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MPW biology > 4.1.1 Communicable diseases, disease prevention & the immune system > Flashcards

4.1.1 Communicable diseases, disease prevention & the immune system Flashcards

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1
Q

what is a pathogen?

A

A pathogen is a microorganism that causes infectious disease in a host organism

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2
Q

what is an infectious disease?

A

a disease which can be passed from one organism to another, of the same or different species

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3
Q

What are the 4 things pathogens can be?

A

bacteria, viruses, Protoctista or fungi

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4
Q

what is a vector?

A

a living or non-living thing that transmits a pathogen from one organism to another i.e. insect or water

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5
Q

what is type of cell is bacteria and what is cell size?

A

prokaryotic microorganisms
1‐2μm in length

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6
Q

give an example of a bacterial infection

A

Tuberculosis

lung damage and immune system suppression

can be fatal if not treated successfully with antibiotics

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7
Q

label this bacterium cell

A
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8
Q

what is the size of a virus?

A

0.02‐0.3μm

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9
Q

What is a virus?

A

genetic material surrounded by a protein coating and sometimes a membrane

Non-living (no metabolic processes)

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10
Q

why is a virus not considered to be living?

A

they lack their own metabolic processes - i.e respiration

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11
Q

give an example of a virus infection

A

Influenza / flu

flu viruses infect, kill the ciliated epithelial cells in the trachea and bronchi

airways become vulnerable to secondary infection by bacteria

Can be fatal, especially in the very young, old and chronically ill.

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12
Q

what is a protoctista?

A

small eukaryotic organisms, often unicellular

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13
Q

give an exmaple of a protoctista infection

A

Malaria

transmitted by a female mosquito (vector)

causes recurring fevers and organ damage

can be fatal

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14
Q

what is a fungus?

A

unicellular or multicellular eukaryotic organisms, that are heterotrophic and have chitin cell walls; they reproduce using spores

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15
Q

give an exmaple of a fungal infection

A

athlete’s foot

the fungus digests the moist skin between the toes

causing itching and cracking of the skin

can be cured with antifungal cream.

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16
Q

how does a virus cause harm to the body?

A

Viruses takeover their host cells by inserting their genetic material into the host’s DNA; the host cells are then forced to produce more viruses, which eventually cause the cells to burst open (killing those cells), releasing the virus particles

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17
Q

how do protoctista cause harm to the body?

A

Protoctista may enter host cells and digest parts of them as a source of nutrition

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18
Q

how do fungi cause harm to the body?

A

they digest body cells by secreting enzymes onto them

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19
Q

how do bacterium cause harm to the body?

A

secrete toxins which cause physical damage (e.g. cell membrane destruction) or metabolic disruption (e.g. enzyme inhibition) in host cells.

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20
Q

what are the two forms of pathogen transmission?

A

Direct and indirect transmission

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21
Q

what are the three sub-catagories of direct pathogen transmission?

A

Direct contact

Inoculation

Ingestion

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22
Q

what are the three sub-catagories of indirect pathogen transmission?

A

Fomites

Droplet infection

Vectors

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23
Q

what is direct transmission?

A

the transfer of the pathogen straight from one host organism to another, without the involvement of a specific vector

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24
Q

what is indirect transmission?

A

this means the transfer of the pathogen from one host to another via some other object/organism

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25
Q

what is direct contact transmission?

A

skin‐to‐skin contact

direct body fluid contact

transfer of microorganisms from faeces on hands

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26
Q

what is inoculation transmission?

A

direct transfer of microorganisms into the host’s bloodstream

ie cracks in the skin, needle-sharing or animals bites

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27
Q

what is ingestion transmission?

A

intake of pathogens in food/drink

contaminated food or water supplies or due to the hand‐to‐mouth transfer

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28
Q

what is fomite infection?

A

these are non‐living (and usually immovable) objects that transfer the pathogen

Touch - one host to another

door knobs, taps or floors

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29
Q

what is droplet infection transmission?

A

When pathogens from one host leave the body in small liquid droplets (of saliva and/or mucus) during sneezing or coughing

Droplets inhaled into the lungs of the new host

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30
Q

what is vector transmission?

