4.1 DIsease and the Immune System Flashcards

1
Q

what is a pathogen

A

an organism that causes disease

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2
Q

what is disease

A

a condition that impairs the normal functioning of an organism

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3
Q

what are the 4 types of pathogen

A

bacteria, virus, fungus and protoctista

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4
Q

outline bacteria as a pathogen

A
  • prokaryotic organisms
  • only some are pathogenic
  • can be classed by:
    1) their basic shapes
    2) their cell walls (Gram positive will turn purple blue once stained, and Gram negative will appear red
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5
Q

outline viruses as a pathogen

A
  • non-living
  • genetic material surrounded by protein
  • bacteriophages are viruses which attack bacteria, by taking over the cells biochemistry and using them to replicate and make more viruses
  • all pathogenic
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6
Q

outline protoctista (protista) as a pathogen

A
  • single-celled eukaryotic organisms and cells grouped into colonies
  • small amount are pathogens
  • parasitic (use people and animals as their host organism)
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7
Q

outline fungus as a pathogen

A
  • not too bad in animals, but cause devastation in plants
  • eukaryotic organisms, often multicellular, can be single
  • can be saprophytes (feed on dead or decaying matter)
  • or parasites (feed on living matter, and are pathogenic)
  • produce loads of tiny spores when reproducing, so can spread rapidly
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8
Q

what are the 2 modes of action of pathogens

A

damaging host tissue directly:
- viruses, which take over cell metabolism, by inserting viral genetic DNA into host cell, reproducing more viruses and bursting the cell
- protoctista, which enter cells and break them as they reproduce
- fungus, which digest and destroy living cells
producing toxins which which damage host tissue:
- bacteria, which produce toxins which poison or damage the host cells
- fungi can also do this

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9
Q

what are the 3 bacterium diseases

A
  • Tuberculosis:
    affects animals, particularly humans and cattle (destroying lung tissue and suppressing the immune system)
  • Bacterial Meningitis:
    affects humans
  • Ring Rot:
  • affects plants, such as potatoes and tomatoes
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10
Q

what is a communicable disease

A

disease that can spread between organisms via use of pathogens

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11
Q

what are the 3 viral diseases

A
  • HIV/AIDS:
    affects humans, and begins with HIV, which destroys the immune system, so you’re more likely to get other infections too, called a retrovirus
  • Influenza:
    affects animals, including humans, which leaves the airways open to secondary infection through destroying ciliated epithelial cells, mutate regularly
  • Tobacco Mosaic Virus:
    affects plants, mainly tobacco and tomato
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12
Q

what are the 3 fungal infections

A
  • Black Sigatoka:
    affects banana plants, turning the leaves black
  • Ringworm:
    affects cattle and other mammals, creams enough to cure the crusty, itchy patches
  • Athlete’s foot:
    affects humans, a form of ringworm
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13
Q

what are the 2 protoctista diseases

A
  • Potato/Tomato Late Blight:
    affects potatoes and tomatoes
  • Malaria:
    affects animals, including humans, spread by mosquitoes as a vector, with female mosquitoes taking 2 blood meals for protein when laying eggs, passing on the virus (easily prevented by removing standing water where they breed, insecticides, nets, window and door screens, and long sleeved clothing)
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14
Q

what are the two ways that communicable diseases can spread

A
  • direct transmission: disease is transmitted directly from one organisms to another
  • indirect transmission: when a disease is transmitted from one organism to another via an intermediate
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15
Q

explain how direct transmission can occur

A
  • droplet infection (coughing or sneezing tiny droplets of mucus or saliva directly onto someone)
  • sexual intercourse, kissing or contact of bodily fluids
  • direct skin to skin contact through touching
  • inoculation (through a break in the skin), such as sharing needles or bites
  • ingestion of contaminated food or drink
  • faeces on hand
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16
Q

give examples of direct transmission at play

A
  • HIV transmitted directly between humans via sexual intercourse
  • Athlete’s foot spread via touch
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17
Q

explain how an indirect transmission can occur

A
  • fomites (inanimate objects like bedding or socks)
  • airborne/droplet infections, when minute droplets of saliva and mucus stay in the air, and are later inhaled
  • vectors (another organism/host), or water
  • food
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18
Q

examples of indirect transmission at play

A
  • potato/tomato late blight: spread when spores are carried between plants, first in air and then water
  • malaria: spread via mosquitoes, which are vectors as they dont cause the disease themselves, but just spread it between organisms
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19
Q

what are factors which affect disease transmission

A
  • overcrowded living conditions
  • climate
  • social factors
  • poor nutrition and compromised immune system
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20
Q

example of overcrowding increasing the spread of communicable disease

A

TB:
- spread directly via droplet infection and indirectly ad bacteria can remain in air for long periods of time, and infect new people
- infection increases when loads of people live crowded together in a small space

