Mycobactreria Flashcards

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1
Q

Leprosy is also called

A

Hansen disease

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2
Q

Leprosy (Hansen disease) is caused by

A

Mycobacterium leprae

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3
Q

Mycobacterium leprae - stracture

A

acid-fast bacillus

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4
Q

Mycobacterium leprae - reservoir in US

A

amradilos

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5
Q

Mycobacterium leprae - area of infection

A

it likes cool temperatures (infect skin and superficial nerves - glove and stocking loss of sensation

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6
Q

Mycobacterium leprae - in vitro

A

cannot grow

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7
Q

Leprosy (Hansen disease) - how many forms and which

A
  1. Lepromatous

2. Tuberciloid

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8
Q

Leprosy (Hansen disease) - lepromatous form - clinical manifestation

A

presents diffusely over the skin, with leonine (lion-like) facies, and is communicable

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9
Q

Leprosy (Hansen disease) - lepromatous form - immune system

A

low cell-mediated immunity with humoral Th2 response

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10
Q

Leprosy (Hansen disease) - Tuberciloid form - clinical manifestation

A

limited to few hypoesthetic. hairless skin plaques

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11
Q

Leprosy (Hansen disease) - Tuberciloid form - immune system

A

high cell-mediated immunity with a largely Th1 type response response

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12
Q

Leprosy (Hansen disease) - Treatment

A

dapsone with rifampin for tuberciloid dorm

clofazimin is added n lepromatous form

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13
Q

primary tuberculosis is caused by

A

infection with Mycobacterium tuberculosis of a Nonimmune host (usually host) (infection of previous unexposed individual)

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14
Q

secondary tuberculosis is caused by

A
  1. reinfection (infection with Mycobacterium tuberculosis of a partially immune hypersensitized host - usually adult)
  2. Reactivation due to immunosuppression
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15
Q

primary tuberculosis - lesion

A

Ghon complex: Hilar nodes + Ghon focus (calcified TB granuloma forming a nodule) usually in lower to middle lung

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16
Q

secondary tuberculosis after reactivation - lesion

A

fibrocaseous cavitary lesion (usually upper lobes)

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17
Q

Primary tuberulosis may lead to

A
  1. heals by fibrosis (immunity and hypersensitivity/PPD+)
  2. progressive lung disease (hiv/malnutrition)
  3. Miliary tuberulosis –> Death
  4. Preallergic lymphatic or hematogenous dissemination (dormant tubercle bacilli in several organs/reactivation in adult life)
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18
Q

Extrapulmonary tuberculosis - sites?

A
  1. CNS (parencymal tuberculoma or meningitis)
  2. Vertebral body (Pott disease)
  3. Lymphadenitis
  4. Renal
  5. GI
  6. Adrenals
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19
Q

Reactivation of tuberculosis in the lung lead to

A
  1. secodary tuberculosis fibrocaseous cavitary lesion (usually upper lobes)
  2. extrapulmonary tuberculosis
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20
Q

TB - primary tuberculosis occurs most commonly in

TB - secondary tuberculosis occurs most commonly in

A

1ry: children
2ry: adults

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21
Q

priamry tuberculosis - next step (and proportions)

A
  1. healing by fibrosis calcification (more than 90%)

2. Progressive 1ry tuberculosis esp on AIDS, malnutrition (less than 10%

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22
Q

Pott disease

A

tb in vertebral body

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23
Q

CNS TB?

A

parencymal tuberculoma or meningitis

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24
Q

TB - PDD positive if

A
  1. current infection or past exposure

2. false positive with BCG vaccination (further workup required)

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25
Q

TB - PDD negative if

A
  1. no infection
  2. anergic (steroids, malnutrition, immunocompromised)
  3. sarcoidosis
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26
Q

tests to diagnose TB

A
  1. PPD

2. Interferon-γ release assays (IGRA)

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27
Q

PPD vs Interferon-γ release assays (IGRA)

A

IGRA has fewer false positives from BCG vaccination

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28
Q

Mycobacteria - bugs?

