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Mpharm > Immunology > Flashcards

Immunology Flashcards

1
Q

How can pathogens enter the body?

A

Eyes, mouth, nose, urogenital tract, rectum and damaged skin

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2
Q

Immune system definition?

A

The collection of organs, tissues, cells and cell products whose role it is to differentiate self from non-self

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3
Q

Four key processes of the immune system?

A

Prevention
Recognition
Elimination
Memory

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4
Q

What are the three lines of defence?

A

Barriers
Innate
Adaptive

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5
Q

How does the skin provide a barrier to pathogens?

A

The tough outer layer of cells that produce keratin
The oleic acid on the skin can kill some bacteria
The skin (also tears and saliva) can secrete lysozymes to break down the outer wall of some bacteria

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6
Q

How do mucosal membranes provide a barrier to pathogens?

A

Secrete mucus to trap small particles and pathogens
Some have cilia to sweep mucus and particles out

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7
Q

How long does the innate immune system take to respond?

A

Around 12 hours

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8
Q

What activates the innate immune system?

A

Cells recognising common generic components of pathogens

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9
Q

What is the distinguishing feature of the innate immune system?

A

Inflammation

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10
Q

What are pattern recognition receptors?

A

They bind to pathogen associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs)

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11
Q

An example of a pattern recognition receptor?

A

Toll-like receptors

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12
Q

What happens when a DAMP/PAMP binds to a toll-like receptor?

A

The receptor activates a cascade signalling pathway resulting in recruitment of other immune cells and inflammatory pathways

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13
Q

How many types of toll-like receptors are in humans?

A

10

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14
Q

Toll-like receptor structure?

A

An extracellular domain which is involved in recognition of microbial products
An another domain in the cytoplasm that recruits the different signalling molecules that activate the transcription of genes involved in inflammation and antimicrobial defences

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15
Q

What do toll-like receptors 1, 2, 4 and 6 recognise?

A

Bacterial lipids

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16
Q

What do toll-like receptors 3, 7 and 8 recognise?

A

Viral RNA

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17
Q

What does toll-like receptor 9 recognise?

A

Bacterial DNA

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18
Q

What do toll-like receptors 5 and 10 recognise?

A

Bacterial or parasitic proteins

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19
Q

Cells involved in the innate immune system?

A

Mast cells
Dendritic cells
Macrophages
Natural killer cells
Complement proteins
Basophils
Eosinophils
Neutrophils

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20
Q

What is usually the first cell on the site of infection?

A

Macrophage

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21
Q

What are granulocytes?

A

Phagocytic cells with granules inside

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22
Q

Types of granulocytes?

A

Neutrophils
Eosinophils
Basophils
Natural killer cells

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23
Q

What is the most common type of granulocyte?

A

Neutrophils

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24
Q

What does the nucleus of a neutrophil look like?

A

Multilobed

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25
Q

What recruits neutrophils to sites of infection?

A

Activated macrophages
Peptide fragments of cleaved complement proteins
Some PAMPs

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26
Q

How are macrophages different to neutrophils?

A

Much larger
No granules
Longer lived
Can ingest larger microbes such as protozoa

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27
Q

What does the nucleus of an eosinophil look like?

A

Bi-lobed

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28
Q

How do eosinophils work?

A

In groups

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29
Q

What can granulocytes bind to?

A

Toll-like receptors
Receptors for antibodies produced by the adaptive immune system
Receptors for complement proteins

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30
Q

How do granulocytes engulf their targets?

A

1) binding to any ligand activates the granulocyte, increasing its killing power
2) this also causes a release of cytokines to attract more white blood cells
3) actin polymerisation induced at the site
4) granulocytes plasma membrane surrounds the pathogen to engulf it in a large membrane called a phagosome

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31
Q

What do the granules in granulocytes do?

A

Fuse with phagosome membrane and release contents (lysozyme and hydrolases) to digest the pathogens cell wall
Granules also contain defensins that destabilise pathogen membranes
NADPH oxidase complexes form on the phago-lysosomal membrane. A respiratory burst (transient increase in oxygen consumption) by the phagocyte allows the NADPH oxidase complexes to produce toxic oxygen-derived compounds such as superoxide (02-), hypochlorite (HOCL) and hydrogen peroxide (H2O2) to damage the pathogen

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32
Q

Do neutrophils and macrophages survive the chemical and enzymatic processes of engulfing pathogens?

A

Macrophages do
Neutrophils usually do not

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33
Q

What can neutrophils do as a last resort to kill a pathogen?

A

Eject its DNA in a sticky web that can trap pathogens to stop them from escaping

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34
Q

What causes pus?

A

Dead neutrophils and deal pathogens

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35
Q

Why can pus sometimes be green or yellow?

A

A release of copper-containing compounds and myeloperoxidase from the dead neutrophils

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36
Q

What can down-regulate the expression of immune system recognition molecules on the surface of cells?

A

Viruses and cancer
So cells with low expression are likely to be infected or transformed

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37
Q

How do natural killer cells recognise their targets?

A

By the low expression of immune system recognition receptors on the surface of a cell

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38
Q

How do natural killer cells destroy their targets?

A

By persuading them to undergo apoptosis
Phagocytes destroy apoptotic bodies that are left behind

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39
Q

What are the four symptoms of inflammation?

A

Dolor (pain)
Rubor (redness)
Calor (heat)
Turgor (swelling)

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40
Q

How does inflammation occur?

A

1) macrophage recognises and engulfs a pathogen
2) cytokines are released
3) cytokines allow vasodilation
4) this allows recruited immune cells to exit blood vessels into tissue so they can target invading pathogens
5) blood clotting occurs at microvessels to stop bacteria from entering the bloodstream

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41
Q

Where are mast cells found?

A

In particular mucosal tissue, not circulating

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42
Q

What do mast cell granules contain?

A

Histamine
Heparin
Leukotrienes
Other mediators

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43
Q

What receptor do mast cells express?

A

FcϵR

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44
Q

How do mast cells release mediators?

A

1) An antibody is bound to the mast cell receptor
2) when the antigen binds to the antibody, lysozymes fuse with the cell wall to break it down
3) the mediators are released

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45
Q

What are the two subdivisions of the adaptive immune system?

A

Humoral
Cell-mediated

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46
Q

How long does it take the adaptive immune system to respond?

A

~ 24 hours

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47
Q

Cells involved in the adaptive immune system?

A

T-cells
B-cells
Antigen-presenting cells

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48
Q

Cells involved in the humoral immune response?

A

B-cells and the antibodies they produce

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49
Q

Structure of an antibody?

A

Tetrameric with four polypeptide chains
Two identical heavy chains and two identical light chains are held together by covalent disulfide bonds at the hinges between the heavy and light chains

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50
Q

What do the heavy chains of the antibody bind to?

A

B-cells to trigger a reaction

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51
Q

What do the light chains of an antibody bind to?

A

The antigen that is specific to that antibody

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52
Q

Where are B-cells matured?

A

Bone marrow

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53
Q

What can mature B-cells differentiate into when they are activated?

A

Memory B-cells
Plasma/effector B-cells

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54
Q

What do memory B-cells do?

A

Look for pathogens

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55
Q

What do effector B-cells do?

A

Produce antibodies

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56
Q

How to resting B-cells differentiate into effector B-cells?

A

When their membrane-bound receptor binds to the antigen
This causes a massive increase in the endoplasmic reticulum allowing secretion of ~ 5000 antibodies per second

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57
Q

What is another word for antibodies?

A

Immunoglobulins

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58
Q

How many classes of antibodies are in humans?

A

Five

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59
Q

IgG structure?

A

Monomer

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60
Q

IgG location?

A

Free in the blood plasma

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61
Q

What percentage of circulating immunoglobulins are IgGs?

A

80%

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62
Q

The function of IgGs?

