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Microimmunology > Mycobacteria > Flashcards

Mycobacteria Flashcards

1
Q

What species cause infection?

A 
M. tuberculosis
- causes tuberculosis in humans 
- TB = tubercle bacilli
- humans are the only konwn resevoir
M. bovis
- Cuases tuberculosis in cows
- Humans can be infected by drinking unpasteurized milk
M. avium
- Can cause a tuberculosis-like illness in humans, particularly in AIDS patients
M. leprae 
- causative agent of leprosy in humans
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2
Q

True or false?

Tuberculosis is the 2nd leading cause of death after AIDS

A

True

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3
Q

Who was M. tuberculosis isolated by?

A

Robert Koch in 1882

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4
Q

General info on M. tuberculosis

A

Obligate human pathogen, intracellular pathogen, Non-motile, rod shaped, obligate aerobe
- can be grown, but takes 4-6 weeks to get small colonies (generation time >15h)

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5
Q

Mycobacteria have high [mycolic acid] in the cell envelope, what is the significance of this?

A
  • Resistance to many antibiotics
  • resistance to killing by acidic and alkaline compounds
  • Resistance to osmotic lysis via complement deposition
  • Resistance to lethal xidative stress and promotes survival inside of macrophages
  • Impermeability to stains and dyes
  • Acid fast (resists common stains)
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6
Q

What is an acid fast stain?

A
  • Stained with the basic dye carbol-fuchsin with slow heating (to melt wax)
  • Washed with EtOH and HCL
  • Counterstained with methylene blue
  • Acid-fast organisms appear red, whereas non-acid fast organisms appear blue
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7
Q

What is Stage 1 of tuberculosis?

A
  • transmission from inhalation of droplets from an infected host (coughing/sneezing)
  • can generate 3000 droplet nuclei (can contain 3 bacteria)
  • small droplets can stay airborne for a while and inhaled directly into lungs
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8
Q

What is stage 2 of tuberculosis?

A
  • 7 - 21 days after initial exposure
  • alveolar macrophages phagocytize TB cells
  • TB can multiply in unactivated macrophages
  • Macrophages will lyse and release TB cells to infect more macrphages
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9
Q

What is stage 3 of tuberculosis?

A
  • infected macrophages form granulomas - TB inhibits fusion of phagosome with lysosome to survive and grow in the macrophage
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10
Q

What are granulomas?

A
  • Tubercles of immune cells trying to destroy invading pathogens
  • Represents a balance between the pathogen and host (latent infection)
  • Macrophages at the centre are harder to activate by T cells
  • activated macrophages can kill TB and present to T cells
  • Macrophages cause caseous necrosis and dead cells maintain a cheese like appearance
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11
Q

What is stage 4 of tuberculosis?

A
  • Some macrophages remain infected
  • Tubercle grows, erosion of granuloma in airway provides the route of transmission (cough)
  • Deterioration of host immunity can result in a life threatening infection (active TB)
  • Caseous centre can liquefy leading to cavitation (hole/cavity in lung)
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12
Q

What is the difference between pulmonary and extra pulmonary TB?

A

Pulmonary = contagious (75%)
- Progressive, irreversible lung destruction can occur and bacteria may enter bloodstream
- Latent carriers do not transmit the infection (single inhaled bacteria can infect though)
Extra pulmonary = non-contagious (25%)
- more likely to occur in immunocompromised individuals
- can infect: bone, joints, liver, spleen, GI tract and brain
- Systemic spread can cause miliary TB (fatal)

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13
Q

What % of infected people develop disease?

A

10%
Symptoms = long cough with thick and possibly bloody mucus, fever, chills, fatigue, weight loss, chest pain, shortness of breath, pallor (pale skin, white death)

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14
Q

What are symptoms of Extra pulmonary TB?

A

They can vary depending on where TB spread to

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15
Q

What is the testing and diagnosis for TB?

A

TB test = PPD (purified protein derivative)

  • a person is infected if they convert from negative to positive on a TB skin test
  • positive = red, swollen circle at 48h
  • delayed-type hypersensitivity
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16
Q

What do negative and positive results for the TB test mean?

