fibres are numerous in wound repair?

A

a scar forms

105
Q

what are 2 types of phagocytes?

A
  • neutrophils
  • macrophages
106
Q

what is an antigen-presenting cell?

A

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

107
Q

what is a clonal selection?

A

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

108
Q

what are cytokines

A

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

109
Q

what are opsonins?

A

proteins that bind to the antigen on a pathogen and then allow phagocytes to bind
- a type of antibody that is non-specific

110
Q

what do neutrophils contain?

A
  • Lysosomes
  • mitochondria
  • ribosomes
  • lobed nucleus
  • well-developed cytoskeleton
  • receptors
111
Q

why do neutrophils have a well-developed cytoskeleton?

A

To help the cell change shape to engulf the pathogen and move lysosomes and vacuoles around the cell

112
Q

what is the process of phagocytosis?

A

1) phagocyte is attracted by chemicals released by cytokines
2) phagocyte binds to the opsonins on the antigen of the pathogen
3) phagocyte engulfs the pathogen to form a phagosome
4) lysosomes move towards and fuse with the phagosome to produce a phagolysosome which releases lytic enzymes that break down the pathogen
5) After digestion the antigen combines with the MHC in the cytoplasm
6) The Antigen complex is displayed on the plasma membrane of the phagocyte

113
Q

what is a neutrophil?

A

A type of white blood cell that engulfs foreign matter and traps it in a large vacuole which fuses with lysosomes to digest the foreign matter

114
Q

Why did neutrophils have a multi-lobed nucleus?

A

to allow the cell to squeeze through narrow gaps

115
Q

what do dead neutrophils form?

116
Q

What are macrophages?

A

a large long long lived phagocytic cell that remains in tissues
- they initiate the specific response

117
Q

What are macrophages called when they are in the blood?

118
Q

Where are macrophages found?

A

Some migrate around the body but most remain stationary in certain tissues such as the kidney, lungs and brain

119
Q

What is phagocytosis?

A

the engulfing of pathogens by phagocytes

120
Q

what are phagolysosomes

A

phagocytes binded to a lysosome

121
Q

what do phagolysosomes release?

A

lytic enzymes that break down the pathogen

122
Q

What are examples of specific immune responses?

A

T cells
B Cells

123
Q

What is a cell mediated response?

A

The release of T cells, which act on pathogens inside the cell

124
Q

What are the 4 types of T cell?

A
  • T helper
  • T killer
  • T regulatory
  • T memory
125
Q

Where do T cells develop?

A

In the thymus

126
Q

What are characteristics of lymphocytes?

A
  • white blood cells
  • smaller than phagocytes
  • large nucleus
  • produced in bone marrow
  • transported in blood
  • specialised receptors on plasma membrane
127
Q

When do T and B cells gain cell surface receptors?

A

During the maturation process

128
Q

What are receptors on T and B cells?

A

Transmembrane glycoproteins that stretch across the membrane, with a specific shape in the extracellular region

129
Q

Can B cells and T cells have the same antigen?

130
Q

What to T helper cells release?

A

Cytokines such as interleukins

131
Q

What do the T helper cells’ cytokines stimulate?

A
  • B cells to develop
  • T killer cells
  • phagocytosis by phagocytes
132
Q

What to T killer cells do?

A
  • Attack and kill the host body cell with foreign antigen on it.
  • produce the chemical perforin
133
Q

What does perforin do?

A

Kills the pathogen by making holes in the cell surface membrane, increasing permeability

134
Q

What do T memory cells do?

A

provide long-term immunity

135
Q

what do T memory cells do when they mmet a pathogen?

A

divide rapidly to produce many T killer clones which destroy the pathogen

136
Q

What do T regulator cells do?

A

shut down the immune response once the pathogen has gone, to prevent autoimmunity

137
Q

how do T cells know when pathogens have invaded?

A

the cells present the foreign antigen to then as an antigen-presenting cell

138
Q

what is the process of T cell activation?

A

1) antigen presentation
2) clonal selection
3) clonal expansion
4) antibody production

139
Q

what is antigen presentation?

A

the APC engulfs the pathogen, then presents its antigens on its plasma membrane

140
Q

what is an APC?

A

antigen presenting cell

141
Q

what is clonal selection?