A

a living or non-living thing that transmits a pathogen from one organism to another i.e. insect or water

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31
Q

what factors can increase the change of infection?

A

Overcrowded living/working conditions

Ineffective waste disposal

Poor nutrition

Weakened immune system (old age, hiv etc)

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32
Q

how do healthy plants get infected?

A

Direct transmission - healthy plant directly contacts part of an infected plant

Indirect transmission - Soil contamination and Vectors

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33
Q

what is soil contamination?

A

new plants can be infected when pathogens (e.g. bacteria and viruses) or their reproductive spores (from Protoctista or fungi) remain in the soil following the decay of previously infected plants

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34
Q

what three factors must be present for plant diseases to occur?

A

the pathogen

a susceptible host

favourable environmental conditions

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35
Q

what other factors can increase plant infection?

A

Climate change

Damp, warm conditions

Low mineral availability

low biodiversity

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36
Q

what are the two types of defence mechanisms against pathogen infection?

A

primary non‐specific defences and secondary specific immune response

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37
Q

Describe the primary non‐specific defences

A

always present and are activated rapidly upon exposure to a pathogen, but are not specific to any particular type of pathogen

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38
Q

give some examples of the primary non‐specific defences

A

Skin

Lysozymes

Wound repair

Blood clotting:

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39
Q

what is an opsonin?

A

these molecules bind to pathogens and increase the chance that the pathogens will be engulfed by a phagocyte. The phagocytes have receptors in their plasma membranes that recognise and bind to opsonins that have attached to pathogens; following the binding of the opsonin to its receptor, phagocytosis is triggered and the associated pathogen is engulfed by the phagocyte’s plasma membrane

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40
Q

what is an agglutinin?

A

these molecules bind to pathogens and then to each other, causing the pathogens to clump together. Agglutinated pathogens cannot attach to or enter body cells and cannot reproduce. Phagocytes can now engulf multiple pathogens simultaneously

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41
Q

what is an anti-toxin?

A

molecules bind to and neutralise toxins, thus acting as antitoxins since the toxins now cannot enter body cells or bind to their receptors/targets.

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42
Q

what is an antibody?

A

Y-shaped glycoproteins made by B cells of the immune system in response to the presence of an antigen

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43
Q

what are antibodies also known as?

A

immunoglobulins

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44
Q

what does each and every antibody have?

A

complementary binding sites that enable attachment to a specific antigen

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45
Q

how would you describe the binding site of an antibody?

A

highly specific

each antibody can only recognise and bind to one particular type of antigen only, since the shapes must fit together to form the antigen‐antibody complex

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46
Q

describe the structure of an antibody

A

four polypeptide chains

2 (identical) heavy chains + 2 (identical) light chains

disulphide bonds

Y-shaped

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47
Q

what region of the antibody binds with the complementary antigen?

A

The variable region

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48
Q

what part of the antibody binds with a complementarty recptor?

A

The constant region

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49
Q

where are the recpetors complementary to the antibodies found?

A

Neutrophils or macrophage (white blood cells)

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50
Q

what is the region between the variable and constant region called?

A

hinge region

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51
Q

what is the function of the hinge region?

A

allows flexibility in the antibody structure such that its variable region could bind to more than one antigen simultaneously

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52
Q

Label this

A
53
Q

What are the 4 main ways an antibody can fight pathogens?

A
  1. Once attached, pathogen cannot atach and enter host cells or reproduce
  2. Opsonification - antibody acts as an opsonin, increasing the chance of phagocytosis.
  3. Agglutination - the affected pathogens to clump together (cannot enter cells or divide)
  4. Acts as an anti-toxin - stops toxins from entering cells
54
Q

what is a phagocyte?

A

blood cells that are capable of engulfing pathogens and digesting them

55
Q

what are the two types of phagocytes?

A

neutrophils and macrophages

56
Q

Describe a neurophil

A

lobed nucleus - allows cell to squeeze

granular cytoplasm - may lysosomes

many mitochndoroa and extensive cytoskeleton

57
Q

describe a macrophage

A

rounded nucleus

They are antigen presenting cells

58
Q

what is an antigen-presenting cells (APC)?

A

once it has engulfed and digested a pathogen, some of the antigens combine with a protein called MHC in the cytoplasm of the antigen-presenting cells.

