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Immunity, Infection and Haematology > Bacteria & Infection response > Flashcards

Bacteria & Infection response Flashcards

1
Q

What does overgrowth of Clostridium difficile lead to?

A

Antibiotic-associated colitis (AAC)

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2
Q

What are bacteria?

A

Prokaryotes (lack cell nucleus) –> DNA is free in the cytoplasm of the cell

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3
Q

What are the two types of bacteria?

A

Gram positive and gram negative

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4
Q

What is distinguished by Gram stain?

A

structure of bacterial cell wall

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5
Q

What is the process of gram stain?

A
  1. Bacteria stained with crystal violet stain and iodine

2. Cells washed with alcohol and counterstained with safarin

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6
Q

How do gram positive bacteria appear?

A

Purple - they retain the crystal violet iodine copmlex

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7
Q

How do gram negative bacteria appear?

A

Pink - complex is removed by the alcohol wash and stained with safarin

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8
Q

What is the structure of a gram positive cell wall?

A

Thick cell wall made up of peptidoglycan on the outside of the cell membrane which retains the crystal violet dye

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9
Q

What is the structure of a gram negative cell wall?

A

Have a thin layer of peptidoglycan sandwiched between two cell membranes
Outer membrane is heavily modified with sugars to produce lipopolysaccharide (LPS) or endotoxin

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10
Q

What is LPS responsible for?

A

LPS is a very potent activator of the immune system and is largely responsible for endotoxic shock (e.g. in meningococcal sepsis)

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11
Q

What is the peptidoglycan cell wall required for?

A

Integrity of the cell

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12
Q

What is the significance of the production of peptidoglycan?

A

It is the target for several commonly used antibiotics e.g. penicillin

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13
Q

What does MALDI-TOF MS stand for?

A

Matrix-assisted laser description ionisation-time of flight mass spectrometry

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14
Q

What does MALDI-TOF MS involve?

A

The bacteria colony is exposed to a laser beam which ionises the sample. Analysis of the mass of the fragmentation products generated allows the identification of the organism by comparison to a data base.

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15
Q

What are the 5 things bacteria need to do to cause disease?

A
  1. Attach to the host
  2. Invade the tissue
  3. Acquire nutients and grow
  4. Avoid the host immune response
  5. Cause damage (–> symptoms)
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16
Q

What are virulence factors?

A

Factors that allow bacteria to cause disease to the host

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17
Q

How can bacteria attach to the host?

A

Appendages (pilli/fimbrae)
By attaching to specific host receptors the bacteria can induce their own uptake into pathways to allow intracellular survival rather than killing

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18
Q

What do bacteria have that help with invasion into host cells?

A

Type 3 secretion systems

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19
Q

What is an example of nutrient acquisition in cells?

A

Iron

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20
Q

What are siderophores?

A

Molecules produced by bacteria which have high affinity for iron and can scavenge iron from host molecules

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21
Q

How is immune evasion achieved?

A

Inhibition of apoptosis
Inhibition of phagocytosis
Inhibition of complement activation
etc

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22
Q

What are the two mechanisms by which damage to the host can be mediated?

A

Direct and indirect mechanisms

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23
Q

What does the direct mechanism of damage involve?

A

Usually mediated by production of toxins e.g. membrane damaging toxins, neurotoxins such as tetanus and botulinum

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24
Q

What does the indirect mechanism of damage involve?

A

Overactivation of inflammation. Molecular mimicry where microbial components are similar to host e.g. Group A streptococci and acute rheumatic fever where antibodies to streptococcal proteins cross react with heart, lung and kidney antigens.

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25
Q

What is toxic shock syndrome associated with?

A

Staphylococcal aureus toxin

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26
Q

What are some examples of gram positive bacteria?

A

Staphylococcus

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27
Q

What are some examples of gram negative bacteria?

A

H. pylori
Vibrio cholerae
Salmonella

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28
Q

What are the four main ways pathogens can enter the body?

A
  1. Skin breach
  2. Gastrointestinal tract
  3. Respiratory tract
  4. Genito-urinary tract
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29
Q

What type of epithelium lines the mouth, pharynx and upper oesophagus?

A

Stratified squamous epithelium

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30
Q

What is a common cause of renal failure in children?

A

Failure or the vesicourteric valve to prevent reflux of urine into the ureter

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31
Q

How does the innate immune system recognise pathogens?

A

Through Pattern recognition receptors and complement

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32
Q

How does the adaptive immune system recognise pathogens?

