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Block 4 > HRR: mycobacterial infection > Flashcards

HRR: mycobacterial infection Flashcards

1
Q

What are the general characteristics of mycobacteria?

A

They’re non-motile obligate aerobes that do not form spores. They have complex cell walls with a bunch of peptidoglycans, lipids, and polysaccharides.

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2
Q

What are some lipids found in mycobacteria cell walls?

A

Mycolic acids and lipoarabinomannan.

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3
Q

What does the cell wall do for mycobacteria?

A

Makes them poorly penetrable; they’re like hard balls of wax.

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4
Q

What is the staining property of mycobacteria?

A

Acid fast.

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5
Q

What determines whether a disease develops following human exposure to mycobacteria?

A

The pathogenicity of the species and the person’s immune system.

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6
Q

What is the leading infectious disease killer?

A

TB.

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7
Q

How is TB spread?

A

Person to person.

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8
Q

TB is normally a ___ presentation.

A

Subacute.

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9
Q

Why is TB difficult to treat?

A

It requires multiple months of multiple antibiotics, and may become resistant to antibiotics.

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10
Q

What is the time frame for tuberculosis growth?

A

3-4 weeks in culture.

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11
Q

Tuberculosis is resistant to…

A

Disinfectant and drying.

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12
Q

What is tuberculosis sensitive to?

A

Heat.

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13
Q

What features allow tuberculosis to hang out in the air?

A

Their droplet nuclei are resistant to drying; this is partly a function of their waxiness.

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14
Q

What is the primary manifestation of TB?

A

Pulmonary disease; it often forms cavity lesions in the upper lobe and apical region. These cavities have billions of mycobacteria.

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15
Q

Who is more likely to develop cavities with TB: immunocompetent or immunocompromised?

A

Immunocompetent! The immunocompromised don’t develop the cavities.

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16
Q

What is TB spondylitis?

A

It is typically found in children and causes an anterior wedging of the spine.

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17
Q

Describe TB meningitis.

A

Happens in young kids or the immunocompromised. Can pick off cranial nerves and is highly inflammatory. It is diagnosed by lumbar puncture and imaging.

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18
Q

What is an implication of GU TB?

A

Infertility.

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19
Q

GI TB can mimic which condition?

A

Crohn’s disease.

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20
Q

If someone is infected with TB, what routes are possible?

A

Most people’s immune system can control TB and prevent them from being sick; the TB will remain latent. The other options include progressive primary/early disseminated TB in which the person becomes sick within 1-2 years following exposure, or reactivation TB in which someone gets sick years later.

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21
Q

Describe the process of infection with progressive primary TB.

A
  1. We breathe in bacteria, which then travel to the alveoli and are not killed by macrophage. 2. There is a lack of control by the innate response. 3. The bacteria invade interstitial lung tissue. 4. Dendritic cells transport bacteria to lymph nodes and there is T and B cell recruitment. 5. The acquired immune response is unable to control the infection, and progressive primary TB occurs.
22
Q

Describe the process of controlling TB infection.

A
  1. We breathe in bacteria, which travel to the alveoli and are not killed by macrophages. 2. The innate immune response, T cells, and B cells control the infection within granulomas. 3. You continue with latent infection, unless a lack of control causes reactivation TB.
23
Q

Describe the composition of granulomas in TB.

A

A caseous center of bacteria surrounded by a layer of activated macrophages and an outer layer of T and B cells.

24
Q

What cytokines are important for maintaining granulomas and preventing them from breaking open and causing issues?

A

IFN-gamma, IL-12, TNF-alpha.

25
Q

What are the ways to detect TB?

A

Visualization vs acid fast stain, detection of nucleic acid on PCR, and culture.

26
Q

How do we treat TB?

A
  1. Intensive phase: 2 months of rifampin, isoniazid, pyrazinamide, ethambutol.
  2. Continuation phase: 4 more months of just rifampin and isoniazid.
27
Q

Which TB drug cannot be replaced by another drug and is considered the most important?

A

Rifampin.

28
Q

How does TB drug resistance develop?

A

Spontaneous mutations.

29
Q

Describe the TB skin test.

A

An intradermal injection of antigens that, in a previously sensitized person, sets off a local immune response. If local inflammation is seen it’s indicative of previous sensitization.

30
Q

Describe the cell mediated immunity TB test.

A

Blood cells from a sample are stimulated with antigen and incubated overnight. The quantity of IFN gamma is then detected.

31
Q

Which TB test tells you about the state of disease?

A

Neither!

32
Q

How can we intervene to control TB from a public health standpoint?

A
  1. BCG vaccine prevents infection as well as rapid progression to disease.
  2. Treatment of latent TB can prevent development of active disease.
    1. Early diagnosis and treatment to prevent further infection.
33
Q

Which vaccine is mycobacterium bovis used for?

A

TB.

34
Q

Describe the TB vaccine.

A

A live attenuated vaccine derived from M bovis.

35
Q

What is the target population for the TB vaccine?

A

Young kids; doesn’t really work in adults.

36
Q

What are the 3 treatment regimens for latent TB?

A
  1. 12 weeks of once weekly isoniazid and rifampin.
  2. Rifampin daily for 4 months.
  3. Isoniazid daily for 6-9 months.
37
Q

Where can we cultivate leprosy?

A

Foot pads of mice and armadillos.

38
Q

What is found in the cell wall of mycobacterium leprae?

A

Phenolic glycolipid 1 (PGL1).

39
Q

How is leprosy transmitted?

A

Respiratory droplets from nasal secretion.

40
Q

What are the two forms of leprosy?

A

Lepromatous and tuberculoid.

41
Q

Which form of leprosy is characterized by poor immune function?

A

Lepromatous.

42
Q

Describe the presentation of lepromatous leprosy.

A

Infiltrated skin lesions, mucus membrane ulcers, cartilage destruction, bacteria-laden histiocytes aka foam cells. Just a bunch of bacteria in general.

43
Q

Describe tuberculoid leprosy.

A

Occurs when there is good cell-mediated immunity. There are very few bacteria but lots of inflammation that impacts the nerves and skin. There is granulomatous inflammation of nerve trunks, giant cells, skin lesions.

44
Q

How is leprosy diagnosed?

A

Clinically and confirmed by AFB staining.

45
Q

Describe M kasasii.

A

Slow growing bacteria that presents very similar to TB and does not have person-to-person transmission.

46
Q

Describe M marinum.

A

Slow growing bacteria. It is present in water and causes ‘fish tank granulomas.’ Presents with bluish skin lesions after water exposure that won’t go away.

47
Q

Describe M avium intracellular complex.

A

A slow growing environmental bacterium that can cause pulmonary disease in those with abnormal structure, disseminated disease in HIV, and lymphadenitis in children.

48
Q

Describe M ulcerans.

A

Slow growing bacteria that is associated with contaminated water. It has a lipid toxin called mycolactone that causes necrosis, but it isn’t painful.

49
Q

Describe M fortuitum.

A

A rapid grower that causes skin infections and can be associated with common source exposure such as nail salons.

50
Q

Describe M abscessus.

A

Can cause skin and devastating pulmonary infections in those with structural disease, kids, and those with cystic fibrosis. Hard to treat.

51
Q

Describe M mucogenicum.

A

Catheter associated bloodstream infection and post-traumatic skin lesions.

Block 4 (28 decks)

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