The MHC then carries and inserts the antigen to the plasma membrane of the APC

59
Q

what does the insertion of an antigen in the APC membrane allow for?

A

recognition by, and stimulation of, other white blood cells

60
Q

what is an antigen?

A

an identifying chemical on the surface of a cell that triggers an immune reponse.

61
Q

what are the seven steps of phagocytosis?

A
  1. A phagocyte may be attracted to a pathogen due to detection of chemical signals that it is releasing, or may contact the pathogen initially through a random collision within the blood
  2. Antigens on the pathogen may bind directly to receptors on the cell surface membrane of the phagocyte; this is considered non‐specific, in that the phagocyte is only recognising that antigens as non‐self (i.e. not belonging to the individual’s own body cells) ‐ but is not recognising them as specific antigens from a specific pathogen.
    Alternatively, the pathogen may already have opsonin molecules (e.g. antibodies) bound to its surface; in this case, these opsonins will be recognised and will bind to receptors on the phagocyte’s membrane.
  3. This triggers the cell surface membrane of the phagocyte to wrap around the pathogen, engulfing it. The cytoskeleton is responsible for pushing the membrane around the pathogen; this process requires a great deal of energy from ATP.
  4. Eventually, the membrane fuses with itself, leaving the pathogen entirely surrounded by membrane. The pathogen is now said to be enclosed within a phagocytic vacuole or phagosome.
  5. The phagocyte has many lysosomes in its cytoplasm, containing hydrolytic enzymes (e.g. proteases and lipases). The membrane of a lysosome now fuses with the membrane of the phagosome, such that the enzymes come into contact with the pathogen. This is called a phagolysosome
  6. The pathogen is digested by the enzymes, killing it. Useful products pass into the cytoplasm of the phagocytes; any undigested material may be egested viaexocytosis.
  7. If the phagocyte is a macrophage, antigens from the pathogen are combined with MHC proteins and then inserted into the macrophage’s cell surface membrane, such that the macrophage becomes an antigen‐presenting cell. Antigen presentation is important in stimulating other white blood cells during a specific immune response.
62
Q

what causes the trigger of the specific immune system?

A

The detection of a particular pathogen/antigens by the immune system

63
Q

what is the specific immune response described as?

A

Active or acquired

64
Q

what are the names of the two types of lymphocytes

A

B-lymphocytes

T-lymphocytes

65
Q

where do B lymphocytes mature?

A

Bone marrow

66
Q

where do T lymphocytes mature?

A

Thymus (its in the chest)

67
Q

What are the three things B-lymphocytes do?

A

B effector cells

Plasma cells

B memory cells

68
Q

what are B effector cells?

A

each B cell produces one specific type of antibody, inserting these into their own cell surface membrane to act as receptors. When these antibodies/receptors come into contact with their complementary antigen, that particular B cell is stimulated/activated (in a process called clonal selection) and divides by mitosis (clonal expansion) into a large number of cells. Most of the cells produced now differentiate into plasma cells, whilst a smaller number become memory cells.

69
Q

what is a plasma cell?

A

these are B cells that have become specialised to produce and secrete a specific antibody in massive quantities at a very high rate. Plasma cells have large amounts of RER, lots of mitochondria and many Golgi bodies.

70
Q

what are B memory cells?

A

these are long‐lived cells that provide immunological memory. They retain the ability to recognise a specific antigen that has been encountered previously and the ability to produce the corresponding antibody. These cells are responsible for a much more rapid and stronger (‘secondary’) immune response on any subsequent occasion that the antigen is encountered.

71
Q

what is a t-killer cell?

A

these cells can kill host body cells that are infected with viruses, by releasing an ‘oxidative burst’ of harmful chemicals including hydrogen peroxide; these T killer cells recognise the infected body cells by the fact that there will be antigens from the viruses ‘displayed’ in the cell surface membrane of such cells.

T killer cells can also kill some types of pathogen directly, by release of perforin molecules; these cause a lethal dramatic increase in the pathogen’s membrane permeability.

72
Q

what is a t-helper cell?

A

these do not directly kill pathogens but enhance the strength of an immune response via cell signalling.

