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A Level Biology > Chapter 12 - Communicable Diseases > Flashcards

Chapter 12 - Communicable Diseases Flashcards

1
Q

structure of HIV?

A

HIV has attachment proteins embedded in a lipid envelope

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2
Q

HIV replication?

A
  • HIV replicates inside T helper cells
  • to do this, HIV first binds to the CD4 proteins on the T helper cell plasma membrane
  • the capsid then fuses w the T helper cell membrane and & the RNA n enzymes enter the cell
  • reverse transcriptase then converts the viral RNA to DNA - which integrates into the T helper cell’s genome in the nucleus
  • the new DNA is then transcribed to generate mRNA
  • This codes for HIV viral proteins & moves out of the nucleus to be translated by the T helper cell ribosomes
  • new RNA which will be used as genetic material for new virus particles is also synthesised from the intergrated DNA
  • new RNA & viral proteins r put together to make new HIV particles
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3
Q

how does HIV cause AIDS?

A

by killing T helper cells or interfering w their functions - when this happens the immune system is severely compromised bc other immune cells can’t function properly

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4
Q

what would happen w/o T helper cells?

A

cytotoxic T cells can’t be instructed to kill infected cells and plasma cells can’t produce specific antibodies

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5
Q

HIV doesn’t directly kill ppl but it…

A

instead just weakens the immune system so it can’ fight other infections

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6
Q

why is HIV diff to treat?

A

due to its high rates of mutation & bc its diff to get drugs inside T cells

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7
Q

why can’t antibiotics be used for viruses?

A

viruses don’t have any metabolic mechanisms or cell cell structures for antibiotics to disrupt

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8
Q

what is the virus responsible for flu?

A
  • the influenza virus
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9
Q

influenza virus structure?

A
  • contains RNA, which is unusually separated into 8 strands
  • has a phospholipid envelope which contains 2 imp proteins embedded into it: Haemagglutinin (HA) and neuraminidase (NA) - both also antigens
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10
Q

what does HA do?

A

plays a role in allowing to virus to enter the host cell

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11
Q

what does NA do?

A

plays a role in allowing the virus to leave the host cell

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12
Q

how does influenza virus actually make us ill?

A

attacks mucous membranes in the upper respiratory tract causing fever, coughing sore throat

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13
Q

what are hyphae?

A

fungi have specialised long filament structures (look hair like), one filament = hypa

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14
Q

how do fungi reproduce?

A

hyphae release spores

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15
Q

why are all fungi defined as parasites?

A

they can’t photosynthesise so all fungi are defined as parasites bc they take nutrients from the host

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16
Q

how do fungi cause symptoms?

A
  • in some fungal infections, the fungus lives in the ski of an animal where its hyphae grow under the skin and form a mycelium
  • the hyphae grow to the surface of the skin and release spores -> this results in redness and irritation
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17
Q

fungal infections in plants?

A
  • in fungal diseases, the fungi live in the vascular tissue where they can gain nutrients
  • damage is caused when the hyphae release enzymes such as cellulase which digests plant cellulose in the cell wall
  • the enzymes digest surrounding vascular tissue & cause decay -> causes the leaves of the plant to die
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18
Q

protozoan pathogens?

A
  • protozoa are unicellular eukaryotic organisms
  • reproduce sex & asex
  • many are parasites
  • protozoa enter host cells and feed on the contents which allows them to gro
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19
Q

malaria?

A
  • caused by the protozoan parasite Plasmodium

- life cycle of plasmodium involves 2 diff hosts: humans, mosquitos

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20
Q

what is a vector?

A

an organism which carries a pathogen from one host to another

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21
Q

life cycle of plasmodium? (mosq)

A
  • when the mosq. feeds on the blood of an infected human, it takes the plasm when its in its sex repro stage
  • when the plasm is in its sex rep stage its called a gametocyte
  • whilst the gameocytes are in the mosq., they develop into sporozoites which is the infective form of Plas
  • mosq then feeds on a healthy human and injects sporozoites into the blood
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22
Q

life cycle of a plasmodium? (human - part 2)

A
  • sporozoites travel to the liver and reproduce asex to produce merozoites
  • which are then released into the blood & infect RBCs where they reproduce again both sex & asex
  • this causes RBCs to burst which prevents O2 from being transported around the body
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23
Q

malaria treatment?

A
  • diff to treat w drugs bc cannot attack the plasmodium when inside RBCs
  • Quinine & artemisinin are anti-malarial drugs - but they are becoming less effec due to plasmodium developing resistance
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24
Q

the most effective treatment for malaria?

A

to use several antimalarial drugs in combination

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25
Q

malaria prevention?

A
  • sleep under nets = mosquitoes feed between dusk and dawn
  • put a film of oil on the water mosquito larvae are in= mosquitos lay their larvae in H20 and this lowers the surface tension so larvae can’t get O2
  • introduce fish to water = eat mosquito larvae
  • sterilise male mosquitos with X rays = after they mate, no offspring
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26
Q

Bacterial meningitis + septicaemia ?

A
  • the bacterial infection can spread to the blood (from brain) causing septicaemia (blood poisoning) which leads to death unless treated immediately
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27
Q

ring rot infects?

A

causes the vascular tissue to decay and decreases the yield of potatoes & tomatoes

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28
Q

TB infects?

A

macrophages in the lungs & inhibits their lysosomes so it can survive

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29
Q

primary TB?

A
  • a person infected w TB for the first time, will get primary TB
  • in this, the person’s lungs will get infected & they will exp fatigue, fever, weight loss
  • in a healthy person, PTB will eventually be controlled by the immune system & won’t develop further
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30
Q

STB?

A
  • In an immunocompromised person, TB may develop further into STB
  • in STB, phagocytic cells accumulate around the infected macrophage
  • this causes cell death and produces a lesion called a granuloma which causes the lung tissue to b damaged
  • granulomas can cause chest pain and eventually lead to death
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31
Q

TB can also be ?

A

latent which means its present in the body but not actively replicating so it causes no symps

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32
Q

what is indirect transmission?

A

when a pathogen is transmitted via vector

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33
Q

direct transmission can occur via: direct physical contact?

A

direct physical contact w an infected person/ contaminated surface ➡ can be minimised by regular handwashing & keeping surfaces clean

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34
Q

direct transmission can occur via: ingestion of contaminated food/ water?

A

➡ treat drinking water & careful washing and cooking of food

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35
Q

direct transmission can occur via: droplet infection?

A

➡ by using a tissue to cover the mouth and nose when coughing and sneezing

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36
Q

direct transmission can occur via: spores?

A

spores carried in air/ if spores are present in soil ➡wearing masks and washing skin after contact w soil

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37
Q

indirect trans: plants?

A

can occur in plants, via insects

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38
Q

primary defences defintion?

A

non-specific defences that prevent pathogens entering the body

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39
Q

physical primary defences?

A

PD e.g. skin, mucous and expulsive reflexes are all classed as physical PDs bc they protect against physical damage

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40
Q

PD: skin?