A
  1. Mycobacterium tuberculosis
  2. Mycobacterium avium-intracellulare
  3. Mycobacterium scrofulaceum
  4. Mycobacterium marinum
  5. Mycobacterium leprae
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29
Q

Mycobacterium tuberculosis - clinical manifestation

A

TB - fever, night sweats, weight loss, cough (non-productive or productive), hemoptysis

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30
Q

TB - cough - non-productive or productive?

A

both

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31
Q

Mycobacterium avium-intracellulare - causes

A

disseminated non-TB disease in AIDS

32
Q

Mycobacterium avium-intracellularee - prophylaxis

A

azithromycin when CD+ cound under 50

or rifabutin

33
Q

Mycobacterium scrofulaceum causes

A

cervical lymphadenitis in children

34
Q

Mycobacterium marinum causes

A

hand infection in aquarium handlers

35
Q

Cord factor is found in

A

the cell wall of Mycobacterium (in virulent stains) –> creates a “serpentine cord” appearance in virulent M. tuberculosis

36
Q

Cord factor - function

A

inhibits macrphage maturation and induces releases of TNF-α

37
Q

Mycobacterium - Sulfatides?

A

surface glycolipids inhibit phagolysosomal fusion

38
Q

Mycobacteria - bugs and diseases

A
  1. Mycobacterium tuberculosis –> TB
  2. Mycobacterium avium-intracellulare –> disseminated non-TB disease in AIDS
  3. Mycobacterium scrofulaceum –> cervical lymphadenitis in children
  4. Mycobacterium marinum –> hand infection in aquarium handlers
  5. Mycobacterium leprae –> Leprosy (Hansen disease)
39
Q

Ziehl-Neelsen (carbol fuschin) stains

A

Acid-Fast bacteria (Nocardia, Mycobaceria) and protozoa (Cryptosporidium oocysts)

40
Q

mycobacteria - special characteristic of the structure (and clinical relevance)

A

cell wall are high in mycolic acid - detected by carbolfuchin in acid-fast stain

41
Q

Special culture requirements - Mycobabterium Tuberculosis - media?

A

Lowenstein-Jensen agar

42
Q

M. tuberculosis - prophylaxis and treatment

A

prophylaxis: isoniziad
treatment: 1. rifampin 2. Isoniazid 3. Pyrazinamide 4. Ethambutol (RIPE)

43
Q

M. intracellulare-avium - prophylaxis and treatment

A

prophylaxis: azithromycin, rifabutin
treatment: Azithromycin or clarithromycin + ethambutol
Can add rifabutin or ciprofroloxacin

44
Q

M leprae - prophylaxis and treatment

A

prophylaxis: N/A
treatment: Long-term treatment with dapsone and rifampin for tubrrculoid form. Add clofazimine for Lepromatous form

45
Q

Antimycobacterial drugs - groups and drugs

A
  1. Mycolic acid synthesis –> isoniazid
  2. Arabinoglycan synthesis (Arabinosyl tranferase) –> ethambutol
  3. mRNA synthesis (DNA-dependent RNA polymerase) –> Rifamycins (rifabutin, rifampin)
  4. Intracellular (unclear mechanism) –> pyrazinamide
  5. streptomycin
46
Q

mycobacterial cell is composed by - from outer to inner

A

outer - acyl lipids, complex free lipids - mycolic acid - arabynogalactan - peptidoglycan - inner

47
Q

Rifamycins - drugs and mechanism of action

A

Rifampin, rifabutin

inhibit DNA-dependent RNA polymerase

48
Q

Rifamycins - drugs and clinical use

A

Rifampin, rifabutin

  1. Mycobacterium tuberculosis treatment
  2. Leprosy: delay resistance to dapsone
  3. Meningicoccal prophylaxis
  4. Chemoprophylaxis in contacts of children with H. influenzae type B
  5. Can add in M. Avium-intracellulare (rifabutin)
  6. M. Avium-intracellulare prophylaxis
49
Q

