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My Packs: (UWO) (MICROIMM 2500) > (Section C: Bacteriology) Lecture 21 > Flashcards

(Section C: Bacteriology) Lecture 21 Flashcards

1
Q

What are the 4 forms of Mycobacteria mentioned?

A
  1. M. tuberculosis
  2. M. leprae
  3. M. bovis
  4. M. avium
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2
Q

Mycobacterium tuberculosis

A
  • Causes tuberculosis in humans
  • “TB” = Tubercle Bacilli
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3
Q

Mycobacterium leprae

A

Causes Leprosy in humans

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4
Q

Mycobacterium bovis

A

Causes tuberculosis in cows, rarely in humans
* Humans can be infected via unpasteurized milk
* Leads to extrapulmonary tuberculosis

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5
Q

Mycobacterium avium

A

Causes tuberculosis-like illness in humans, particularly in patients with AIDS

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6
Q

What are the two types of Tuberculosis infection?

A
  • Latent
  • Active
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7
Q

How much of the population has latent TB?

A

2 billion (1/4 of the world’s population)

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8
Q

TB is contagious and spreads…

A

Through the air by people with active TB

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9
Q

How many people with latent TB will develop active TB in their lifetime?

A

~10%

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10
Q

How many people die from TB each year?

A

1.6 million

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11
Q

Mycobacterium tuberculosis
* Type of pathogen
* Generation time

A
  • Intracellular pathogen (lives within macrophages
  • Slow generation time of >15 hr
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12
Q

Can M. tuberculosis be grown in labs?

A

Yes
* Takes 4-6 weeks to get small colonies
* Must be grown on specialized media

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13
Q

What is unusual about the cell envelope of M. tuberculosis?

A

High concentrations of mycolic acid

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14
Q

What characteristics does mycolic acid impart on M. tuberculosis?

A
  • ‘Waxy’ layer
  • Impermeability to stains and dyes (require acid fast staining)
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15
Q

The unusual cell envelope of M. tuberculosis is associated with resistance to:

A
  1. Some antibiotics
  2. Osmotic lysis via complement desposition (resistance to complement pathway)
  3. Lethal oxidative stress (allows survival inside of macrophages)
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16
Q

Describe the process of:

Acid Fast Stain

A
  1. Stained with carbo-fuchsin dye with slow heating (why)
  2. Washed with ethanol and HCl
  3. Counter stained with methylene blue
  4. Differentiate acid-fast vs non-acid fast

  1. Slow heating will melt the waxy cell envelope to allow staining
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17
Q

In Acid Fast Stain:

What do acid-fast organisms appear like? Non-acid fast organisms?

A

Acid-fast organisms: Red
Non-acid fast organisms: Blue

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18
Q

“Acid fastness” is due to the presence of…

A

Mycolic acid

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19
Q

Spread and progression of tuberculosis:

Stage 1

A

Transmission
* Inhalation of droplets from infected host (coughing, sneezing)

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20
Q

Coughing and sneezing can generate —- droplet nuclei
* Droplet nuclei can contain — bacteria

A
  1. 3000
  2. <10
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21
Q

How big are droplets from coughing and sneezing? What property do they have?

A

Small diameter (~5μm)
* Stay airborne for extended time
* Can be directly inhaled into lungs

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22
Q

Spread and progression of tuberculosis:

Stage 2

A

Phagocytosis of TB cells by lung (alveolar) macrophages

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23
Q

How do TB cells escape phagocytosis and continue infection?

(5 points)

A
  1. Blocks acidification of the phagosome
  2. Inhibits fusion of lysosome to the phagosome
  3. Multiplies in macrophages
  4. Macrophages lyse = release TB cells to infect more
  5. Delays dendritic cell migration to lymph nodes
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24
Q

ESX secretion system

A

Enable the transport of select bacterial molecules across the thick Mtb cell envelope

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25
Q

How many ESX systems exist in Mtb?

A

5

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26
Q

What functions do the molecules secreted by ESX secretion systems have?