A
  • made up of mainly cells called keratinocytes
  • over 30 days, keratinocytes migrate out to the top of skin
  • as they do, the cytoplasm is replaced w keratin - keratinisation
  • these cells die by the time they reach the skin surface- where they act as a barrier to pathogens
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41
Q

PD: skin flora?

A
  • a large no. of harmless microbes called skin flora live on the skin
  • they prevent pathogens from colonising on the skin by competing w them for nutrients
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42
Q

what is a scab?

A
  • when a blood clot dries- it forms a temp seal called a scab which allows the skin to repair
  • to repair the skin under the scab, fibrous collagen is deposited & new cells from stem cells in the epidermis
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43
Q

what is more exposed to pathogens?

A

exchange surfaces - thinner

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44
Q

expulsive reflexes?

A
  • areas which r at risk of infection are very sensitive to pathogens and their toxins - airways
  • when these sen areas are irritated, they respond w an expulsive reflex
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45
Q

e.g.s of non specific chemical defences?

A

saliva and tears

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46
Q

NSDs - lysozyme?

A
  • kills bacteria by breaking down the bacterial cell wall, eventually the bacterial cell swells up w fluid and water, burst open and die
  • the lysis of the pathogen prevents its entry
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47
Q

what is inflammation?

A

the swelling and redness of tissue caused by infection

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48
Q

what does histamine do?

A

causes vasodilation which makes the capillary walls in the tissues more permeable to WBCs -> this allows more WBCs to get out of the blood and into the site of infection

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49
Q

vasodilation causes?

A

more TF to be produced which causes swelling - oedema

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50
Q

most non specific defences are aimed at?

A

bacteria

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51
Q

interferon?

A
  • the chemical interferon is also a non specific defence against viruses, protozoa, and some bacteria
  • infected cells produce interferons which diffuse to surrounding cells where it prevents microbes from multiplying -> does this by inhibiting microbial protein synthesis
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52
Q

Monocytes?

A
  • precursors to macrophages

- are present in the blood, when they enter the tissues, they become macrophages

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53
Q

where are monocytes and neutrophils made?

A

bone marrow

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54
Q

how do neutrophils/ macrophages work?

A
  • when ANY pathogen infects a tissue, neutrophils arrive 1st and each neutrophil can engulf 5-20 pathogenic cells
  • neutrophils die quickly after a few days whereas macrophages are long lived cells - 2 -3 months
  • when the neutrophil die, macrophages then arrive at the infected tissue and each can engulf 100 pathogens
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55
Q

what allows APCs to form?

A
  • a few special cells like macrophages don’t completely destroy the pathogen & instead save the pathogen antigen
  • macrophages & other special cells which do this r called APCs
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56
Q

phagocyte specialisations?

A
  • have well developed cytoskeletons to help them change shape to engulf the pathogen & move lysosomes around
  • many mitochondria - energy for cell movement
  • many ribosomes - synthesise lysosome enzymes
  • have a lobed nucleus to help them squeeze thru narrow gaps between cells in the tissues
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57
Q

what is an antibody?

A

specific protein released by plasma cells that can attach to pathogenic antigens (
a.k.a immunoglobulins)

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58
Q

the constant region of antibodies?

A

is always the same in all antbodies and can bind to receptors present on immune cells

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59
Q

each antibody has __ variables regions?

A

2

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60
Q

function of antibodies?

A
  • role is not to destroy pathogens directly, they’re just proteins, but to help immune cells destroy pathogens more effectively
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61
Q

when pathogens are clumped together, they also find it harder to?

A

enter host cells

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62
Q

why do plants make the perfect host for pathogens to invade?

A

they photosynthesise so they make their own sugars

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63
Q

what do plants not have?

A

immune systems to fight off invading pathogens

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64
Q

plant defences can b?

A

physical/ chemical/ active/ passive

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65
Q

what are passive plant defences?

A

exist all the time, even b4 infection occurs and prevent the entry and spread of pathogens e.g. cell walls

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66
Q

what are active plant defences?

A

only induced when the pathogen is detected

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67
Q

passive: cell wall?

A

acts as a physical barrier but also releases antipathogenic chemicals

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68
Q

passive: waxy cuticle?

A

prevent water collecting on the surface of plants - w/o H2O pathogens struggle to survive

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69
Q

passive: bark?

A

bark on trees contains anti-pathogenic chemical defences e.g. tannins

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70
Q

plant defences: phloem?

A
  • callose prevents the flow in the sieve tube of the phloem and prevents the spread of pathogens
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71
Q

plant defences: xylem?

A

a balloon like swelling in the xylem called a tylose can block the xylem vessel + also prevent the spread of pathogens

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72
Q

how does a plant know its being invaded?

A

there r spec chemicals in the cell walls of plant cells which can detect invading pathogens (mainly by binding to them)

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73
Q

how does the plant respond after detecting pathogen?

A

⬆ the strength of it’s physical defences + releasing more anti-pathogenic chemicals

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74
Q

active plant defences?

A
  • add more cellulose to CW to strengthen
  • ⬆ no. of oxidative bursts - produces O radicals, can damage pathogens
  • close stomata to prevent further entry
  • may inclu cell necrosis (deliberate cell death around site of infection) ➡ the pathogen’s access to H2O and nutrients cut off
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75
Q

role of leukocytes?

A

recognise foreign material + provide immunity against it

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76
Q

immunity definition?

A

the ability of an organism to resist infection by protecting against disease- causing micro-organisms or their toxins that invade the body.

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77
Q

2 types of leukocytes?

A
  • non spec immune cells: Macrophages + neutrophils

- specific immune cells: T+B lymphocytes

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78
Q

macrophages and neutrophils?

A

can’t tell the difference between specific antigens and produce a response against any infection

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79
Q

T and B lymphocytes?

A

Produce an adaptive response - they adapt their response so it’s appropriate for the destruction of a specific pathogen

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80
Q

how are T+B cells similar and how are they different?

A
  • T and B cells come from stem cells in the bone marrow -> then mature in diff places: T in the Thymus and B in the bone marrow
  • the role of them is to provide specific and long term protection
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81
Q

where are antibodies present?

A

in the plasma and can bind to specific antigens free in bodily fluids or antigens on cells

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82
Q

B lymphocytes are involved in?

A
  • humoral immunity

- the antibodies are present on bodily fluids, which is a.k.a humour traditionally

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83
Q

T lymphocytes?

A

have specific receptors on their plasma membranes which are specific to antigens - these receptors can only bind to antigens present on a body cell (infected)

  • cell mediated immunity
  • can only detect an antigen if it’s presented to them by another cell - APCs, infected body cells (host cells), transplanted cells, cancer cells
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84
Q

what is cell mediated immunity?

A
  • the recognition of antigens by T lymphocytes & subsequent T lymphocyte response
  • antibodies not involved
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85
Q

what can a T lymphocyte not do?

A

recognise a free antigen

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86
Q

what does Perforin do?