T helper cells secrete specific cytokine cell signalling molecules called interleukins, following contact between their CD4 receptors and the antigens of a specific pathogen that are being displayed by an Antigen Presenting Cell (e.g. a macrophage).

The interleukins released by T helper cells bind to complementary receptors on other white blood cells, triggering various responses depending on the cell type:
o in B cells, antibody production/secretion is increased;
o macrophages are attracted to the site of interleukin release and have increased rate of engulfing/digesting pathogens that already have antibodies attached;
o for other types of T cell, the interleukins released by T helper cells stimulate clonal expansion, i.e. mitosis to increase the number of T cells.

73
Q

what is a t-memory cell?

A

these are long‐lived cells which provide immunological memory. They have receptors (essentially antibodies) in their cell surface membranes; when these encounter the same pathogen’s antigens in future, rapid clonal expansion (via mitosis) is stimulated, producing a very large number of T killer cells that can specifically kill that pathogen (or, in the case of viruses, body cells containing pathogens).

74
Q

what is a t-reguator cell?

A

T regulator cells – these cells act to supress immune system activity, which is important in shutting down a specific immune response when the pathogen has been removed from body.

T regulator cells are also important in the recognition of self‐antigens on body cells and thus the avoidance of autoimmune diseases.

Cell signalling via interleukins and other types of cytokines is important in these aspects of immune system regulation and control.

75
Q

what is immunity?

A

the ability to destroy a particular pathogen as soon as it enters the body, avoiding the onset of disease symptoms

76
Q

how do we describe immunity?

A

highly specific

you can be immune to one pathogen, but remain susceptible to another similar pathogen, if its antigens are a different shape

77
Q

what are the 4 specific types of immunity?

A

Passive or Active

Natural or Artificial

78
Q

Describe Active-Natural immunity

A

Natural active immunity is that involving the rapid production of large quantities of a specific antibody by the body’s own plasma cells, following exposure to a pathogen whose antigens have been recognised by T and B memory cells; this is a secondary immune response and occurs when there has been previous infection by that pathogen.

This form of immunity is long‐lived, since it involves memory cells which retain the ability to recognise the pathogen in future and make the required antibodies again, if needed.

79
Q

Describe Active-Artificial immunity

A

Artificial active immunity is when large quantities of a specific antibody are rapidly produced by the body’s own plasma cells, following exposure to a pathogen whose antigens have been recognised by T and B memory cells because these antigens had previously been introduced to the body via a medical procedure, usually vaccination.

The vaccination had transferred antigens into the blood in a safe form (e.g. on dead or weakened pathogens); this triggered a primary immune response which led to the production of memory cells. This form of immunity is therefore long‐lived: the (real) pathogen will be recognised in future and will stimulate a secondary immune response, whereby plasma cells will rapidly make large quantities of the appropriate antibodies.

80
Q

Describe Passive-Natural immunity

A

Natural passive immunity is when readymade antibodies are naturally transferred from one individual to another, without any medical procedure. This gives the recipient immediate immunity to any pathogens that the donor had immunity to already.

Examples: babies receiving antibodies from their mother, across the placenta and by consuming early breast milk

Notice that in this case the individual receiving the antibodies is NOT gaining the ability to make these antibodies themselves in future, since no immune response is actually taking place and no memory cells are being produced; consequently, this form of immunity is short‐lived (lasting only a few months)

81
Q

Describe Passive-Artifical immunity

A

Artificial passive immunity is when ready‐made antibodies are deliberately transferred into an individual’s blood via a medical procedure, giving immediate immunity to a specific pathogen.

Example: antibodies from an animal can be injected (or given via transfusion) into a human’s blood if that human has been exposed to a potentially lethal pathogen.

In this case the individual receiving the antibodies is NOT gaining the ability to make these antibodies themselves in future, since no immune response is actually taking place and no memory cells are being produced; consequently, this form of immunity is short‐lived (lasting only a few months) – though it could of course be living‐saving in an emergency.

82
Q

give an exmaple of active-natural

A

infection

83
Q

give an exmaple of active-artificial

A

injected of live pathogen

84
Q

give an exmaple of passive-natural

A

antibodies from mothers breast milk or antibodies across the placenta

85
Q

give an exmaple of passive-artificial

A

injection of antibodies or antitoxin directly

86
Q

what is a vaccination?