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21
Q

examples of climate increasing the spread of communicable diseases

A
  • potato/tomato late blight, which is especially common in wet summers, as spores need water to spread
  • malaria, which is most common in tropical countries, which are humid and hot, the ideal conditions for mosquitoes to breed
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22
Q

examples of social factors increasing the transmission of communicable diseases

A

HIV:
- limited access to good healthcare means people are less likely to be diagnosed and treated for HIV, and the most effective anti-HIV drugs are less likely to be available, so virus is more likely to be spread
- limited health education, to inform people about how HIV is transmitted and how it can be avoided, e.g. through safe-sex practises like using condoms

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23
Q

direct transmission of communicable diseases in plants

A

direct contact of a healthy plant with any part of a diseased plant

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24
Q

indirect transmission of communicable diseases in plants

A
  • soil contamination: infected plants can leave pathogens and spores in the soil, which can infect the next crop (also with compost, if can survive the composting cycle)
  • vectors: wind, water (swimming through the surface film of water on leaves), animals (e.g. insects and birds as they feed) and humans (hands, clothing, fomites and during transportation)
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25
Q

what affects the transmission of communicable diseases in plants

A
  • varieties of crops susceptible to disease
  • overcrowding, increasing the likelihood of contact
  • poor mineral nutrition reducing resistance
  • damp, warm conditions
  • climate change (increases rainfall and wind, vectors moving to different area)
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26
Q

what are the physical defences plants have against pathogens

A
  • leaves and stems have a WAXY CUTICLE, providing a physical barrier against pathogen entering, and may stop water from collecting on leaf, reducing risk of infection by pathogens transferred between plants in water
  • plant cells themselves are surrounded by a CELL WALL, forming a physical barrier to any pathogens that make it past the waxy cuticle
  • plants produce a polysaccharide called CALLOSE: gets deposited between cell walls and plasma membranes during times of stress (pathogen invasion). the depositions make it harder for pathogens to enter the cell. depositions at the plasmodesmata (small channels in the cell wall) may limit spread of viruses between cells
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27
Q

what are the plant chemical defences against pathogens

A
  • produce ANTIMICROBIAL CHEMICALS, including antibiotics which kill pathogens and inhibit their growth
  • e.g. producing saponins, thought to destroy the cell membranes of fungi and other pathogens
  • e.g. producing phytoalexins, which inhibit the growth of fungi and other pathogens
  • also secrete chemicals which are TOXIC TO CHEMICALS, which reduce the amount of insect-feeding in plants, and therefore reduce the risk of infections by plant viruses carried by insect vectors
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28
Q

what do primary, non-specific defences do

A

prevent pathogens from entering an organisms and causing disease

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29
Q

what does non-specific mean when talking about animal defences

A

defences that work in the same way for all pathogens

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30
Q

how does the skin work as a barrier to prevent infection

A
  • acts as a physical barrier, blocking pathogens from entering the body
  • acts as a chemical barrier, producing chemicals (sebum) that are antimicrobial and can lower pH, inhibiting the growth of pathogens
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31
Q

how does the mucus membrane act as a barrier to prevent infection

A
  • protect the body openings that are exposed to the environment (mouth, nostrils, ears, genitals and anus)
  • some membranes secrete mucus, a sticky substance that traps pathogens and contains antimicrobial enzymes (lysozymes)
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32
Q

how does blood clotting act as a barrier to prevent infection

A
  • a blood clot is a mesh of protein (fibrin) fibres
  • blood clot plug wounds to prevent pathogen entry and blood loss
  • formed by a series of reactions/cascade of events that take place when platelets (fragments of cells in the blood) are exposed to damaged blood vessels, releasing substances that form the fibrin
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33
Q

