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MM- Bacteria > Tuberculosis Summary > Flashcards

Tuberculosis Summary Flashcards

1
Q

M.prototuberculosis evolved into?

A

7 different lineages

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2
Q

Lineage 2 is associated with which region?

A

East Asia

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3
Q

Lineage 3 is associated with which regions?

A

India and East Africa

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4
Q

Lineage 4 is associated with which region?

A

Europe

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5
Q

Lineages 5 and 6 are associated with which regions?

A

West Africa

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6
Q

Mycolic acid length?

A

C60-C90

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7
Q

What is mycolic acid?

A

Beta-hydroxy fatty acid with alpha alkyl side chain

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8
Q

Ketomycolates fold into which conformation?

A

W conformation

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9
Q

Describe the W conformation?

A

4 chains in parallel

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10
Q

What are the 4 types of receptors on macrophages?

A

Scavenger receptors
Opsonising receptors (FcR and complement receptors)
Innate immune sensors (TLR)
C-type lectin (mannose binding lectin, DC-Sign, dectin-1, dectin-2)

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11
Q

What are some examples of opsonins?

A

Surfactants SP-A and SP-D
IgG
Complement proteins e.g. C3b

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12
Q

Complement receptor 3 Mtb complex results in?

A

Phagosome arrest

Prevents respiratory burst

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13
Q

TLR2 recognises?

A

19kDa LP
Lipomannan LM
Lipoarabinomannan LAM

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14
Q

Granuloma formation is aided by which cytokines?

A

IL-12
IFN-g
TNF-alpha

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15
Q

Granuloma formation is suppressed by which cytokine?

A

IL-10

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16
Q

How can Mtb prevent destruction in macrophages?

A

Phagosomal maturation arrest

Prevention of phagolysosome formation

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17
Q

Ways that Mtb can prevent destruction in macrophages?

A

Receptors involved in Mtb uptake
Altering the phagosomal lumen
Altering in the phagosomal membrane

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18
Q

Receptors involved in Mtb uptake?

A

CR3-Mtb complex prevents respiratory burst and leads to phagosome maturation arrest

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19
Q

Altering the phagosomal lumen?

A

SapM
PknG
Urease C
LAM

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20
Q

What is SapM?

A

Secretory phosphatase

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21
Q

How does SapM work?

A

Need phosphatidylinositol-3-phosphate (PI3P) on the surface in order to allow phagolysosome fusion. SapM dephosphorylates PI3P and leads to phagosome maturation arrest.

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22
Q

What is PknG?

A

It is a secretory kinase

Serine/threonine kinase

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23
Q

How does PknG work?

A

It is a secretory kinase

It prevents phagosome-lysosome fusion

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24
Q

How does LAM work?

A

Prevents the increase of intracellular Ca2+ which prevents phagosome maturation

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25
Q

Urease C?

A

It leads to the production of ammonia which can neutralise the acidic phagosome

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26
Q

Alteration of the phagosomal membrane?

A

V-ATPase

Able to prevent acidification of the phagosome

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27
Q

Phagosomal arrest does not occur in?

A

Activated macrophages

28
Q

What activates macrophages?

A

Opsonins binding opsonin receptors
IFN-gamma
TNF-alpha

29
Q

Phagosome is acidified to what pH?

A

~4.5

30
Q

What are γδ T cells?

A

They are non-classical T cells and are involved in recognising lipid antigens

31
Q

γδ T cells can recognise antigens without?

A

Without the need for antigen to be presented on MHC

32
Q

What are CD1 restricted T cells?

A

Recognise lipid antigen e.g. LAM, mycolic acid antigens presented on CD1 molecules.
Non-classical presentation of antigen on CD1

33
Q

What are non-oxidative mechanisms of macrophage microbicidal activity?

A

Autophagy- Immunophagy

Apoptosis

34
Q

The immunological induction of autophagy is known as ?