A

Most abundant antibody in primary and secondary immune response
Can cross the placenta to provide passive immunisation to the foetus

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63
Q

Structure of IgM?

A

Pentamer

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64
Q

Location of IgMs?

A

The surface of the B-cell
Free in blood plasma

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65
Q

The function of IgMs?

A 
Antigen receptor on the B-cell membrane 
The first class of antibodies released by B-cells during the primary response
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66
Q

IgD structure?

A

Monomer

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67
Q

Location of IgDs?

A

Surface of the B-cell

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68
Q

The function of IgDs?

A

The cell surface receptor of mature B-cells
Important in B-cell activation

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69
Q

Structure of IgA?

A

Dimer

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70
Q

Location of IgAs?

A

Saliva, tears, milk and other body sections

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71
Q

The function of IgAs?

A

Protect mucosal surfaces
Prevent attachment of pathogens to epithelial cells
Colostrum

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72
Q

Structure of IgE?

A

Monomer

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73
Q

Location of IgEs?

A

Secretion by plasma cells in skin and tissues lining the gastrointestinal and respiratory tracts

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74
Q

The function of IgEs?

A

When bound to antigens, it binds to mast cells and basophils. This triggers the release of histamine that contributes to inflammation and some allergic responses

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75
Q

What is agglutination?

A

The clumping together of pathogens in the presence of antibodies that bind them together
Particularly IgMs

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76
Q

Why is agglutination important in medical terms?

A

Blood transfusions
If the recipient has antibodies to the type of blood received, this can cause agglutination and death

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77
Q

What blood can an O recipient receive?

A

O

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78
Q

What blood can an A recipient receive?

A

A
O

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79
Q

What blood can a B recipient receive?

A

B
O

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80
Q

What blood can an AB recipient receive?

A

Any

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81
Q

Who can receive rhesus negative blood?

A

Anyone

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82
Q

Who can receive rhesus positive blood?

A

Only those who are rhesus positive

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83
Q

Where do T-cells develop?

A

In the thymus from thymocytes

Haemopoietic stem cells in bone marrow –> common lymphoid progenitor cells –> thymocytes –> T-cells

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84
Q

Structure of a T-cell receptor?

A

Two light chains called alfa and beta have a constant portion and a variable portion. At the bottom, there are two anchor points bound by a disulfide bond which go into the T-cell membrane

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85
Q

What are major histocompatibility complexes?

A

On the surface of cells
Involved in interacting with T-cells and activating immune response

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86
Q

What are the types of major histocompatibility complexes?

A

Type 1 and type 2

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87
Q

Where are class 2 major histocompatibility complexes found?

A

Only on classic antigen-presenting cells such as macrophages, dendritic cells and B-cells

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88
Q

Where are class 1 major histocompatibility complexes found?

A

All nucleated cells of the body but in different levels

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89
Q

What major histocompatibility complex would present a cytosolic pathogen to the surface?

A

Class 1

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90
Q

What major histocompatibility complex would present a intravascular pathogen to the surface?

A

Class 2

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91
Q

What major histocompatibility complex would present an extracellular pathogen/toxin to the surface?

A

Class 2

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92
Q

What type of T-cell do class one major histocompatibility complexes present to?

A

Effector CD8 T-cells

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93
Q

What type of T-cell do class two major histocompatibility complexes present to?

A

Effector CD4 T-cells

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94
Q

What are the three types of T-cell?

A 
Treg CD4 (regulatory)
Th CD4 (helper)
Tc CD8 (cytotoxic)
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95
Q

What do T-helper cells do?

A

Activate macrophages, dendritic cells and B-cells. Maintain cytotoxic T-cell activity by secreting a variety of cytokines

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96
Q

What do T-regulatory cells do?

A

They inhibit the function of T-helper cells, cytotoxic T-cells and dendritic cells

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97
Q

What do cytotoxic T-cells do?

A

They kill the infected host by persuading them to undergo apoptosis

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98
Q

What is inflammatory disease?

A

Chronic inflammation- persistent inflammatory status

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99
Q

What can cause inflammatory disease?

A

Pathogens
Tumours
Autoimmunity
Atherosclerosis
Heart disease
Obesity
Any kind of tissue damage

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100
Q

What are the two types of inflammatory bowel disease?

A

Ulcerative colitis
Crohn’s disease

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101
Q

What causes inflammatory bowel disease?

A

Immune reaction to commensal bacteria of the gut (self microbiota)

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102
Q

How does Crohn’s disease occur?

A

Typically Phagocytic cells in the gut are looking for harmful bacteria to get rid of
In Crohn’s disease, the phagocytes take helpful bacteria and introduce them to the macrophage
Cytokines and chemokines are the produced

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103
Q

Cytokines/chemokines typically involved in Crohn’s disease?

A

IL12
IL6
EGF beta
IL beta
IL 23

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104
Q

What type of T-cells are produced by cytokines/chemokines in Crohn’s disease?

A

T-helper 1 and 17 cells rather than regulatory T-cells

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105
Q

What do T-helper 1 cells produce? (Crohn’s)

A

Chemokines- to recruit macrophages
IFN gamma- which induces expression of vascular adhesion molecules. Activates macrophages which increase the release of inflammatory mediators
TNF alfa and LT- causes local tissue damage. Increase expression of adhesion molecules on local blood vessels
IL-3/GM-CSF- stimulated monocyte production by bone marrow stem cells

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106
Q

What causes coeliac disease?

A

Gluten is made up of a protein called gliadin
Gliadin is attached by tissue transglutaminase to deamidate it
This triggers the body to react and antibodies to bind
This complex is then shown on the antigen-presenting cell
This activates the T-cell which releases IFN gamma which causes inflammation and damage to epithelial cells in gastrointestinal tract
IFN gamma also activates B-cells to produce IgA to anti-gliadin, anti-endomysium and anti-tTg
T-cells will activate natural killer cells which again damage epithelial cells
Leading to flattening of the gastrointestinal tract, which leads to decreased absorption

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107
Q

What is rheumatoid arthritis?

A

Chronic inflammation of the joints
Can affect haematologic, cardiovascular and respiratory systems

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108
Q

What is the Fc region of an antibody?

A

The bottom of the Y-shape section that binds on to the receptor cell that activates a response if the antibody is activated

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109
Q

What causes Rheumatoid Arthritis?

A

Antibodies are produced which react to the Fc region of IgG
IgM-IgG complexes are created
This causes massive agglutination
These agglutinated complexes are deposited in the joints
When these complexes build-up, the complement cascade is activated, which when leads to a type 3 sensitivity reaction

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110
Q

What is hypersensitivity?

A

Adaptive responses generated against harmless pathogens

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111
Q

What does autoimmune mean?

A

Where the immune system attacks the host. Can have genetic and environmental factors

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112
Q

How many majn types of allergic reactions are there?

A

4

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113
Q

What is a type-I allergic reaction?

A

IgE binds to a soluble antigen This triggers mast cell activation Histamines are released

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114
Q

Examples of type-I allergic reactions?

A

Allergic rhinitis, allergic asthma, atopic eczema, anaphylaxis, some drug allergies

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115
Q

What is a type-II allergic reaction?

A

IgG can trigger two different pathways: 1) IgG can bind to a cell or matrix associated antigen, leading to activation of complement and receptor cells, phagocytes and NK cells. (causes some drug allergies such as penicillin) 2) IgG binds to a cell surface receptor altering the signalling from the cell. (can cause chronic urticaria)

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116
Q

What is a type-III allergic reaction?

A

IgG binds to a soluble antigen Activates complement and phagocytes IgG-antigen complex is formed within a blood vessel compartment This can lead to cell lysis and other cells are attracted into the blood vessel

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117
Q

Examples of a type-III allergic reaction?

A

Serum sickness Arthus reaction

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118
Q

What is a type-IV allergic reaction?