A

make a hole in the plasma membrane

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87
Q

what is an immunological memory?

A

if a pathogen returns, memory T cells detect it and produce a rapid response

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88
Q

role of T regulatory cells?

A

to inhibit the immune response when the pathogen has been destroyed

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89
Q

the primary immune response is?

A

the initial response caused by 1st infection➡ takes a long time as there r many steps

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90
Q

what happens when the body is infected a 2nd time by the same pathogen?

A
  • antibodies have to be made again

- secondary immune response

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91
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

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92
Q

the primary immune response - what happens?

A
  • the IS has never come across the pathogen B4
  • to produce specific antibodies, B lymphocytes have to undergo clonal selection + expansion
  • the correct B lymphocyte has to differentiate into plasma cells and memory cells
  • this process takes a long time & symptoms usually appear
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93
Q

the secondary immune response - what happens?

A
  • when the same pathogen invades the body a second time, there r already memory cells in blood
  • these quickly recognise the spec antigens from the same pathogen
  • is quicker as clonal selection & expansion r skipped
  • usually quick enough to prevent any symptoms from appearing
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94
Q

what normally happens during lymphocyte development?

A
  • any lymphocytes spec to self-antigens are normally destroyed
  • but sometimes, by mistake, they r not destroyed leaving some lymphocytes in the body which react to self antigens
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95
Q

Autoimmune disorders?

A

where ur IS mistakenly attacks your own body

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96
Q

what causes ADs?

A

exact causes unknown but they include both genetic and environmental factors

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97
Q

arthiritis?

A

antibodies attack membranes around the joint

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98
Q

lupus?

A

antibodies attack proteins in the nucleus of cells, meaning it can occur in any part of the body where there r cells w a nucleus

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99
Q

+s of antibodies?

A
  • most r produced naturally by microorganisms such as fungi, some are produced synthetically in labs
  • B4 them, ppl would often die if simple wounds got infected w bacteria
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100
Q

antibiotic resistant?

A
  • the overuse has led to the spread of resistance in bacteria
  • some bacteria are resistant to multiple antibiotics - multiple resistant bacteria -> most common in hospitals and thus are a big threat to patients
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101
Q

overcoming antibiotic resistance?

A
  • prescription is tightly controlled - only given to patients when they are the only way an infection can be treated
  • patients are strongly advised to finish the whole course so all the bacteria are destroyed
  • infection control measures are taken in hospitals to prevent bacteria spreading
  • produce new - the only way to overcome AR - slow tho
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102
Q

infection control measures inclu?

A

regular hand washing. rules preventing drs from wearing long sleeves, watches, ties

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103
Q

observations of wildlife have also led to?

A

new drugs being discovered - e.g.s monkeys and citrus oil

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104
Q

drugs from plants: theophylline?

A

found naturally in cocoa beans, used to treat asthma bc it relaxes SM

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105
Q

How are drugs derived from plants?

A
  • the compounds produced by plants can b extracted and analysed to find the main, active ingredient
  • this active ingredient can then b conc + manufactured into a commercially available drug by scientists
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106
Q

why is it imp to maintain plant biodiversity?

A

as there is an ⬆ chance of discovering new drugs

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107
Q

personalised med - plants?

A

the DNA of plants and microorganisms can be screened to see if it encodes for new medical compounds which can be made into drugs

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108
Q

vaccination use?

A

The immune response can be stimulated to be more effective against a specific infection

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109
Q

why are vaccines needed?

A

The immune response alone is not effective enough to prevent some infections
Infections that the immune response is ineffective against include smallpox and measles

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110
Q

what is vaccination?

A
  • Vaccination = a way of stimulating an immune response so that immunity is achieved
  • Is a precautionary measure to prevent people from contracting a disease
  • Vaccines protect against pathogens & are very specific to a single organism (each vaccine works towards one specific pathogen)
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111
Q

How Vaccination works

A
  • Disease usually kills the host bc the primary immune response is too small & slow
  • When the actual pathogen invades the vaccinated host for the first time, the memory cells differentiate into plasma cells
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112
Q

live vaccines?

A

Live vaccines contain whole live microorganisms which have similar antigens to the pathogen BUT THIS IS NOT THE REAL PATHOGEN!! Just similar antigens - e.g. the virus that causes cowpox was used in the smallpox vaccine

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113
Q

pathogen fragment vaccines?

A

Pathogen fragment vaccines contain only specific antigens that stimulate the IS

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114
Q

features of vaccination programs?

A
  • Involves vaccinating almost all of the population
  • This makes the majority of the pop immune to the pathogen so it’s difficult for the pathogen to be transmitted - this is called herd immunity
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115
Q

what is herd immunity and why is it important?

A
  • Herd immunity = occurs when the vaccination of a sig proportion of the pop provides protection for the individuals who have not developed immunity
  • Herd immunity protects non-immunised people because it is highly unlikely that they will come into contact w an infected person
  • Herd immunity is v imp as it’s not possible to immunise everyone in a pop like babies
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116
Q

what is ring vaccination?

A

Sometimes when a new case of disease is reported, everyone in the immediate vicinity of the case is vaccinated - this is called ring vaccination

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117
Q

to prevent epidemics what needs to happen?

A
  • Some vaccination programmes can fail in the long term - some pathogens can mutate their antigens so memory cells produced by vaccination do not recognise them anymore
  • To prevent epidemics, vaccines have to be changed regularly
  • New modified vaccines specific for mutated antigens are made every year
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118
Q

What is immunity?

A

Immunity = the ability of an organism to resist infections

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119
Q

what is active immunity?

A

Active immunity occurs when specific antibodies are produced by the individuals own IS

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120
Q

what is natural immunity?

A

Natural is achieved thru normal life processes - e.g. immunity through a regular infection

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121
Q

what is artificial immunity?

A
  • Artificial is usually induced by medical intervention and the individual does not suffer any symptoms of a disease - e.g. vaccination, injection of antibodies made by another indiv
122
Q

what r the non spec immune responses?

A
  • skin
  • Mucous membranes
  • Lysozymes
  • Blood clotting + wound repair
  • fever
  • inflammation
  • phagocytosis
123
Q

non spec immune responses that keep pathogens out?

A
  • skin
  • Mucous membranes
  • Lysozymes
  • Blood clotting + wound repair
124
Q

non spec immune responses once pathogens are in the body?

A
  • fever
  • inflammation
  • phagocytosis
125
Q

fever?

A
  • when a pathogen invades body, cytokines stimulate hypothalamus to ⬆ body temp ➡ useful bc:
  • inhibits pathogen reproduction
  • spec immune response works faster
126
Q

inflammatory response?

A
  • inflammation at the site of the wound, which is categorised by pain, heat, redness, swelling of tissue
  • mast cells activated + release histamines + cytokines
  • if infection is widespread, can cause a whole body rash
127
Q

what do histamines do?

A
  • make BV walls more leaky so BP is forced out - now TF. TF causes oedema and pain.
  • mave BVs dilate, causing heat and redness, preventing pathogens reproducing
128
Q

what do cytokies do?

