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Hilary week 1 > TB > Flashcards

TB Flashcards

1
Q

What is the leading killer of HIV infected patients?

A

TB

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2
Q

What lifestyle choice increases risk of TB?

A

smoking

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3
Q

what treatment is used for TB?

A

every day fro siz months is isoniazid and rifampicin.

For first two months as well, pyrazinamide and ethambutol.

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4
Q

Issues with drugs for TB?

A

drug toxicity, along with long term use makes adherence poor.

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5
Q

what are multidrug restistant TB resistant to normally? HOw long does alternative treatment last?

A

resistant to isoniazid and rifampicin.

20 months and with lower success.

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6
Q

What are extensively resistant drugs resistant to?

A

resistant to isoniazid and rifampcicin and another drug.

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7
Q

Why does m.TB primarily infect the lungs?

A

Becuase its an obligate aerobe, lik high O2 tissue concentration.

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8
Q

What other parts of the body does disseminated (extrapulmonary) Tb affect?

A

the lymph nodes, the CNS, bone and joints.

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9
Q

How slow is the mTB generation time?

A

18hrs

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10
Q

What are the four layers of the thick wall of mTB made up of?

A

capsule- proteins/peptides and polysaccharidess.
Mycolic acid layer, bound to underlying arabinogalacta.
Peptidoglycan cell wall which is heavily cross linked.

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11
Q

What benefit does complex lipid cell wall give?

A

protection against drying- long survival.

resistant to chemicals and lysozyme.

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12
Q

What dye is used for diagnosis?

A

acid fast stain (carbolfuchsin) stains thick cell wall (mycolic acid)

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13
Q

3 outocmes with after TB bacilli have reached alveolar?

A

active diease
latent disease (can later become active in 5-10%, or 10% risk of this in HIV patients each year).
Eradication

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14
Q

In what cell does m TB replicate?

A

In lung macrophages following its phagocytosis.

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15
Q

What happens characteristically to the infected lung macrophages?

A

They form large multi nuclear cells and granulamas. They become ‘foamy’.

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16
Q

describe what the containment and escape phase of granulomas looks like?

A

T cells surround th macrophages adifferentiated into epithelioids- containment in latent stage.
Escape the blood vessels are broken down leading to rupture of granuloma and active disease.

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17
Q

4 different memory responses in Tb?

A

Tcm Tem, Trm and Brm (resident memory cells are in the lungs.

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18
Q

What does AECs stand for and how do they help to fight TB?

A
  • airway epithelial cells in the upper respiratory tract.
  • Recognise mTB via PRRs, secrete cytokines and can -present antigen to MAIT cells via MR1?
  • Can also control the composition of the airway surface liquid
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19
Q

What does ASL stand for and how does it protect against TB?

A

airway surface liquid, contains AMPS e.g. cathelldicin, Beta defensins, and cytokines.

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20
Q

What is the a chain of the semi invariant MAIT cell TCR?

A

Va 7.2

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21
Q

What do MAIT cells recognise?

A

riboflavin derivative 5-OP-RA presented on MR1.

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22
Q

what effector functinos of MAIT cells could contribute to mTB protection?

A

cytotoxic effects and cytokine relesas e.g. of IFN-y and IL-17.

23
Q

MAIT cells are mostly CD8+ or DN, what about CD4+ MAITS in active infection and latent infection?

A

CD4 MAITS upregulated in active infection.
In latent infection CD8+ MAITS predominate.
Overall in active infection the MAITS in circulation are reduced (going to the tissues?)

24
Q

Why might MAIT cells not be protective in macaques?

A

because of slow Mtb regernation , or due to immune evasion by mTB?

25
Q

What are the roles of type 1 and type 2 epithelial cells?

A

type 1 line alveoli involved in gas exchange.

type 2 produce AMPs, and realise surfactant prtoeins (SP-A and SP-D?).

26
Q

What two aspects of phagocytosis could be targeted for bacterial escape?

A

endosome acidification, and phagosome lysosome fusion.

27
Q

4 ways macrophages can contribute to mTB control?

A

1) phagocytosis
2) cytokine production and inflammation.
3) ROS and nitrogen species/toxic metals.
4) via cell death- macroautophagy and apoptosis.