A

Three ways: 1) Th1 cell binds to soluble antigen leading to macrophage activation and cytokine release (such as contact dermatitis or tuberculin reaction) 2) Th2 cell binds to soluble antigen leading to IgE production, eosinophils activation and mastocytosis. Causing inflammatory mediator release (such as chronic asthma or chronic allergic rhinitis) 3) Tc cell binds to cell-associated antigen leading to cytotoxicity leading to apoptosis of cells. (such as graft rejection)

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119
Q

What is atopy?

A

A predisposition to developing allergies. It can be both environmental and genetic factors

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120
Q

What is the major normal role of IgE?

A

Clearing worm infections

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121
Q

Environmental factors that affect allergy?

A

Changes in exposure to animals or soil microorganisms Changes in intestinal microbiota Reduced childhood exposure to pathogens

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122
Q

If mast cells degranulate in the blood, what symptoms could occur?

A

Anaphylaxis

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123
Q

If mast cells degranulate in the skin, what symptoms could occur?

A

Acute urticaria

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124
Q

If mast cells degranulate in the eye/nose, what symptoms could occur?

A

Seasonal rhinoconjunctivitis (hay fever)

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125
Q

If mast cells degranulate in the mucosal lining of the airways, what symptoms could occur?

A

Asthma

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126
Q

Genetic factors of allergy?

A

Some people are more prone to IgE production rather than IgG production

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127
Q

Properties of an airborne allergens that often cause allergies?

A

Proteins Low doses Low molecular weight Highly soluble Stable Contain peptides that bind to MHC II

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128
Q

How does mast cell activation affect gastrointestinal tract tissue?

A

Increased fluid secretion Increases peristalsis caused by inflammation

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129
Q

How does mast cell activation affect eye/nasal/airway tissue?

A

Decreased diameter due to inflammation Increased mucus secretion

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130
Q

How does mast cell activation affect blood vesell tissue?

A

Increased blood flow Increased permeability Increased fluid in tissues to increased flow of lymph to lymph nodes Increased cells and protein in tissues Increases effector response in tissues This can all lead to hypotension then anaphylaxis shock

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131
Q

Risk factors for food allergies?

A

Immature mucosal immune system Early introduction of solid foods Hereditary increase in mucosal permeability IgA deficiency Genetically determined bias towards TH2 environment GI infections Polymorphisms of Th2 cytokine or IgE receptor genes

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132
Q

How can targeting mediator action treat allergic reactions?

A

Inhibit the effect of the mediators on specific receptors Inhibit the synthesis of particular mediators Such as antihistamines, beta-blockers and lipoxygenase inhibitors (montelukast)

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133
Q

How can targeting chronic targeting sites of inflammation treat allergic reactions?

A

General anti-inflammatory effect Such as corticosteroids

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134
Q

How can targeting the Th2 response treat allergic reactions?

A

Introduction of regulator T cells to build up exposure and tolerability

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135
Q

How can targeting IgE treat allergic reactions?

A

A drug can bind to the IgE Fc region to prevent IgE binding to the Fc region on mast cells Omalizumab

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136
Q

What is autoimmunity?

A

The breaking of self-tolerance

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137
Q

How is self-tolerance achieved?

A

Usually, antigen-specific receptors generated at random by recombination are screened for self-reactivity and any that react receive a negative signal leading to inactivation or death. Cells have lots and lots of antigens, so lymphocytes become tolerant

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138
Q

Pathoimmunology of psoriasis?

A

Autoreactive T cells against skin associated antigens

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139
Q

Pathoimmunology of rheumatoid arthritis?

A

Autoreactive T cells against antigens of joint synovium

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140
Q

Pathoimmunology of Graves’ diseases?

A

Autoantibodies against the thyroid-stimulating hormone receptor

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141
Q

Pathoimmunology of Hashimoto’s disease?

A

Autoantibodies and autoreactive T cells against thyroid antigens

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142
Q

Pathoimmunology of systemic lupus erythematosus?

A

Autoantibodies and autoreactive T cells against DNA, chromatin proteins, and ubiquitous ribonucleoprotein antigens

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143
Q

Pathoimmunology of Sjogren’s syndrome?

A

Autoantibodies and autoreactive T cells against ribonucleoprotein antigens

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144
Q

Pathoimmunology of Crohn’s disease?

A

Autoreactive T cells against intestinal flora antigens

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145
Q

Pathoimmunology of multiple sclerosis?

A

Autoreactive T cells against brain antigens

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146
Q

Pathoimmunology of type 1 Diabetes Mellitus?

A

Autoreactive T cells against pancreatic islet cell antigens

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147
Q

Examples of organ-specific autoimmune disease?

A

Type 1 diabetes mellitus Multiple sclerosis Crohn’s disease Psoriasis Graves’ disease Myasthenia Gravis

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148
Q

Examples of systemic autoimmune disease?

A

Rheumatoid arthritis Scleroderma Polymyositis Systemic lupus erythematosus

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149
Q

How can infection break self-tolerance?

A

Cell/tissue destruction: release of sequestered self-antigen causes activation of non-tolerised cells (sympathetic ophthalmia) Molecular mimicry: if bacterial/viral cell structures have similar protein structures to self-cells, it can cause the production of cross-reactive antibodies or T cells (rheumatic fever, Lyme arthritis)

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150
Q

Where are sequestered antigens hidden in the body?

A

Brain Testes Eyes Uterus (so the fetus isn’t attacked)

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151
Q

What happens if sequestered antigens are released? (eye example)

A

Trauma to the eye results in the release of sequestered intraocular antigens These antigens are carried to lymph nodes and activate T cells Effector T cells return via the bloodstream and encounter the antigens in both eyes Leading to autoimmune disease in both eyes

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152
Q

Why is there not a type-I autoimmune response?

A

IgE is not involved in autoimmunity, only allergy

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153
Q

What is a type-II (cell surface/matrix antigen) autoimmune response?

A

The antibody binds to an antigen on self-cell Leading to cellular destruction via the membrane attack complex

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154
Q

What is a type-II (receptor) autoimmune response?

A

The antibody binds to cell surface receptor This either prevents endogenous ligand from binding or mimics the effect of the ligand, sending cell signalling into overdrive

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155
Q

Examples of type-II (cell surface/matrix antigen) autoimmune diseases?

A

Autoimmune hemolytic anaemia Autoimmune thrombocytopenic purpura Goodpasture’s syndrome Pemphigus Vulgaris Acute rheumatic fever

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156
Q

Examples of type-II (receptor) autoimmune diseases?

A

Graves’ disease Type 2 Diabetes Mellitus Myasthenia gravis Chronic urticaria

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157
Q

What is graves’ disease?

A

Autoimmune B cells make antibodies against TSH receptors that also stimulate thyroid hormone production Thyroid hormones bind to the pituitary gland to shut down TSH production but do not affect autoantibody production, which causes excessive thyroid hormone

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158
Q

What is Myasthenia Gravis?

A

Antibodies bind to acetylcholine receptors which are then internalised and degraded So there are fewer receptors to measure the influx of sodium, and also, the antibodies binding can antagonise sodium being able to bind to and remaining receptors So there is no muscle contraction

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159
Q

What is a type-III autoimmune response?

A

Antibodies bind to soluble antigens forming a circulating immune complex The complex is often deposited in vessel walls of joints and kidneys This initiates a local inflammatory response

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160
Q

Examples of type-III autoimmune diseases?

A

Rheumatoid arthritis Mixed essential cryoglobulinemia

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161
Q

What is rheumatoid arthritis?

A

B cells are responsible for an autoantibody called rheumatoid factor Large immune complexes form, which are then phagocytosed by APC’s and augment the inflammatory response They secrete TNFa and IL-6, which amplify the ongoing immune response

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162
Q

What is a type-IV autoimmune response?

