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APO506 - MICROBIOLOGY & IMMUNOLOGY > WEEK 2: Tuberculosis > Flashcards

WEEK 2: Tuberculosis Flashcards

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1
Q

what are the symptoms of tuberculosis? - late stage disease

A

Breathlessness​

Chest Pains​

Persistent cough​

Coughing up blood​

Night sweats​

Tiredness​

Loss of appetite​

Loss of weight​

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2
Q

what does TB look like in an x-ray?

A

Usually see clouded areas in upper lobe or superior segment of lower lobe​

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3
Q

name the bacteria causing TB

A

Mycobacterium tuberculosis complex

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4
Q

how many people globally are estimated to carry ‘latent’ TB?

A

2 billion people

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5
Q

what year was the first antibiotic effective against TB discovered?

A

1943

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6
Q

what was the first antibiotic effective against TB called?

A

streptomycin

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7
Q

how many people infected with Mycobacterium tuberculosis are asymptomatic?

A

an estimated 90%

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8
Q

how does TB infection process begin?

A

with the inhalation of droplet nuclei expectorated from the respiratory tract of active TB sufferer

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9
Q

what are the 4 potential outcomes of inhaling TB bacilli?

A
  1. Initial host response can kill all bacteria​. No chance of active TB ever developing​
  2. Organisms begin to multiply immediately causing primary tuberculosis.​
  3. Bacilli become dormant & never cause disease – Latent infection. Patient has positive tuberculin skin-test​
  4. Latent organisms eventually grow with resultant clinical disease – Reactivation TB​
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10
Q

why is infection of TB with HIV the strongest risk factor for progression?

A

TB increases levels of HIV-1 replication, propagation and genetic diversity​. Therefore, co-infection provides reciprocal advantages to both pathogens

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11
Q

what is lymphatic TB?

A

TB in the lymphatic system - often affects women and children

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12
Q

what is pleural TB?

A

just outside the lung in chest cavity

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13
Q

what is cutaneous TB?

A

infection of TB that shows in the skin

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14
Q

how does TB get around the body?

A

haematogenous spread (through blood)

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15
Q

what bacteria causes TB?

A

mycobacterium tuberculosis complex

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16
Q

what are actinomycetes?

A

the genus class related to the gram-positive bacteria

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17
Q

TB is described as a diderm - what does that mean?

A

it has 2 outer membranes

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18
Q

what do mycolic acids do for the TB bacteria membrane?

A

forms the bases for outer membrane lipid bi layer - these inter-collate with complex bio active lipids and form a really hydrophobic membrane. Protects bacteria from drugs and disinfectants and toxic agents

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19
Q

what are mycolic acids

A

made from 2 long fatty acids, and they form a very impermeable membrane

20
Q

how is mycobacteria stained?

A

with a Ziehl-Neelsen stain. Looks red

21
Q

how are TB cells recognised by the immune system?

A

CD1 genes (MHC i like proteins) present TB lipid antigens to T cells

22
Q

how many estimated deaths were caused by TB in 2020?

A

1.5 million

23
Q

is mycobacterium tuberculosis an extra or intracellular pathogen?

A

intracellular

24
Q

what usually happens when a macrophage engulfs a pathogen?

A

acidification occurs - pH is lowered

25
Q

what happens when macrophages first engluf TB pathogen?

A

TB pathogen resists acid in macrophage

26
Q

why is a granuloma formed?

A

after the bacteria are ingested by the macrophages, they survive inside. This internalisation triggers an inflammatory response and brings other wbc’s to the area and forms a granuloma.

27
Q

how is the caseous centre of a granuloma formed?

A

tissue inside granuloma dies and forms this caseous centre.

28
Q

what attracts arrival of T lymphocytes?

A

IL-8

29
Q

why does exponential bacterial growth slow down?

A

the area becomes solid so there’s no access to nutrients and oxygen

30
Q

if you have a good cell mediated (CMI) immunity, what is the outcome?

A

effective CD4+ and CD8+ T cell activation of macrophages, activated macros can better kill TB and any surviving dormant TB contained within microscopic granuloma.

31
Q

if you have a poor cell mediated (CMI) immunity, what is the outcome?

A

macros around caseous legion stay poorly activated. TB continues intracellular growth, kills infected macros by delayed hypersensitivity response. Caseous necrosis, granuloma grows and is physically visible

32
Q

how many outcomes of TB have a poor CMI?

A

5-10% infections - children and immunocompromised adults.

33
Q

what is stage 4 for a poor CMI?

A

around 4-5 weeks, lung self damage. Infected macrophages spread, dissemination via lymphatics to thoracic lymph node and blood

34
Q

what are the 4 stages of TB?

A

the initial macrophage response, the growth stage, the immune control stage, and the lung cavitation stage

35
Q

what is DOTS?

A

directly observed treatment

36
Q

what is the cause of drug resistant TB?

A

it is the result of interrupted, erratic or inadequate TB therapy

37
Q

what are some requirements for DOTS?

A

political commitment from local government, standardised treatment with supervision (every drug dose to be observed by trained healthcare worker), effective drug supply and and management systems

38
Q

what are some disadvantages to DOTS?

A

DOTS difficult to deliver, reliance on smear microscopy has only a 60% detection rate, efforts to control TB fail in high burden areas

39
Q

what is latent TB?

A

a dormant enclosed infection that does not cause any symptoms.

40
Q

what is MDR TB?

A

multi-drug resistant TB

41
Q

what is XDR TB?

A

extensively drug resistant TB

42
Q

how is TB treated effectively?

A
  • make sure drugs work against specific strain
  • multiple medications used together
  • medications used for entire course of therapy
43
Q

what drugs are used to treat TB infection?

A
  • Rifampin ​
  • Isoniazid​
  • Ethambutol​
  • Pyrazinamide
44
Q

why does TB spread in the upper lobes of the lungs?

A

oxygen is greatest here and TB is a strict aerobe.

45
Q

how is TB tested for?

A

purified protein derivative (PPD) intradermal skin test or interferon gamma release assay (IGRA)

APO506 - MICROBIOLOGY & IMMUNOLOGY (10 decks)

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