how does inflammation act as a barrier to prevent infection

A
  • swelling, pain, heat and redness
  • triggered by tissue damage,
  • mast cells in damaged tissues are activated, and release molecules
  • release histamines, which increase the permeability of the blood vessels, so they start to leak fluid into the surrounding areas (now tissue fluid)
  • this causes swelling (and pain) and helps to isolate any pathogens that may have entered the damaged tissue
  • histamines also cause vasodilation, widening of the blood vessels, which increases blood flow to the affected area
  • increases temperature and stops pathogens from reproducing
  • cytokines also present, which attract white blood cells to the area to fight off any pathogens that may be present
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34
Q

explain how wound repair acts as a barrier to prevent infection

A
  • skin is able to repair itself in an event of an injury, and reforms a barrier against pathogen entry
  • surface is repaired by an outer layer of skin cells dividing and migrating to the edges of the wound
  • the tissue below the wound then contracts to bring the edges of the wound close together
  • it is repaired using collagen fibres, too many fibres and you’ll end up with a scar
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35
Q

how do expulsive reflexes act as a barrier to prevent infection

A
  • coughing and sneezing
  • sneeze: when mucus membranes in the nostrils are irritated by things such as dust and dirt
  • cough: stems from an irritation in the respiratory tract
  • both are an attempt to expel foreign objects, including pathogens from the body
  • happen automatically
  • vomiting and diarrhea too
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36
Q

what are phagocytes

A

specialised white blood cells that engulf and destroy pathogens

  • 2 types: neutrophils and macrophages, present in blood and tissue
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37
Q

what is pus

A

dead neutrophils and pathogens

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38
Q

what are antigens

A

molecules (usually proteins or polysaccharides) found on the surface of cells)

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39
Q

what happens when a pathogen invades the body

A
  • the antigens on its cell surface are identified as foreign, activating cells in the immune system
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40
Q

what does the immune system involve

A
  • non-specific response: happens in the same way for all microorganisms, whatever the foreign antigen present
  • specific response: is antigen-specific and is aimed at specific pathogens
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41
Q

what is involved in the specific stage of immune response

A

white blood cells - called T and B lymphocytes

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42
Q

what is the first stage of the immune response (non-specific)

A

phagocyte engulfs the pathogen

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43
Q

what is a phagocyte

A

a type of white blood cell that carries out phagocytosis (engulfment of pathogens)
- found in the blood and tissue

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44
Q

what is a neutrophil

A

a type of phagocyte
- the first white blood cells to respond to a pathogen inside the body
- move towards a wound in response to signals from cytokines

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45
Q

explain phagocytosis

A

1) phagocyte recognises the antigen on a pathogen (identified as non-human/foreign) - made easier via presence of opsonins
2) the cytoplasm of the phagocyte moves round the pathogen, engulfing it
3) pathogen is now contained in a phagosome (a type of vesicle found in the cytoplasm of phagocytes)
4) a lysosome (organelle containing digestive enzymes) fuses with the phagosome (phagolysosome), and the enzymes break down the pathogen
5) the phagocyte will then present the pathogens antigens, sticking the antigens on its surface to activate other immune system cells
6) when a phagocyte is doing this, it acts as an antigen-presenting cell APC

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46
Q

what is the role of opsonins in the process of phagocytosis

A
  • molecules in the blood that attach to foreign antigens to aid phagocytosis
  • bind to the pathogens and “tag” them so that they are more easily recognised by phagocytes:
  • work in different ways, e.g. hiding negative charged on the membranes of pathogens, making it easier for the negatively charged phagocyte to get closer to the pathogen
  • most phagocytes have receptors on their cell membranes that bind to common opsonins, and the phagocyte can then engulf the pathogen
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47
Q

how do cytokines assist in phagocytosis

A
  • released by phagocytes that have engulfed the pathogen (cells at the site of the wound)
  • cell-signalling messenger molecules that inform other phagocytes that the body is under attack
  • stimulates the WBCs to move towards the area of attack
  • also increase the body temperature
  • and stimulate the specific immune system
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48
Q

what is the second stage of the immune response

A

phagocytes activate T lymphocytes

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49
Q

what is a T lymphocyte

A

another type of white blood cell
- contain a plasma membrane containing cytoplasm and a large nucleus, and surface covered in receptors - each T lymphocyte has a different receptor on its surface
- its receptors bind to antigens presented by antigen-presenting cells