A

attract phagocytes to the site

129
Q

what ois phagocytosis

A
  • phagocytes engulf + destroy pathogens ➡ 2 main types: neutrophils and macrphages
  • Phagocytes build up at site of infection + attack pathogens
130
Q

stages of phagocytosis?

A

1) pathogens produce attractive chemicals
2) phagocytes recognise non-human proteins
3) engulfs the pathogens encloses it in phagosome
4) phagosome combines w a lysosome to form phagolysosome
5) enzymes from lysosome destroy + digest pathogen

131
Q

lysozymes?

A

in tears, urine, stomach acid. Prevent pathogens getting into body

132
Q

skin?

A
  • has a skin flora of healthy microorganisms that outcompete pathogens for space
  • also produces sebum ➡ inhiits the growth of pathogens
133
Q

mucuous mebranes?

A
  • many of the body tracts - incl airways r lined w it
  • secrete mucus - traps microorganisms + contains lysosomes ➡ destroy bacterial and fungal cell walls
    • contain phagocytes ➡ remove remaining pathogens
134
Q

blood clotting + wound repair?

A
  • cut means pathogens can get in
  • when platelets come into contact w collagen in skin/ wall of blood vessel, they adhere + secret: Thromboplastin( enzyme that triggers a cascade of reactions resulting in the formation of a blood clot) & Serotonin (makes SM in the walls of BVs contract, so they narrow and reduce the supply of blood to the area)
  • Clot dries, forming a scab, epithelial cells below scab start to grow, sealing wound permanently, damaged BVs regrow
  • Collagen fibres deposited
135
Q

communicable diseases can be classified accord to the 4 types of disease causing pathogens in animals & plants:

A
  • bacteira, virus, protoctista, fungi
136
Q

types of non communicable diseases?

A
  • genetically inherited: CF
  • developmental: Down’s Syndrome
  • mental health disorders
  • cancers
  • age assoc: Dementia
137
Q

bacterial diseases need to know?

A
  • Tuberculosis
  • Bacterial meningitis
  • Ring Rot
    (TBR)
138
Q

Viral diseases need to know?

A
  • HIV/ AIDS
  • Influenza
  • TMV
    (HIT the virus)
139
Q

protoctist diseasd need to know?

A
  • Malaria
  • Potato/ Tomato blight
    (MP)
140
Q

Fungal diseases need to know?

A
  • Black Sigatoka
  • Ringworm
  • Athletes foot
    (BRA)
141
Q

Tuberculosis?

A
  • Caused by Mycobacterium tuberculosis and M. bovis
    TB damages and destroys lung tissue and suppresses the immune system, so the body is less able to fight off other diseases
  • In people, TB is both curable (by antibiotics) and preventable (by improving living standards & vaccination)
  • Worldwide, in 2012, around 8.6 million people had TB of which 1.3 million died, HIV/AIDS increases likelihood of developing TB
142
Q

Bacterial Meningitis?

A
  • Streptococcus pneumonia or Neisseria meningitidis
  • Meninges infected - the outer covering of the brain and spinal cord & can spread to the rest of the body causing Septicameia
  • A blotchy red/purple rash that does not disappear when a glass is pressed against it is a symptom of septicemia
  • Antibiotics will cure the disease if presented early, vaccines can protect against some forms of bacterial meningitis
  • Mainly affects very young children and teenagers, 10% die, 25% permanent damage
143
Q

Ring Rot?

A
  • Caused by the gram + bacterium Clavibacter michiganensis
  • Damages leaves, tubers, fruit, can destroy up to 80% of the crop
  • No cure
  • Once a bacterial ring rot infects a field, it can’t be used to grow potatoes again for 2 years
144
Q

HIV/ AIDS?

A
  • Human Immunodeficiency Virus causes Acquired Immunodeficiency Syndrome
  • Targets T helper cells and gradually destroys the immune system so affected people are open to other infections
  • Retrovirus with RNA as its genetic material, contains reverse transcriptase which transcribes the RNA to a single strand of DNA to produce a single strand of DNA in the host cell which interacts with the genetic material of the host cell
  • Transfers through body fluids (unprotected sex, sharing needles, contaminated blood products and from mothers to babies during pregnancy, birth or breastfeeding)
  • No cure + no vaccine but anti-retroviral slow
  • Sub-Saharan Africa
145
Q

Influenza?

A
  • Kills ciliated epithelial cells, leaving airways open to 2ndry infections
  • Deaths from secondary viral infection common e.g. pneumonia
  • Easily mutates = vaccine difficult
  • Can be zoonotic, affects young, old and people with chronic illnesses especially
146
Q

Tobacco Mosaic Virus?

A
  • Affects tobacco plants and 150 other species e.g. peppers, tomatoes
  • Stunts growth and reduces yield
  • No cure but resistant strains, careful management, chemical treatments can reduce infection risk
147
Q

Malaria?

A
  • Caused by Plasmodium, spread by bites of infected Anopheles mosquitoes
  • Complex life cycle w 2 hosts - mosquitoes and people
    Invades red blood cells, liver, brain
  • 200 million people are reported to have malaria every year, 600,000 die
  • No vaccine but preventative measures - insecticides, removing standing water, mosquito nets, door and window screens, long sleeved clothing
148
Q

potato/ tomato blight?

A
  • Caused by the fungus like protoctist oomycete Phytophthora infestans
  • The hyphae penetrate host cells, destroying leaves, tubers, fruits, causing £millions of damage
  • No cure but resistant strains, careful management, chemical treatments can reduce infection risk
149
Q

Black Sigatoka?

A
  • Banana disease caused by the fungus Mycosphaerella fijiensis which attacks and destroys the leaves
  • Leaves turn black and cannot photosynthesise
  • No cure, but resistant strains and fungicides
150
Q

ringworm?

A
  • Fungal disease affecting mammals including cattles, dogs, cats, humans
  • In cattle, usually caused by Trichophyton verrucosum which infects skin
  • Antifungal creams
151
Q

Athletes foot?

A
  • Human fungal disease caused by Tinia pedia which digests the warm, moist skin between the toes
  • Antifungal creams
152
Q

How do pathogens cause harm?

A
  • in 2 main ways: directly damaging the host’s cells or producing toxins which damage host cells.
153
Q

how can pathogens directly damage the host’s cells?

A
  • Different types of pathogens attack and damage the host tissues in different ways:
  • Viruses - take over the cell metabolism. The viral genetic material is inserted into the host DNA. The virus then uses the host cell to make new viruses which then burst out of the cell, destroying and then spread to infect other cells
  • Some protoctista - also take over cells and break them open, as the new generation emerge, but they don’t take over the genetic material of the cell, instead, simply digest and use the cell contents as they reproduce
  • Fungi - digest living cells and destroy them
154
Q

how do pathogens cause harm by producing toxins?

