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MM- Bacteria > Tuberculosis > Flashcards

Tuberculosis Flashcards

1
Q

How many people fell ill with TB and how many people died from TB in 2015?

A
  1. 4 million people fell ill

1. 8 million died from TB

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2
Q

Over 95% of TB deaths occur where?

A

In low and middle income countries

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3
Q

TB infections are most common in which countries?

A 
India
South Africa
Nigeria
China
Pakistan
Indonesia
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4
Q

How many people are latently infected with TB?

A

~2 billion

1/3 of the world’s population

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5
Q

What mycobacteria cause tuberculosis?

A

MTBC: Mycobacterium tuberculosis complex

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6
Q

What mycobacterium causes leprosy?

A

Mycobacterium leprae

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7
Q

What mycobacterium causes Buruli ulcers?

A

Mycobacterium ulcerans

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8
Q

What bacteria make up the mycobacterium tuberculosis complex?

A 
MBTCA
M= microti
B= bovis
T= tuberculosis
c= canetti
a= africanum
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9
Q

Which mycobacterium led to the BCG vaccine?

A

Mycobacterium bovis

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10
Q

Prototuberculosis developed into?

A

Different lineages

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11
Q

How did the different linages of TB form?

A

Through regions of deletion

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12
Q

Where are different lineages found?

A

Different lineages are found in different parts of the world. They have a phylogeographic population structure with different lineages associated with different human populations

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13
Q

Which lineage is most common in Europe?

A

Lineage 4

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14
Q

Which lineages are most common in West Africa?

A

Lineages 5 and 6

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15
Q

Which lineage is most common in India/East Africa?

A

Lineage 3

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16
Q

Which lineage is most common in East Asia?

A

Lineage 2

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17
Q

Lineage 2 is most common in?

A

East Asia

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18
Q

Lineage 3 is most common in?

A

India/East Africa

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19
Q

Lineages 5 and 6 belong to which member of the MTBC complex?

A

Mycobacterium africanum

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20
Q

Which lineages form a monophyletic group?

A

2,3,4

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21
Q

Lineages 2,3,4 form a monophyletic group through which unique deletion?

A

tbD1

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22
Q

Which region of deletion produces lineages 5 and 6?

A

RDL9

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23
Q

What is the MTBC?

A

Mycobacterium tuberculosis complex

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24
Q

Nucleotide sequence similarity in MTBC?

A

99.9% similarity at nucleotide level. Have host tropism and phenotypic and pathogenic differences.

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25
Q

When did TB arise as a human pathogen?

A

~70,000 years ago

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26
Q

What are some key features of mycobacteria?

A
  • aerobic
  • microaerophilic
  • non-motile
  • bacilli
  • slow growing
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27
Q

TB doubling time?

A

24 hours

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28
Q

Mycobacterium staining procedure is known as the?

A

Acid fast staining

Ziehl-Neelsen

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29
Q

What is another name for the acid fast staining procedure?

A

Ziehl-Neelsen

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30
Q

Steps in the acid fast staining procedure?

A

Add carbol-fuchsin dye
Decolorise with acid-alcohol or acid-acetone solutions
Add methylene blue counter stain to stain any cells which are not acid fast

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31
Q

Why are mycobacterium called acid fast?

A

They maintain the red colouration from the carbol-fuchsin dye as they resist decoloration by acid-alcohol and acid-acetone solutions

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32
Q

Describe the cell envelope of gram negative bacteria?

A 
Plasma membrane
Periplasmic space
Thin peptidoglycan layer
Periplasmic space
Outer membrane with lipopolysaccharide
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33
Q

Describe the cell envelope of gram positive bacteria?

A

Plasma membrane
Thick peptidoglycan layer
Teichoic acids

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34
Q

What can be used to stain gram positive cells?

A

Crystal violet

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35
Q

What can be used to stain gram negative cells?

A

Counter stain safranin

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36
Q

Describe the mycobacterium cell envelope structure?

A

Plasma membrane
PIM= phosphatidylinositol mannosides
Peptidoglycan then this is covalently linked to arabinogalactan
Arabinogalactan is covalently linked to mycolic acid
Inner leaflet of the outer membrane= mycolic acid
Outer leaflet of the outer membrane= extractible lipids including PIM and LAM= lipoarabinomannan
Capsule made of lipids, proteins and polysaccharides

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37
Q

What is mycolic acid?

