Tuberculosis Flashcards

1
Q

What is the leading single infectious killer in adults world-wide (excluding HIV)

A

Tuberculosis

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2
Q

How many people got TB in 2019?

A

10 mil

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3
Q

Why are mycobacteria hard to grow, diagnose & treat?

A

Mycobacteria are slow growing and have a lipid rich wall making them difficult to treat with antibiotics. They are hard to culture and therefore, hard to diagnose.

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4
Q

What 8 countries accounted for 2/3rds of the total new cases of TB

A
India
Indonesia
China
Philippines
Pakistan
Nigeria
Bangladesh
South Africa
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5
Q

What is the relationship and effect of TB and HIV concurrent illness?

A
  • HIV makes people more likely to get TB
  • TB makes those with HIV more likely to die
  • TB is still curable in HIV
  • TB makes HIV progress more rapidly
  • HIV patients have a higher mortality with TB
  • HIV makes TB more difficult to diagnose
  • HIV drugs and TB drugs interact
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6
Q

how is TB transmitted?

A

Spread in aerosols from infected individuals lung to another or via spitting or sneezing on plates or hands

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7
Q

what do we mean by smear positive and smear negative in TB? what effect does this have on transmissibility?

A

If we can’t see the bacteria in the sputum, we say they are smear negative, if we can see the bacteria in sputum, we say they are smear positive.
Smear positive = 27/50% of household contacts become infected (more infectious)
Smear negative = <5% household contacts become infected (less infectious)

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8
Q

how is bovine tb spread?

A

through cows and unpasteurised milk drinking. more common in butchers or abattoir workers.

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9
Q

why are mycobacteria good at surviving intracellularly?

A

they have a waxy outer coat so they can survive in phagolysosomes.

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10
Q

pathology of TB

A
  • Bacilli are taken in lymphatics to hilar lymph nodes and the adaptive immune response is activated
  • Macrophages and lymphocytes seal in, contain and kill majority of infecting bacilli in a granuloma to stop further replication of the bacteria or make the bacteria go into a dormant stage = latent TB
  • Primary infection is contained but cell mediated immune response persists
  • Latent TB = no clinical disease, may be tiny granulomata that become calcified, detectable CMI to TB on tuberculin skin test
  • If immune response is not strong, the granuloma does not work to suffocate the mycobacteria
  • As granuloma grows it develops into a cavity (more likely in apex of lung as there is more air and less blood supply and immune cells which is favourable for the bacteria)
  • The cavity is full of TB bacilli which are expelled when the patient coughs
  • Bacilli + macrophages coalesce to form a granuloma this is called the primary (ghon) focus
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11
Q

When there is a primary (goon) focus + mediastinal lymph nodes enlarged what is this called?

A

Ghon complex

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12
Q

Presentation of TB (systemic features)

A
weight loss
night sweats
low grade fever
anorexia
malaise
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13
Q

Presentation of TB (pulmonary features)

A

Chronic cough >3 weeks
Chest pain
breathlessness
haemoptysis

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14
Q

Presentation of TB (extra-pulmonary features)

A

lymph node tb, miliary tb

Bone pain, swelling of joint or Potts disease

Abdominal TB - ascites, abdominal nodes, ileal malabsorption

GU TB: epididymitis, frequency, urgency, haematuria

CNS TB: meningitis, CN palsy, tuberculoma

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15
Q

natural course of tb infection?

A
  • At some point there is a primary infection which can develop into primary disease (5% cases) (either specific organ which is usually the lung or all over the body)
  • This can lead to dormant TB and at some point it can re-activate and the patients can develop disease (post-primary disease)
  • Post primary disease usually occurs wherever the dormant TB were hiding (usually lung)
  • Those who have had TB can become re-infected even after being treated and lead to disease again and some die from TB
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16
Q

What percentage of people have been identified to have latent TB?

A

25%

17
Q

Diagnosing active TB?

A
Microbiology, microscopy, PCR, culture
Sputum
Urine
CSF
Pleural fluid
Biopsy specimens of lymph nodes, peritoneum, bone brain etc.

Other non-specific
- prolonged inflammatory. response, normochromic normocytic anaemia, thrombocytosis, raised eSR or CRP, low albumin, hypercalcaemia, sterile pyruria.

18
Q

diagnosing latent tb?

A

Not possible to find dormant bacteria so we use TB skin test where we inject a protein derived from organism into the dermis and it stimulates a reaction if the person has been exposed (doesn’t distinguish between BCG used in vaccine)

Interferon gamma release assays - antigens specific to M tuberculosis which does distinguish between BCG and TB.

19
Q

What is the standard UK treatment for TB?

A

Rifampicin - 6m
Isoniazid - 6m
Pyrazinamide - first 2m
Ethambutol - first 2m

20
Q

what is DOTS?

A

directly observed treatment short-course. It is the TB strategy from WHO to have successful treatment of TB. It involves 5 main things, one of which is giving medication in a supervised fashion.

21
Q

What is a common side effect for TB drugs?

A

hepatitis

22
Q

why is the course of antibiotics so long for TB and why are so many drugs used?

A

Most bacteria are killed within weeks but a group of mycobacteria are dormant and can re-activate so using a combination of drugs means most can be effectively killed.

23
Q

In the UK, what percentage of patients are thought to have isoniazid resistance and MDR to TB drugs?

A

7% isoniazid

1% MDR

24
Q

Why is drug resistant TB worse?

A

DR TB is more difficult to treat, more side effects from IV/IM injections required, >20m treatment and increased relapse rate

XDR TB is now present in many countries and is very difficult to treat with a very high mortality.

25
Q

Newer drug for TB with potential?

A

Bedaquiline

26
Q

What is the ‘end TB strategy’?

A

END TB strategy: 95% reduction by 2035 in TB deaths, 90% reduction in TB incidence.

27
Q

Prevention of TB?

A
  • Active case finding to reduce infectivity
  • Detection and treatment of latent TB with a short course of abx
  • Vaccination: neonatal BCG for those in high risk groups.