A
  • Most bacteria produce toxins which damage the host cells, causing disease. Some bacterial toxins break down cell membranes, some damage/inactivate enzymes and some interfere with the genetic material so cells don’t divide
  • Some fungi produce toxins which also cause disease
155
Q

Direct transmission in animals?

A
  • Direct contact
  • Inoculation
  • Ingestion
156
Q

Direct contact?

A

Transfer of body fluids – kissing, sexual intercourse.

157
Q

Inoculation?

A

Through broken skin
From an animal bite
Through a puncture wound/ sharing needles

158
Q

Ingestion?

A

Contaminated food or drink

Transferring pathogens from the hands to mouth

159
Q

direct transmission in plants?

A

Involves direct contact of a healthy plant with any part of a diseased plant e.g. ring rot, TMV, tomato and potato blight, black sigatoka

160
Q

Indirect transmission in animals?

A
  • Fomites
  • Droplet infection
  • Vectors
161
Q

Fomites?

A

Inanimate object – bedding, socks etc

162
Q

Droplet infection?

A

Droplets of saliva or mucus which contain pathogens

163
Q

Vectors?

A

A vector transmits communicable pathogens from one host to another - often animals, or water

164
Q

indirect transmission in plants?

A

soil contamination & vectors

165
Q

Soil contamination?

A

Pathogenic viruses and bacteria, and spores from protoctists and fungi remain in soil

166
Q

vectors?

A

Wind, water, animals, humans

167
Q

factors affecting transmission in animals?

A
  • Overcrowding
  • Poor nutrition
  • Compromised immune system
  • Poor waste disposal
  • Climate change
  • Culture and infrastructure
  • Socioeconomic factors
168
Q

factors affecting transmission in plants?

A
  • Planting susceptible crops
  • overcrowding
  • Poor mineral nutrition
  • Damp, warm conditions
  • Climate change
169
Q

plant physical defences against pathogens?

A

callose and lignin

170
Q

callose+ lignin?

A
  • Callose is papillae act as barriers preventing the entry of pathogens into plant cells around the site of infection
  • callose + lignin deposited in cell walls - lignin for mechanical strength
  • Blocks sieve plates
  • Deposited in plasmodesmata between infected cells and their neighbours
171
Q

plat chemical defenses against pathogens?

A
  • insect repellent
  • insecticides
  • antibacterial compounds
  • antifungal compounds
  • anti-oomycetes
  • toxins
172
Q

insecticides?

A

E.g. pyrethrins & caffeine

173
Q

insect repellent?

A

E.g. pine resin and citronella from lemon grass

174
Q

antibacterial compounds?

A

Including antibiotics - e.g. phenols, antibacterial gossypol, defensins, lysosomes

175
Q

antifungal compounds?

A

Phenols - antifungals : antifungal gossypol, caffeine, saponins, chitinases

176
Q

anti-oomycetes?

A

E.g. glucanases

177
Q

toxins?

A

Some plants make chemicals that can be broken down to form cyanide compounds when the plant is attacked

178
Q

neutrophils & macrophages?

A
  • Neutrophils engulf and destroy pathogens, and eventually die themselves. They are short lived cells with a relatively straightforward function.
  • Macrophages engulf and destroy pathogens, but are much longer lived and can become APCs - antigen presenting cells.
179
Q

antigens are?

A
  • molecules on the surface of a pathogen that are ‘non self’

- these are also excreted by the pathogen into the blood or TF

180
Q

how do antigens trigger the SIR?

A
  • when they are recognised by receptors on the surface of lymphocytes
  • A macrophage can engulf a pathogen and ‘present’ the antigen molecules on its surface, using a protein called MHC - the major histocompatibility complex.
  • This increases the chances of the antigen being recognised, triggering the specific immune response.
181
Q

why is blood a useful diagnostic tool?

A

the different components of blood can be identified and counted using a microscope and blood smear.

182
Q

what would a blood smear from a patient suffering from leukaemia look like?

A

elevated numbers of leukocytes, including many immature cells

183
Q

what is the specific immune response?

A

A complex set of responses that are specific to the pathogen that has entered the body

184
Q

what does the SIR involve?

A

lymphocytes

185
Q

how many types of lymphocyte are there?

A

2, which are involved in 2 different subdivisions of the specific immune response

186
Q

B lymphocytes ?

A

(B cells) - these mature in the bone marrow and are responsible for the humoral*, or antibody mediated response.

187
Q

T lymphocytes?

A

T lymphocytes (T cells) - these are produced in the bone marrow, like all blood cells, then mature in a gland called the thymus. These cells are responsible for the cell mediated response.

188
Q

how do viruses trigger the SIR?

A
  • Viruses infect body cells by injecting viral DNA and causing the cells to produce viral proteins.
  • These viral proteins appear on the surface of body cells, and act as antigens, triggering the specific immune response.
189
Q

How do antigens trigger the humoral response?

A
  • A pathogen can be an independent organism like a bacterium, a protoctist or a fungus.
  • These cells have ‘non-self’ molecules on their surface, and they excrete ‘non-self’ molecules into the blood or tissue fluid.
  • The antigen molecules here are extracellular - found outside normal body cells.
  • These antigens activate B lymphocytes, triggering the humoral or antibody mediated response
190
Q

how do antigens trigger the cell mediated response?

A
  • Intracellular antigens - found in or on the surface of ‘normal’ body cells activate T lymphocytes
  • Cell mediated response can be triggered by: virus invaded cells, transplanted cells, mutated body cells
191
Q

antibodies are a.k.a?

A

immunoglobulins

192
Q

antibodies - structure?

A
  • Y shaped molecule, with the 2 antigen binding sites at the end of the ‘arms’ of the Y.
  • The end of the ‘arms’ are different for each antibody, and form the variable region of the molecule.
  • The ‘stalk’ of the Y is the same for each antibody, and forms the constant region.
  • The mol 4 subunits - 2 short, light chains, and 2 longer, heavy chains. The chains are chains of amino acids, as theses are protein molecules. The chains are held together by disulphide bonds.
  • A hinge region makes the molecule flexible, allowing it to bind 2 separate antigen molecules on the surface of 2 separate pathogens
193
Q

Antibodies can act as what to defend the body against pathogens?

A
  • Agglutinins
  • Opsonins
  • anti-toxins
  • Also, a pathogen coated in antibodies cannot effectively invade host cells
194
Q

Opsonins?

A

molecules that ‘tag’ pathogens allowing phagocytes to easily recognise them. Phagocytes have receptors that bind to the constant region of antibodies that have ‘tagged’ pathogens

195
Q

Agglutinins?

A

molecules that cause pathogens to agglutinate (stick together) which makes the pathogens less effective and easier to destroy by phagocytes.

196
Q

Anti-toxins?/

A

Anti – toxins – molecules that neutralise the effect of toxins by binding to them. Antibodies can also bind to free antigens, neutalising them

197
Q

for both subdivisions of the IS, there are 4 main stages?

A
  • Clonal selection
  • Clonal expansion
  • Differentiation
  • Effects
198
Q

Clonal Selection?