A 
Negative = not infected, immune compromised or not infected long enough
Positive = Latent or active TB or BCG vaccinated (chest x-ray for upper lobe "shadowing" = lesions)
17
Q

How deadly is TB if untreated?

A

will kill 2/3 people

18
Q

What is the treatment for TB?

A

6 months of antibiotics for the short treatment (slow growth = long treatments)
Multiple Antibiotics:
- Rifampin (inhibits RNA polymerase)
- Isonazid (inhibits mycolic acid synthesis)

19
Q

Why give 2 or more drugs?

A

10^11 bacteria possible in tubercle (hube amount)

- minimizes development of resistance (has to develop 2 of them)

20
Q

What is the difference between MDR-TB and XDR-TB?

A

multi-drug resistant TB = MDR-TB
- resistant to the first 2 most effective first-line therapeutic drugs, isoniazid and rifampin
Extensively-drug resistant TB = XDR-TB
- Also resistant to the most effective 2nd-line therapeutic drugs used commonly to treat MDR-TB
- XDR-TB has been found globally and can be untreatable

21
Q

What is BCG and why does it result in a false positive on the TB test?

A

Bacille Calmette-Guerin

  • living vaccine prepared from attenuated M. bovis which shares antigenicity with TB
  • controversial du to variable efficacy (~80% or more)
  • leaves large scars (only recommneded if at high risk of exposure)
22
Q

Which is more widely spread HIV/AIDS or TB?

A

People living with HIV = 33.3 million

People living with TB = 2 billion people

23
Q

What is leprosy?

A

Chronic diesase caused by M. leprae (Hansen’s disease)

  • slow growth (incubation period ~5 years)
  • Causes permanent damage to skin, nerves, limbs and eyes
  • rare in developed countries
  • 2 million people are permanently disabled bny leprosy (mainly tropical developing countries)
24
Q

What does M. leprae share with M. tuberculosis?

A

Both are Gram+ acid fast, rod shaped, aerobic and have waxy cell envelopes (mycolic acid)

25
Q

Where can M. leprae grow?

A
  • foot pads of mice (low #s)
  • Systemic infection in armadillp (10^10 per gram of infected tissue)
  • M. leprae infects macrophages of skin and schwann cells in nerves
26
Q

What is more infectious TB or leprosy?

A

Leprosy is much less infectious

  • Despite this victims of leprosy have been ostracized (killed, rejected by family, etc.)
  • This may be because lesions in TB are hidden, but in leprosy they are visible
27
Q

What are the 2 major forms of leprosy and what % of people will develop the disease?

A

Tuberculoid and lepromatous

- 95% will not develop disease

28
Q

What is Tuberculoid Leprosy?

A
  • cell-mediated immunity present
  • macrophage can contain the bacteria
  • lesions with “anesthetic” areas
  • loss of hair and pigmentation
  • tuberculin positive
  • bacterial cells are not recoverable from lesions
  • can be self limiting
29
Q

What is Lepromatous leprosy?

A
  • Cell-mediated immune responses are absent
  • Macrophages are not activated
  • M. leprae survives and multiplies in macrophages and Schwann cells
  • damges nerves = loss of sensation leads to inadvertant traumatic lesions
  • Can cause loss of eyebrows, thickening and enlarged nares, ears and cheeks (lion-like appearance)
  • lesions can become secondarioly infected resulting in disfigurements and mutilation
30
Q

What is the spread and progression of leprosy?

A
  • Transmission is not well understood
  • Close (direct) contact for long time periods is hypothesized
  • most exposed individuals do not develop disease (host genetics may be important)
31
Q

Is leprosy treatable, and how if so?

A
  • Yes, with multiple antibiotics for 6 months to a year
  • Dapsone (1940) used until resistance developed (1960s)
  • In 1980 MDT - dapsone, rifampin, clofazimine
  • After one does of MDT (multi-drug therapy) patients no longer transmit the disease
32
Q

Is Leprosy still stigmatized today?

A

Yes, people are still very fearful of the disease due to the appearance of victims

Microimmunology (10 decks)

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