Chapter 5 Flashcards

1
Q

How does mycobacteria look like?

A

Slender rod shaped

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2
Q

What feature makes mycobacteria resistant to destruction by neutrophils?

A

Waxy Cell Wall

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3
Q

Can mycobacteria be destroyed by neutrophils? What can phagocytose it? Can it still live on?

A

No. Macrophages. Can proliferate in macrophages

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4
Q

What two ways can you identify mycobacteria?

A
  1. Ziehl Nielsen
  2. Resist decolorisation (Acid fast Bacili)
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5
Q

Can other mycobacteria from M. Tb cause disease?

A

Yes. Less virulent but in immunosuppresed and those with pre existing lung disease

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6
Q

What is the main difference between primary and secondary TB?

A

Where the immune reaction is predominant

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7
Q

Can Secondary TB look like primary TB?

A

yes. when pt has poor immune system

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8
Q

Outcomes of TB?

A
  1. Primary and Secondary TB may heal or spread
  2. Within lung, TB often spreads via bronchi, lymphatics or into pleural space
  3. If TB enters blood supply, the patient develops miliary TB (can be limited to pulmonary circulation or spread to multiple organs)
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9
Q

What determines severity of TB?

A

Host factors and bacterial factors balance

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10
Q

How does immunity come about in TB?

A
  1. Host develops targeted cell-mediated immunity
  2. Antigens presented to CD4 T cells which secrete cytokines and activate macrophages to kill bacteria
  3. Immune response comes at the cost of hypersensitivity and accompanying tissue destruction
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11
Q

What is the pathogenesis of primary TB?

A

Occurs in unsensitised host

  1. Following inhalation, infection and necrosis at the periphery of the lung, often just beneath the lung (‘Ghon focus)
  2. Bacteria are then converted to local lymph nodes at the lung hilum where there is immune recognition - they enlarge through granulomatous inflammation and caseation

*lung lesion often small, lymph node involvement more evident
*these early changes may produce no significant symptoms

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12
Q

What happens if cell mediated immunity controls the infection?

A

Area of caseation heals and only residual evidence of infection may be small calcified nodule at site of infection

Viable organisms may lie dormant in these foci for decades = latent TB
(do not have active disease and cannot transmit)

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13
Q

What happens if cell mediated immunity does not control the infection?

A

Progresses with severe pneumonia and dissemination

Contining enlargement of caseating granulomas in the lymph nodes

Spread occurs by the enlarging nodes eroding through the walls of a bronchus (tuberculous bronchopneumonia) or into a thin walled blood vessel (miliary TB)

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14
Q

What happens in miliary TB?

A

Foci erodes into blood vessels (ie. into pulmonary artery), forms a small granuloma surrounding the organism

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15
Q

What is the pathogenesis of secondary TB?

A

Occurs in previously exposed, sensitised people; common presentation in immunocompetnent adults

  1. Acquire ‘new’ organisms or re-activation of primary complex
  2. Usually occurs in the apex, but may reactivate elsewhere if other organs were seeded during primary infection
  3. Rapid mobilisation of defence reaction at site of entry and increased tissue destruction
  4. Immune system recognises the infection in the lung and tries to contain it there - relatively little lymph node involvement
  5. Apical lesion (Assmann focus) begins as a central area of caseous necrosis surrounded by granulomas
  6. Destruction of lung tissue along with bacteria results in cavitation
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16
Q

Explain the two outcomes of secondary TB

A
  1. Healing
    - in adults with vigorous immune responses, healing of the apical lesion occurs, leaving a central area of caseous necrotic material (may still contain bacteria) surrounded by a thick, dense collagenous wall which often calcifies (fibrocaseous TB)
    - if the patient’s immune response weakens later in life and there are residual organisms, this latent TB can lead to spreading infection (reactivated fibrocaseous TB)
  2. Progression
    - progressive enlargement of the apical lesion, continued destruction of lung tissue
    - erosion into blood vessels or airways
    - spread (bronchopneumonia, miliary TB)