A

when the ‘right’ B or T cell is selected by receptors binding to specific antigens.

199
Q

Clonal Expansion?

A

when the selected cell divides rapidly by mitosis, making multiple copies of the cell.

200
Q

Differentiation?

A

when the B or T cells differentiate into different types of cell.

201
Q

Effects?

A

the different types of cell carry out some sort of effect - destroying pathogens, producing antibodies etc…

202
Q

The humoral response summary?

A
  • B cells respond to extracellular antigen molecules – either on the surface of pathogens like bacteria and fungi, or free in the blood plasma or tissue fluid.
  • B cells with the right complementary B cell receptor bind to specific antigen molecules – clonal selection.
  • Clonal selection then stimulates B cells to divide rapidly by mitosis – clonal expansion
  • B cells then differentiate into plasma and memory B cells
203
Q

the cell mediated repsonse summary?

A
  • T cells respond to body cells that have changed in some way: (infected by virus, mutation, transplanted)
  • T cells with the right complementary T cell receptor bind to specific antigen molecules on the surface of the infected / mutated / transplanted cells – clonal selection
  • Clonal selection then stimulates T cells to divide rapidly by mitosis – clonal expansion
  • T cells then differentiate into killer, helper and memory T cells
204
Q

what do T regulator cells do?

A

supress the IS, acting to control and regulate it. They stop the Immune response once a pathogen as been eliminated, and make sure the body recognises self antigens and does not set up an autoimmune response. Interleukins are imp in this control

205
Q

what are communicable diseases caused by?

A

infective organisms known as pathogens,

206
Q

what do viruses do?

A
  • invade living cells where the genetic material of the virus takes over the biochem of the host cell to make more viruses
  • reproduce rapidly and evolve by developing adaptations to their host, which makes them very successful pathogens
  • considered to be the ultimate parasite
207
Q

how do plant diseases threaten ppl?

A

bc when crop plants fail ppl suffer: may starve, economies may struggle & jobs are lost. Threaten ecosystems too

208
Q

how can climate change affect the transmission of communicable diseases in animals?

A

this can introduce new vectors and new diseases, e.g. inc temps promote the spread of malaria as the vector mosquito species is able to survive over a wider range

209
Q

how can culture & infrastructure affect the transmission of communicable diseases in animals?

A

in many countries traditional medical practices can increase transmission (e.g. FGM)

210
Q

how can socioeconomic factors affect the transmission of communicable diseases in animals?

A

e.g. lack of trained health workers and insufficient public warning when there is an outbreak of disease can effect trans rates.

211
Q

(indirect trans in plants) vectors?

A
  • wind
  • water
  • animals (carrying pathogens and spores fro, one plant to another as they feed
  • humans - pathogens and spores are transmitted by hands, clothing, fomites, farming practices and by transporting plants and crops around the world
212
Q

how does climate change affect the trans of communicable diseases in plants?

A

incr rainfall and wind promote the spread of diseases: changing conditions allow animal vectors to spread to new areas: drier conditions may reduce the spread od disease

213
Q

how do plants defend themselves against pathogens?

A
  • waxy cuticle of leaves, bark on trees, cellulose cell walls act as barriers preventing pathogen entry. Plants don’t heal tissue like they seal it off and sacrifice it, can replace it as continually growing at meristems
214
Q

plant physical defences - callose?

A
  • within mins of an initial attack, callose is synthesised and deposited between the cell walls and th cell membrane in cells next to the infected cells. These callose papillae act as barriers preventing pathogens entering plant cells around the site of infection
  • large amounts of a callose continued to be deposited in cell walls after initial infection. Lignin is added making mechanical barrier stronger
  • blocks sieve plates, sealing off infected part and is deposited in plasodesmata between infected cells and their neighbours, sealing them off
215
Q

(human) expulsive reflexes?

A
  • coughs and sneezes eject pathogen laden mucus from the gas exchange system, while vomiting and diarrhoea expel the contents of the gut along with any infective pathogen,
216
Q

how can the type of immune response be identified in from a blood smear?

A

identifying the no.s of diff types of lymphocytes

217
Q

what is the role of cytokines?

A
  • phagocytes that have engulfed a pathogen produce ^
  • act as cell-signalling molecules, informing other phagocytes that the body is under attack & stimulating them to move to the site of infection or inflammation.
  • can also ⬆ body temp and stimulate the SIS
218
Q

what is the role of opsonins?

A
  • chemicals that bind to pathogens and ‘tag’ them so they can be more easily recognised by phagocytes
  • phagocytes have receptors on their cell membranes that bind to common opsonins, and the phagocyte then engulfs the pathogen
  • antibodies
219
Q

what are antibodies made up of?

A
  • 2 identical long polypeptide chains - the heavy chains & 2 much shorter identical chains - light chains
  • the chains are held together by disulfide bridges & there are also disulfide bridges within the polypeptide chains holding them in shape
220
Q

how do antibodies bind to antigens?

A
  • w a protein based lock and key mechanism
  • the binding site is an area of 110 amino acids on both the heavy and light chains known as the variable region
  • when binds, forms an antigen-antibody complex
221
Q

what does the hinge region of the antibody provide?

A

the molecule w flexibility allowing it to bind 2 separate antigens, one at each of its antigen binding sites

222
Q

types of T lymphocyte?

A
  • T helper cells
  • T killer cells
  • T memory cells
  • T regulatory cells
223
Q

T helper cells ?

A
  • have CD4 receptors on their cell surface membranes which bind to the the surface antigens on ACPs.
  • produce interleukins (a type of cytokine- a cell signalling mol) which stimulate the activity of B cells which ⬆ antibody production, stimulates production of other types of T cells and attracts and stimulates . macrophages to ingest pathogens.
224
Q

T killer cells?

A

destroy the pathogen carrying the antigen. Produce perforin which kills the pathogen by making holes in the CM so it is freely permeable.

225
Q

T memory cells?

A

live for a long time, are part of the immunological memory. If they meet an antigen a 2nd time, they / rapidly to form a large no. of clones of T killer cells that destroy the pathogen

226
Q

the main types of B llymphocyte>

A
  • plasma cells
  • B effector cells
  • B memory cells
227
Q

Plasma cells?

A

produce antibodies to a particular antigen and release them into the circulation.

228
Q

B effector cells?

A

these / to form the plasma cell clones

229
Q

B memory cells?

A

these live for a v long time, provide the immunological memory. Are programmed to remember a spec antigen & enable the body to make a very rapid response when a pathogen carrying that antigen is carried again.

230
Q

Macrophages are?

A

Cells that engulf and destroy pathogens and present antigen molecules on their surface using MHC proteins.

231
Q

T helper cell are?

A

A lymphocyte that uses CD4 receptors to bind to APCs. The cells then become activated and secrete interleukins

232
Q

Interleukins / cytokines are?

A

These molecules activate the process of clonal expansion in both B and T cells, as well as phagocytosis by macrophages and neutrophils

233
Q

Humoral response is?