A

Vaccination (or inoculation) is a medical procedure intended to result in the development of artificial active immunity to a specific pathogen.

87
Q

what is immunisation?

A

the process of developing immunity, i.e. the intended consequence of vaccination

88
Q

what does vaccination involve?

A

the deliberate injection into the blood of antigens from a pathogen (in safe form): the vaccine could be made of dead pathogens or pathogens that have been modified to weaken them so that they cannot cause disease (attenuated pathogens); alternatively, purified antigens or modified versions of the pathogen’s toxins could be injected.

89
Q

what is the mechansim for vaccination?

A
  1. The vaccine, containing antigens from the pathogen in a safe form, is injected into the blood.
  2. The antigens now trigger a primary immune response (just as if the person was infected with the real, live pathogen): this results in the clonal selection and expansion (by mitosis) of B and T cells that are able to produce antibodies of the complementary shape to the introduced antigens.
  3. Crucially, the primary immune response results in the formation of B and T memory cells. These will remain in the person’s blood long term.
  4. If the real pathogen is encountered in future, a secondary immune response is triggered: the memory cells recognise this pathogen from the shape of its antigens. Clonal selection and expansion occur and the large numbers of plasma cells formed will rapidly produce very large quantities of the relevant antibody.
  5. The pathogen is destroyed before it can reproduce or do any damage to body cells. The person therefore does not experience any symptoms of disease and is described as being immune to that pathogen.
  6. For some types of vaccine, ‘booster’ injections are needed in order to trigger additional memory cell formation and thus ensure that immunity is reliably maintained throughout the person’s lifetime.
90
Q

what is herd immunity?

A

if a high proportion of a population is vaccinated (e.g. 95%) then it is very unlikely that the pathogens will be able to spread from person to person, since most people are immune.

91
Q

what is an epidemic and pandemic, and how do we stop them?

A

epidemic - when a communicable disease spreads rapidly and infects a high proportion of people in a given area

pandemic - when a communicable disease spreads to many people across a number of different countries and continents

mass vaccination of those in the affected area can be effective at preventing the disease spreading

Considerable financial resources, organisation and cooperation between governments, healthcare providers and charities are required for such programmes to be successful

Education can also be crucial, e.g. parents may not allow their children to be vaccinated if they don’t understand that the vaccine helps to prevent (not cause!) the spread of disease.

92
Q

What is cell-mediated response?

A

a response that attacks body cells that have undergone modification or damage.

93
Q

what does a cell-mediated repsonse consist of?

A

This would include the responses involving T lymphocytes against virus‐infected body cells or against cells with DNA damage (i.e. mutations, which could lead to uncontrolled cell division and hence cancer).

94
Q

what can occur after a organ transplant?

A

Immune responses against cells in a transplanted organ (e.g. a kidney), that can lead to the rejection of the organ in the recipient’s body, are also in this category.

95
Q

summaries cell-mediated immunity in 4 steps

A
  1. Antigen presentation: macrophages (which are able to act as APCs) engulf and digest pathogens, then display the antigens from the pathogen (in association with MHC proteins) in their own cell surface membrane.
  2. Clonal selection: some T lymphocytes have receptors that fit the displayed antigens on the APC (i.e. the receptor can bind to the antigen as the shape of the receptor is complementary to the antigen); these particular T lymphocytes are therefore now activated.
  3. Clonal expansion: the selected T lymphocytes undergo mitosis to produce a large number of identical cells (a clone), all of which have receptors that fit the relevant antigen. This process is stimulated by the interleukins (cell signalling molecules) produced by activated T helper cells.
  4. Differentiation and responses: some T lymphocytes become T killer cells that destroy body cells infected with the pathogen; some become T helper cells that produce interleukins to stimulate phagocytosis or to increase mitosis in selected T or B cells; some become T memory cells which survive long term and recognise the pathogen upon reinfection.
96
Q

what is a humoral repsonse?

A

a response to antigens that are in body fluids rather than in/on body cells, for example a response to antigens that are on the surface of a pathogen in the bloodstream.