Rifamycins - action on leprosy

A

delay resistance to dapsone

50
Q

Rifamycins - toxicity

A
  1. Minor hepatotoxicity
  2. Drug interactions (increases cytochrome P-450) - esp rifampin
  3. orange body fluids (nonhazardous side effect)
51
Q

Rifamycins - drugs interaction by

A

increases cytochrome P-450 - esp rifampin

52
Q

Rifamycins - HIV

A

RIfabutin favored over rifampin in HIV patients due to LESS cytochrome P-450 stimulation

53
Q

Rifampin vs rifabutin according to side effects

A

Rifampin increases P450 much more than Rifabutin

54
Q

Rifamycins - resistance

A

mutation reduce drug binding to RNA polymerase

–> monotherapy leads to resistance

55
Q

Isonizid (INH) - mechanism of action / aka

A

Bacterial catalase peroxidase (encoded by KatG) needed to convert Isonizid (INH) to active metabolite –> decreases synthesis of mycolic acid. aka: INH

56
Q

what is needed to convert Isonizid (INH) to active metabolite

A

Bacterial catalase peroxidase (encoded by KatG)

57
Q

Isonizid (INH) - clinical use

A
  1. Mycobaterium tuberculosis prophylaxis

2. Mycobaterium tuberculosis treatment

58
Q

Isonizid (INH) - resistance

A

Mutation leading to underexpression of KatG (bacterial catalase peroxidase)

59
Q

bacterial catalase peroxidose is encoded by

A

KatG

60
Q

Isonizid (INH) - toxicity

A
  1. hepatotoxicity
  2. P-450 inhibition
  3. drug induced SLE
  4. vitamin 6 - pyridoxine (B6) deficiency (–> peripheral neuropathy, siderblastic anemia)
61
Q

Isonizid (INH) - solution of toxicity

A

vitamine 6 (Pyridoxine) can prevent neurotoxicity and anemia

62
Q

Isoniazid - half-lives

A

different Isonizid (INH) half-lives in fast vs slow acetyators

63
Q

Pyrazinamide - mechanism

A

mechanism uncertain
Pyrazinamide is a prodrug that is converted to tha active compound pyrazinoic acid
WORKS BEST at acidic ph (eg. in host phagolysosomes)

64
Q

Pyrazinamide - active compound

A

pyrazinoic acid

65
Q

Pyrazinamide - clinical use

A

treatment of Mycobacterium Tuberculosis

66
Q

Pyrazinamide - toxicity

A
  1. hyperuricemia

2. hepatotoxicity

67
Q

Ethambutol - mechanism of action

A

decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltranferase

68
Q

Ethambutol - clinical use

A
  1. treatment of Mycobacterium Tuberculosis

2. treatment of Mycobacterium acium-intracellulare

69
Q

Ethambutol - toxicity

A

Optic neuropathy (red green color blindness)

70
Q

M. tuberculosis and M.avium-intracellulare - prophylaxis and prevention

A

M. TUBERCULOSIS:
prophylaxis: isonizid
treatment: 1. rifampin 2. Isoniazid 3. Pyrazinamide 4. Ethambutol (RIPE)
M. avium-intracellulae
prophylaxis: azithromycin, rifabutin
treatment: Azithromycin or clarithromycin + ethambutol
Can add rifabutin or ciprofroloxacin

71
Q

M leprae - prophylaxis and treatment

A

prophylaxis: N/A
treatment: Long-term treatment with dapsone and rifampin for tubrrculoid form. Add clofazimine for Lepromatous form

72
Q

TB - PDD positive if

A
  1. current infection or past exposure

2. false positive with BCG vaccination (further workup required)

73
Q

TB - PDD negative if

A
  1. no infection
  2. anergic (steroids, malnutrition, immunocompromised)
  3. sarcoidosis
74
Q

Streptomycin - mechanism of action

A

inerferes with 30S compoment of ribosome

75
Q

Streptomycin - clinical use

A

M. tuberculosis

76
Q

Streptomycin - adverse effects

A
  1. Tinnitus
  2. Vertigo
  3. ataxia
  4. nephrotoxicity