Bacteria- Ch23 Mycobacteria Flashcards

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1
Q

what is in the cell wall of mycobacteria

A

mycolic acids

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2
Q

describe the type of microbe mycobacteria is

A
  • gram positive
  • weak staining: use acid fast stain or specific fluorescent detection
  • facultative intracellular growth in macrophages
    -obligate aerobe
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3
Q

how is mycobacteria transferred

A

airborne- as few as 10 cells can result in infection

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4
Q

what are reservoirs for mycobacteria

A

humans

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5
Q

describe an acid fast stain

A

hot carbol fuchsin

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6
Q

describe the mycobacterial cell wall structure

A

cord factor- glycolipid

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7
Q

what are virulence factors for mycobacteria

A

-structural mycobacterial cell wall components- mycolic acid moiety
-inhibition of phagolysosome fusion

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8
Q

what does mycolic acid slow cord like growth result from

A

adherence of cell surface lipid mycolic acids and glycolipids

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9
Q

what does the virulence of mycobacteria result from

A

they provide a challenge to the immune response such as CD4+ T cells and macrophages because the disease is caused by the immune response not by the mycobacteria itself

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10
Q

what potentiates cord factor effects

A

sulfatides

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11
Q

how long does mycobacteria last in the body

A

lifelong, once infected you may be asymptomatic but never cured

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12
Q

what does a CMI to mycobacterium tuberculosis look like

A

TB granuloma surrounded by puncate nuclei of lung tissue and inflammatory leukocytes. central area of necrosis where nuclei have been destroyed

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13
Q

effective CMI is capable of _________ infection by M tuberculosis

A

localizing and stopping

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14
Q

what is the typical result of aerosol transmission of mycobacterium tuberculosis

A

chronic TB

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15
Q

what is the exception to aerosol transmission to mycobacterium tuberculosis

A

young children under 5 have a high risk for developing progressive TB due to insufficient immune system development

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16
Q

what are the outcomes of untreated TB

A

-91% no disease
-6% clinical TB (2% pulmonary + 3% extrathoracic + 1% both)
- 3% progressive systemic disease and death

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17
Q

what is another name for acute TB and what is it caused by

A

secondary tuberculosis or galloping consumption caused by endogenous reactivation of prior infection

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18
Q

what is endogenous reactivation of acute TB stimulated by

A

stress, malnutrition and HIV

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19
Q

what does the disease of mycobacterium tuberculosis arise from

A

tissue destruction by our immune defenses and not by damage caused by the bacterial infection

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20
Q

what causes impaired lung function in mycobacterium tuberculosis infections

A

the repeated attempts to remove foci of infection by lung macrophages cause the granulomatous lung tissue

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21
Q

what is breathing impairment in TB due to

A

the macrophage induced tissue destruction

22
Q

what is the mantoux reaction

A

a positive tuberculin test to subdermal PPD (processed protein derivative of the cell wall of the opportunistic intracellular pathogen mycobacterial tuberculosis)

23
Q

what is a positive test and strongly positive test in the mantoux reaction

A

-positive test: >10 mm redness
- strongly positive: >20 mm red

24
Q

what is the vaccination for mycobacteria

A

exposure to living attenuated mycobacterium, known as bacille calmette guerin (BCG) a derivative of M bovis

25
Q

what type of vaccine is BCG vaccine

A
  • little virulence in humans (infectious in immune compromised people)
  • some protective immunity ( when given to young children)
26
Q

why is BCG vaccination discouraged in the USA

A

because it gives a positive tuberculin test, thus removing an important diagnostic screening tool

27
Q

what type of disease is TB

A

opportunistic

28
Q

what has caused a recent increase in TB

A

HIV and AIDS

29
Q

what is the number for world wide latent M tuberculosis infections

A

~ 2 billion
-USA: 13 million

30
Q

what is the number for world wide TB deaths

A

~ 1.6 million/ year
-USA: 500

31
Q

what are the treatments for TB

A

isoniazid

32
Q

what are the preferred targets for mycobacterium leprae

A

peripheral nerves

33
Q

what happens in a Th1 response to mycobacterium leprae

A

-tuberculoid
-macrophages kill nerves
-macules and plaques without sensation
-good prognosis for recovery not infectious

34
Q

what happens in a lepromatous infection

A

bad prognosis for recovery
-highly infectious

35
Q

what happens in loss of CMI to mycobacterium leprae and what is this type of response called

A

-CTL lysis and loss of tissue including nerves
- AKA Th2 response

36
Q

what do histology slides of m leprae look like

A

beaded acid fast rods

37
Q

describe a tuberculoid plaque

A

without sensations, resulting from macrophage action after TH1 cytokine (IFNgamma activation)

38
Q

what happens in Th2 leprosy

A

cytokine (IL4) activation of CTL tissue lysis

39
Q

what is the multidrug therapy for tuberculoid and lepromatous leprosy

A

dapsone + rifampin +clofazimine

40
Q

describe tuberculoid granuloma

A
  • no or few bacteria
  • low infectivity
  • ag- specific Th1
  • no Ag specific IgG
  • normal Ig level
41
Q

describe leprosy

A
  • many bacteria inside macrophages
  • high infectivity
  • extensive tissue damage
  • no T- response to Ag
  • sometimes Ag- specific IgG
  • hyper Ig level
42
Q

what are the virulence factors, clinical features, treatment, and epidemiology for M. tuberculosis

A
  • ability to survive and live in lung macrophages
  • pulmonary and extrapulmonary tuberculosis
  • mutlidrug therapy for 6-12 months
  • aerosol, all ages, highest risk if immune compromised such as HIV
43
Q

what are the virulence factors, clinical features, treatment, epidemiology for M. leprae

A

-ability to survive and live in macrophages
- tuberculoid-to- lepramatous leprosy
- multidrug therapy for 2+ years
- close physical contact

44
Q

all pathogenic mycobacterial species have ________ growth rates

A

very slow

45
Q

when is isoniazid used other than mycobacterium infections

A

prophylactically upon conversion to a positive mantoux reaction

46
Q

what does ethambutol do

A

inhibitor of enzymes that synthesize non-mycolic acid cell wall components

47
Q

what does pyrazinamide do (PZA)

A

mechanism of action is unknown

48
Q

what type of microbe is nocardia

A
  • gram positive
  • partially acid fast
  • poor stinaing
  • mycolic acid in cell wall: partially acid fast
49
Q

what is the difference between nocardial mycolic acid and mycobacterial mycolic acid

A

-nocardial: 50-62 x C
- mycobacterial: 70-90 x C

50
Q

what are the virluence factors for nocardia

A

-opportunistic pathogen in immuno compromised patients
- antiphagocytic virulence factors of strictly aerobic nocardia
- intracellular survival and growth
- catalase
- superoxide dismutase

51
Q

what are the clinical features, treatment and epidemiology for nocardia

A
  • bronchopulmonary cutaneous infections and brain abscesses
  • sulfonamides, amikacin, carbapenems, or cephalosporins
  • opportunistic pathogen if pulmonary disease of T deficiency