A

MHC molecules, T cell receptors, B cell receptors (antibody)

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33
Q

What do Pattern Recognition Receptors (PRRs) recognise?

A

General patterns on non-mammalian cells - Pathogen Associated Molecular Patterns (PAMPs)

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34
Q

What are Toll-Like Receptors (TLRs)?

A

A major group of PRRs

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35
Q

What are the 3 surface TLRs?

A

TLR-2, TLR-4, TLR-5

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36
Q

What does TLR-2 recognise?

A

Peptidoglycan, bacterial lipoproteins, lipoteichoic acid, porins

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37
Q

What does TLR-4 recognise?

A

lipopolysaccharide (LPS) from gram(-) cell wall, fungal mannans, parasitic phospholipids, heat-shock proteins, viral envelope proteins

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38
Q

What does TLR-5 recognise?

A

Bacterial flagellin

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39
Q

What are the intracellular/endosomal TLRs?

A

TLR-3, TLR-7, TLR-8, TLR-9

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40
Q

What does TLR-3 recognise?

A

viral dsDNA

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41
Q

What does TLR-7 recognise?

A

viral ssRNA

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42
Q

What does TLR-8 recognise?

A

G-rich oligonucleotides

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43
Q

What does TLR-9 recognise?

A

viral and bacterial unmethylated CpG sequences of DNA

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44
Q

What are other common PRRs?

A

NOD-2, RIG-I, MBL

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45
Q

What does NOD-2 recognise?

A

muramyl dipeptide from bacterial peptidoglycan

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46
Q

What does RIG-I recognise?

A

viral RNA

47
Q

What does MBL (Mannose Binding Lectin) recognise?

A

microbial glycoproteins and glycolipids,can be soluble and trigger complement activation or attached to macrophages and trigger phagocytosis

48
Q

What is the end result of TLRs binding to PAMPs?

A

upregulation of inflammatory cytokines

49
Q

What do genetic defects in Myd88 or IRAK4 result in?

A

immunodeficiency characterised by recurrent pyogenic infection

50
Q

What are the three ways in which the complement cascade can be triggered?

A

Classical pathway, lectin binding pathway, alternative pathway

51
Q

How is the classical pathway activated?

A

Following recognition of antigen-antibody complexes, and through CRP

52
Q

What is the main pathway of complement activation during the adaptive immune response to a pathogen?

A

Classical pathway

53
Q

What do local macrophages release following infection?

A

cytokines that alert the immune system of attack

54
Q

What do IL-1B and IL-6 do?

A

Released into tissue fluids and act on the liver to induce the release of soluble acute phase proteins

55
Q

What are the two acute phase proteins involved in the lectin pathway?

A

Mannose Binding Lectin (MBL) and C-Reactive Protein (CRP)

56
Q

What do MBL and CRP do?

A

They are soluble PRRs that recognise common constituents of bacterial cell walls, triggering complement activation

57
Q

What does MBL recognise and bind to?

A

mannose

58
Q

What does CRP recognise and bind to?

A

Phosphorylcholine

59
Q

During the innate response, which pathway does the lectin pathway support?

A

The alternative pathway

60
Q

What is the main complement activation pathway when infected with a previously unknown pathogen?

A

alternative pathway

61
Q

What is the alternative pathway activated by?

A

endotoxin and bacterial cell walls

62
Q

What does the activation of alternative pathway rely on?

A

Soluble C3 spontaneously hydrolysing to insoluble C3b

63
Q

What does insoluble C3b bind to?

A

any nearby microbial/membrane surface

64
Q

What is the result of C3b binding?

A

Activation of the rest of the complement cascade

Microbe becomes covered in C3b molecules, promoting opsonisation

65
Q

Where is C3 convertase found?

A

On the surface of the mirobe

66
Q

What does C3 convertase do?

A

Split molecules of soluble C3 to insoluble C3b

67
Q

How does C3b help in the amplification loop?

A

Bound C3b molecules form more C3 convertases (via the alternative pathway)

68
Q

How is the complement system controlled?

A

Inhibition by control enzymes

69
Q

What do the control enzymes of complement cascade do?

A

cleave C3b to an inactive form called iC3b

70
Q

What are 2 examples of control enzymes?

A

Factor H, Factor I

71
Q

What is absence of control enzymes associated with?

A

Low levels of circulating C3 and an increased risk of infections esp. Neisseria meningitidis

72
Q

A patient with 2 episodes of Neisseria meningitid has complement investigations undertaken. A defect in what factor/test is most likely?