A
  • the body has to pick the T cell with the complementary antigen
  • the APC secretes a chemical which stimulatees T helper cells to become active
142
Q

what is clonal expansion?

A

T cells undergo mitosis to form many more clones, which then differentiate into different types of T cells, B cells are stimulated

143
Q

what do T helper cells release?

A
  • chemicals that stimulate the division and differentiation of B cells into plasma cells
144
Q

what is antibody production?

A

the stimulated B cells form plasma cells, which secrete the appropriate antibody

145
Q

what is the humoral response?

A

B lymphocytes (B cells) attack pathogens that are outside the cell

146
Q

where do B cells develop?

A

in the bone marrow

147
Q

How can B cells be activated?

A
  • by an antigen
  • by T helper cells
148
Q

What do B cells respond to?

A
  • large molecules with a repeated structure
  • soluble antigens such as protein molecules
149
Q

Where are T and B cells formed?

A

In the bone marrow

150
Q

What lymphocyte is in humoral immunity?

151
Q

What lymphocyte is involved in cell mediated immunity?

152
Q

What are B and T cells formed from?

A

Stem cells

153
Q

Where are T and B cells mainly found?

A

In the lymphatic system

154
Q

What do B and T cells produce?

A
  • memory cells
  • plasma cells
155
Q

What do B cells secrete?

A

Antibodies

156
Q

How are the pathogens identified in humoral immunity?

A

Free floating antigens in the bloodstream

157
Q

How are pathogens identified in cell mediated immunity?

A

Antigens on the surface of the cell

158
Q

How do T and B cells divide?

159
Q

How are pathogens killed in humoral immunity?

A

By secreted antibodies

160
Q

How are pathogens killed in cell mediated immunity?

A

By T killer cells

161
Q

What are the 2 types of white blood cell?

A

Phagocytes
Lymphocytes

162
Q

What do lymphocytes do?

A

Produce antibodies

163
Q

What do phagocytes do?

A

Ingest bacteria by endocytosis

164
Q

What are antibodies?

A
  • proteins that bind to a specific antigen
165
Q

What are antigens?

A

Foreign substances that stimulate antibody production

166
Q

What are polyclonal antibodies?

A

The many antibodies produced as pathogens have many different antigens on their surface

167
Q

What are antibodies also called?

A

Immunoglobulins

168
Q

What is the v region on an antibody?

A
  • variable region
  • shape is specific to the shape of antigen
169
Q

What is the c region on the antibody?

A
  • constant region
  • is the same in all antibodies of that class
170
Q

What is the role of the hinge in an antibody?

A

Allows flexibility

171
Q

What are the 6 components of an antibody?

A
  • light chain
  • heavy chain
  • variable region
  • constant region
  • hinge region
  • disulfide bridge
172
Q

What are the 4 types of antibody defence?

A
  • agglutination
  • toxin neutralisation
  • preventing pathogens from binding to host cells
  • opsonisation
173
Q

What is the process of agglutination of pathogens?

A
  • each antibody has 2 binding sites so binds to 2 pathogens at once
  • the pathogens clump together preventing it functioning
  • phagocytosis of multiple pathogens
174
Q

What is the process of toxin neutralisation?

A

The antibody acts as antibodies to the toxins produced by bacteria, the toxin is neutralised so no longer harmful.
Toxin-antobody complexes are phagocytosised

175
Q

How do antibodies prevent pathogens from binding to host cells?

A

Antibodies bind to the pathogens antigens, blocking the cell surface membranes receptors so the pathogens can’t attack or attach to the host cell. Then phagocytosis

176
Q

What is opsonisation?

A

Antibodies attach to bacteria making the identifiable to phagocytes

177
Q

Are opsonins specific?

A

Some are as they bind to specific antigens
Some aren’t as they stick to any foreign molecules

178
Q

What is the primary immune response?

A

The initial response caused by a first induction.

179
Q

What is the secondary immune response?

A

A more rapid and vigorous response caused by a second or subsequent infection by the same pathogen.

180
Q

What happens during the primary immune response?

A
  1. Pathogen and his body antigens initiate immune response
  2. LAG PERIOD: 10-17 days after antigen enters the body, antibodies appear in the blood. There are symptoms of the infection.
  3. Plasma cells don’t remain in the body for long, but they fight off the infection successfully. So the antibody concentration decreases.
  4. After exposure, the T and B lymphocytes produce memory cells, which remain in the body for a long time.
181
Q

What happens during the secondary immune response?

