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Global Health BSc 2018/19 - CDMM1 > TB - 1-4 > Flashcards

TB - 1-4 Flashcards

1
Q

What is the incidence of TB worldwide?

A

10 million new cases worldwide in 2017 (WHO)

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2
Q

How many cases of the incidence of global TB have HIV?

A

1.2 million - high incidence in SSA as linked with HIV

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3
Q

Which is more prevalent: latent TB or active TB?

A

More people with latent TB than active

1 in 7 people have latent TB

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4
Q

Which 6 countries account for 60% of TB cases worldwide?

A

India, Pakistan, Indonesia, China, Nigeria, South Africa

Half of cases are rifampicin resistant

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5
Q

What is the trend in TB incidence compared to mortality?

A

TB deaths falling faster than TB incidence but people still getting latent TB in LMICs
Decline in incidence rates since 2010 exceeded 4% per year in several high TB burden countries

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6
Q

What is the definition of elimination in a TB setting?

A

< 1 case per million/year

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7
Q

What is the definition of pre-elimination in a TB setting?

A

< 10 cases per million/year

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8
Q

Why is there a high incidence of TB in former Soviet Union countries?

A

Collapse of the healthcare system + therefore poor access to healthcare
Civil unrest, inequality + poverty

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9
Q

What is the definition of Multi-Drug Resistance TB?

A

Resistant to rifampicin + isoniazid

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10
Q

How many people have MDR-TB?

A

Roughly 460 000

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11
Q

Where is MDR-TB significantly prevalent in?

A

Russia, China + India

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12
Q

What HIC country is TB still prevalent in?

A

UK!
8.9 new cases per 100 000
In 2017, lowest number of new TB cases for past 30 years

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13
Q

What % of migrants have MDR-TB in the UK?

A

70%; 30% Native - marginated or economically suffering

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14
Q

What are the 5 outcomes of an exposed person to TB?

A

1) Uninfected - insufficient infecting dose + mucosal barriers
2) Cleared - Innate response but no B cell response
3) Contained - local immune response but not detectable systematically
4) Latent TB infection - Innate + adaptive immunity
5) Active TB infection - 5% of all people exposed

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15
Q

What is the natural course of Mtb infection?

A

Disease most likely occurs in the first few years of infection + then declines e.g. S Korea + Taiwan have an increased prevalence in the elderly as they were exposed when they were young + now reactivated when their immune systems are weak

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16
Q

What are the predisposing factors to TB?

A 
HIV
Malnutrition
Diabetes
Alcoholism
Deficiency of TNF-a --> encourages pro/anti-inflammatory balance
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17
Q

What is the innate immune response to TB?

A

TB recognised by PRRs on macrophages in the lung
Macrophage activated and causes a local response
Cytokines released to induce adaptive response

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18
Q

What is the adaptive response to TB?

A

TB travels to lymph nodes + activates dendritic cells
Dendritic cells activate T cells - T cell priming
T cells go to the lung and activate IFN-gamma which increases macrophage response and all gather to the lung
There a protective granuloma forms - causes symptoms - If any present, this is latent TB
This then turns into transmissive granuloma whereby it bursts if immune system can’t handle it - active TB

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19
Q

When does the first immune response to TB occur?

A

Usually 8 -12 days post infection

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20
Q

Describe why there is a symbiosis between TB and immune response

A

If there is an impaired immune response e.g. from HIV, malnutrition, diabetes, alcoholism - disease
If tissue damage e.g. pro inflammatory > anti-inflammatory - disease, transmission (problem with forming TNF-alpha so no granuloma forms
If balance between pro-inflammatory = anti-inflammatory - equilibrium so no disease

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21
Q

What are the 2 diagnostic tests for TB?

A

TST (Tuberculin skin test) + IGRA (Interferon gamma release assay)

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22
Q

How does a TST work?

A

If antibodies produced before will produce a positive TST result + cause an inflammatory response

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23
Q

What are the weaknesses of TST?

A

Can’t differentiate between latent or active TB
False +ve if exposed to other mycobacterium e.g. in the soil (cross-reactivity)
False +ve for BCG as it contains tuberculin

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24
Q

What are the strengths of IGRA?

A

Strong specificity for antigens in Mtb that are not in BCG - Less likely to get false positives
However, more costly + require work in the lab

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25
Q

What is the WHO Tb strategy?

A

END TB 2015-2030

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26
Q

What is in the END TB 2015-2030 strategy?

A 
WHO Tb strategy 
Vision: world free of TB
Goal: reduce TB epidemic
95% reduction in deaths
90% reduction in incidence
0%  to suffer catastrophic costs = >40% of total income
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27
Q

Who should be tested following the WHO End TB strategy?

A

Should systematic test for LTBI and treat

Definitely test and treat: HIV, Exposed, Healthcare workers

28
Q

Does the WHO use IGRA/TBT?

A

Yes, if no IGRA still use TBT

High incidence, high burden

29
Q

What is the PHE strategy for TB?

A

Collaborative TB Strategy for England 2015-2020

30
Q

What does the Collaborative TB Strategy for England 2015-2020 entail?

A

Voluntary screening:

Migrants from countries of incidence > 50/100 000 year

31
Q

What is the problem with the Collaborative TB Strategy for England 2015-2020?

A 
GP registration?
Undocumented migrants
Adherence
Language
Accessibility
Loss to follow up - refer to cascade of care
32
Q

What does PHE say in terms of screening for TB?

A

IGRA + TST

Low incidence, high burden

33
Q

What type of vaccine is the BCG?

A

Live attenuated

34
Q

What is the gold standard vaccine for TB?

