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microbiology > mycobacteria > Flashcards

mycobacteria Flashcards

1
Q

mycobacteria gram

A

positive, weakly

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2
Q

mycobacteria acid of cell wall

A

mycolic acid

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3
Q

mycobacteria cell growth and O2 use

A 
Facultative intracellular growth (in macrophages)
Obligate aerobe (growth in lung macrophages)
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4
Q

reservoir/ transmission for mycobacteria

A
  • Humans are reservoir

* airborne transmission (as few as 10 cells can result in infection)

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5
Q

growth rates of pathogenic mycobacteria

A

slow

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6
Q

Acid-fast stain

A

used with mycobacteria

use of hot carbol fucshin to adhere to mycolic acid, stains red

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7
Q

important components/ virulence factors of mycobacteria cell wall

A

mycolic acid
cord factor
arabinogalactan
lipoarabinomanan

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8
Q

mycolic acid and cord factor of cell wall
results in?
correlated with?

A

Cord-like growth results from adherence of cell surface lipid mycolic acids and glyco-lipids

Slow, cord-like growth strongly correlates with virulence.

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9
Q

Virulence of M.tuberculosis and M.leprae due to?

A

virulence results from the challenge that they provide to the immune response (typically DTH: CD4+ T-cells + macrophages) because (in most cases) the disease is caused by the immune response, NOT by the mycobacteria.

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10
Q

Virulence Factors of M.tuberculosis and M.leprae

A 
Facultative intracellular growth in macrophages 
mycosides 
sulfatides 
cord factor 
adenylate cyclase 
arabinogalactan/ lipoarabinomannan 
mycolic acid
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11
Q

CMI to Mycobacterium tuberculosis; granuloma

A

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

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12
Q

mycobacterium tuberculosis: life long?

A

Mycobacterium tuberculosis is a “life-long” pathogen: once infected, you may be asymptomatic but never cured

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13
Q

o Mycobacterium tuberculosis tranmission

A

aerosols

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14
Q

Effective CMI to M.tuberculosis capable of?

exception?

A

Effective CMI is capable of localizing and stopping infection by M.tuberculosis. Chronic TB is typical.

Exception: young children under 5 years have a high risk for developing progressive TB due to insufficient immune system development/activation.

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15
Q

OUTCOMES of untreated primary TB [results for non-immune-compromised patents]:

A
  • 91% no disease
  • 6% clinical TB (2% pulmonary + 3% extrathoracic + 1% both)
  • 3% progressive systemic disease and death
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16
Q

secondary tuberculosis

A

reemergence after primary infection
However, acute (‘open’) TB [also known as “secondary tuberculosis” or in older terms “galloping consumption” caused by “endogenous reactivation” of prior infection - while rare (life-time risk is assessed as <12% for carriers, or less) it is VERY contagious!
Isolation of acute TB cases is mandatory.
Endogenous reactivation is stimulated by stress, malnutrition and HIV

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17
Q

tuberculosis disease/ symptoms arise from?

A

Actually, the “disease” (except for the infection risk of “Open TB”) arises from tissue destruction by our immune defenses and not by damage caused by the bacterial infection.

The repeated attempts to remove foci of infection by lung macrophages cause the granulomatous lung tissue that impairs lung function.

Breathing impairment in TB is not due to tuberculosis bacilli but by the macrophage-induced tissue destruction

18
Q

Mantoux Reaction

A

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

Positive test: >10 mm redness
Strongly positive: >20mm red

19
Q

Vaccination to mycobacterium

A

Exposure to living attenuated mycobacterium, known as Bacille Calmette-Guérin (BCG), a
derivative of M.bovis (which may be identical to M.tuberculosis based on whole genome sequencing):
• little virulence in humans (but infectious in immune-compromised persons)
• some protective immunity (when given to young children)
• BCG vaccination is discouraged in USA because it gives a positive tuberculin test, thus removing an important diagnostic screening tool. (And M.bovis causes disease in immune-compromised persons.)

20
Q

TB opportunistic?
recent increase
overall decrease

A

opportunistic disease

HIV infections, with its Acquired Immune Deficiency Syndrome (AIDS),
has caused a recent increase.

Better living standards, with help of the BCG vaccine and antibiotic protocols, have
reduced TB death rates dramatically

21
Q

main Treatment for TB

A

isoniazid: block mycolic acid synthesis

22
Q

Mycobacterium leprae: diverse CMI responses

A

diversity of responses can determine prognosis

effective CMI: healthy

Th1 response: tuberculoid, macrophages kill nerves; macules and plaques without sensation, good prognosis, not contagious

Loss of CMI (or TH2-response, CTL lysis and loss of tissue, including nerves): lepromatous, bad prognosis/ highly contagious

23
Q

Mycobacterium leprae intra or extracellular?

preferred target?

A

M.leprae is an obligate intracellular pathogen

Peripheral nerves are preferred target tissue for infection and cytolysis

24
Q

Histology: tuberculoid vs lepramatous leprosy

A

more growth of cells in lepramatous leprosy

25
Q

Tuberculoid plaque

A

Tuberculoid plaque: without sensation, resulting from macrophage action after TH1 cytokine (IFNg) activation

good prognosis

26
Q

Lepromatous Leprosy

A

TH2 Leprosy:
• cytokine (IL4) activation of CTL tissue lysis

bad prognosis

27
Q

leprosy treatments

A

Multidrug therapy: Dapsone + rifampin + clofazimine

Rising resistance is becoming a problem

28
Q 
TH1 (tuberculoid) vs TH2 (leprosy) M.leprae responses
bacteria level?
infectivity? 
T response? 
IgG? 
Ig level?
A 
Tuberculoid granuloma
• no or few bacteria
• low infectivity
• Ag-specific TH1
• no Ag-spec IgG
• normal Ig level
Leprosy
• many bacteria inside macrophages
• high infectivity
• extensive tissue damage
• no T-response to Ag
• sometimes Ag-spec IgG
• hyper-Ig level
29
Q

M.tuberculosis main virulence factor

A

Ability to survive and live in lung macrophages

30
Q

M.tuberculosis clinical presentation

A

pulmonary (and
extrapulmonary)
tuberculosis

31
Q

M.tuberculosis treatment/ length

A

multidrug therapy

6-12 months

32
Q

M.tuberculosis epidemiology

A

Aerosol
(person-to-person) All ages
Highest risk if immune compromised (HIV)

33
Q

M.leprae main virulence factor

A

survival in macrophages

34
Q

M.leprae clinical presentation

A

tuberculoid-tolepramatous

leprosy

35
Q

M.leprae treatment/length

A

mutli drug

2 years

36
Q

m. leprae epidemiology

A

contact dependent

37
Q

All pathogenic mycobacterial species growth rates

A

All pathogenic mycobacterial species have (very) slow growth rates

38
Q

Nocardia gram

A

Gram+ (poor staining)

39
Q

Nocardia acid fast

A

mycolic acid in cell wall: “partially acid-fast”

Test to distinguish Nocardia from fungal look-alikes

40
Q

Nocardia as a pathogen

A

Opportunistic pathogen in immuno-compromised patients

41
Q

Nocardia virulence factors
main action?
which spp?

A

Antiphagocytic Virulence Factors of strictly aerobic Nocardia sp

catalase 
superoxide dimutase 
cord factor
prevent lysosomal acidification
slow growth
42
Q

Nocardia clinical presentation

A

bronchopulomanry
cutaneous infections
brain abcesses

microbiology (42 decks)

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