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Micro Exam #2 > Pathogens with Respiratory Transmission > Flashcards

Pathogens with Respiratory Transmission Flashcards

1
Q

Three primary bacteria discussed in this packet

A

Mycobacterium
Mycoplasma
Corynebacterium

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2
Q

Staining used for mycobacterium?

A

Acid-Fast

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3
Q

Describe the growth of mycobacteria?

A 
Very Slow (18hours)
Growth from one pole
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4
Q

Significance of mycobacteria growth time?

A

Culturing is too slow for diagnosis

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5
Q

mycobacterial structure associated with virulence?

A

Serpentine Cord Formation

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6
Q

Describe the mycobacterial cell wall

A

Made with mycolic acids (very hydrophobic

Waxy part of outer layer

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7
Q

Significance of mycolic acids in mycobacterium? (2)

A

Acid-Fastness

Prevents lysozyme or complement attack

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8
Q

What is Freund’s Adjuvant?

A

The waxy part of the outer layer of mycobacteriua

Antigenic

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9
Q

What is LAM? Why do we care?

A

Lipoarabinomannan

Stimulates cytokine production by mammalian host

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10
Q

TB promotes what other disease?

A

HIV

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11
Q

Symptoms of mycobacterium tuberculosis?

A

Fatigue, Fever, Night Sweats, Weight Loss, Hemoptysis

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12
Q

Primary presentation of mycobacterium tuberculosis?

A 
Exudative lesion (edema, inflammation)
Usually Unnoticed
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13
Q

Three potential responses to exudative lesions?

A

Healing
Necrotizes lung
Productive Lesion

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14
Q

A productive lesion will cause a _____ to occur. This can cause these two responses.

A

Granuloma

Encasing or Spreading (via lymph, bronchi, or blood)

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15
Q

Encases granulomas run the risk of

A

Reactivation

Leads to multiple granulomas, fibrination of lung

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16
Q

Mycobacterium tuberculosis spread in the blood can lead to …

A

Miliary TB

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17
Q

What is caseum?

A

Necrotic tissue damaged by inflammatory response and lack of vascularization

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18
Q

Why are caseum especially bad in mycobacterial infection?

A

The hollowed areas they leave behind may allow encapsulated TB to escape

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19
Q

Prevalence of TB?

A

2B people in the world infected (30%)

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20
Q

TB at risk populations in the US? (5)

A 
Minorities and Immigrants
Co-Existing Infection (esp. HIV)
Homeless
Very Young or Old
Travelers in High Risk Areas
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21
Q

How is TB spread?

A

Person-to-Person via respiratory droplets

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22
Q

What does TB do when in the body?

A

Attach to alveolar macrophages and invade
Prevent Phagolysosome fusion
Cytotoxicity from cord factor
Cytokine-mediated inflammation

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23
Q

T or F. TB always presents with primary symptoms of the lungs.

A

False. Rarely primary extrapulmonary symptoms will occur.

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24
Q

Two sites where long term TB retention may occur.

A

Granulomas and Bone Marrow.

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25
Q

Two tests used to detect TB?

A

Mantoux (PPD) Test

QuantiFERON-Gold assay (IGRA)

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26
Q

How does a Mantoux (PPD) Test work?

A

Intradermal Protein Injection

Sensitivity within 72 hours indicates that Tmem cells were present

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27
Q

How does a QuantiFERON-Gold assay work?

A

Tests for releave of IFN-g from peripheral lymphocytes when exposed to TB antigen

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28
Q

Best method of diagnosing TB?

A

PCR

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29
Q

Two ineffective means of diagnosing TB?

A

Culture (too slow)

Acid-fast sputum stain (requires massive inf. to detect)

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30
Q

What does a IGRA+ or PPD+ patient with no symptoms and normal X ray indicate? What should you do?

A

Latent TB

Latent TB MUST be treated

31
Q

Drug therapy commonly used to treat tuberculosis patients?

A

INH, Rifampin, Pyrazinamide, Ethambutol daily for 6-9 months

32
Q

Drug therapy commonly used for latent TB?

A

Just INH

33
Q

What non-chemical treatment method is important in some patients?

A

Directly Observed Therapy

34
Q

Why might someone except to see TB+ patients very commonly in other countries?

A

Other parts of the world vaccinate for TB

35
Q

How do you treat XDR-T patients? (3)

A

Meropenem + Clavulanate
Linezolid is effective, but almost always causes adverse events
Bedaquiline

36
Q

Two manifestations of mycobacterium leprae?

A

Tuberculoid Leprosy

Lepromatous Leprosy

37
Q

Describe tuberculoid leprosy (paucibacillary).

A

Macular Lesions

Nerves on One Side (occasional bilateral) Involved

38
Q

Describe lepromatous leprosy (multibacillary)

A

Progressive Nodular Lesions

Bilateral Nerve Death –> Bone Resorption/Extremity Loss

39
Q

Which form of leprosy is rare in the modern era

A

Lepromatous

40
Q

Describe the skin markings seen on patients with mycobacterium leprae

A

Whitened, anaesthetized skin area with red ring around it

41
Q

Most mycobacterium leprae cases come from what parts of the world? How is it transmitted?