A

BCG

35
Q

When was BCG made?

A

In 1921, cultured from Mycobacterium. bovis and took 11 years

36
Q

How available is the BCG?

A

Widely available - different countries have different stocks due to controversial efficacy

37
Q

When should people be vaccinated?

A

Before 1 year old as more efficacious in infants due to immunological maturation

38
Q

What are the strengths of the BCG?

A

Safe
Widely available
Works in kids and provides immunity against TB meningitis
Cures bladder cancer and improves outcomes in leprosy
Cheap

39
Q

What are the weaknesses of BCG?

A

Doesn’t work in high-incidence countries but works in HICs - tragedy of BCG
Too many different strains of vaccine - variable efficacy: 0-80%
Fridge storage
Doesn’t work in lifelong immunity
Injectable
Don’t have anything for LTBI/ATBI
Can’t be used in immunocompromised patients

40
Q

Why is there a variability in efficacy of the BCG?

A

Cross-reactivity with previous mycobacterium exposure e.g. in the soil
Strain variation - no horizontal transmission so lost genes of Mtb
Nutritional
Other infections
Population genetics

41
Q

What are the 5 new TB candidates?

A 
MTBVAC
M72/AS01
MVA85A
VPM1002
H4:IC31
42
Q

What are the characteristics of MTBVAC?

A

Live attenuated - first and only Mtb live vaccine
Safe
TB + HIV -ve

43
Q

What are the characteristics of M72/AS01?

A

Conjugate/subunit - most promising candidate
Safe
High efficacy (54%) in adults
Can be used in TB or HIV +ve

44
Q

What is the most promising TB Vaccine candidate?

A

M72/AS01
Broom (2018) - Very good and worth investing in vaccines as vaccines cost less than the burden of TB
Needs more funding

45
Q

What are the characteristics of MVA85A?

A

Used as a BCG booster but failed

Large Phase III RCT w/ 3000 people in S. Africa but failed - lots of money was invested

46
Q

What are the characteristics of VPM1002?

A

Recombinant protein based on BCG, Used in kids/adolescents
Ongoing trials since 2012/2015
TB + HIV - ve

47
Q

What are the characteristics of H4: IC31?

A

BCG re-vaccination
Nemes et al did 3 armed RCT and found BCG was better than H4:IC31 > Placebo
Generally still low efficacy

48
Q

What did Kaufmann, 2011 say about vaccination?

A

Vaccines are expensive so need acknowledge this
MDRTB is a huge problem but nothing is being done
Need predictors of how trials are doing e.g. MVA85A

49
Q

What is a key driver to the problems of HIV + MDR-TB?

A

HIV epidemic

Young children have similar presentations for TB as HIV Patients due to an immature immune system

50
Q

What is the incidence of TB in Africa?

A

High due to also high HIV burden

51
Q

What are the issues with HIV TB coinfection?

A

Less likely classical presentation, more likely extra pulmonary (more serious), X ray change variable, tests less sensitive, false -ves

52
Q

What is the treatment regime for TB?

A 
RIPE
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol 6/12 months minimum
53
Q

What is an extensively drug resistant TB?

A

Resistant to isonniazid and rifampicin AND any fluoroquinolone + at least one of three injectable second-line drugs

54
Q

Why is MDRTB more prevalent in the former Soviet Union countries?

A

Due to collapse of the healthcare system

55
Q

What are the interventions to control MDR/XDRTB?

A 
Invest in R&amp;D for new vaccines, drugs + diagnostics
Optimise MDR + XDRTB management
Prioritise infection control
Address global workforce crisis
Address lab costs
Ensure access to high quality drugs
Finance - abolish barriers to care
Restrict availability of anti-TB drugs for efficacy
The Three I's for TB/HIV (WHO)
DOTS (End TB Strategy 2015)
Patient activism/education
56
Q

What is the challenge to R&D for new vaccines, drugs + diagnostics?

A

Dx takes time as TB must be grown
New molecular targets in diagnostics
Costly
Not always easy to detect pathogen - children

57
Q

What is the challenge to prioritise infection control?

A

In high prevalence settings, many hospitals have high rates of undiagnosed TB
Natural ventilation proven benefit + UV light

58
Q

What is the challenge to addressing the global workforce crisis?

A

Migration of healthcare workers - spread globally (Williams 2015)

59
Q

What are the 3 I’s for TB/HIV (WHO)?

A

Intensified case finding
Isoniazid Preventative therapy (IPT) - Treating those with LTBI with isoniazid for 9 months
Infection control for TB

60
Q

What is causing the TB burden in the migrant population?

A

Reactivation of remotely-acquired latent TB infection following migration from high TB burden, LICs + migrated to HICs, low TB burden countries

61
Q

Historically, what have HICs focused on combating TB control?

A

Focused on combating active TB but with an increasing migrant population where TB burden lies in LTBI, new mechanisms to tackle this burden are needed

62
Q

What does evidence suggest HICs do to control TB?

A

LTBI screening post-arrival and Rx to certain migrant groups

Barriers to access + implementation + sub-optimal Rx must still be overcome to achieve elimination

63
Q

What is the most effective mechanism to screen?

A

Pre-arrival screening for active TB
Targeted post arrival screening for LTBI in migrants from intermediate/high burden settings
Single step IGRA

64
Q

What are the challenges to post-arrival screening for LTBI?

A

Limited uptake - loss in the cascade of care
Acceptance
Completion of therapy

65
Q

How do foreign-born individuals bear the TB burden in HICs?

A

Disproportionate

Reactivation of LTBI is important in migrants

Global Health BSc 2018/19 - CDMM1 (12 decks)

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