A
  1. As a result of the specific immune response, there B and T memory cells in the blood.
  2. The memory cells recognise specific antigens and the immune response is much faster, with rarely any symptoms.
  3. It takes a few days for the antibody concentration to increase, but it is much higher and longer lasting response
182
Q

Why can’t you remain immune forever?

A

T and B memory cells only have a limited lifespan.

183
Q

How can immunity be maintained?

A

Continue exposure is required to maintain constant immunity by making more memory B and T cells.

184
Q

summarise the primary immune response.

A
  • First exposure to pathogen
  • slow response
  • activates T and B cells
  • symptoms
  • produces antibodies
  • triggered by invasion.
185
Q

summarise with secondary immune response.

A
  • Subsequent exposure to pathogen
  • fast response
  • T and B memory serves activated
  • No symptoms
  • produces antibodies
  • triggered by invasion.
186
Q

What happens during the lag phase?

A

Clonal selection and making lymphocytes.

187
Q

Summarise plasma cells.

A
  • Primary immune response
  • secrete antibodies directly
  • only survive a few days
  • Slow response.
188
Q

summarise memory cells.

A
  • Secondary immune response
  • circulate in the blood and tissue fluid.
  • Divide rapidly after encountering pathogen from the primary response rapidly.
  • rapid response.
189
Q

Summarise T memory cells.

A
  • Last long after infection
  • recognise a vast number of antigens
  • expand to large numbers on exposure
  • produce more interleukins than normal tea helper cells.
190
Q

Summarise B memory cells.

A
  • Working inconjunction with memory T helper cells - produce antibodies even faster and in greater numbers
  • become plasma cells quicker.
191
Q

What is natural immunity?

A

Immunity achieved through normal life processes.

192
Q

What is artificial immunity

A

immunity achieved as a result of medical intervention.

193
Q

what is active immunity.

A

Where the immune system is activated and manufactures antibodies.

194
Q

What is passive immunity?

A

Immunity achieved when antibodies are passed to the individual through breastfeeding or injection.

195
Q

What is active natural immunity?

A

Community provided by antibodies in the immune system as a result of exposure to the Antigen.

196
Q

What is passive natural immunity?

A

immunity resulting from exposure to antibodies rather than the antigen, such as the antibodies provided via the placenta or breast milk.

197
Q

What is active artificial immunity?

A

Immunity provided by antibodies made from the immune system as a result of a vaccination Containing a weakened dead or similar pathogen. causing the body to produce antibodies and memory cells against the Antigen.

198
Q

What is passive artificial immunity

A

Immediate short term immunity from the injection of antibodies that aren’t produced by the recipient cells.

199
Q

Compare and contrast active and passive immunity.

A

Active immunity is long term as a memory cells are produced. It is a result of the body being exposed to an antigen and takes time for immunity to occur.

Passive immunity is short term and has an immediate response. It’s caused by the body being exposed to antibodies rather than an antigen when memory cells are not produced.

200
Q

What types of immunity are short term?

A

Passive natural and passive artificial.

201
Q

What types of immunity are long term

A

Active natural and active artificial

202
Q

What is vaccination?

A

A way of stimulating an immune response to the immunity is achieved.

203
Q

What is an epidemic?

A

The rapid spread of disease for high proportion of the population

204
Q

How are vaccinations given?

A

Usually injected, but some are taken orally.

205
Q

What could be in a vaccine?

A
  • Whole live organism
  • an attenuated version of the pathogen
  • a dead pathogen
  • a preparation of antigens from the pathogen
  • toxoid.
206
Q

What is attenuated mean?

207
Q

What are vaccination programmes?

A

Methods of preventing epidemics, where local health authorities, governments and world bodies organise vaccination programmes to prevent the spread of disease and work to eradicate it

208
Q

what are examples of diseases that can be vaccinated against.

A
  • covid 19
  • measles
  • mumps
  • rubella
  • typhoid
  • cholera
209
Q

What is herd immunity?

A

Using vaccination to provide immunity to almost all the population, this only applies to diseases spread from person to person.