A
  1. Damage to the phagosome membrane
  2. Other functions that inhibit the immune responses

Multiple functions

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27
Q

Spread and progression of tuberculosis:

Stage 3

A

Infected macrophages may form granulomas

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28
Q

What are TB granulomas?

A

“Tubercles” of immune cells that try to destroy invading pathogens
* Typically comprised of macrophages

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29
Q

What do TB granulomas represent?

A

Latent infection
* A balance between the pathogen and the host

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30
Q

How do granulomas work?

A
  • T cell activated macrophages can kill TB
  • Activated T cells secrete cytokines (IFN-gamma) to activate macrophages
  • Macrophages at the center of the granuloma ramin harder to activate
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31
Q

Caseous necrosis

A

Chronic inflammation that causes “cheese-like” necrosis

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32
Q

Spread and progression of tuberculosis:

Stage 4

A

Active tuberculosis
* Some macrophages remain unactivated and infected, tubercle grows
* Erosion of granuloma into airway leads to transmission
* Deterioration of host immunity results in life-threatening infection

33
Q

The caseous center of granulomas can liquefy, leading to…

A

Cavitation

34
Q

Extrapulmonary tuberculosis

A

Infection outside the lungs
* Can infect multiple organ systems (bone, joints, liver, spleen, gastrointestinal tract and brain)

35
Q

Who is more likely to get extrapulmonary tuberculosis?

A
  1. Immunocompromised individuals (HIV infected patients etc.)
  2. Young children
36
Q

Miliary tuberculosis

A

Widespread dissemination occurs, almost always fatal

37
Q

What is the test for tuberculosis?

A

Tuberculin test
* PPD (purified protein derivative) from M. tuberculosis

38
Q

Tuberculin test
* Immune response
* Positive result

A
  • T cell-mediated response
  • Positive result is a red and swollen circle at 48 hrs
39
Q

In a TB skin test, how is person determined to be infected?

A

If they convert from negative to positive on a TB skin test

40
Q

What could positive and negative results mean on a TB skin test?

A

Positive:
* Latent/active TB
* BCG vaccinated
* Previously infected

Negative:
* Not infected
* Immune compromised (e.g. AIDS)
* Not infected long enough

41
Q

What other diagnosis methods are used to diagnosis M. tuberculosis?

A
  • History
  • Chest X-ray (shows upper lobe “shadowing”, indicates lesions)
  • Staining of sputum and culturing
  • Interferon-gamma response assay
42
Q

True or False:

Active TB can kill 1 out of 3 people if untreated

A

False, active TB can kill ~2 out of 3 people if untreated

43
Q

Why are TB treatments very long?

A

Due to the slow growth of the bacteria

44
Q

How is tuberculosis treated?

A

Generally, multiple types of antibiotics are used
* Rifampin
* Isoniazid

45
Q

Rifampin

A

Inhibits RNA polymerase

46
Q

Isoniazid

A

Inhibits mycolic acid synthesis

47
Q

MDR-TB

A

Multi-drug resistant TB
* Defined as being resistant to the two most effective first-line therapeutic drugs (isoniazid and rifampin)

48
Q

XDR-TB

A

Extensively-drug resistant tuberculosis
* Also resistant to the most effective second-line therapeutic drugs used commonly to treat MDR-TB

49
Q

How prevalent is XDR-TB?

A

Found in all regions of the world

50
Q

BCG

A

“Bacille Calmette-Guerin”
* A living vaccine prepared from attenuated M. bovis

51
Q

How is the M. bovis attenuated in the BCG vaccine?

A
  • Lacks ESX-1 secretion system
  • Shares antigenicity with TB
52
Q

Why is the BCG vaccine controversial?

A

Variable efficacy (~80% to much less) for pulmonary TB

53
Q

True or False:

BCG vaccinated individuals can give a false positive for the tuberculin test

A

True

54
Q

What happens as a side effect of BCG vaccine?

