TB and mycobacterial infection Flashcards

1
Q

how is TB related to poverty

A

increased rates where poverty is
TB causes poverty for individual and family - because long term illness when cant make money

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the mycobacteria that cause TB

A

M. tuberculosis (effects humans)
M. bovis (1% of human TB is caused by M bovis – look for it in cattle/badgers)
M. africanum
M. microti
M. canetti

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is TB transmitted

A

Classic TB presentation is in chest – can get it everywhere in the body.

Cant pass on if in bones for e.g.
Can pass in cough, sneeze, speaks, sings (laryngeal TB)

Aerosol transmission – droplet size small so hangs like fog in the air.
transmission happens when inhale droplet nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
A

Stain the red organisms – sputum smear positive mycobacterium
But don’t know whether its actually TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are some non TB mycobacteria

A

M chelonae (in fish) (right)
M abscessus and CF (hard to eradicate, would stop transplant for CF)
M avium eg HIV
M chimaera-vascular bypass device
NOT ALL AFB are TB!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what changes the probability that TB will be transmitted

A

Infectiousness of person with TB disease
Environment in which exposure occurred
Length of exposure
Virulence (strength) of the tubercle bacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how to prevent TB transmission

A

Isolate infectious persons
Provide effective treatment to infectious persons as soon as possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

summarise latent TB

A

1/4-1/3 of world’s population have latent TB
-> risk of developing active disease
Post TB infection, 10% lifetime risk for active TB =dogma; 30-50% active TB if HIV positive
Latent infection: prevent active TB = diagnosis +chemoprophylaxis
Fever+Wt loss+Night sweats+cough (2-3 wks)
Disease can occur decades later but rare
TB grows very slow – about once a day (every 18hr) – so always interval between being infected and having active TB

Don’t always have all of the symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

summarise latent TB

A

1/4-1/3 of world’s population have latent TB
-> risk of developing active disease
Post TB infection, 10% lifetime risk for active TB =dogma; 30-50% active TB if HIV positive
Latent infection: prevent active TB = diagnosis +chemoprophylaxis
Fever+Wt loss+Night sweats+cough (2-3 wks)
Disease can occur decades later but rare
TB grows very slow – about once a day (every 18hr) – so always interval between being infected and having active TB

Don’t always have all of the symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do you diagnose latent TB

A

Mantoux with PPD or
gamma interferon release assays (IGRA) - count gamma releasing T cells – a lot of spots = likely to be affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the incubation period for TB

A

3-9 months and almost always under two years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

why are rates of ltent TB overestimated

A

reflects immunoreactivity to either past or present infection.

Does not indicate the presence of live bacteria, as reactivity can persist after infection has been cleared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

do you need rx for latent TB

A

If its getting towards 3yrs since had infective contact – probably don’t need treatment – but let people know if going to be immunosuppressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the treatment of drug sensitive TB

A

2mo:
* Isoniazid
* Rifampicin
* Pyrazinamide
* Ethambutol

For 4 months
* Rifampicin and Isoniazid

daily, PO (or 3x/wk)
total 6mo
12mo for TB meningitis
Baseline checks incl CXR, LFT, FBC, UandE, CRP,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the limits of TB detection of different methods?

A

Microscopy ZN stain – smear – know infectious

Flurescnet based microscopy – bit more sensitivity

Solid culture – takes 4-6wks
Liquid culture 2wks
Molecylar tech – a daY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is MDRTB

A

resisytance to Rifampicin and Isoniazid

16
Q

where is most MDRTB

A

india
china
russian federation

17
Q

problem with MDRTB

A

treat for 18mo-24mo
Drugs toxic
Much more expensive – and it is a disease of poverty

18
Q

why is there MDRTB

A

Resistant happens as a natural phenomenon
But give multiple drugs – unlikely to get resistance clinically

18
Q

why is there MDRTB

A

Resistant happens as a natural phenomenon at rate of:
* INH = 1 in 10(6)
* RIF = 1 in 10(8)
* EMB = 1 in 10(6)
* Strep = 1 in 10(6)
* INH + RIF = 1 in 10(14)

But give multiple drugs – unlikely to get resistance clinically
The greater the burden of disease, the larger the bacillary population and the greater the risk for harboring drug-resistant mutants and acquiring drug resistance.

19
Q

how do you analyse resistance to TB meds

A

phenotypically ie microbiologically – TB grow in liquid, if grow with Abx - then resistant

Amplify DNA:

molecular line probe assays - PCR amplification of genes associated with resistance -> hybridisation with DNA probes on membranes -> development, reading adn interpretation of results

PCR based: Line probe assays (TB, RIF, INH from sputum eg
Genotype MTBDRplus
GenXpert (TB, RIF from sputum)
LAMP, WGS
DIAGNOSTIC TARGET PRODUCT PROFILES

20
Q

use of whole genome sequencing in TB

A
21
Q

what is (next generation sequencing) NGS and WGS

A

WGS and NGS are used synonymously but are not the same
WGS – is sequencing the genetic material
Next gen sequencing is the method
Take out DNA – smash into pieces – sequence them – stick along reference

22
Q

what is the benefit of WGS for TB

A

identify resistance w/o microbiology because that is dangerous

still need phenotype to know what drugs to use for the resistant ones

23
Q

what are compensatory mutations in TB

A

Drug resistance TB had other mutations that made it still efficient at functioning – so are as fit as drug sensitive TB – so these strains wont just burn out

24
Q

what is deeplex

A

targeted NGS but focues only on the key 14 genes associated with resistance

can usually get enough sputum for this straight from the sputum

24
Q

what is deeplex

A

targeted NGS but focues only on the key 14 genes associated with resistance

can usually get enough sputum for this straight from the sputum

25
Q

problem for second line drugs fro TB

A

cant use WGS to determine susceptability - still need culture