A

Mycolic acid= beta hydroxy fatty acid with alpha-alykl side chain

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38
Q

What is mycolic acid?

A

A beta hydroxy fatty acid with an alpha-alkyl side chain

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39
Q

Mycolic acid length?

A

C60-C90

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40
Q

Mycolic acid can form different?

A

Conformations

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41
Q

Why does mycolic acid need to fold into different conformations?

A

Full length mycolic acid would be too large for the inner leaflet of the outer membrane

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42
Q

Which mycolic acid conformation decreases the permeability of the inner leaflet and how?

A

W conformation of keto-mycolates. Folds into four chains in parallel. The tight packing aids the formation of an impermeable barrier

43
Q

Mycobacterium tuberculosis infectivity?

A

Very infectious

Only a single particle is needed for infection

44
Q

Which cells first phagocytose the mycobacterium tuberculosis bacilli?

A

The resident alveolar macrophages

45
Q

What are the four categories of receptors found on macrophages?

A

Scavenging receptors
Opsonising receptors
C-type lectin receptors
Innate immune sensors

46
Q

What are opsonising receptors?

A

Fc receptors or complement receptors

47
Q

What are c-type lectin receptors?

A

Mannose binding lectin
dectin-1
dectin-2
DC-SIGN

48
Q

What does TLR2 recognise?

A 
19kDa lipoprotein (LP)
LAM= Lipoarabinomannan
LM= Lipomannan
49
Q

TLR2 signals via which pathway?

A

Myd88

50
Q

TLR2 leads to the production of what?

A

Causes macrophages to produce IL-12

51
Q

One of the major receptors you need to know on macrophages for phagocytosis?

A

CR3

Complement Receptor 3

52
Q

Tuberculosis-complement receptor 3 complex causes what?

A

Prevents respiratory burst

Blocks phagosome maturation

53
Q

What are neutrophil NETs made out of?

A

DNA, histones, nucleosomes

54
Q

What does NET stand for?

A

Neutrophil Extracellular Traps

55
Q

What are lymphatic endothelial cells?

A

They line lymphatic vessels

The bacteria can hide in the lymph node and cause disease when conditions are more favourable

56
Q

Which cytokines aid granuloma formation?

A

Pro-inflammatory cytokines:
TNF-alpha
IL-12
IFN-gamma

57
Q

Which cytokines prevent granuloma formation?

A

Anti-inflammatory cytokines

IL-10

58
Q

Which CD4+ response is important for granuloma formation?

A

Th1 response

59
Q

How is the Th1 response activated?

A

Th0–>Th1

Stimulated by IL-12

60
Q

Describe the granuloma structure?

A

Necrotic area in the centre known as the caseum
You then have lots of innate immune cells including: dendritic cells, foamy macrophages, multinucleated giant cells, NK cells and neutrophils.
These are surrounded by a ring of lymphocytes

61
Q

What are the main lymphocytes?

A

Mainly CD4+, CD8+, CD1 and γ/δ T cells

62
Q

What is the caseum?

A

Necrotic centre
Has a ‘cheese-like’ appearance
Dead macrophages are found here
Rich in lipids

63
Q

Macrophages can become?

A

They can fuse to from large multinucleated cells

They can differentiate to become foamy macrophages

64
Q

Foamy macrophages are?

A

Lipid rich

65
Q

Foamy macrophages have lost?

A

Their phagocytic and bactericidal activities

66
Q

Where is mycobacterium tuberculosis found in the granuloma?

A

Extracellularly in the caseum

Intracellularly in foamy macrophages

67
Q

Why is the bacteria found in the caseum and in foamy macrophages?

A

They are lipid rich

68
Q

What are the conditions within the caseum like?

A

Reduced vasculature
Low oxygen levels
This is why it is good that mycobacterium tuberculosis is a microaerophile

69
Q

Reduced oxygen and nutrient levels lead to?

A

A reduction in metabolic activity

Reduction in cell division/proliferation

70
Q

What can cause the latent infection to then re-activate?

A

Immunosuppression
HIV
Ageing
Malnutrition

71
Q

What is the role of vitamin D?