A

Immunophagy

35
Q

Autophagy process?

A

Formation of an autophagosome

The autophagosome is a double membrane- can surround the Mtb and fuse with the lysosome for degradation

36
Q

When is autophagy activated in cells?

A

In times of stress/ starvation

37
Q

What is autophagy used for in cells that are not infected?

A

In times of starvation, organelles that are not being used/ proteins can be degraded and recycled to provide nutrients using autophagy

38
Q

Describe the antibiotic treatment and length of treatment for DOTS?

A

Directly observed treatment- short course
6 months
2 months: Rifampin, pyrazinamide, isoniazid and ethambutol
4 months: Rifampin and isoniazid

39
Q

Describe the antibiotic treatment and length of treatment for DOTS-Plus

A

24 months+

Use of second line drugs such as fluoroquinolone

40
Q

What is MDR TB?

A

Resistant to rifampin and isoniazid

41
Q

What is XDR TB?

A

Extensively drug resistant
Resistant to rifampin and isoniazid
Also resistant to fluoroquinolone and another second line antibiotic

42
Q

Which antibiotics are prodrugs?

A

Pyrazinamide and isoniazid

43
Q

Which antibiotics are cell wall synthesis inhibitors?

A

Ethambutol and isoniazid

44
Q

Which drug has great penetrative capabilities?

A

Pyrazinamide

45
Q

Which drug has poor penetrative capabilities?

A

Clofazimine

46
Q

What is the new TB antibiotic drug?

A

Bedaquiline

47
Q

Bedaquiline action?

A

Inhibits ATP synthase

48
Q

Action of rifampin?

A

Inhibits DNA dependent RNA polymerase

Prevents transcription

49
Q

Resistance to rifampin

A

Mutations in rpoB gene

50
Q

Action of isoniazid?

A

Cell wall synthesis inhibitor

Prevents mycolic acid synthesis mainly through inhibition of InhA

51
Q

Isoniazid prodrug activation?

A

Via catalase peroxidase encoded by katG

52
Q

Isoniazid resistance?

A

Mutations in katG and inhA genes

53
Q

Pyrazinamide action?

A

Energy inhibitor
Disrupts membrane potential
In acid pH uncharged protonated pyrazinoic acid and protons cross the membrane and disrupt membrane potential

54
Q

Pyrazinamide prodrug activation?

A

Pyrazinamidase enzyme

55
Q

Pyrazinamidase enzyme is encoded by?

A

pncA

56
Q

Resistance to pyrazinamide?

A

Mutations in pncA

57
Q

Ethambutol action?

A

Cell wall synthesis inhibitor
Prevents arabinogalactan synthesis
Inhibits arabinosyl transferases

58
Q

Resistance to ethambutol?

A

Mutations in the gene encoding arabinosyl transferases

59
Q

Streptomycin action?

A

Protein synthesis inhibitor

Binds to and blocks 30S subunit of the ribosome and associated 16S rRNA

60
Q

Streptomycin resistance?

A

Mutationsin 16S rRNA

61
Q

Fluoroquinolone action?

A

DNA replication inhibitor

Can inhibit action of DNA gyrase or topoisomerase IV

62
Q

Quinolone antibiotic resistance?

A

Mutations in DNA gyrase

63
Q

Pharmacodynamic considerations?

A

Impact of the drug on the organism

Ability of the antibiotic to clear infection and act on bacterial cells, especially those persisters

64
Q

Pharmacokinetic considerations?

A

Impact of the organism on the drug

Ability of the drug to penetrate the granulomas

65
Q

Why are the granulomas hard for antibiotics to penetrate?

A

Caseum where the bacteria are found has low vascularity

66
Q

Why are some cells hard for antibiotics to impact?

A

As these cells may be persisters. Many drugs only work effectively on active bacteria. Some bacilli in the granuloma are in a dormant state with low proliferative ability and low metabolic activity.

MM- Bacteria (7 decks)

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