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Stage 2: Inflammation > TB > Flashcards

TB Flashcards

1
Q

What is a characteristic of mycobacterium that other gram positive bacteria don’t have?

A

They have a thick layer of mycolic acid on the outside of the cell which makes the bacteria very resistant to environmental effects (can survive a long time in dust and intracellularly)

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2
Q

What are the effects of mycobacterium’s slow generation time of 15-20 hours?

A
  • Takes a long time to diagnose in the lab (culture based)
  • Chronicity of infection
  • Virulence
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3
Q

What is the key property of mycolic acid with staining?

A
  • It confers the unique property of acid fastness
  • Long thin pink rods indicate mycobacterium
  • The acid and alcohol wash has washed away everything else on the slide but not mycobacterium
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4
Q

Describe the spread of M. TB

A
  • Airborne spread via droplet nuclei (tiny)
  • Generated in alveoli
  • Remains in the air for a long time if someone coughs
  • Deposit in alveoli
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5
Q

What happens in 90% of primary TB infections?

A
  • The bacteria are phagocytosed by alveolar macrophages, forming a granuloma
  • If this drains to local lymph nodes it can cause lymphadenitis
  • The contained infection in the granuloma leads to latent TB
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6
Q

What happens to 10% of individuals with latent TB?

A
  • The lesions progress after some time to (plaque then) cavitation which destroys lung tissue (CD8 and NK cells?)
  • This is post-primary/reactivation TB
  • Half of these individuals will have this within 2 years of infection
  • For others, it may take up to 50 years
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7
Q

What happens to 5% of people with primary TB infection?

A

The immune system won’t contain the initial infection and will progress to classic pulmonary TB within 2 years

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8
Q

What percentage of M. TB infections go on to become active TB?

A

10%

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9
Q

What is the risk of progression/reactivation of TB in AIDS?

A

10% per year (rather than 10% lifetime risk)

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10
Q

What else can TB do?

A

Disseminate at any time (even when latent) to any body site via blood/lymphatics esp. if immunocompromised or < 2

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11
Q

What kind of disease is TB and why?

A

Immunopathological disease

  • If have no T cells (AIDS) don’t get cavitation and tissue destruction
  • However, the infection can’t be contained so get rapid dissemination and death
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12
Q

What is a significant risk factor for reactivation/progression with dissemination?

A

CD4 depletion

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13
Q

What is the biggest pathogenic determinant in mycobacteria?

A

Mycobacterial cell wall - predominant genes associated with pathogenicity are those involved in mycolic acid synthesis

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14
Q

How can you test for TB when it is latent?

A
  • Positive tuberculin skin tests
  • IGRA (interferon gamma release assay)
  • No symptoms
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15
Q

What are the systemic signs/symptoms in TB?

A
  • Weight loss
  • Malaise
  • Fever
  • Night sweats
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16
Q

What are pulmonary signs/symptoms in TB?

A
  • Non productive cough
  • Primary TB pleural effusion/pleurisy leading to SoB (reduced intra-thoracic volume and effective air space) - otherwise SoB more likely to be other infection
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17
Q

What are pulmonary symptoms in late TB?

A
  • Haemoptysis - when have bad cavitation

- SoB

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18
Q

What can happen in fulminant TB?

A

Haemoptysis and massive pulmonary haemorrhage due to cavities eroding onto pulmonary artery

19
Q

What are extra-pulmonary findings in TB?

A
  • Cervical lymphadenitis
  • Meningitis
  • Osteomyelitis
  • Renal/gut TB (can get TB anywhere + granulomas)
20
Q

What radiological findings are there in primary TB?

A
  • Hilar lymphadenopathy (due to primary TB of hilar lymphnodes) - different from normal hilar shadow of pulmonary artery and vein
  • Consolidation (upper lobe)
  • Pleural effusion in primary TB lesion is sub-pleural on outside of lung
21
Q

What radiological findings are there in post-primary TB?

A
  • Cavitation (destruction, abscesses) - dense white scarring
  • Fibrosis (scarred lung tissue, contracts down and get shrunken lungs)
  • Upper lobe predominance (spread to both lungs)
  • Tracheal tug due to loss of lung volume in advanced TB
22
Q

How would you diagnose TB in the context of pleurisy and pleural effusion?