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50
Q

explain the second stage of the immune response

A
  • the receptor on the surface of a T lymphocyte meets a complimentary antigen on a APC
  • binds to it (means each T lymphocyte will bind to a different antigen
  • this activates the T-lymphocyte - CALLED CLONAL SELECTION
  • T lymphocyte then undergoes CLONAL EXPANSION, where it divides to produces clones of itself
  • different T lymphocytes have different functions
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51
Q

what are the different types on activated T lymphocyte cells

A

T helper cells
T killer cells
T regulatory cells
- some will also become memory cells

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52
Q

what is a T helper cell

A

they release substances to activate B lymphocytes and T killer cells

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53
Q

what is a T killer cell

A

attach to and kill cells infected with a virus

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54
Q

what are T regulatory cells

A

suppress the immune response from other white blood cells, helping to stop the immune system cells from mistakenly attacking the host’s body cells

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55
Q

what is the third main stage in the immune response

A

T lymphocytes activate B lymphocytes, which divide into plasma cells

56
Q

what is a B lymphocyte

A

another type of white blood cell
- made of plasma membrane containing the cytoplasm and nucleus
- covered with proteins called antibodies
- these antibodies bind to antigens to form an antigen-antibody complex

57
Q

explain the third stage of the immune response

A
  • each B lymphocyte has a different shaped antibody on its surface
  • when the antibody on the surface of a B lymphocyte meets a complementary shaped antigen, it binds to it (each B lymphocyte will bind to a different antigen)
  • this, along with substances released from T helper cells (a type of cytokine called interleukins), activated the B lymphocyte - another example of CLONAL SELECTION
  • the activated B lymphocyte divides by mitosis into plasma cells and memory cells - another example of CLONAL EXPANSION
58
Q

what is the basis of cell signalling

A
  • how cells communicate
  • a cell may release or present a substance that binds to the receptors on another cell, causing a response of some kind in the other cell
59
Q

why is cell signalling especially important in the immune response

A

it helps to activate all the different types of white blood cells that are needed

60
Q

explain an example of cells signalling in the immune response involving T helper cells and B lymphocytes

A
  • T Helper cells will release a type of cytokine called interleukins
  • this binds to receptors on B lymphocytes
  • this activates the B lymphocyte
  • so T helper cells are signalling to the B lymphocyte that there is a pathogen in the body
61
Q

what is the fourth stage of the immune response

A

plasma cells make more antibodies to a specific antigen

62
Q

what is a plasma cell and what occurs in this fourth stage of the immune response

A
  • plasma cells are clones of the B lymphocyte, meaning they are identical
  • they secrete loads of the antibody, specific to the antigen, into the blood
  • these antibodies will bind to the antigens on the surface of the pathogens to form lots of antigen-antibody complexes
63
Q

what is the structure of an antibody

A
  • glycoproteins
  • made of 4 polypeptide chains, 2 heavy and 2 light chains
  • each chain has a variable region at the slanted end at the top, and a constant region
  • the variable regions of the antibody form the antigen binding sites (the shape of the variable region is complementary to a particular antigen (so the variable region differs between antibodies)
  • the hinge region (where the heavy chains start to bend) allow flexibility when the antibody binds to the antigen
  • the constant regions allow to binding to receptors on the immune system cells, e.g. phagocytes
  • it is the same (has the same sequence of amino acids) in all antibodies
  • disulfide bridges hold the polypeptide chains of the protein together
64
Q

what are the 3 ways that antibodies help to clear infections

A
  • agglutinating pathogens
  • neutralising toxins
  • preventing the pathogen binding to human cells
65
Q

how do antibodies agglutinate pathogens

A
  • each antibody has 2 binding sites, so an antibody can bind to 2 pathogens at a time
  • this clumps together the pathogens
  • the phagocytes then bind to the antibodies and phagocytose lots of pathogens all at once
  • antibodies that behave in this way are called agglutinins
66
Q

how do antibodies neutralise toxins

A
  • like antigens, toxins have different shapes
  • antibodies called anti-toxins can bind to the toxins produced by pathogens
  • this prevents toxins from affecting human cells, so the toxins are neutralised/inactivated
  • the toxin-antibody complexes are also phagocytosed
67
Q

how to antibodies prevent pathogens from binding to human cells

A
  • when antibodies bind to antigens on a pathogen, they may block the cell surface receptors that the pathogens need to bind to the host cell
  • this means pathogens can’t attach to or infect the host cell
68
Q

what is a primary response

A

when a pathogen enters the body for the first time, the antigens on its surface activate the immune system