A

CD4+ helper T cells recognise antigen in complex with MHC II The APC’s are macrophages that stimulate proliferation of further CD4+ helper T cells CD4+ helper T cells release other Th cytokines mediating the response Activated CD8+ T cells destroy target cells on contact

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163
Q

Examples of a type-IV autoimmune disease?

A

Type 1 Diabetes Mellitus Rheumatoid arthritis Multiple Sclerosis Crohn’s disease Coeliac disease

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164
Q

Coeliac disease symptoms?

A

Loss of gastrointestinal villi Severe inflammation of the intestinal wall Increase number of intestinal lymphocytes

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165
Q

Coeliac disease cause?

A

Peptides normally produced from gluten do not bind to MHC II Transglutaminase (tTG) modifies the peptides (gliadin), so they can bind The bound peptide activates gluten-specific CD4+ cells The activates T cells can kill mucosal epithelial cells by binding Fas (important receptor in cytotoxic killing)

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166
Q

Types of eukaryotes?

A

Humans Plants Protozoa Fungi Algae

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167
Q

Types of prokaryotes?

A

Bacteria Archaea

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168
Q

Types of acellular organisms?

A

Viruses

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169
Q

Features of bacteria?

A

Unicellular Lack nucleus Found everywhere that there is moisture Reproduce asexually Cell wall contains peptidoglycan

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170
Q

Features of archaea?

A

Unicellular Lack nucleus Found everywhere that there is moisture Reproduce asexually Cell wall contains other polymers NOT peptidoglycan

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171
Q

Features of fungi?

A

eukaryotic Obtain food from other organisms Possess a cell wall Can be multi or unicellular

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172
Q

Types of fungi?

A

molds and yeasts

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173
Q

Features of molds?

A

multicellular Grow as long filaments Reproduce by sexual and asexual spores

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174
Q

Features of yeasts?

A

unicellular Reproduce by budding or sexual spores

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175
Q

Features of algae?

A

Multi or unicellular Photosynthetic Simple reproductive structures Categorised on the basis of pigmentation, storage products and cell wall composition

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176
Q

Features of protozoa?

A

Unicellular Eukaryote Similar to animals in nutrient need and cellular structure Live freely in water Some live in animal hosts Capable of locomotion

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177
Q

How can protozoa move?

A

Pseudopodia Cilia Flagella

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178
Q

Features of viruses?

A

Need an electron microscope to see Acellular Obligatory parasites (cannot survive on their own) Composed of DNA or RNA and a protein coat

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179
Q

What characteristics of life do viruses show?

A

Some can react to environmental stimuli (antiviral resistance) But cannot grow, reproduce, metabolise and do not have a cellular structure

180
Q

Who is Antoni van Leeuwenhoek (1632-1723)?

A

Father of protozoology and bacteriology First, highly precise simple microscopes Animacules and beasties

181
Q

Who is Linnaeus (1758)?

A

Publication of Systema Naturae Species categorisation- organisms that can interbreed to produce viable offspring Two kingdoms: Plantae and Animalia

182
Q

The order of categorising organisms?

A

Domain Kingdom Phylum Class Order Family Genus Species

183
Q

Who to correctly write the genus and species?

A

in italics

184
Q

What happened during the golden age of microbiology (1800-1900)

A

Search for answers if spontaneous life is possible (Aristotle proposed) What causes fermentation What causes disease How can prevent infection and disease

185
Q

How was the spontaneous generation of life disproven?

A

Redi’s maggots on meat experiment (maggots only when the meat was open to flies) Needham’s gravy in flask experiment Pasteur’s swan-necked flask experiment

186
Q

Who is Louis Pasteur (1822-1895)?

A

Father of microbiology Contested theory of spontaneous generation of life Proved yeast cells cause fermentation Showed anaerobic bacteria caused wine spoilage Developed pasteurisation Industrial microbiology

187
Q

Who is Robert Koch (1843-1910)?

A

Father of the microbiology lab Formulated Koch’s postulates Revolutionised the lab Lab and medical microbiology Disease aetiology

188
Q

What are Kock’s postulates?

A

Microbes isolated from dead sick rat -> microbes grown in culture and identified -> microbes injected into healthy rat -> disease is reproduced -> second animal then has microbes isolated and identified

189
Q

Antisepsis definition?

A

Reduction in the number of microorganisms/viruses on living tissue

190
Q

Examples of antisepsis products?

A

Iodine Alcohol Usually reduced strength disinfectants so safe to use of living tissue

191
Q

Aseptic definition?

A

An environment or procedure free of pathogenic contaminants

192
Q

Examples of aseptic conditions?

A

Preparation of surgical field Hand washing Flame sterilisation of lab equipment

193
Q

Degerming definition?

A

Removal of microbes by mechanical means

194
Q

Examples of degerming?

A

Handwashing Alcohol swabbing at the site of injection

195
Q

Disinfection definition?

A

Destruction of most microorganisms and viruses on nonliving tissue

196
Q

Examples of disinfectants?

A

Phenolics Bleach Alcohols Aldehydes Soaps

197
Q

Pasteurisation definition?

A

Use of heat to destroy pathogens and reduce the number of spoilage microorganisms in food and drink

198
Q

Sanitisation definition?

A

Removal of pathogens from objects to meet public health standards

199
Q

Examples of sanitisation?

A

Washing cutlery in boiling water in restaurants

200
Q

Sterilisation definition?

A

Destruction of all microorganisms and viruses in or on an object

201
Q

How can antimicrobials destroy pathogens?

A

Inhibit cell wall production Inhibit protein synthesis Inhibit nucleic acid synthesis Block biosynthetic pathways Disrupt bacterial membranes

202
Q

Methods to control environmental microbes?

A

Heat Chemical Refrigeration/freezing Dessication/lyophilisation Ionising radiation 

203
Q

What is moist heat microbial control?

A

Used to disinfect, sanitise and sterilise Denatures proteins and destroys cytoplasmic membranes More effective than dry heat Methods include: boiling, autoclaving, pasteurisation and ultra-high temperature sterilisation

204
Q

What is dry heat microbial control?

A

Used for materials when moist heat cannot be used Dentures proteins and oxidises metabolic and structural chemicals Requires higher temperatures for a longer time than moist heat Incineration is the ultimate means of sterilisation

205
Q

What is refrigeration/freezing microbial control?

A

Decreases microbial metabolism, growth and reproduction; chemical reactions take place slower at lower temperatures, and liquid water is not available Susceptibility to refrigeration and freezing of microbes can vary Psychrophilic microbes can multiple in refrigerated foods Slow freezing is more effective than quick freezing Only holts growth does not kill

206
Q

What is dessication/lyophilisation microbial control?

A

Drying/freeze drying Drying inhibits growth due to the removal of water Lyophilisation used for long term preservation of microbial cultures

207
Q

What is radiation microbial control?

A

Wavelengths must be shorter than 1nm Ejects electrons from atoms to create ions Ions disrupt hydrogen bonding, oxidise double covalent bonds and create hydroxide ions Hydroxide ions denature other molecules Electron beams are effective at killing but do not penetrate well Gamma rays penetrate well but require hours to kill microbes

208
Q

What is biosafety level 1?

A

Handling pathogens that do not cause disease in healthy humans

209
Q

What is biosafety level 2?

A

Handling of moderately hazardous agents

210
Q

What is biosafety level 3?

A

Handling of microbes in safety cabinets

211
Q

What is biosafety level 4?

A

Handling of microbes that cause severe or fatal disease

212
Q

Why is it easier to develop antibiotics compared to antifungal/antiprotozoan?

A

Bacteria are prokaryotes and, therefore, the most different to human cells

213
Q

What are antibiotics?

A

A substance produced by microorganisms that in low concentrations inhibit the growth of another microorganism. Majority are based on naturally occuring compounds. They may be semi-synthetic or synthetic

214
Q

Features of an ideal antibiotic?