A
  • Pleural tap

- Pleural biopsy

23
Q

What is the most common site for TB?

A

Intra-thoracic (53% pulmonary)

24
Q

What is the second most common site for TB?

A

Extra-thoracic lymph node TB (23.1%) e.g. cervical

25
Q

What are other common sites for TB?

A

GI tract, spine, other bones, TB meningitis

26
Q

What causes the broken down caseous material in cavitary TB?

A
  • Immune response and NK cells
  • Local tissue destruction
  • Macrophages break up and release cytotoxic chemicals leading to tissue destruction
27
Q

How would cervical lymph node TB present?

A
  • Swollen, inflamed, soft and fluctuant cervical lymph node with abscess formation
  • Just above collar bone, just outside insertion of SCM in collar bone v likely to be TB
28
Q

What type of TB tends to occur in immunocompromised patients?

A

Military TB

  • Don’t get cavitation
  • Miliary seed type granulomas in the lung
29
Q

What happens in spinal TB?

A
  • TB osteomyelitis
  • Destruction of discs and bone
  • These vertebrae eventually collapse leading to kyphosis spine and the patient is hunched over
  • This is Pott’s disease (typical of spinal TB)
30
Q

What happens in TB basal meningitis?

A
  • Inflammation
  • Thick adherent white plaques cause occlusive meningitis which blocks CSF flow
  • Hydrocephalus is common
31
Q

How do you diagnose TB?

A

1) Clinical samples - sputum/lavage, tissue, blood
2) Microscopy
3) Solid/liquid Culture - takes weeks, highest sensitivity
4) PCR - also detects rifampin resistance, v rapid (2 hours), can do directly on sputum, but less sensitive than culture
5) Speciation

32
Q

Why do you need 4 agents to treat drug-sensitive TB?

A
  • The mutation rate to single agents in TB is high

- A high number will already inherently have rifampicin or isoniazid resistance

33
Q

What drugs and for how long do you use to treat drug-sensitive TB?

A

1) Rifampicin (6-12 months)
2) Isoniazid (6-12 months)
3) Pyrazinamide (2 months)
4) Ethambutol (1-2 months)

34
Q

What are 3 less effective second-line agents only used in drug-resistant TB?

A
  • Levofloxacin
  • Streptomycin
  • Clarithromycin
35
Q

What is TB mono-resistance?

A

Resistance to one first line anti-TB drug only

36
Q

What is TB poly-resistance?

A

Resistance to > 1 first line anti-TB drug, other than isoniazid and rifampicin

37
Q

What is TB multi-drug resistance?

A

Resistance to at least both isoniazid and rifampicin (most effective drugs) - if resistant to both of these, mortality increases significantly

38
Q

How might you have to treat someone with extensive drug resistance?

A

Pneumonectomy (treated as if before TB therapy)

39
Q

What is DOT?

A

Directly observed therapy (bc if not compliant will get resistance)

40
Q

What are some other non-TB mycobacteria (generally skin and soft tissue or bone infections)?

A
  • M.avium
  • M.fortuitum
  • M.marinum
  • M.leprae
  • M.ulcerans
  • M.kansasii - similar to typical TB
41
Q

What is granulomatous inflammation?

A
  • Protective response to chronic infection or foreign material, preventing dissemination and restricting inflammation through formation of a granuloma
  • Distinctive pattern of the chronic inflammatory reaction
42
Q

What are causes of granulomatous inflammation?

A

1) Fungal infections
2) TB
3) Leprosy
4) Schistosomiasis
5) Foreign material
6) Autoimmune diseases
7) RA
8) Crohn’s
9) Sarcoidosis

43
Q

What happens during granulomatous inflammation in active pulmonary TB?

A
  • M.TB lives in macrophages (intracellular) in the lung so bc the immune system can’t clear bacteria they form granulomas to prevent the spread
  • Put down fibrin to wall off the infected macrophages
  • Granulomas impair lung function and oxygen exchange
  • Top of lung typically affected

Stage 2: Inflammation (39 decks)

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