69
Q

what is the speed of the immune response, and why

A

slow
- there aren’t many B lymphocytes that can make the antibody needed to bind to it
- eventually the body will produce enough of the right antibody to overcome the infection
- in the meantime, the infected person will show symptoms of the disease

70
Q

what do memory T lymphocytes do

A
  • remember the specific antigen on the pathogen
  • and will recognise it the second time round
71
Q

what do memory B lymphocytes do

A
  • record the specific antibodies needed to bind to the antigen
72
Q

how do memory cells make a person immune

A

their immune system has the ability to respond quickly to a second infection

73
Q

what is the secondary immune response

A
  • if the same pathogen enters the body again, the immune system will produce a quicker and stronger immune response
74
Q

how is the secondary response quicker than the first

A
  • clonal selection occurs quicker
  • memory B lymphocytes are activated and divide into plasma cells that produce the right antibody to the antigen
  • memory T lymphocytes are activated and divide into the correct type of T lymphocyte to kill the cell carrying the antigen
  • often able to get rid of the pathogen before you show any symptoms
75
Q

what would a graph of antibody concentration and times of infection show

A
  • time/days on x-axis
  • concentration of the right antibody in the blood on the y-axis
  • after first exposure to antigen, line is still close to 0 for a long time before increasing, then slowly heading down to still a level above 0
  • long interval stays here
  • after second exposure, conc. of antibody increases straight away and much more rapid and levels off again higher than before
76
Q

what is the difference between pathogen entry, speed of response, cells activated and symptoms in primary and secondary response

A

PATHOGEN: enters first time/enters second time
SPEED OF RESPONSE: slow/fast
CELLS ACTIVATED: B and T lymphocytes/ memory cells
SYMPTOMS: yes/no

77
Q

what is a blood smear

A

a sample of blood smeared over a microscopic slide

78
Q

why are stains added to blood smears

A

to make different cells easy to see

79
Q

what are you likely to see when you look at a blood smear sample

A
  • red blood cells
  • white blood cells
  • platelets (tiny fragments of cells involved in blood clotting)
  • some will have granules and so will look grainy in their cytoplasm, others wont
80
Q

how would you identify red blood cells in a sample

A
  • most are red blood cells (erythrocytes)
  • easy to spot, no nucleus
81
Q

how would you identify a neutrophil (type of phagocyte)

A
  • nucleus looks like interconnected blobs - MULTI-LOBED nucleus
  • grainy cytoplasm
82
Q

how would you identify a lymphocyte

A
  • much smaller than a neutrophil
  • nucleus takes up most of the cell
  • very little cytoplasm, not grainy either
  • cannot distinguish between T or B lymphocyte under light microscope
83
Q

how would you identify a monocyte

A
  • the biggest white blood cell
  • type of phagocyte
  • kidney-bean shaped nucleus
  • non-grainy cytoplasm
84
Q

what is active immunity

A

when your immune system makes its OWN antibodies after being stimulated by an antigen

85
Q

what are the two types of active immunity

A

natural and artificial

86
Q

what is natural, active immunity

A
  • when you become immune after catching a disease
  • e.. if you have measles as a child, you wont get it again in later life
87
Q

what is artificial, active immunity

A
  • when you become immune after being given a vaccination (containing a harmless dose of the antigen
88
Q

what is passive immunity

A

immunity you get after being GIVEN antibodies made from a different organism
- your immune system doesn’t produce any antibodies of its own

89
Q

what are the wo types of passive immunity

A

natural and artificial

90
Q

what is natural, passive immunity

A

when a baby becomes immune due to the antibodies it receives from its mother, via placenta or breast milk

91
Q

what is artificial, passive immunity

A

when your body becomes immune after being injected with antibodies from someone else
- e.g. if you contract tetanus, you can be injected with antibodies against the toxin, collected from blood donations