A

Appropriate spectrum of activity No toxicity to host Low chance of resistance developing Does not induce hypersensitivity Rapid and extensive tissue distribution Relatively long half-life Free of drug-drug interactions Convenient administration Inexpensive Chemical stable

215
Q

What is MIC?

A

Minimum inhibitory concentration: the minimum concentration of antibiotic required to inhibit growth of test organism

216
Q

What is MBC?

A

Minimum bactericidal concentration: minimum concentration of antibiotic required to kill test organism

217
Q

Examples of antimicrobials that inhibit cell wall synthesis?

A

Penicillin Cephalosporins Vancomycin Isoniazid Echinocandins

218
Q

Examples of antimicrobials that inhibit DNA/RNA synthesis?

A

nucleotide analogues, e.g. Tenofovir Quinolones Rifampicin

219
Q

Examples of antimicrobials that inhibit general metabolic pathways?

A

Trimethoprim Sulfonamides (e.g. Sulfamethoxazole) Dapsone

220
Q

Examples of antimicrobials that disrupt cytoplasmic membranes?

A

polymyxins (Colistimethate) Polyenes (amphotericin B, nystatin)

221
Q

Examples of antimicrobials that inhibit protein synthesis?

A

Aminoglycosides Tetracyclines Macrolides Chloramphenicol

222
Q

Antibiotic resistance definition?

A

The inability to kill or inhibit the organism with clinically achievable drug concentrations

223
Q

Reasons a microbe may be resistant?

A

May be innate May be acquired due to mutation or acquisition of foreign DNA

224
Q

Factors that can accelerate the development of antibiotic resistance?

A

Inadequate levels of antibiotics at the site of infection Duration of treatment too short Overwhelming numbers or organisms Misuse of antibiotics

225
Q

Features of a prokaryote nucleoid?

A

No membrane Single chromosone Circular DNA Only one copy except in division No histones Sometimes have plasmids

226
Q

Prokaryotic ribosomes contain what subunits?

A

30s and 50s

227
Q

What RNA strands do 50s subunits contain?

A

5s and 23s

228
Q

What RNA strands do 30s subunits contain?

A

16s

229
Q

How are the ribosomes subunits named?

A

‘S’ refers to a unit of density called the Svedberg unit. A measurement of the sedimentation rate when the molecules in question are centrifuged

230
Q

What are endospores?

A

A dormant, tough, and non-reproductive structure produced by certain bacteria. Usually triggered by stress in Gram-negative bacteria. The spores can reactive themselves when the conditions become more favourable

231
Q

What does gram-positive mean?

A

The peptidoglycan cell wall is the top layer of the bacteria

232
Q

What does gram-negative mean?

A

The peptidoglycan is sandwiched between two membranes

233
Q

What are bacteria cell walls made of?

A

Most are peptidoglycan with B-lactam bonds, but some bacteria do not have a cell wall

234
Q

How does a Gram-stain work?

A
235
Q

What colour do gram-negative bacteria stain?

A

Red/pink

236
Q

What colour do gram-positive bacteria stain?

A

purple

237
Q

Prokaryotic cell membranes do not contain…

A

sterols So less fluid

238
Q

What do gram-negative outer membranes contain?

A

additions molecules such as porins and endotoxins

239
Q

What is the glycocalyx?

A

The slime capzule

240
Q

What is the purpose of the glycocalyx?

A

Protection again phagocytosis and desiccation Allows biofilm formation

241
Q

What is the glycocalyx made of?

A

Usually polysaccharides

242
Q

What is biofilm formation?

A

A biofilm is a thick layer of prokaryotic organisms that have aggregated to form a colony. The colony attaches to a surface with a slime layer which aids in protecting the microorganisms

243
Q

What are fimbriae?

A

hair-like projections, external to the cell wall, that allow bacteria to stick to the cells they infect.

244
Q

What is the most common type of bacteria to have fimbriae and pili?

A

gram-negative

245
Q

What is a pili?

A

Short rigid structures on bacteria. For attachment and also the transfer of plasmids

246
Q

What is the flagella?

A

Long protein filament with a hollow core coming off bacteria. Can be singular or numerous

247
Q

Function of bacterial flagella?

A

Movement

248
Q

How many phyla of prokaryotes are there?

A

28 (2 archaea and 26 bacteria)

249
Q

How are prokaryotes classified?

A

Based on rRNA information. Bergey’s manuals of determinative and systematic bacteriology

250
Q

What are the two types of gram-negative?

A

Proteobacteria and nonproteobacteria

251
Q

What are the two types of Gram-positive?

A

Low G+C and high G+C

252
Q

What does low/high G+C mean?

A

their DNA typically has fewer/more G and C DNA bases than A and T bases as compared to other bacteria. High GC are more stable due to more hydrogen bonds (three rather than two)

253
Q

What shape are cocci?

A

Spherical

254
Q

What shapes are bacilli?

A

Rod-like

255
Q

Examples of Gram-positive bacilli?

A

Bacillus Lactobacillus Listeria

256
Q

Examples of Gram-positive cocci?

A

Streptococcus Staphylococcus Enterococcus

257
Q

Staphylococcus vs streptococcus vs enterococcus regarding structure?

A

Staph: grape-like Strep: straight chain Entero: usually pairs

258
Q

Examples of Gram-negative proteobacteria?

A

Nitrogen fixers (rhizobium) Sulpher reducers (Neisseria) Pseudomonads Bdellovibrio Helicobacter

259
Q

Examples of Gram-negative nonproteobacteria?

A

Chlamydias Spirochetes Cyanobacteria

260
Q

What can affect microbial growth?

A

Temperature Pressure Nutrients Oxygen pH

261
Q

What are the four phases of bacterial growth in a lab?

A

Lag Log Stationary Death

262
Q

What is the lag phase of bacterial growth?

A

Where the bacteria is growing and preparing to divide

263
Q

What is the log phase of bacterial growth?

A

Rapid multiplication of bacteria

264
Q

What is the stationary phase of bacterial growth?

A

Bacteria are still dividing but at a similar rate of bacteria death

265
Q

What is the death phase of bacterial growth?

A

Bacteria start to die off

266
Q

What is binary fission?

A

In the process of binary fission, an organism duplicates its genetic material, or deoxyribonucleic acid (DNA), and then divides into two parts (cytokinesis), with each new organism receiving one copy of DNA

267
Q

How do bacteria divide?

A

Binary fission

268
Q

What is mutualism?

A

Both the bacteria and the host benefit, for example, bacteria in the colon

269
Q

What is commensalism?

A

The bacteria benefits, but the host does not receive benefits or harm, such as staphylococcus on the skin.

270
Q

What is parasitism?

A

The bacteria benefits, but the host is harmed, such as tuberculosis in the lungs.

271
Q

What are opportunistic pathogens?

A

Usually, normal microbiota that are introduced to unusual sites if the body. Immune suppression Changes in microbiota

272
Q

Features of staphylococcus?

A

Gram-positive cocci Grape-like arrangements Facultatively anaerobic Non-motile Low G+C

273
Q

Common species of staphylococcus?

A

Aureus Epidermidis

274
Q

Diseases caused by staphylococcus?

A

Food poisoning Impetigo Scalded skin syndrome Conjunctivitis Toxic shock syndrome Bacteremia

275
Q

Features of streptococcus?

A

Gram-positive cocci Arranged in chains Facultatively anaerobic Non-motile Low G+C

276
Q

Species of streptococcus?

A

Pyogenes agalactiae Pneumoniae

277
Q

Diseases caused by streptococcus?

A

Impetigo Conjunctivitis Tonsillitis Pharyngitis Otitis media Scarlet fever Meningitis Pneumonia Miscarriage

278
Q

What does lipid A in the outer membrane of Gram-negative bacteria trigger?

A

Fever Vasodilation Inflammation Shock Blood clot formation

279
Q

What does facultatively anaerobic/aerobic mean?

A

Prefers one but can live in both

280
Q

Features of Neisseria?