210
Q

What is required for herd immunity to be effective?

A

Most of the population to be vaccinated.

211
Q

What is ring vaccination?

A

you vaccinate all the people in the immediate vicinity of the new cases?

212
Q

When is ring vaccination used?

A

When a new case of the disease is reported.

213
Q

Where is ring vaccination used?

A

In hospitals or to control the spread of livestock disease.

214
Q

How can viruses change their surface antigens?

A
  • antigenic drift
  • antigenic shift
  • cross breeding
215
Q

What is antigenic drift?

A

Small changes in the antigen shape within the same strain of virus

216
Q

What is antigenic shift?

A

Major change in the antigens within the same strain

217
Q

What is virus cross breeding?

A

Different strains of virus invading the same cell form new viruses with antigens from different strains

218
Q

What are some issues with vaccines?

A
  • different strains have different antigens
  • new strains require new vaccines to be made
219
Q

What is an auto immune disease?

A

When the immune system attacks a part of the body, as the immune system can’t recognise self-antigens. So the antibodies start to attack our own antigens

220
Q

What are the causes of auto immune disease?

A

Unknown but could be a combination of genetic and environmental factors

221
Q

What are 2 examples of autoimmune disease?

A
  • lupus
  • arthritis
222
Q

What are antibiotics?

A

A chemical that prevents the growth of microorganisms, can be antibacterial or antifungal

223
Q

How do antibiotics work?

A

They interfere with the metabolism of bacteria without the metabolism of human cells being affected. This is selective toxicity

224
Q

What do bacteriostatic antibiotics do?

A

Keep the numbers static so they can’t reach harmful levels

225
Q

What do bactericidal antibiotics do?

A

They kill the bacteria outright

226
Q

What bacterial processes can antibiotics inhibit?

A
  • cell wall synthesis
  • transcription
  • translation
  • DNA synthesis
  • cell surface membrane function
  • synthesis of folic acid
227
Q

What are risks of antibiotics?

A
  • allergic reactions
  • side effects
  • antibiotic resistance
228
Q

What can cause antibiotic resistance ?

A

The overuse and misuse of antibiotics have enabled microorganisms to develop resistance.

229
Q

Why do mutant genes have an immediate effect on bacteria?

A

They have only one copy of each gene

230
Q

What are 2 examples of antibiotics resistance bacteria?

A
  • MRSA
  • c-diff ( clostrifium difficile )
231
Q

How does antibiotic resistance occur in bacteria?

A
  1. Genetic variation in bacteria population due to genetic mutations make some bacteria naturally resistant
  2. Selection pressure, the sensitive strains die, and more resistant survive
  3. Resistant strains pass allele for antibiotic resistance to lots of offspring
  4. It is an example of natural selection
232
Q

How do bacteria develop resistance?

A
  • by acquiring genes from other bacteria
233
Q

What genes can they counteract ?

A
  • the enzyme penicillinase, which breaks down penicillin making them harmless
  • membrane components that reduce the inflow of antibiotics into the cell
234
Q

Why are new drugs needed?

A

Because new diseases are emerging, many diseases have no effective treatment. Some antibiotic treatments are becoming less effective.

235
Q

How can you reduce antibiotic resistance?

A
  • minimise use
  • good hygiene
  • ensure course is completed
236
Q

What is MRSA?

A

A bacteria that causes serious wind infections, which is resistant to many antibiotics such as methacillin

237
Q

What is C diff?

A

Her bacteria found in the gut that affects the digestive system and produces a toxin causing sickness, diarrhoea and cramps.

238
Q

Why do we need to find new sources of medicine?

A
  • New diseases are emerging
  • some diseases have no effective treatments
  • Antibiotics are coming less effective
  • Scientists fear previous diseases that were curable may return
239
Q

What are sources of new medicines?

A
  • Plants
  • fungi
  • microorganisms
  • animals.
240
Q

Why is biodiversity important for new medicines

A

Plants could contain compounds for new sources of medicines.

241
Q

How can new drugs be discovered and developed?

A
  1. likely compounds identified from organisms
  2. genetic analysis of orgamisms to search for genes
  3. finding molecules that fit
  4. modifying existing drugs
  5. researching the ways microorganisms cause disease

OCR A BIOLOGY (24 decks)

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