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Microimm 2500 > Tuberculosis and Leprosy > Flashcards

Tuberculosis and Leprosy Flashcards

1
Q

What type of bacteria is the cause of tuberculosis and leprosy?

A

mycobacteria

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2
Q

M. tuberculosis

A
  • causative agent of tuberculosis in humans

- often called TB (tubercle bacilli)

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3
Q

M.bovis

A
  • causes tuberculosis in cows, rarely in humans

- humans can be infected by the consumption of unpasteurized milk leading to extrapulmonary TB

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4
Q

M. avium

A
  • can cause tuberculosis-like illness in humans, particularly in AIDS patients
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5
Q

M. leprae

A

causative agent of leprosy in humans

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6
Q

What fraction of the world is affected with latent TB?

A
  • 1/4 (carrier to the disease)
  • 5-10% of these people with develop active TB in their lifetime
  • greater rates in countries without access to medical care/treatment
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7
Q

How does TB spread?

A

through the air; if not treated, each person with active TB can infect 10-15 people a year

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8
Q

What is the leading killer among people living with HIV?

A

TB

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9
Q

The pathogen: Mycobacterium tuberculosis

A
  • isolated by Robert Koch in 1882
  • intracellular pathogen (lives inside macrophages)
  • can be grown in the lab on specialized media but takes 4-6 weeks to get small colonies
  • slow generation time of > 15hrs
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10
Q

Mycobacterium tuberculosis - what is the cell wall made of?

A
  • have unusual cell envelope with high concentrations of mycolic acid - “waxy”
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11
Q

What is the cell wall of M.tuberculosis resistant to?

A
  • many antibiotics
  • killing by acidic and alkaline compounds
  • osmotic lysis via complement deposition
  • lethal oxidative stress promoting survival inside of macrophages
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12
Q

Why is the Acid Fast stain used for mycobacteria?

A

the waxy, lipid-rich cell envelope (very hydrophobic) resists common strains (Gram

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13
Q

Acid Fast Stain

A
  • stained with carbol-fuchsin dye with slow heating (to melt the wax)
  • washed with EtOH and HCl
  • counter stained with methylene blue
  • acid-fast organisms appear red whereas non-acid fast organisms appear blue
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14
Q

Acid-fastness is due to the presence of ____?

A

mycolic acid

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15
Q

Stage 1 of Tuberculosis

A
  • transmission from inhalation of droplets from an infected host, usually by coughing or sneezing
  • coughing/sneezing can generate 3000 droplet nuclei; droplet nuclei contain ~3 bacteria
  • small diameter droplets can stay airborne for extended periods of time
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16
Q

T/F: Latent TB can still be transmitted.

A

FALSE - only active TB can be transmitted

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17
Q

Stage 2 of Tuberculosis

A
  • begins 7-21 days after initial exposure
  • phagocytosis of TB cells by lung (alveolar) macrophages
  • TB inhibits the fusion of the lysosome to the phagosome and can multiply in macrophages
  • macrophages will lyse and release TB cells to infect more macrophages
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18
Q

What is a key virulence property of M. Tuberculosis?

A

the ability to survive within the host macrophage

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19
Q

Stage 3 of Tuberculosis

A
  • infected macrophages may form granulomas
  • TB granulomas are “tubercles” of immune cells that try to destroy invading pathogens (typically formed by macrophages)
  • the granuloma represents a “balance” between the pathogen and the host (latent infection)
  • T cell activated macrophages can kill TB
  • activated T cells can secrete cytokines (IFN-gamma) to activate the macrophages
  • macrophages at the center of the granuloma remain harder to activate by T cells
  • chronic inflammation cause “cheese-like” necrosis caseous necrosis
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20
Q

Stage 4 of Tuberculosis

A
  • some macrophages remain unactivated and infected
  • the tubercle grows
  • erosion of the granuloma into the airway provides the route of transmission
  • deterioration of host immunity can result in a life threatening infection (active tuberculosis)
  • the caseous centre can liquefy leading to cavitation
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21
Q

Pulmonary Tuberculosis

A
  • 75%
  • progressive, irreversible lung destruction can occur, and the bacteria may enter the bloodstream
  • it is thought that a single inhaled bacterium can infect
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22
Q

Extra pulmonary tuberculosis

A
  • more likely to occur in immunocompromised individuals
    can infect: bone, joints, liver, spleen, gastrointestinal tract and brain
  • systemic spread, called miliary tuberculosis, is almost always fatal
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23
Q

What percent of TB infected people develop the active disease?

A

5-10%

24
Q

What are the Symptoms of Tuberculosis

A
  • often non specific
  • a prolonged (> 2 weeks) cough with thick and possibly blood in mucus
  • fever, chills, night sweats
  • fatigue and weakness
  • chest pain and shortness of breath
  • loss of appetite and weight loss (“consumption”)
  • pallor, meaning pastiness or pale skin (“the white death”)
  • extra pulmonary depends on where TB has spread
25
Q

Testing and Diagnosis of TB

A
  • tuberculin test (PPD = purified protein derivative from M. tuberculosis)
  • T cell mediated response
  • positive test result is a red swollen circle at 48 hr
  • a person is considered infected if the CONVERT from negative to positive on a TB sin test
26
Q

What could a negative result in a TB test mean?