97
Q

what does a humoral repsonse consist of?

A

Humoral immunity involves B lymphocytes and the release of antibodies (produced by plasma cells) into body fluids.

98
Q

summarise humoral immunity in 4 steps

A
  1. Antigen presentation: an APC that has engulfed and digested the pathogen displays the pathogen’s antigens its own cell surface membrane.
  2. Clonal selection: some B lymphocytes have receptors (essentially antibodies held in their cell surface membranes) that fit the antigens displayed by the APC; these particular B lymphocytes are now activated.
  3. Clonal expansion: the selected B lymphocytes undergo mitosis to produce a large number of identical cells (a clone), all of which have receptors that fit the relevant antigen. This process is stimulated by the interleukins (cell signalling molecules) produced by activated T helper cells.
  4. Differentiation and responses: most of the B cells become plasma cells that produce and secrete massive quantities of the correct antibody into the blood or tissue fluid [See previous section for the action of antibodies]; some instead become B memory cells which survive long term and recognise thepathogen upon reinfection.
99
Q

Describe the primary immune repsone

A

antigen is being detected for the first time

The processes of clonal selection and expansion are relatively slow

takes a while before there are enough plasma cells producing enough of the correct antibodies to destroy all the pathogens

pathogen has reproduced and caused damage to body cells. Hence in this scenario, disease symptoms appear during the time that the primary immune response is taking place

occurs when a pathogen infects the body for the first time, but can also be triggered by injection of a vaccine containing dead/weakened pathogen or its antigens

B and T memory cells produced, enabling a secondary immune response to take place if the same antigens are detected again in future

100
Q

draw the primary immune response graph

A
101
Q

Describe the secondary immune repsonse

A

occurs when a pathogen’s antigens are recognised by the B/T memory cells that were produced during the primary immune response (i.e. that which was triggered on a previous exposure to this pathogen or, at least, its antigens). This time, the processes of clonal selection and expansion occur much more quickly.

Compared to a primary response, secondary responses are characterised by a shorter delay before antibody secretion by plasma cells begins, a faster rate of antibody production and the production of a far greater total quantity of antibodies.The pathogen is therefore eliminated very rapidly, before it has had time to reproduce or damage body cells; hence disease symptoms are avoided.

If a person is capable of a secondary immune response to a particular pathogen (due to the presence of memory cells that formed during previous exposure to its antigens), they can be described as having immunity to that pathogen.

This immunity can be acquired naturally (by previous infection) or artificially (via vaccination). Immunity is highly specific to a pat hogen with a particular type/shape ofantigen.

102
Q

what is an autoimmune disease?

A

the immune system begins to attack the individual’s own body cells as if they were pathogens

103
Q

how do we diagnose an autoimmune disease?

A

blood test: there will be antibodies present that are specific to self‐antigens found in the plasma membranes of particular body cells

104
Q

how do autoimmune diseases operate?

A

antibodies present that are specific to self‐antigens found in the plasma membranes of particular body cells.

These antibodies are the product of a humoral response (by B lymphocytes that have undergone clonal selection, expansion and differentiation into plasma cells). However, much of the cell damage that occurs in autoimmune disease is due to a cell‐mediated response: T killer cells will destroy healthy body cells (e.g. via release of hydrogen peroxide) if antigens on these cells have (incorrectly) been identified as ‘foreign’

105
Q

how do we treat autoimmune diseases?

A

The obvious treatment for autoimmune diseases is immunosuppressant drugs, i.e. medicines that decrease white blood cell production and/or activity.

However, the substantial loss of immune system function that results from this treatment (though it may decrease the severity of symptoms relating to the autoimmune disease) will leave the individual vulnerable to infections, e.g. flu.

106
Q

give an example of an autoimmune disease

A

Arthritis (specifically the form known as rheumatoid arthritis)

pain and stiffness of movement in joints such as those in the hands and feet

there is no known cure, but treatments which can reduce the severity of symptoms include immunosuppressant drugs, anti‐inflammatory drugs and painkillers

107
Q

what are antibiotics?

A

which kill bacteria and thus that are able to cure communicable diseases that are caused by bacterial infection

108
Q

how do antibiotics work?