A

Gram-negative Non-motile Diplococci Glycocalyx True pathogen

281
Q

Species of Neisseria?

A

Gonorrhoeae Meningitidis

282
Q

Diseases caused by Neisseria?

A

Meningitis Gonorrhoea

283
Q

What bacteria causes impetigo?

A

Staphylococcus aureus Streptococcus pyogenes

284
Q

What bacteria can cause conjunctivitis?

A

Staphylococcus Streptococcus Haemophilus influenzae Neisseria gonorhorreae Moraxella (although mainly viral)

285
Q

What bacteria can cause tonsilitis?

A

Streptococcus pyogenes

286
Q

What bacteria can cause otitis media?

A

Various respiratory microbiota Streptococcus pneumoniae Haemophilus influenzae Moraxella cattarhalis (viruses)

287
Q

What bacteria can cause meningitis?

A

Neisseria meningitidis Streptococcus pneumoniae Haemophilus influenzae Listeria monocytogenes Streptococcus agalactiae

288
Q

What bacteria causes pertussis?

A

Bordetella pertussis

289
Q

Features of Rickettsias?

A

Obligate intracellular Gram-negative coccobacillus multiply within eukaryotic cells Non-motile

290
Q

What diseases can Rickettsias cause?

A

Spotted fever Typhus

291
Q

Features of chlamydias?

A

Gram-negative Obligate intracellular Oval-shaped Some lack a cell wall

292
Q

Diseases caused by chlamydias?

A

Chlamydia Pneumonia

293
Q

Features of spirochaetes?

A

Gram-negative Helically coiled shape Have special flagella called endoflagella Motile

294
Q

What diseases can spirochaetes cause?

A

Lyme disease Syphilis

295
Q

Features of vibrios?

A

Gram-negative Curved rod-shaped Facultative anaerobes Live in water

296
Q

What diseases can vibrios cause?

A

Cholera Vibriosis

297
Q

Characteristics of virus’?

A

Minuscule, acellular infectious agent having either DNA or RNA •Causes many infections of humans, animals, plants, and bacteria •Causes most of the diseases that plague the industrialized world •Cannot carry out any metabolic pathway •Neither grow nor respond to the environment •Cannot reproduce independently •Recruit the cell’s metabolic pathways to reproduce No cytoplasmic membrane or organelles

298
Q

What type of genetic material do viruses’ have?

A

Either DNA or RNA but not both

299
Q

What are capsids?

A

Provide protection for viral nucleic acid •Means of attachment to host’s cells •Composed of proteinaceous subunits called capsomeres

300
Q

What are the three basic viral shapes?

A

•Helical •Polyhedral •Complex

301
Q

Viral envelope characteristics?

A

Acquired from host cell during viral replication or release ◦Envelope is portion of membrane system of host •Composed of phospholipid bilayer and proteins ◦Some proteins are virally coded glycoproteins (spikes) •Envelope’s proteins and glycoproteins often play role in host recognition

302
Q

How can viruses be classified?

A

Morphology Serology Genetic material (Baltimore classification system)

303
Q

Six types of virus genome?

A

ds DNA ds RNA ss positive-sense DNA ss negative-sense DNA ss positive-sense RNA ss negative-sense RNA

304
Q

Examples of cancers caused by viruses?

A

•Burkitt’s lymphoma •Hodgkin’s disease •Kaposi’s sarcoma •Cervical cancer

305
Q

What is a bacteriophage?

A

Type of virus that infects bacteria

306
Q

What is positive sense RNA?

A

Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell

307
Q

What is negative sense RNA?

A

Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA polymerase before translation

308
Q

What are the two types of viral replication cycles?

A

Lytic Lysogeny

309
Q

What is lysogeny?

A

the viral DNA gets integrated into the host’s DNA but viral genes are not expressed but can later be expressed

310
Q

Steps of viral replication?

A

1.Attachment 2.Entry 3.Uncoating 4.Replication 5.Assembly and release

311
Q

Signs and symptoms of viral conjunctivitis?

A

Itchy eyes Tearing Redness Discharge Light sensitivity

312
Q

What pathogens can cause viral conjunctivitis?

A

Most common = adenovirus Most problematic = human herpes virus

313
Q

Treatment for viral conjunctivitis?

A

Usually self-limiting unless caused by herpes, and then antivirals such as aciclovir, idoxuridine, vidarabine and trifluridine can be used

314
Q

How to diagnose viral conjunctivitis?

A

Can usually tell by symptoms but referral to a specialist if herpes suspected

315
Q

How to prevent viral conjunctivitis?

A

Avoid touching the eye Use separate towels and linen

316
Q

How to tell between viral and bacterial tonsilitis?

A

Both will have red, swollen tonsils and throat redness, but bacterial will also have white spots, swollen uvula, and grey furry tongue

317
Q

Signs and symptoms of viral otitis media?

A

Severe to pain in the ear

318
Q

Pathogen that causes viral otitis media?

A

Adenovirus

319
Q

How to diagnose viral otitis media?

A

Symptoms are usually diagnostic

320
Q

How to treat viral otitis media?

A

Self-limiting No treatment

321
Q

Pathogen that usually causes viral meningitis?

A

Enterovirus

322
Q

How is viral meningitis spread?

A

Respiratory droplets and faeces

323
Q

How to diagnose viral meningitis?

A

Characteristic signs with the absence of bacteria in CSF

324
Q

Signs and symptoms of cold sores?

A

Slow spreading skin lesions Usually recurrent

325
Q

What pathogen causes cold sores?

A

Human herpes virus 1

326
Q

Pathogenesis of cold sores?

A

Painful lesions caused by inflammation and cell death Cause fusion of cells to form syncytia

327
Q

What is syncytia?

A

When a virus causes multiple cells to fuse together. This means the virus can move from cell to cell without exposing itself to the immune system. Such as in HHV and RSV

328
Q

How to diagnose cold sores?

A

Usually by symptoms Immunoassays can be used

329
Q

Treatment for cold sores?

A

Chemotherapeutic drugs such as aciclovir can help control the disease but does not cure it

330
Q

Symptoms of hand, foot and mouth disease?

A

Cold-like symptoms Loss of appetite Mild fever A non-itchy red rash with bumps or fluid-filled sacks around hands and feet (but can be elsewhere) Painful mouth ulcers

331
Q

Pathogens that cause hand, foot and mouth disease?

A

Most common: Coxsackievirus A16, A6, A10 Most serious: enterovirus 71

332
Q

Symptoms of respiratory syncytial virus?

A

Fever Runny nose Coughing

333
Q

Pathogenesis of respiratory syncytial virus?

A

Virus cause syncytia to form in the lungs Immune response to virus further damages the lungs

334
Q

How to diagnose respiratory syncytial virus?

A

Immunoassay

335
Q

Examples of how antivirals can inhibit metabolic pathways?

A

Amantadine can prevent viral uncoating Some drugs can interfere with an enzyme HIV needs in its replication cycle, such as boceprevir and darunavir

336
Q

Main ways antivirals can work?

A

Inhibit metabolic pathways Inhibition of nucleic acid synthesis Prevention of viral attachment

337
Q

Types of drugs that can inhibit viral nucleic acid synthesis?

A

Nucleotide analogues Reverse transcriptase inhibitors

338
Q

How do nucleotide analogues work?

A

Interfere with functions of nucleic acids Distort shapes of nucleic acids and prevent further replication, transcription and translation Mainly used for viruses but can also be effective against rapidly dividing cancer cells

339
Q

How do reverse transcriptase inhibitors work?

A

Act on the enzyme that HIV uses in its replication cycle

340
Q

Characteristics of fungi?

A

Eukaryotes Non-motile under any conditions, grow toward food Chitin based cell wall No chlorophyll The vegetative (non-fruiting) body of a fungus is called the thallus

341
Q

Types of fungi?