A
  • not infected
  • immune compromised (e.g. AIDs)
  • not infected long enough
27
Q

What could a positive result in a TB test mean?

A
  • latent or active TB
  • BCG vaccinated
  • previously infected
28
Q

What would happen if you got a positive TB skin test?

A
  • careful history and chest X-ray
  • X-ray: typical upper lobe “shadowing” = lesions
  • calcified granulomas may be seen on an X-ray
  • staining of sputum for acid fast bacilli and culturing
29
Q

What are the hallmark of TB?

A

Lesions

30
Q

Treatment of TB

A
  • if untreated, active TB kills 2/3 of people
  • six months of antibiotics for short treatment (slow growth means long treatments)
  • multiple types of antibiotics are used
31
Q

What does the antibiotic Rifampin do?

A

inhibits RNA polymerase

32
Q

What does the antibiotic Isoniazid do?

A

inhibits mycolic acid synthesis

33
Q

Why do you give two or more drugs for the treatment of TB?

A

if you have bacterial cells resistant to one, you have a backup to kill the others.

34
Q

Multi-Drug Resistant TB

A

being resistant to the two most effective first-line therapeutic drugs, isoniazid and rifampib

35
Q

Extensively-Drug Resistant TB

A
  • also resistant to the most effective SECOND-line drugs commonly used to treat MDR-TB
  • found in all regions of the world
  • strains have be virtually untreatable
36
Q

Spectinamides

A
  • chemically modified from spectinomycin
  • narrow spectrum = high specificity for TB
  • not pumped out of TB cells
  • low toxicity for host cells
  • works in mice
  • presents antibiotic from being pumped out from bacteria
  • inhibits the ribosomes but doesn’t get pumped out of transporter
37
Q

“bacille Calmette-Guerin” (BCG)

A
  • a living vaccine prepared from attenuated M. bovis
  • BCG shares antigenicity with TB
  • controversial due to variable efficacy (~80% or much less for pulmonary TB)
  • effective against miliary TB
  • vaccinated individuals get a false positive for the tuberculin test
  • vaccination leaves large scars
  • recommended for individuals with high risk to exposure
38
Q

Tuberculosis and HIV/AIDS

A
  • Individuals infected with HIV are ~25-times more likely to develop active tuberculosis
  • One third of the persons living with HIV infection are co-infected with TB
  • TB is a leading killer of HIV-positive people
    ~ 400,000 deaths per year are HIV/TB coinfections
39
Q

What bacteria causes leprosy?

A

Mycobacterium leprae

40
Q

what is another name for leprosy?

A

Hansen’s disease

41
Q

What type of progression (slow/fast) does leprosy have?

A

slow - incubation period ~ 5years (if exposed to the bacteria, takes this long to develop the disease)

42
Q

Where can leprosy cause damage?

A

permanent damage to skin, nerves, limbs, and eyes

43
Q

T/F: Leprosy is very rare in developed countries

A

True

44
Q

Approximately how many people are permanently disable by leprosy?

A

2 million

45
Q

Describe M. leprae

A
  • gram positive acid fast
  • rod shaped
  • waxy cell envelope (mycolic acid)
  • cannot be cultivated in vitro (less well-studied than M.tuberculosis)
  • can grow in food pads of mice (low numbers)
  • causes systemic infection in the armadillo
46
Q

What part of the body does M. leprae infect?

A

macrophages of skin and Schwann cells in nerves

47
Q

Stigma around leprosy

A
  • victims have been ostracized
  • lesions of leprosy are visible whereas in tuberculosis they are hidden
  • BUT, leprosy is much less infectious than TB
48
Q

Is leprosy just as, less, or more infectious than TB?

A

less

49
Q

What are the two major forms of leprosy?

A

Tuberculoid and Lepromatous

50
Q

Tuberculoid Leprosy

A
  • cell-mediated immunity present
  • macrophage can contain the bacteria
  • light coloured lesions with “anesthetic” areas
    sometimes loss of hair and pigmentation
  • patients become tuberculin positive (active T cell-mediated responses)
  • bacterial cells are generally not recoverable from lesions
  • Tuberculoid Leprosy can be self-limiting
51
Q

Lepromatous Leprosy

A
  • cell-mediated immune responses are absent
  • macrophages are not activated
  • M. leprae survives and multiples in macrophages and Schwann cells
  • Schwann cells provide myelin insulation to peripheral nerves
  • due to nerve damage and loss of sensation leads to inadvertent traumatic lesions on the face and extremities
  • can cause loss of eyebrows, thickening and enlarged nares, ears and cheeks “lion like” appearance
  • lesions can become secondarily infected, eventually resulting in bone resorption, disfigurements and mutilation
52
Q

Spread and Progression of Leprosy

A
  • transmission is not well understood
  • probably close (direct) contact for extended periods of time - inhaled droplets?
  • most exposed individuals do not develop disease – host genetics likely plays an important role
53
Q

Treatment of Leprosy

A
  • highly treatable with antibiotics
  • multiple drugs are used (6 months to 1 year)
  • patients no longer transmit the disease after one dose of MDT
54
Q

What drugs consist of MDT and when was it introduced?

A

1980s

- dapsone, rifampin, clofazimine

55
Q

What drug was used to treat leprosy in the 1940s and why was it stopped?

A

dapsone, but resistance developed in the 1960s

Microimm 2500 (8 decks)

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