A

interfere with metabolic processes or cell wall structures that are only present in bacteria, hence they do not damage human cells

109
Q

what is antibiotic resistance?

A

When an antibiotic is used on a population of bacteria, most bacteria will be killed. However, due to random mutations that have already occurred, a small number of bacteria might be resistant to the drug; these bacteria (only) are able to survive and reproduce, passing on their resistance alleles to the next generation. This natural selection mechanism repeats over many generations.

In favourable conditions, bacteria can divide by binary fission every 20‐30 minutes, hence it does not take long for a large population of resistant bacteria to build up; these bacteria have all inherited the alleles for resistance and so cannot be killed by the antibiotic that is present in their environment. i.e MRSA

110
Q

what speeds up/causes antibiotic resistances?

A

antibiotics are routinely given to farm animals in some counties

antibiotics are often being prescribed unnecessarily for minor infections (that the
immune system of an otherwise healthy person would effectively deal with anyway)

in some countries, antibiotics are readily available without prescription, including
via the internet, leading to people taking them when they are not the most
appropriate treatment

failure to complete a course of antibiotics, which increases the chance that bacteria
with moderate levels of resistance survive rather than be destroyed

very few new antibiotics (that, when tested, prove effective and safe for use in
humans) have been discovered in recent years

failure to implement effective hygiene practices in hospitals and elsewhere means
that infections spread to more people and so more use of antibiotics is required.

111
Q

how can we slow down antibiotic resistance?

A

ban the routine use of antibiotics in farm animals (already true in the UK);

only prescribe antibiotics for serious infections;

ensure that antibiotics are not readily available (e.g. for purchase online without
prescription) and so decrease their inappropriate use;

educate patients so they understand that a course of antibiotics should always be
completed;

fund research into the discovery/development of new antibiotics, e.g. by screening compounds from plants/microorganisms or by rational drug design

develop and implement better hygiene practices in hospitals and public places so
that infections are less likely to spread and there will be less need for antibiotic use.

112
Q

give an exmaple of a naturally occuring drug

A

Penicillin ‐ an antibiotic from Penicillium crysogenum fungus

or

Vancomycin ‐ an antibiotic isolated from a soil fungus.

113
Q

How do we discover new drugs?

A

Screening of databases of compounds

Rational drug design

Pharmacogenetics

114
Q

what is Screening of databases of compounds

A

once a drug target has been identified (e.g. an enzyme or receptor), computer software can be used to (virtually) test thousands of compounds in order to find those which (in theory) may bind to it; the shortlist of candidate drugs is then tested for real in living cells or whole organisms

115
Q

what is Rational drug design

A

this involves the identification of a drug target (e.g. an enzyme or receptor), the modelling of its precise 3D shape and chemical properties (particularly the active site or other binding site), followed by the design of possible molecules that may be able to bind to this target (using sophisticated computer software).

Chemists then attempt to synthesise the compounds that are the potential new drugs, so that the properties of these can be tested in living cells or whole organisms.

Alternatively, it may be possible to genetically modify bacteria (or other organisms) so that they can produce the required compounds; this is a form of synthetic biology and is likely to be the preferred approach if complex drug molecules are to be mass produced at low cost.

116
Q

what is Pharmacogenetics?

A

this is where an individual’s genotype (their specific combination of alleles) is analysed and used as a basis for selecting which type of drug will be most effective in treating the disease they have.

This is a form of personalised medicine; as research in this area progresses, it is likely to become increasingly important in healthcare provision, allowing medicines to be selected that have the best chance of success in each individual patient.

117
Q

Do plants have immune systems?

A

Nah G

118
Q

what do plants have to combat pathogens?

A

receptors that can detect molecules that pathogens have produced or that detect the breakdown products from damage to their own cell walls

When a pathogen is thus detected, genes are switched on in the nucleus that code forenzymes involved in fighting the pathogen. For example, enzymes may be produced that synthesis callose and lignin (which strengthen the cell walls).

Cell signalling molecules pass from the affected cells into adjacent cells (through plasmodesmata), triggering pre‐emptive responses which will defend those cells from imminent attack by the pathogens.

119
Q

what are the three examples of plant defence we must know?