A

Alternative pathway defect

73
Q

What does C3b activate?

A

C5 convertase

74
Q

What does C5 convertase activate?

A

the terminal lytic pathway components C5-9

75
Q

What makes up the Membrane Attack Complex (MAC)?

A

C5b-9

76
Q

What is the MAC?

A

A transmembrane channel

77
Q

How does the MAC cause destruction?

A

Allows water uptake into the cell resulting in swelling and ultimately destruction of the cell

78
Q

What are the 4 function of complement activation?

A

Opsonisation, cell lysis, mast cell degranulation, neutrophil chemotaxix

79
Q

What causes opsonisation?

A

Surface bound C3b and iC3b

80
Q

What is C3b recognised by?

A

Complement Receptor 1 (CR1)

81
Q

What is iC3b recognised by?

A

Complement Receptor 3/4 (CR3/4)

82
Q

Where are CR1 and CR3/4 expressed?

A

On neutrophils and macrophages

83
Q

What causes cell lysis?

A

formation of MAC

84
Q

What causes mast cell degranulation?

A

C3a

85
Q

How do C3a act on mast cells?

A

Mast cells express C3a receptors

86
Q

What causes neutrophil chemotaxis?

A

C5a is able to attract neutrophils to site of complement activation

87
Q

What are the two main complements tests undertaken frequently?

A

C4 and C3

88
Q

What does a high complement level reflect?

A

Infection, not a natural response

89
Q

What do patients with a low C4 suffer from?

A

Recurrent infection

90
Q

What type of bacteria do patients with a low C4 suffer from?

A

Encapsulated bacteria

91
Q

Which pathway is responsible for killing bacteria such as pneumococcus?

A

Classical pathway

92
Q

How many alleles is C4 made up of?

A

4

93
Q

What is a common immune complex disease?

A

Lupus

94
Q

What could cause a low C4?

A

C1 inhibitor deficiency (Hereditary angioedema)

95
Q

When is C1 inhibitor used?

A

At the beginning of the classical pathway, to block C1 formation
Also an enzyme that works in the bradykinin pathway

96
Q

What does bradykinin do to vessels?

A

Increase intravascular permeability (as well as vasodilation)

97
Q

What does bradykinin result in?

A

Oedema (swelling) due to fluid movement

98
Q

What are the acquired causes of a low C4?

A

Consumption or increased activation of the classical pathway - lupus, cryoglobulinaemia, rheumatoid vasculitis, ANCA positive vasculitis

99
Q

What does a low C3 often present with?

A

Meningitis

100
Q

What is the most common acquired low C3?

A

Post-streptococcal glomerulonephritis in paediatrics

101
Q

What are the cells of the innate immune system?

A

Dendritic cells, monocytes, macrophages, neutrophils, eosinophils, basophils, mast cells, NK cells

102
Q

Where are dendritic cells found?

A

all tissues

103
Q

What is the main function of dendritic cells?

A

presentation of antigen to naive T cells

104
Q

How can dendritic cells be activated?

A

Local tissue injury - to take up fluid and particles from their surroundings

105
Q

What does activation of dendritic cells cause them to do?

A

Migration to secondary lymphoid tissues

106
Q

What do dendritic cells do in the secondary lymphoid tissues?

A

Present to T lymphocytes the antigen derived peptide/MHC complexes

107
Q

What are the 3 functions of dendritic cells?

A
  1. Pick up and process antigens, and present them on their MHC class I and class II molecules
  2. Migrate to the T cell rich areas of secondary lymphoid tissues where naive and memory T cells circulate, and where they present antigens to specific T cells
  3. Transmit danger signals through molecules like TLR that help determine the type of T cell response that is programmed
108
Q

What do follicular dendritic cells capture?

A

They capture native non-degraded antigens through complement and antibody and presents this antigen to B cells in B follicles

109
Q

Where are dendritic cells most abundant?

A

Body surface

110
Q

What are Langerhans cells?

A

Tissue dendritic cells that have not taken up antigen

111
Q

What induces Langerhans cells to start to take up material from their surroundings?

A

Local tissue injury which causes release of chemical mediators

112
Q

How do Langerhans cells take up material?

A

In pinocytotic vesicles

113
Q

What do Langerhans cells have that help with phagocytosis?

A

Receptors that allow them to recognise bacteria and induce phagocytosis

114
Q

Which type of cell can engulf cells, including phagocytes, which are undergoing apoptosis?

A

Langerhans cells

Immunity, Infection and Haematology (6 decks)

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