A

The response caused by antigen molecules or pathogens in the blood plasma or tissue fluid. B cells are activated.

234
Q

Cell mediated response?

A

The response caused by infected, mutated or transplanted cells. T cells are activated.

235
Q

T and B receptors?

A

Receptors on the surface of lymphocytes that have many different shaped antigen binding sites. When antigen binds to the ‘right’ receptor, clonal selection occurs.

236
Q

Clonal expansion is?

A

Rapid division by mitosis, as well as differentiation. Immediately follows clonal selection and is further amplified by interleukins.

237
Q

Plasma B cells?

A

Cells that secrete 2000 antibody molecules per second.

238
Q

Killer T cells?

A

Cells that secrete perforin which forms holes in the membranes of pathogens and infected cells, making them freely permeable and killing them.

239
Q

Antigen molecules?

A

Protein, glycoprotein or polysaccharide molecules associated with pathogens that bind to B and T cell receptors causing clonal selection.

240
Q

Abs acting as opsonins?

A

Antibodies ‘tag’ the surface of pathogens by binding to antigen molecules. This increases and stimulates phagocytosis by neutrophils and macrophages.

241
Q

Abs acting as anti toxins

A

Antibodies neutralise toxins secreted by pathogens by binding to them

242
Q

Abs acting as agglutinins?

A

Antibodies cause pathogens to agglutinate, enabling phagocytes to engulf and destroy many pathogens at once.

243
Q

Lysosome?

A

An organelle containing hydrolytic enzymes.

244
Q

Phagosome?

A

The vesicle formed when a phagocyte engulfs a pathogen.

245
Q

Phagolysosome?

A

The vesicle formed when lysosomes fuse with a phagosome.

246
Q

Memory B and T cells?

A

Cells that quickly stimulate clonal expansion of B and T cells after a second infection by a pathogen.

247
Q

MHC proteins?

A

The proteins that bind to antigen molecules in macrophages and present the antigen molecules on the cell’s surface.

248
Q

Primary response?

A
  • the response that happens on first exposure to a pathogen.
249
Q

Secondary response ?

A

the response that happens on second and consequent exposure to the same pathogen.

250
Q

why does a person get ill after the initial exposure to a pathogen but not 2nd exposure?

A
  • Immediately after the initial exposure, the pathogen becomes established and causes symptoms – the person becomes ill.
  • This is because of the time taken for lymphocytes to undergo clonal selection and expansion.
  • After the second exposure, memory cells immediately undergo clonal expansion, and the pathogen is destroyed before symptoms are shown.
  • The person has developed active immunity to the pathogen.
251
Q

How many types of immunity are there?

A

4 different types of immunity, divided into 2 groups, active and passive.

252
Q

active immunity?

A

If your immunity has been caused by exposure to antigen molecules, and you have actively developed memory cells, then this is active immunity.

253
Q

passive immunity?

A

If you have received antibodies from an external source and have not developed memory cells, then this is passive immunity.

254
Q

both active and passive immunity can be ?

A

natural or artificial

255
Q

How does Natural Active immunity develop?

A
  • immune system develops T and B memory cells
  • 2nd time - IS recognises antigens and destroys
  • Active bc body has acted to produce antibodies
256
Q

e.g.s of Natural Active immunity?

A

infection

257
Q

How does Natural Passive immunity develop?

A
  • new born baby IS can’t make antibodies for 1st few months

- Antibodies cross placenta to baby

258
Q

e.g.s of Natural passive immunity?

A

Colostrum very high in antibodies

259
Q

How does Artificial active immunity develop?

A
  • vaccination
  • small amounts of vaccine inserted into blood
  • primary immune response triggered
  • if live pathogens enter, SIR triggered
  • prevents epidemic
260
Q

e.g.s of Artificial active immunity ?

A

injection of live or attenuated pathogen

261
Q

How does artificial Passive immunity develop

A
  • antibodies are formed in 1 indiv, extracted, injected into blood stream of another
262
Q

artificial Passive immunity e.g.?

A
  • tetanus - ppl infected w it will be injected w tetanus antibodies from a horse.
  • Rabies
263
Q

vaccines may contain?

A
  • killed/ inactivated bacteria and viruses
  • attenuated strains of live bacteria/ viruses
  • toxin mols that have been altered and detoxified
  • Isolated antigens extracted from the pathogen
  • genetically engineered antigens
264
Q

what is an epidemic?

A

when a disease spreads quickly through a population at a local or national level.

265
Q

what is a pandemic?

A

when an outbreak spreads further afield, across countries and continents. Ease of international travel has increased the risk of pandemics in recent times.

266
Q

when an epidemic occurs?

A

a mass vaccination programme will help slow or prevent the spread of the pathogen.

267
Q

why do vaccines have to be changed freq?

A

to keep up with the continually mutating nature of pathogens, especially viruses.

268
Q

what is herd immunity?

A
  • When a percentage of the population has been vaccinated (usually ~95%), then the disease is very unlikely to occur or spread – the population is said to have herd immunity.
  • If the % drops below this level, then outbreaks become much more likely.
269
Q

what is vaccine hesitancy?

A

a reluctance to have vaccinations, often based on false or misleading evidence or beliefs.
The actions of these people can directly cause deaths, often of individuals who cannot be vaccinated, like very young children.
By getting vaccinated, you are not just protecting yourself, but those around you to

270
Q

why do autoimmune diseases occur?

A
  • T regulator cells suppress the immune system, controlling and regulating it.
  • They stop the immune response once a pathogen has been eliminated, and ensure the body recognises ‘self’ antigens.
  • Sometimes this system doesn’t work effectively and an autoimmune disease can occur. This is when the immune system responds against ‘self’ antigen molecules, and destroys body cells inappropriately.
271
Q

what are some causes of auto-immune diseases?

A
  • not well understood, but:
  • Genetic predisposition – the condition ‘runs in the family’
  • Abnormal response to a mild pathogen, or normal body microorganisms
  • Malfunction of T regulator cell system
272
Q

Type 1 diabetes?

A
  • affects insulin secreting cells of the pancreas

- Treatment: insulin injections, pancreas transplants, immunosupressant drugs

273
Q

Rheumatoid arthritis?

A
  • joints- especially in the hands, wrists, ankles and feet

- T: no cure, anti-inflammatory drugs, steroids, immunosupressants, pain relief

274
Q

Lupus?

A
  • often affects skin and joints and causes fatigue
  • can attack any organ in the body inclu kidneys, liver, lungs or brain
  • T: no cure, anti-inflammatory drugs, steroids, immunosupressants, ect
275
Q

Paclitaxel ?

A

a drug used to treat breast cancers – reduces cell division by affecting microtubule formation

276
Q

Ziconotide?

A

a pain relief drug 1000 times more effective than morphine – but only safe when delivered intrathecally – directly into the cerebrospinal fluid

277
Q

Digoxin?

A

a heart drug used to treat atrial fibrillation and other heart conditions.

278
Q

why are humans looking for new sources of medications?