92
Q

what are the characteristics of active immunity

A
  • requires exposure to the antigen
  • it takes a while for protection to develop
  • protection is long-term
  • memory cells are produced
93
Q

what are the characteristics of passive immunity

A
  • no exposure to antigen
  • protection is immediate
  • protection is short-term
  • memory cells are not produced
94
Q

what abnormal immune response results in an autoimmune disease developing

A
  • an organisms immune system isn’t able to recognise self-antigens (antigens present on the organisms own cells)
  • so the immune system treats these self-antigens as foreign antigens
  • and launches an immune response against the organisms own tissues
95
Q

what are examples of autoimmune diseases

A
  • LUPUS: causes by the immune system attacking cells in the connective tissues, damaging the tissues and causing painful inflammation
  • affects skin and joints, as well as organs such as heart and lungs
  • RHEUMATOID ARTHRITIS: caused by immune system attacking cells in the joints, causing pain and inflammation
96
Q

what are characteristics of autoimmune diseases in terms of time affected

A
  • usually chronic (long-term)
  • can often be treated, but not cured
97
Q

whilst the primary response is still taking place, do you still suffer from the disease, and what can be done about it

A
  • YES
  • while your B-lymphocytes are busy dividing to build up their numbers to the deal with the pathogen
  • vaccines can help avoid this
98
Q

how do vaccines prevent you from getting any symptoms of a disease

A
  • they contain substances that cause your body to produce memory cells against a particular pathogen, without the pathogen causing disease
  • so you can become immune without getting any symptoms
99
Q

what are epidemics

A

mass outbreaks of disease

100
Q

how can epidemics be prevented with vaccines

A
  • a large percentage of the population is vaccinated
  • which means that even the people who have not been vaccinated are unlikely to catch the disease
  • as there is no one to catch it from
  • = HERD IMMUNITY
101
Q

what substances are present in vaccines

A
  • could be ANTIGENS: can be free or attached to a dead or attenuated (weakened) pathogen
  • could be mRNA: designed to code for antigens found on the pathogen, meaning when the mRNA enters the body cell, it provides instructions for some cells to produce these antigens, triggering memory cells to be made
102
Q

what do booster vaccines do

A
  • given later, e.g. after several years
  • to make sure memory cells have been produced
103
Q

what is the difference between vaccination and immunisation

A

VACCINATION: the administration of a substance designed to stimulate the immune system
- IMMUNISATION: the process by which you develop immunity

104
Q

what is the link between vaccination and immunisation

A

vaccination CAUSES immunisation

105
Q

how can vaccines be administered

A
  • injected
  • taken orally
  • in an aerosol
106
Q

what are routine vaccines

A

vaccines offered to everybody

107
Q

what are examples of routine vaccines

A
  • MMR: protection against measles, mumps and rubella (usually given to children as an injection around 1 year old, and again before they start school) - contains attenuated measles, mumps and rubella viruses
  • Meningitis C vaccine: protects against the bacteria that causes Meningitis C (first given as an injection to babies at 3 months, then boosters given to 1-year-olds and teenagers
108
Q

what is an example of a vaccination programme and vaccine that changes every year

A

influenza vaccine

109
Q

why does the influenza vaccine change every year

A
  • the antigen on the surface of the influenza virus changes regularly
  • forming new strains of the virus
  • memory cells produced from the vaccination of one strain will not recognise the other strains (different antigens) - as the strains are IMMUNOLOGICALLY DISTINCT
  • every year different strains of the influenza virus circulate in the population
  • so a new vaccine has to be made
110
Q

how are new vaccines of influenza developed every year

A
  • labs collect samples of different strains
  • organisations (e.g. WHO and CDC) test the effectiveness of different influenza vaccines against them
  • new vaccines are developed and one is chosen every year that is most effective against the recently circulating viruses
  • governments and health authorities then implement a programme for vaccination using the most suitable vaccines
111
Q

why may some people be given vaccines to protect them from strains causing an epidemic in a different country

A

helps to stop the strain spreading globally

112
Q

what are antibiotics

A

chemicals that kill or inhibit the growth of bacteria

113
Q

how are antibiotics used by humans and why are they useful

A
  • used as drugs to treat bacterial infections
  • useful as they can target bacterial cells without damaging human body cells
114
Q

what was the first antibiotic

A

penicillin
- first to be isolated by Alexander Fleming in 1928

115
Q

since when have antibiotics been used widespread, and why

A
  • since the mid-twentieth century
  • partly due to the successful treatment of soldiers with penicillin in WW2
116
Q

explain how useful antibiotics have been in the last few decades

A
  • very useful
  • been able to deal with bacterial infections pretty easily using antibiotics
  • the death rate from infectious bacterial disease has fallen drastically
117
Q

what are some of the risks of using antibiotics, and what is the biggest

A
  • can cause side effects
  • can cause severe allergic reactions in some people
  • ANTIBIOTIC RESISTANCE
118
Q

explain how antibiotic resistance can develop in a population of bacteria, and what is this an example of