28
Q

What kind of changes are associated with trained innate memory?

A

metabolic reprogramming and epigenetic modifications.

Can be induced by the BCG vaccine as well.

29
Q

Evidence that innate responses alone can be protective?

A

Some individuals with high exposure to mTB never get disease, but also don’t have the memory responses either.

30
Q

Why might there be such a delay for arrival of CD4 and CD8 T cell responses to the lungs and site of infection?

A

Because of slow regeneration? Or situation of infection deep in lungs causes delay?

31
Q

CD4 T cells important for mTB response, what mechanissm are protective?

A

directly activate macrophages and via secretion of IFN-y which increases macrophage killing.

32
Q

CD8 T cells important in later infection, what mechanisms important for mtB responses?

A

perforin granzyme killing, and Fas-FasL as well as IFN-y ecretion.

33
Q

Which two cytokines are most important for the mTb response?

A

IFN-y and TNF-a

34
Q

Why is anti-TNF-a not recommened for patients with TB?

A

Because it increases the liklihood of activation of TB.

35
Q

What other cytokines are imporatnt for mTB response apart from INF-y and TNF-a?

A

IL-17, Il21, Il22 and IL23.

36
Q

What can Th17 responses increase, and why might they be dangerous?

A

INreases neutrophil recruitment, and inflammation.

But increasing too much may contribute in increased lung damage and pathology.

37
Q

Why might Tregs be activated in mTB and what can this impari?

A

Tregs presumably activated to control the specific TH1 responses and lung damage.
But may impair Mtb control

38
Q

unconventional T cells involved in Tb?

A 
ydelta T cells (big IL-17 producers)
invariant NKT (CD1 restricted)
MAIT cells (MR1 presented 5-OP-RA)
HLA-E restricted CD8s
39
Q

what might be a problem with alveolar macrophages?

A

they may not be as bactericidal (for lung protection) making them more permissive.

40
Q

Evidence for and agaisnt B cells in TB?

A

B cell and ab deficiencies aren’t a risk for TB disease.

However, MVA85A vaccine study showed higher specific IgG titres correlated with reduced TB risk.

41
Q

What kind of differences exist between ab in active and latently infected people?

A

functional and glycosylation differences.

42
Q

6 ways Ab can help with protection against TB

A

1) enhance phagocytosis
2) enhance phagosome-lysosomal fusion
3) neutralisation
4) enhance inflammasome
5) induce ADCC
6) also complement activation!

43
Q

what is at the centre and periphery of tubercles? What walls off the granuloma?

A

centre is necrosis containing bacilli.
Periphery are lymphocytes and plasma cell aggregates.
fibroblasts lay down collagen to wall off granuloma.

44
Q

different between langhans cells and epithelioid cells?

A

Langhans are giante multinucleated cells.

epithelioid are macrophages with eosinophilic cytoplasm (foamy?)

45
Q

How does mTb survive in host?

A

interferes with phagosome maturation(e.g. maturation and fusion with lysosomes)

  • Can still fuse with other vesicles for nutrients.
  • escape to the cytosol by creating proes with ESTAT6.
  • decoy molecule secretion and interference with IFN-y signalling.
46
Q

What does mtB inhibition of apoptosis allow?

A

prolonged survival of infected cells allwoign greater number of bacteria to accumulate.

47
Q

What are the bacterial benefits of necrosis?

A

reruitiment of fresh macrophages for growth and expansion.

48
Q

Is cell wall compostin fixed?

A

No it changes with active and lantency, eg. mycoclic acids layer thicker in active disease.

49
Q

What are the two secretion systems for mTB rpoteins?

A

ESX system accross the inner membrane. Or type VII seccretion system across outer membrane.

50
Q

What three important proteins does the virulent ESX1 region encode?

A

ESPG and H, and ESTAT6.

51
Q

What does ESX-3 encode?

A

mycobactin for iron binding and growtn.

52
Q

What is ESX-5 mportant for?

A

secretion of ppe secretory proteins.

ESX 2+4 not essential for growht or virulence

53
Q

How do ESXG and H evade immunity in DCs?

A

by interfering with tranlocation of ESCRT complex mediated mtB antigen fusion with MHC II containing vesicles.

Hilary week 1 (5 decks)

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