A

Mechanical/physical protection via callose deposition

Leaf abscission

Production of chemicals that destroy the pathogens

120
Q

what is Mechanical/physical protection via callose deposition

A

detection of a pathogen rapidly triggers the production of a polysaccharide called callose in the affected cell(s) and those nearby; the callose is deposited in the cell walls, making these walls a less permeable barrier, thus limiting the spread of the pathogen through the tissue. Further spread of the pathogen beyond the immediate cells is also restricted, via the deposition of callose in sieve plates in the phloem and in plasmodesmata, blocking them. Essentially, the infected area is being sealed off (and cells already infected are allowed to die), containing the pathogen and preventing its spread to healthy tissues

121
Q

what is leaf abscission?

A

infected leaves fall off the plant, preventing the pathogen spreading into healthy tissues.

122
Q

what is Production of chemicals that destroy the pathogens in plants?

A

Production of chemicals that destroy the pathogens themselves (e.g. anti‐bacterial or anti‐fungal compounds), that repel the pathogen’s vectors (e.g. production of insect repellents) or that are lethal to the vectors (e.g. production of insecticides or the release of metabolic poisons such as cyanide or ricin, lethal to most living organisms even in tiny doses).

123
Q

how is skin a primary non-specific defence?

A

this acts as a water‐proof, impermeable barrier that is highly effective in preventing the entry of most microorganisms into the blood / body tissues. Nonpathogenic microorganisms that normally grow on the skin may out‐compete pathogens. Sebum (an oily substance secreted by the skin) inhibits pathogen growth

124
Q

how is Mucous membranes a primary non‐specific defences

A

these are the layers of epithelial tissue that line the airways, digestive system etc. The presence of goblet cells means that mucus is secreted, which is sticky and so traps many pathogens; there may also be phagocytes in the mucus, which engulf and digest some pathogens

125
Q

how is Lysozymes a primary non‐specific defences

A

these are enzymes found in tears, stomach acid and urine, capable of digesting the cell walls of bacterial and fungal pathogens.

126
Q

how is Expulsive reflexes a primary non‐specific defences

A

these are actions that remove body fluids containing pathogens from the body, including coughing, sneezing, vomiting and diarrhoea

127
Q

how is blood clotting a primary non‐specific defences

A

the clotting of blood can seal a small wound, such that blood loss from the wound stops and the break in the skin does not become an entry point for pathogens. Blood clotting involves the activation of platelets (via contact with collagen from damaged capillary walls), leading to a cascade of enzyme‐catalysed reactions which culminates in the conversion of (soluble, globular) fibrinogen proteins in the blood plasma into (insoluble, fibrous) fibrin. The mesh of long fibrin threads traps red blood cells, forming the blood clot

128
Q

how is wound repair a primary non‐specific defences

A

once a blood clot has formed at the site of an injury, it dries out to become a protective scab, preventing pathogen entry; underneath the scab, new epidermal tissue grows, tough collagen fibres are deposited and damaged capillaries are repaired. Eventually, the repair of the epidermis is complete and the protective scab falls off.

129
Q

how is inflammation a primary non‐specific defences

A

this is a localised and non‐specific immune response to pathogens, tissue damage or irritants, typically occurring at the site of a wound. Signs of inflammation include feelings of heat and pain, plus redness and swelling. The inflammatory response is coordinated via the activation of mast cells, which secrete signalling molecules called histamines and cytokines:

o Histamines cause dilation of arterioles and hence increased blood flow to the affected region: this is visible as localised redness, accompanied by a rise in temperature which may decrease the reproductive rate of the pathogens, whilst boosting immune system activity;
o Histamines also increase the permeability of capillary walls, increasing tissue fluid formation: this is visible as localised swelling, and may help bring more white blood cells into the affected area;
o Cytokines attract phagocytes to the affected area and stimulate their phagocytic activity: this increases the rate at which any pathogens present will be engulfed and digested.

During an inflammatory response, excess tissue fluid (possibly now containing pathogens) from the affected area drains away as lymph via lymph vessels to the lymph glands (e.g. in the armpits, neck and groin); this build‐up of lymph, plus increased activity of phagocytes and lymphocytes in the lymph glands, results in the glandular tissue swelling and become painful.

MPW biology (26 decks)

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