A

Most are multicellular Some unicellular Yeasts (usually unicellular) Hyphae

342
Q

Growth conditions for fungi?

A

Airborne fungal spores germinate in favourable conditions Spores swell until development of branched hypha 25°c to 37°c Obligate aerobes Yeasts can be facultative anaerobes

343
Q

Fungi sources of food?

A

Heterotrophic by absorption Most are saprotrophic (decaying matter) Some are parasitic (living matter) Some can for mutualistic relationships e.g. lichen with Cyanobacteria

344
Q

How do fungi reproduce?

A

Asexual by mitosis or binary fission Occurs in all fungi to some extent Production of spores, budding, fragmentation Sexual reproduction through meiosis or schizogony Haploid nuclei form and fuse through hyphae touching or spores joining

345
Q

Asexual reproduction in fungi?

A

Aerial hyphae produces a sporangium Sporangium bursts to release spores Spores germinate to produce aseptae mycelium Vegetative mycelium grows and forms hyphae Repeat

346
Q

Sexual reproduction in fungi?

A

Gamete forms at the tip of hyphae Mating hyphae join and fuse Zygosporangium forms Zygosporangium matures Nuclear meiosis occurs Zygosporangium produces an asexual sporangium Spores released from the sporangium Spores germinate

347
Q

Classifications of fungi?

A

Division Zygomycota Division Ascomycota Division Basidiomycota Deuteromycetes

348
Q

Fungal species that can cause superficial/cutaneous disease?

A

dermatophytes Candidate spp.

349
Q

Fungi species that can cause invasive/systemic disease?

A

Aspergillus spp., Candida spp., Pneumocystis, Cryptococcus, Mucor

350
Q

Toxicosis causes by fungi?

A

Mycotoxicosis (aflatoxin)

351
Q

Examples of cutanous infection caused by fungi?

A

Ringworm Athletes foot Fungal nails

352
Q

Nomenclature of ‘ringworm’?

A

Tinea capitas- scalp Tinea corporis- trunk Tinea pedis- athletes foot Tinea cruris- groin

353
Q

How do subcutaneous fungal infections occur?

A

mainly in tropical environments where people walk bare feet Inoculation of cuts Many types

354
Q

Systemic fungal infections?

A

Rare Difficult to diagnose It usually affects the lungs but can occur anywhere High mortality rate Usually, in severely immunocompromised Low virulence Cryptococcal meningitis (cryptococcus neoformans)

355
Q

How to diagnose fungal infections?

A

Tissue sample required Fungi isolated on Sabourauds agar Microscopy Molecular biology techniques such as PCR ELISA serology

356
Q

How do echinocandins work?

A

Inhibition of cell wall synthesis by inhibiting the enzyme 1,3 B-glucan synthase Such as anidulafungin, caspofungin and micafungin

357
Q

Why can we target fungal cell membranes?

A

They contain ergosterol rather than cholesterol found in humans

358
Q

How does amphotericin-B work?

A

Attaches to ergosterol in fungal membranes Amphotericin binds to ergosterol and a hydrophilic group binds to the polar heads of the membrane

359
Q

Examples of polyene antifungals?

A

Amphotericon-B Nystatin

360
Q

how do azoles work?

A

Inhibit the enzyme lanosterol 14a demethylase Lack of ergosterol leads to disruption of cell membrane Such as itraconazole, fluconazole, voriconazole, isavuconazole, posaconazole

361
Q

Types of vaccine?

A

Attenuated live vaccines Inactivated vaccines Subunit vaccines (toxoid) Recombinant vaccines DNA/RNA vaccines

362
Q

Attenuated vaccine features?

A

Active organisms that have lost their virulence Mild infections may occur but not serious Strong memory response Not suitable for the immunocompromised or in pregnancy Mainly for viruses Created by serial passage of the organism within cells Examples include MMR, varicella, flu, rotavirus and BCG

363
Q

Features of inactivated vaccines?

A

Whole agent vaccines Killed by heat or formaldehyde Safer than attenuated but less strong memory response Can cause inflammatory response causing side effects Require adjuvants, high dose or booster Examples polio and Hep A

364
Q

Risks from the attenuated polio vaccine?

A

Can revert to wildtype within the host leading to disease

365
Q

How does the attenuated polio vaccine work?

A

Replicates in the intestines but not the nervous system so created a memory response but not disease

366
Q

Who should have what type of polio vaccine?

A

Countries with low risk give pentavalent inactivated vaccine Countries with high risk give live attenuated vaccine

367
Q

Features of subunit vaccines?

A

Antigenic fragments Often conjugate vaccines Use antigenic polysaccharides from infecting agent Polysaccharide is usually serotype-specific Vaccine should contain serotype that causes disease Polysaccharides are attached to inactivated toxin Can be immunotolerant if too similar to human cell components

368
Q

What does the pneumococcal vaccine protect against?

A

Many serotypes of streptococcus pneumoniae

369
Q

Types of pneumococcal vaccine?

A

Pneumococcal conjugate vaccine for under 2 years Pneumococcal polysaccharide vaccine for over 2 years

370
Q

Features of pneumococcal polysaccharide vaccine?

A

Covers a large number of serotypes (23) Less robust immune response (boosters required) No mucosal immunity provoked so carriage rate is unaffected

371
Q

Features of pneumococcal conjugate vaccine?

A

Only covers 13 serotypes Conjugated to diphtheria toxoid More robust immune response but booster still needed Mucosal immunity triggered so carriage of serotypes reduced and herd immunity possible

372
Q

Examples of outer membrane vesicles used in subunit vaccines?

A

Neisseria meningitis vaccine Outer membrane vesicles are part of the SOS response in bacteria produced by gram-negative bacteria during invasion

373
Q

Toxoid vaccine features?

A

For bacterial diseases such as tetanus and diphtheria where the toxins from the bacteria cause the disease Toxins inactivated by formaldehyde to create toxoids Also possible to inactive toxin by mutating them Caution should be taken that the bacteria is also killed by immune system to they are not carriers

374
Q

Features of recombinant vaccines?

A

antigen DNA inserted into a cell and then grown in a lab for the vaccine. It will not cause the disease but will cause the immune system to react

375
Q

Features of the Hep B vaccine?

A

First recombinant vaccine Developed by P Valenzula in 1986 Produced in yeast cells Required 3 vaccines for full protection Protective for life

376
Q

Features of DNA vaccines?

A

Plasmids containing genes that encode for an antigen are injected into host cells Cells produce the antigen Body mounts a response Still experimental as immune response has not been significant Non currently licensed in UK

377
Q

How could a potential HIV vaccine work?

A

Using salmonella as a vector Salmonella attenuated Plasmids with antigen DNA added to vector Ideal for HIV as both infect M cells in intestinal lining

378
Q

Features of mRNA vaccines?

A

mRNA inside a lipid membrane to protect it when it gets into the body and also to help it enter cells Cells then translates it into the antigen Not capable of combining with the human genetic code Pfizer and Moderna covid-19 vaccines

379
Q

Features of Pfizer covid-19 vaccine?

A

mRNA to encode spike protein delivered in lipid nanoparticles 95% effective Must be stored at -80°C

380
Q

Features of the AstraZeneca covid vaccine?

A

Chimpanzee adenovirus attenuated and recombinantly express spike protein Similar to flu vaccine More stable as only require normal fridge storage 60-90% effective depending on dosage

381
Q

What would an ideal vaccine be like?

A

Produce immune response that triggers memory response Single administration No risk of infection No side effects 100% effective

382
Q

What is passive immunotherapy?

A

Administration of antiserum containing pre-formed antibodies Also includes breast feeding

383
Q

Advantages of passive immunotherapy?

A

Immediate protection against recent infection or ongoing disease

384
Q

Limitations of passive immunotherapy?

A

Can contain antibodies against many antigens Can trigger an allergic reaction known as serum sickness Viral pathogens may contaminate Antibodies degrade relatively quickly

385
Q

Types of vaccine administration?