A

As viruses change and mutate, as bacteria become resistant to more antibiotics, and as more pathogens transfer from animals, humans are constantly on the lookout for sources of new medicines

279
Q

what are possible sources of new medications?

A

Microorganisms
Plants and animals
Personalised medicine - pharmacogenomics
Synthetic biology

280
Q

MRSA stands for?

A

Methicillin
Resistant
Staphylococcus
aureus

281
Q

C. diff stands for ?

A

Clostridium difficile

282
Q

what are 2 antibiotic resistant bacteria?

A

MRSA & C. difficile

283
Q

antibiotic resistance cause

A
  • This is because long term exposure to antibiotics has acted as a selection pressure, selecting for individual bacteria that are naturally resistant to these drugs, because of a random mutation in their DNA.
  • That means these bacteria are more likely to survive and reproduce, and eventually whole populations become resistant.
  • It is a form of natural selection that has been accelerated by humans’ use of antibiotics.
284
Q

The antibiotic dilemma is?

A

Antibiotics are very effective at killing bacteria, so should we use them more and more to save lives… …but the more they’re used, the more bacteria become resistant to them, so should we reduce the use of antibiotics?

285
Q

ACP formation steps?

A
  1. Macrophage is attracted by the antigen molecules the pathogen excretes
  2. The macrophage engulfs the pathogen enclosing in a vesicle called a phagsome
  3. Lysosomes fuse w the phagosome, forming a phagolysosome
  4. Hydrolytic enzymes break down the pathogen, destroying it
  5. Pathogen mols are recycled by the macrophage
  6. Non-self antigen molecules from the pathogen bind to MHC proteins in the cytoplasm of the macrophage
  7. MHC proteins inserted into the CM of the macrophage
  8. this ‘presents’ the antigen mols on the surface of the macrophage
  9. the antigen is then presented to T helper cells which using CD4 receptors become activated
286
Q

What does a full blood count do?

A

provides info ab the kinds and no.s of cells in the blood. RBCs, WBCs, platelets. Abnormalilites in any of these types of cells can indicate the presence of important medical disorders.

287
Q

what can full blood counts show?

A
  • WBC test
  • Neutrophil test
  • Lymphs test
  • RBC test
  • Platelet
288
Q

possible sources of new medications- Plants & animals?

A
  • Docetaxel - originally derived from yew trees ➡ breast cancer
  • Aspirin - sallow bark ➡ pain killer, anti-co-ogulatant, antipyetic, anti-inflammatory
  • Digoxin - based on digitoxin (foxgloves) ➡ heart drug
  • prialt - cone snail venom ➡ pain killer
289
Q

possible sources of new medications- pharmacogenetics?

A
  • personalised medicines
  • the science of interweaving knowledge of drug actions and personalised genetic materials
  • e.g. HER2 gene ➡ trastuzumab
290
Q

possible sources of new medications- microorganisms ?

A
  • Penicillin - commerical extraction, originally from mould, antibiotic
  • Vacomycin - soil fungus ➡ antibiotic
291
Q

possible sources of new medications- synthetic biology?

A
  • using genetic engineering techs, can develop pops of bacteria to produce much needed drugs
  • enables use of bacteria as biological factories
  • mammals have also been genetically modified to produce therapeutic protein in milk
  • nanotech - drug delivery e.g.
292
Q

principles of vaccination?

A
  1. pathogen is made safe
  2. Vaccine is injected into the blood
  3. Primary immune response triggered
  4. If you come into contact a live version of the pathogen, Secondary IR triggered
293
Q

E.g.s of vaccines and how they work - flu?

A
  • the WHO identifies the flu strains most likely to spread in the upcoming season
  • Fragments of these virus strains are incorporated into the new vaccine
  • is commonly administered by injection
  • triggers IS to produce antibodies
  • But the vaccine can’t prepare the Immune system for every kind of flu, or if the original strains have mutated, the antibodies won’t recognise them
294
Q

E.g.s of vaccines and how they work - MMR?

A
  • contains weakened versions of live measels, mumps, rubella viruses
  • works by triggering IS to produce antibodies against M,,M,R
295
Q

E.g.s of vaccines and how they work - Polio?

A
  • 2 vaccines
  • 1 is given w 2 drops into the mouth of a child - the oral polio vaccine, builds protection in the child’s gut
  • other is given w an injection - the inactivated polio virus vaccine, builds protection in the blood
296
Q

what is the problem w antibiotic use?

A

often used for relatively minor infections where the IS of the patient would deal w the infection w no serious difficulty.

297
Q

the development of antibiotic resistance?

A
  • there is an evol race between scientists and bacteria
  • an antibiotic works bc a bacterium has a binding site for the drug
  • if a random mutation during reproduction produces a bacterium that is not affected by the antibiotic, that is the one which is best fitted to survive and reproduce, passing on the antibiotic resistance mutation to the daughter cells. Bactria reproduce very rapidly, so once a mutation occurs it does not take long to grow a big pop on antibiotic-resistant bacteria.
298
Q

how can antibiotic resistance be ⬇ in the long term?

A
  • min. antibiotic use, ensuring every course is completed

- good hygiene in hospitals, care homes and in general -this has a major impact on the spread of all infections

299
Q

solving the problem of antibiotic resistance?

A
  • scientists are working on developing new antibiotics using computer modelling and looking at possible sources in a wide variety of places. but at the moment, antibiotic resistance is building at a faster rate than new antibiotics can be found.
300
Q

cell mediated immunity process?

A
  1. in the non spec response, macrophages engulf & digest pathogens in phagocytes. They process the antigens from the surface of the pathogen to form ACPs
  2. the receptors on some of the T helper cells fir the antigens. These T helper cells become activated and produce interleukins which T cells to / rapidly by mitosis. they form clones of identical activated T cells that carry all the right antigen to bind to a particular pathogen
  3. the cloned T cells may: develop into memory T cells, produce interleukins that stimulate phagocytosis, B cells to /, and stimulate the development of a clone of T killer cells that are epsec for the presented antigen and then destroy infected cells.
301
Q

Describe what happens when a pathogen enters body e.g. Virus?

A
  • cell mediated immunity
  • the T lymphocyte that has the correct receptor to bknd to pathogen’s antigen is selected for through clonal selection
  • clonal expansion occurs
  • this means selected T lymphocyte undergoes mitosis and produces 3 types of T cells: T helper, T memory, T killer
  • T killer cells secret perforin which makes holes in the plasma membrane of the host cell
  • T memory cells stay in the blood for many years and respond quickly to divide & differentiate into helper T and T kiler cels after the pathogen invades a 2nd time
  • T helper cells bind to an APC produced by phagocytosis and release interleukin
  • the interleukins stimulate clonal selection and expansion of B and T lymphocytes, phagocytosis, action of T killer cells
  • as clonal expansion is stimulated in B cells, plasma B cells and memory B cells are produced
  • plasma B cells then produce spec antibodies against the host cell

A Level Biology (28 decks)

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