A

Has been shown to boost the immune system

72
Q

How can mycobacterium tuberculosis prevent destruction within non-activated macrophages?

A

Prevents phagosome maturation and phagosome fusion with the lysosome= prevents phagolysosome formation.

73
Q

What are the three ways in which mycobacterium tuberculosis can prevent destruction in non-activated macrophages?

A

1) Receptors involved in Mtb uptake
2) Alteration of phagosomal lumen
3) Alteration of phagosomal membrane

74
Q

Receptors involved in Mtb uptake to avoid destruction?

A

The CR3-Mtb complex is able to prevent respiratory burst and prevent the maturation of the phagosome

75
Q

Alteration of the phagosomal lumen?

A

sapM
PknG
Urease C
LAM

76
Q

sapM?

A

Phagosomal fusion requires the presence of PI3P on the surface of phagosomes
PI3P= phosphatidylinositol-3-phosphate
sapM is a secretory phosphatase which can dephosphorylate PI3P which arrests phagosome maturation

77
Q

What is sapM?

A

A secretory phosphatase

78
Q

What is PknG?

A

A secretory kinase

Serine/threonine kinase

79
Q

What does PknG do?

A

Blocks phago-lysosome fusion

80
Q

How does LAM prevent degradation in non-activated macrophages?

A

Inhibits cellular increase in Ca2+

Phagosome maturation arrest

81
Q

How does Urease C prevent phagolysosomal maturation?

A

Urease C drives neutralisation of acidification in phagosomes by generation of ammonia, thereby inhibiting phagolysosomal maturation

82
Q

Modification of the phagosomal membrane?

A

Prevention of V-ATPase

By inhibiting its function acidification of the endosome is prevented

83
Q

What is PknG?

A

A secretory serine/threonine kinase
Able to prevent phagolysosome formation
Phagosome and lysosome fusion is prevented

84
Q

What is sapM?

A

It is a secretory phosphatase
Dephosphorylates PI3P= phosphatidylinositol-3-phosphate which is required on the surface of phagosomes. Leads to the arrest of phagosomal maturation

85
Q

Phagosomal arrest does not occur in?

A

Activated macrophages

86
Q

How can macrophages overcome phagosomal arrest?

A

Through activation

87
Q

How are macrophages activated?

A

Recognition of opsonised molecules

IFN-gamma production

88
Q

What pH is the phagosome acidified to?

A

~4.5

89
Q

How can the innate immune response promote the adaptive immune response? Provide an example?

A

Macrophages produce IL-12. This can then stimulate Th0–>Th1 which leads to the production of IFN-gamma which can then activate macrophages

90
Q

What cells predominantly produce IFN-gamma?

A

CD4+ cells

91
Q

CD8+ cells produce what to induce apoptosis/cell death?

A

Granulysin

Perforin

92
Q

γδ T cells recognise antigens without?

A

Without the need for presentation on a major histocompatibility complex

93
Q

γδ T cells recognise what type of antigens?

A

Lipid antigens

94
Q

CD1 restricted T cells recognise?

A

Recognise lipid antigens abundant in the mycobacterial cell walls (LAM, PIM, mycolic acids) presented by the CD1 molecules

95
Q

The T cells have which main two functions?

A
  1. Direct cytotoxic activity

2. Activation of the macrophages

96
Q

Activated macrophage killing pathways?

A

Reactive oxygen and reactive nitrogen species

97
Q

Reactive oxygen pathway?

A

Requires oxygen to make reactive oxygen species including superoxide and hydrogen peroxide

98
Q

Reactive nitrogen pathway?

A

Requires L-arginine as a precursor to make e.g. nitric oxide and nitrogen dioxide

99
Q

How do macrophages kill Mtb?

A

Oxidative and non-oxidative mechanisms

100
Q

Non-oxidative mechanisms?

A

Autophagy- immunophage

Apoptosis

101
Q

Autophagy stimulated by the immune system is known as?

A

Immunophagy

102
Q

How can TB resist death in activated macrophages, what is a mechanism?

A

KatG

103
Q

What is KatG?

A

Catalase peroxidase

104
Q

What can KatG do?

A

Can inactivate reactive oxygen species within phagolysosomes

MM- Bacteria (7 decks)

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