A

Asia and Africa

Long-term contact

42
Q

What organisms can have mycobacterium leprae infections?

A

Humans and Armadillos

43
Q

Describe the pathogenesis of mycobacterium leprae.

A

Inflammatory disease (like TB)
Inflammation damages Nerve Endings
Hyposensitivity can cause soft tissue damage and bone loss

44
Q

How do you treat mycobacterium leprae?

A

Dapsone (sulfone) + Rifampin

45
Q

Significance of M. avium-intracellulare?

A

Most common hospital-acquired bacterial infection of AIDS patients

46
Q

Treatment for M. avium-intracellulare?

A

Clarithromycin + Ethambutol for life

47
Q

How does M. kansasii present?

A

TB-like symptoms in IC patients

48
Q

Describe the physical structure of mycoplasm bacteria

A

Probably the smallest possible free-living entity

No Cell Wall, Membrane Only with Sterols

49
Q

How do mycoplasm generate sterols?

A

They don’t. They take them from the host.

50
Q

Describe what you would see in attempting to culture mycoplasm pneumoniae.

A

Grows Slowly

Tiny Colonies with Depressed centers (Fried Egg Appearance)

51
Q

Describe the clinical presentation of mycoplasma pneumoniae

A

Mild atypical (wheeze+crackle) pneumonia
tracheobronchitis
Insidious Onset
Mild Fever + Dry Cough

52
Q

How is mycoplasma pneumoniae transmitted?

A

Transmitted via respiratory droplets

53
Q

Circumstances in which mycoplasma pneumoniae is more common.

A

Schoolchildren

Winter

54
Q

Describe the pathogenesis of mycoplasma pneumoniae.

A

Proline-rich adhesion protein forms elongated tip, binds epithelial cells.
Protein M blocks the Ab Fab region
Cyotoxic Effects

55
Q

List cytotoxic effects of mycoplasma pneumonia

A

Production of H2O2, O2-

Competition for nutrients

56
Q

How is mycoplasma pneumonia

A

Typically don’t treat if mind

Tetracycline, Erythromycin

57
Q

What drug are you a doof if you give to treat mycoplasma.

A

Penicilin

Mycoplasma don’t have a cell wall

58
Q

Mycoplasma genetalium manifest in what three ways?

A

Normal Flora
Urethral Infections
Genital Infections

59
Q

Manifestations of mycoplasma hominis?

A

10% of salphingitis

Post-partum fever

60
Q

Unique metabolic activity of ureaplasma urealyticum?

A

Requires 10% urea to grow

61
Q

Long term effect of ureaplasma urealyticum metabolism?

A

Generates an alkalinized environment
Causes bladder stones
Bladder stones –> Non-gonococcal urethritis in males

62
Q

Describe the physical structure of Corynebacterium diphtheriae

A

G+ with mycolic acids in outer mem
Club Shaped
Pleomorphic

63
Q

Important diagnostic test for Corynebacterium diphtheriae.

A

Plate on tellurite blood agar, will reduce potassium tellurite to tellurium (turn it black)

64
Q

Clinical presentation of Corynebacterium diphtheriae?

A

Throat Infection – sore throat, fever
“Bull-Neck” – Swollen Lymph Nodes
Pseudomembrane – forms at back of throat and may obstruct airway
Toxin

65
Q

Effects of Corynebacterium diphtheriae toxin?

A

Absorbed in blood – affects heart, liver, kidneys

66
Q

How are toxigenic strains of Corynebacterium diphtheriae identified?

A

Elek immunodiffusion test
Filter paper with antitoxin placed perpendicular to stain streaks
Toxin and Anti-Toxin form precipitate

67
Q

How is Corynebacterium diphtheriae spread?

A

Aerosolized droplets

68
Q

When is Corynebacterium diphtheriae typically acquired?

A

Usually a childhood disease, most adults immune from subclinical exposure (except not really)

69
Q

Mortality rate of Corynebacterium diphtheriae

A

10-25%

70
Q

Describe the pathogenesis of Corynebacterium diphtheriae.

A
  • AB toxin from beta-phage conversion.
  • B binds EGF-like receptor and it internalized. Low pH in vesicle allows hydrolysis, frees the A
  • A binds NAD and ADP, ribosylates EF-2
  • NO PROTEIN SYNTHESIS
71
Q

How does Corynebacterium diphtheriae work its tox genes.

A

High Fe turns off toxAB operon
Free Fe is kept at low levels in the body
Corynebacterium diphtheriae only releases the toxin in the body

72
Q

How is Corynebacterium diphtheriae prevented?

A

DTaP or DPT

Booster before school and every 10 years

73
Q

How is Corynebacterium diphtheriae treated?

A

Quarantine
Equine anti-toxin in large dose
Penicillin/Erythromycin to keep bacteria low

Micro Exam #2 (15 decks)

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