A
  • there is genetic variation in a population of bacteria
  • genetic mutations cause some bacteria to be naturally resistant to an antibiotic
  • BIG ADVANTAGE if able to naturally resist an antibiotic, as it is better able to survive (even in a host who is being treated with antibiotics)
  • means it can live longer and reproduce many more times
  • causes the allele for antibiotic resistance to be passed on to lots of offspring
  • EXAMPLE OF NATURAL SELECTION
  • means that antibiotic resistance spreads and becomes more common in a population of bacteria over time
119
Q

why is antibiotic resistance a problem

A
  • problem for people who become infected with resistant bacteria
  • as can’t easily get rid of them with antibiotics
120
Q

what has the increased use of antibiotics led to

A
  • antibiotic resistance is increasing
  • so we are less able to treat some potentially life-threatening bacterial infections
121
Q

what are superbugs

A

resistant to to most known antibiotics
- becoming MORE common

122
Q

what are the two examples of antibiotic-resistant bacteria, and where are they the most common

A
  • MRSA
  • Clostridium difficile
  • the infections are most common in hospitals, where many antibiotics are used by patients, and patients that are already ill have weakened immune systems
123
Q

what is MRSA

A
  • meticillin-resistant Staphylococcus aureus
  • causes serious wound infections
  • is resistant to several antibiotics, like meticillin
124
Q

what is Clostridium difficile

A
  • infects the digestive system
  • usually causes problems in people that have already been treated with antibiotics
  • the harmless bacteria normally present in the digestive system are killed by the antibiotics, which C.difficile is resistant to
  • the bacteria is able to flourish
  • produces a toxin, causing severe diarrhoea, fever and cramps
125
Q

what are two ways of overcoming the problem of antibiotic resistance

A
  • developing new antibiotics
  • modifying existing antibiotics
  • BUT NOT EASY
126
Q

what are ways to reduce antibiotic resistance from developing in the first place

A
  • doctors are being encouraged to reduce the use of antibiotics, e.g. not to prescribe them for minor infections or to prevent infections (except for people with already weakened immune systems, like the elderly and those with HIV)
  • patients are advised to take all of the antibiotics they’re prescribed to make sure the infection is fully cleared out and all the bacteria have been killed (reducing risk of a population of antibiotic-resistant bacteria developing)
127
Q

give examples of where we manufacture medicinal drugs from natural compounds

A
  • natural compounds found in plants, animals or microorganisms
  • penicillin: obtained from FUNGUS
  • some cancer drugs: SOIL BACTERIA
  • drug treating Alzheimer’s disease: DAFFODILS
128
Q

what could some organisms that haven’t been investigated so far help to develop

A
  • only a small proportion so far investigation
  • other plants and organisms could exist that contain compounds that can be used to treat currently incurable diseases, e.g. AIDS
  • may be used to produce antibiotics
129
Q

why is maintaining biodiversity important for developing drugs

A
  • to protect possible sources of drugs
  • if we don’t protect them
  • some species could die out
  • before we get the chance to study them
  • even if they have already been studies, could still prove useful sources of medicine
  • as we develop new techniques to identify, purify and test compounds
130
Q

what do your genes determine in regards to drugs

A
  • determines how your body responds to certain drugs
  • different people respond to the same drug in different ways
  • makes certain drugs more effective in some people that others
  • PERSONALISED MEDICINE
131
Q

what are personalised medicines

A

medicines that are tailored to an individual’s DNA

132
Q

how do personalised medicines work

A
  • if doctors have your genetic information
  • they can use it to predict how you will respond to different drugs
  • and only prescribe you ones that will be most effective for you
133
Q

how can personalised medicines be used to develop more effective drugs in the future

A
  • by studying the relationship between someone’s genetic makeup and their responsiveness to drugs
134
Q

what is synthetic biology

A

involves using technology to design and make things like artificial proteins, cells and even microorganisms

135
Q

why may synthetic biology be useful

A
  • could be used to develop medicines
  • e.g. scientists are looking at engineering bacteria to destroy cancer cells, whilst leaving healthy body cells intact