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MM- Bacteria > Tuberculosis Drugs > Flashcards

Tuberculosis Drugs Flashcards

1
Q

How many individuals died of TB infection in 2015?

A

1.8 million

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2
Q

How many individuals died of MDR in 2016?

A

240,000

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3
Q

XDR has been observed in how many countries?

A

117 countries

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4
Q

How many individuals were infected with TB in 2015?

A

10.4 million

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5
Q

Why is TB increasing in the UK?

A
  • Immigration
  • Drug resistance
  • Worldwide travel
  • HIV co-infection
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6
Q

When was the first TB antibiotic identified, what was it?

A

Streptomycin 1943

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7
Q

What are symptoms of TB infection?

A
  • Chills
  • Coughing for over 3 weeks
  • Coughing up blood
  • Fever
  • Night sweats
  • Unintentional weight loss
  • Chest pain
  • Difficulty breathing
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8
Q

How can TB be diagnosed?

A
  • Mantoux TST
  • Chest X-ray
  • Alere Determine TB LAM Ag
  • IGRA: QuantiFERON TB Gold
  • Sputum smear microscopy
  • 16S rRNA probes
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9
Q

TST results can be obtained within?

A

48-72 hours

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10
Q

Sputum smear microscopy results can be obtained within?

A

3-6 weeks

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11
Q

Chest X-ray results can be obtained within?

A

Immediately

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12
Q

IGRA results can be obtained within?

A

24 hours

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13
Q

What is IGRA?

A

Interferon Gamma Release Assay

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14
Q

Main issue with TST?

A

False positives due to BCG vaccination

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15
Q

Which test is not impacted by BCG vaccination?

A

Interferon gamma release assay

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16
Q

Main issues with chest X-ray?

A

X-ray exposure is not ideal

Can only identify the late stages of infection

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17
Q

16S rRNA is associated with?

A

30S ribosomal subunit

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18
Q

Prokaryotic ribosome structure?

A

30S small subunit
50S large subunit
70S ribosome

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19
Q

16S rRNA structure?

A

Has conserved regions

Has variable regions which are species/genus specific

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20
Q

How can 16S rRNA be used to identify bacteria?

A
  • Primers to the conserved regions which amplify the variable regions
  • Compare the sequence of the variable regions to known sequence databases
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21
Q

What is used to stimulate the T cell IFN-g production in vitro in the interferon gamma release assay?

A

CFP-10
TB 7.7
ESAT-6

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22
Q

What can detect IFN-G in the IGRA?

A

ELISA technology

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23
Q

Why does is QuantiFERON TB Gold not impacted by BCG?

A

As attenuated mycobacterium bovis has an RD1 deletion which means it lacks the CFP-10 and ESAT-6

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24
Q

Can IGRA distinguish between latent and active infection?

A

No

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25
Q

Can Mantoux TST distinguish between latent and active infection?

A

No

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26
Q

What are we looking for in an effective diagnosis?

A
  • Fast
  • High sensitivity
  • High specificity
  • Reliable
  • Cost effective
  • Safe
  • Easy to perform
  • Can be transportable
  • Not impacted by vaccination
  • Non-invasive
  • Can diagnose infection in children
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27
Q

Why can LAM be detected in the urine of HIV+ TB co-infected individuals?

A

As they have a low CD4+ cell count, TB infection could not be contained, results in disseminated TB disease. LAM is shed by the bacteria in the kidneys and is released into the urine

28
Q

What were the earliest TB treatments?

A

Purple bugle to encourage individuals to cough up blood

TB sanatoriums

29
Q

When was the first TB drug identified and what was it?

A

WWII
1943
Streptomycin

30
Q

DOTS is?

A

Directly Observed Treatment, short course

31
Q

DOTS is how long?

A

6 months

32
Q

2 months with?

A

Rifampicin, isoniazid, pyrazinamide and ethambutol

33
Q

4 months with?

A

Rifampicin and isoniazid

34
Q

Which drugs are cell wall synthesis inhibitors?

A

Isoniazid and ethambutol

35
Q

Which drugs are prodrugs?

A

Isoniazid and pyrazinamide

36
Q

Which drug can penetrate into the caseum?

A

Pyrazinamide

37
Q

Which drug stays in the rim of the granuloma?

A

Clofazimine

38
Q

What does isoniazid do?

A

Prevents mycolic acid synthesis

39
Q

What does ethambutol do?

A

Inhibits arabinosyl transferases

Prevents arabinogalactan synthesis

40
Q

What does pyrazinamide do?

A

Energy inhibitor
De-energises the membrane
Collapses the proton motive force

41
Q

What does streptomycin do?

A

Protein synthesis inhibitor

Blocks 30S ribosomal subunit and associated 16S rRNA

42
Q

What do fluoroquinolones do?

A

DNA synthesis inhibitor, inhibits DNA gyrase and topoisomerase IV activity

43
Q

What does bedaquiline do?

A

ATP synthase inhibitor

44
Q

Promising new drug?

A

Bedaquiline

45
Q

What is required to activate isoniazid prodrug?

A

KatG

Catalase peroxidase

46
Q

What is required to activate pyrazinamide prodrug?

A

Pyrazinamidase

47
Q

What encodes catalase peroxidase?

A

katG gene

48
Q

What encodes pyrazinamidase?

A

pncA gene

49
Q

Resistance to isoniazid?

A

Overexpression of InhA

Mutations in katG or inhA genes

50
Q

Resistance to pyrazinamide?

A

Mutations in pnca

51
Q

Resistance to ethambutol?

A

Mutations in arabinosyl transferases

52
Q

Resistance to rifampin?

A

Mutations in rpoB

53
Q

rpoB gene?

A

DNA dependent RNA polymerase

54
Q

Rifampin action?

A

Prevents transcription by inhibiting the DNA dependent RNA polymerase

55
Q

Resistance to streptomycin?

A

Mutations in the 16S rRNA gene

56
Q

Resistance to fluoroquinolones?

A

Mutations in the DNA gyrase

57
Q

How does pyrazinamide work?

A

Transformed into pyrazinoic acid by pyrazinamidase
In acid pH the uncharged protonated pyrazinoic acid can cross the membrane along with protons, this can de-energise the membrane and lead to collapse of the proton motive force

58
Q

What are drug tolerant bacteria?

A

These are persisters

They have phenotypic resistance

59
Q

What is phenotypic resistance?

A

Same genome as susceptible cells but able to tolerate certain levels of antibiotics

60
Q

What can drive phenotypic resistance?

A

The lack of vascularisation in the caseum

Low nutrients and low oxygen can cause cells to become metabolically inactive and dormant

61
Q

Many antibiotics rely on cells being?

A

Metabolically active

62
Q

Which antibiotic is ineffective on dormant cells?

A

Isoniazid

63
Q

Which type of resistance is genetic?

A

MDR and XDR

64
Q

Types of genetic resistance?

A

Natural intrinsic

Acquired

65
Q

Why is combination therapy required?

A

No single antibiotic in our current arsenal can penetrate every area of the granuloma and target all the different types of bacteria present
To prevent resistance developing

MM- Bacteria (7 decks)

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