A

Cutaneous Subcutaneous Intramuscular Mucosal membrane Oral

386
Q

Advantages of cutaneous vaccine administration?

A

Non invasive

387
Q

Disadvantages of cutaneous vaccine administration?

A

Challenging to get antigens across skin May require shaving and irritation of the skin Still in developmental stage

388
Q

Advantages of intramuscular vaccine administration?

A

Standard at present High blood volume so stimulate immune response

389
Q

Disadvantages of intramuscular vaccine administration?

A

Painful Not normal access of infection

390
Q

Advantages of mucosal membrane vaccine administration?

A

Classic way infections enter the body Stimulate immune response of mucosal membrane

391
Q

Disadvantages of mucosal membrane vaccine administration?

A

Difficult to get antigen to the cells Only for live attenuated vaccines currently

392
Q

Advantages of oral vaccine administration?

A

Classic way infection enters the body Non-invasive Minimal training requires to administer Successful for polio

393
Q

Disadvantages of oral vaccine administration?

A

Difficult to get antigen to the cells Only for live attenuated vaccines currently

394
Q

What are adjuvants in vaccines?

A

Lengthen and strengthen the immune response Such as aluminium hydroxide Mostly in toxoid and subunit vaccines

395
Q

How to administer multiple attenuated vaccines?

A

Must be either at the same time or four weeks apart

396
Q

Vaccines given at 8 weeks old?

A

6-in-1 vaccine first dose (diphtheria, tetanus, pertussis, polio, haemophilia influenzae type B, Hep B) Rotavirus vaccine first dose Meningococcal B vaccine first dose

397
Q

Vaccines given at 12 weeks old?

A

6-in-1 vaccine second dose (diphtheria, tetanus, pertussis, polio, haemophilia influenzae type B, Hep B) Rotavirus vaccine second dose Pneumococcal conjugate vaccine first dose

398
Q

Vaccines given at 16 weeks old?

A

6-in-1 vaccine third dose (diphtheria, tetanus, pertussis, polio, haemophilia influenzae type B, Hep B) Meningococcal B vaccine second dose

399
Q

Vaccines given at 12/13 months?

A

Haemophilus influenza type B/ meningococcal type C vaccine Measles, mumps, rubella first dose Pneumococcal conjugate vaccine booster dose Meningococcal B booster

400
Q

Vaccine given to children aged 2 years to school year 11?

A

Nasal flu vaccine

401
Q

Vaccines given at 3 years and 4 months?

A

Measles, mumps, rubella vaccine booster 4-in-1 pre-school booster vaccine for diphtheria, tetanus, pertussis and polio

402
Q

Vaccines given to teenager?

A

Two doses of human papillomavirus vaccine at least six months apart Teenage booster for tetanus, diphtheria and polio Meningococcal ACWY vaccine

403
Q

Who is eligible for the shingle vaccine?

A

Over 70s as there is a greater risk of post-herpetic neuralgia One injection given with the live vaccine or two with the inactivated vaccine

404
Q

Who is eligible for the polysaccharide pneumococcal vaccine?

A

Aged over 65 Certain long-term health conditions

405
Q

Vaccines for pregnant women?

A

Pertussis any time after 16 weeks Flu vaccine

406
Q

What is an ectoparasite?

A

Lives on the surface of the host

407
Q

What is an endoparasite?

A

Lives within another organism

408
Q

What is an erratic/aberrant parasite?

A

Wanders from its usual site of infection Such as fleas from a cat to a human

409
Q

What is a definitive parasitic host?

A

Holds the adult stage of the parasite where sexual reproduction takes place

410
Q

What is an intermediate parasitic host?

A

Holds the developmental stage of the parasite before transferring it to another host

411
Q

What is a parenthetic parasitic host?

A

Holds the parasite when it is not in a developmental stage. ‘Frozen’

412
Q

Examples of direct effects of parasites on hosts?

A

Blockage of blood vessels Producing toxins Nutrient/fluid deficiency

413
Q

Examples of indirect effects of parasites on hosts?

A

Immunological response Propagation of certain tissues Tissue damage

414
Q

What main phyla of parasites?

A

Protozoa Helminths Arthropods

415
Q

Protozoa main characteristics?

A

Eukaryotic Unicellular Lack a cell wall

416
Q

Main life stages of protozoa?

A

Trophozoites- the active stage Cysts- to survive challenging conditions

417
Q

Name of a trophozoite to cyst conversion?

A

Encystation

418
Q

Name of a cyst to trophozoite conversion?

A

Excystation

419
Q

How do protozoa move?

A

Flagella Cilia Pseudopodia Or not at all

420
Q

Anti-protozoan drugs that inhibit protein synthesis?

A

Lincosamides (clindamycin) Paromomycin

421
Q

Anti-protozoan drugs that inhibit DNA synthesis?

A

Eflornithine Nitroimidiazoles (metronidazole) Pentamidine Quinolones

422
Q

What are helminths?

A

Worms

423
Q

What are the three groups of helminths?

A

Cestodes Trematodes Nematodes

424
Q

What are cestodes?

A

Flatworms (tapeworm)

425
Q

Features of cestodes?

A

Bodies consist of many similar units called proglottids; these are essentially packages of eggs which are regularly shed into the environment Scolex (head) with four suckers and hooks for attachment No respiratory or digestive systems, nutrients are absorbed from teguments that cover the body

426
Q

Cestode lifecycle?

A

Intermediate host (cow/pig) eat grass infected with fertilised eggs Larvae become encrusted in muscle tissue Human eats cow The scolex of the cestode attaches to the intestinal wall Fertilised eggs leave the human via faeces Cycle repeats

427
Q

What are nematodes?

A

Roundworms including threadworms

428
Q

Characteristics of nematodes?

A

Round cross-section Elongated body Reproduce sexually Have a simple digestive system with a mouth at one end

429
Q

Pathogen that causes threadworm?

A

Enterobius vermicularis

430
Q

What shape are threadworm eggs?

A

D-shaped

431
Q

What are trematodes?

A

Flukes (flat, leaf shaped worms)

432
Q

Medically important trematodes?

A

Fasciola Schistosoma

433
Q

Trematode characteristics?

A

Have two suckers for food and attachment Incomplete digestive system Need more than one intermediate host Have large eggs

434
Q

Life cycle of trematodes?

A

Eggs hatch in water Enters snail and develops into sporocyst Sprocycst develops into cercaria and is released into water Cercaria enters human body (when in water) Maturation of worm occurs in liver Worms mate and fertilised eggs pass in faeces

435
Q

Arthropod examples?

A

Ticks Fleas Flies Lice Mites

436
Q

Characteristics of arthropods?

A

Have respiratory, excretory and nervous systems

437
Q

Example of arthropod diseases?

A

Ticks transmit bacteria that cause Lyme disease Tsetse flies transmit trypanosomes that cause sleeping sickness

438
Q

Examples of antihelminthic drugs?

A

Benzimidazoles Iodoquinol Ivermectin Niclosamide Praziquantel Niridazole

439
Q

Mechanism of action of benzimidazoles?

A

Inhibit glucose uptake

440
Q

Mechanism of action of iodoquinol?

A

Inhibits iron uptake

441
Q

Mechanism of action of ivermectin?

A

Blocks neurotransmitters

442
Q

Mechanism of action of niclosamide?

A

Inhibits oxidative phosphorylation of ATP in mitochondria

443
Q

Mechanism of action of praziquantel?

A

Inhibits calcium ion uptake

444
Q

Mechanism of action of niridazole?

A

Prevents nucleic acid replication

445
Q

Mechanism of action of Permethrin?

A

Pyrethroid insecticide that targets the nervous system

446
Q

Mechanism of action of malathion?

A

Organophosphate that targets the nervous system

Mpharm (9 decks)

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