A

Vaccination leaves large scars
* Larger the scar, the more efficient it was

55
Q

What group of individuals are recommended to get the BCG vaccine?

A

Individuals with high risk to exposure of TB

56
Q

Leprosy

A

Chronic disease cause by M. leprae
* Sometimes called Hansen’s disease

57
Q

Leprosy
* Progression time
* Damage
* Prevalence

A
  • Very slow progression (incubation period of ~5 years)
  • Permanent damage to skin, nerves, limbs and eyes
  • Very rare in high-income countries
58
Q

How many people are permanently disabled by leprosy?

A

~2 million
* Mainly in tropical developing countries
* May be a low estimate

59
Q

Mycobacterium leprae
* Gram stain
* Shape
* Envelope

A
  • “Gram positive” acid fast stain
  • Rod shaped
  • Waxy cell envelope (mycolic acid)
60
Q

Why is M. leprae less well-studied than M. tuberculosis?

A

Cannot be cultivated in vitro

61
Q

What cells does M. leprae infect?

A
  • Macrophages of skin
  • Schwann cells in nerves
62
Q

How can M. leprae be grown?

A
  1. Grown in foot pads of mice (low numbers)
  2. Systemic infection in armadillo (10^10 organisms per gram of infected tissue)
63
Q

Leprosy vs. Tuberculosis

A
  • Lesions in tuberculosis are “hidden” (internal)
  • Lesions in leprosy are “visible” (external)

Leprosy is much less infectious than TB

64
Q

What has happened to victims of leprosy historically?

A

Ostracized
* Rejected by family and friends
* Driven out of communities

65
Q

What are the two major forms of Leprosy?

A
  1. Tuberculoid
  2. Lepromatous
66
Q

Tuberculoid Leprosy
* Characteristics
* Signs/symptoms

A
  • Cell-mediated immunity present
  • Light coloureed lesions with “anesthetic” areas
  • Sometimes loss of hair and pigmentation
67
Q

In Tuberculoid Leprosy:

Do macrophages contain the bacteria?

A

Yes they can

68
Q

What result do tuberculoid leprosy patients have on the tuberculin test?

A

Patients become tuberculin positive

69
Q

Are bacterial cells recoverable from lesions in Tuberculoid Leprosy?

A

Generally not

70
Q

What does it mean that Tuberculoid Leprosy is a self-limiting disease?

A

It can resolve on its own

71
Q

Lepromatous Leprosy
* Characteristics
* Signs/symptoms

A
  • Cell mediated immune responses are absent
  • Nerve damage, loss of sensation, traumatic lesions
  • Loss of eyebrows, thickening and enlarge nares, ears and cheeks
  • Lesions can become secondarily infected, eventually resulting bone resorption, disfigurements and mutilation
72
Q

What are Schwann cells?

A

Provide myelin insulation to peripheral nerves

73
Q

Macrophages
* Lepromatous vs Tuberculoid Leprosy

A

Lepromatous:
* Macrophages are not activated

Tuberculoid:
* Macrophages are activated

74
Q

What happens to bacteria in macrophages in Lepromatous Leprosy?

A

M. leprae survives and multiplies in macrophages and Schwann cells

75
Q

Does the bacteria attack and damage Schwann cells in Lepromatous leprosy?

A

No, the bacteria guides the macrophages to self-harm the Schwann cells

76
Q

How is leprosy spread and transmitted?

A

Not well understood
* Requires close and direct contact for extended periods of time
* Most exposed individuals do not develop disease, thus host genetics likely plays an important role

77
Q

What has been the treatment for Leprosy?

A

MDT (multidrug therapy) since 1980s
* Uses 3 antibiotics
* 6 months to 1 year

78
Q

True or False:

Patients can still transmit leprosy after one dose of MDT

A

False, patients are thought to no longer transmit the disease after one dose

79
Q

What is the ultimate goal of MDT?

A

Elimination of leprosy

My Packs: (UWO) (MICROIMM 2500) (30 decks)

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