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Lect 14 Flashcards

(35 cards)

1
Q

Mycobacterium tuberculosis: reservoir and transmission

A
  • humans are only reservoir
  • transmission: aerosol
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2
Q

MTB Strains vary in antibiotic susceptiblity. name the strains

A

MDR strains - multi-drug resistant XDR strains - extensively drug resistant

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3
Q

MTB Bimodal Age Distribution of disease. Name the ages and also what type of dissemination occurs in these patients

A
  • Infants and Older Adults
    • Infants and Immunocompromised - Hematogenous dissemination Can result in meningitis and other symptoms
    • Older - Failure of immune system - Possible reactivation of latent infection
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4
Q

MTB initial infection risk factors

A
  • close contact with TB case: • Many children become infected by caregivers
  • Residence in long-term care facility
  • Low income/inner city housing
  • Alcoholism or IV Drug Use
  • Diabetes mellitus (30% increase over lifetime)
  • Silicosis - pneumoconiosis- inhalation silica dust
  • Immunosuppression
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5
Q

Name the three species that produces human tuberculosis

A
  1. mycobacterium tuberculosis
  2. mycobacterium bovis
  3. mycobacterium aficanum
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6
Q

which mycobacterium is the source of the BCG vaccine

A

mycobacterium bovis

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7
Q

MTB

  • shape
  • motility
  • oxygen?
A
  • bacillus
  • non motile
  • obligate aerobes
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8
Q

MTB is killed by what process that we do to milk

A
  • pasteurization
  • *heat sensitive
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9
Q

where does MTB grow

A
  • intracellular growth - alveolar macrophages
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10
Q

MTB undergo what type of staining

A
  • MTB cells resist normal gram stain: acid fast bacilli
  • harsh treatment is used: ziehl-neelsen or Kinyoun stains
  • MTB cells, once stained, will not decolorize
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11
Q

describe cell wall of mycobacterium tuberculosis

A
  • outer layer: mycolic acid
  • inner layer: peptidoglycan
  • **cell wall Influences staining behavior, produces slow growth phenotype and confounds antibiotic therapy
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12
Q

MTB virulence factors

A
  • No classic virulence factors or toxins
  • structure enables it to persist as an intracellular pathogen
    • mycolic acid: prevent dehydration and may resist H2O2
    • cord factor
      • Mycoside – glycolipid Mycolic acid + disaccharide
    • lipoarabinomannan: Inhibits cell-mediated immunity
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13
Q

MTB infection potential outcomes

A
  1. immediate resolution
  2. primary disease
  3. progressive primary (active disease)
  4. latent infection
  5. endogenous reactivation/secondary disease
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14
Q

how does MTB cause cell and tissue destruction

A
  • After phagocytosis by macrophages, MTB specifically prevents fusion with lysosomes while allowing nutrient-containing vesicles to merge.
  • Innate and cell-mediated host immune responses to MTB produces selfdestruction of cells and tissues
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15
Q

what structure becomes evident 2-6 weeks after MTB infection

A
  • granulomas: areas surrounded by macrophages, fibroblasts, and collagen fibers harboring viable MTB cells
    • over time, can form fibrotic tubercle and calcify-> tubercles or Ghon bodies.
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16
Q

Does person infected with latent TB able to spread disease

A
  • bacteria remain viable in lesions but inactive
  • patients have no symptoms
  • no risk to spread disease
17
Q

what happens to a patient when latent TB becomes reactivated-> secondary TB

A
  • Granulomas: Erode and discharge TB bacilli into bronchi (infectious)
    • Erode blood vessel – hematogenous spread to other body sites – TB can involve any organ
  • signs and symptoms are present; patient is infectious
  • cough, weight loss, fatigue, fever, night sweats, chest pain
18
Q

what is miliary tuberculosis

A
  • results from lymphohematogenous spread of primary infection or via a latent focus with subsequent spread
  • **massive spread of agent
19
Q

What means are available to help aid diagnosis of TB

A
  • skin test
  • xray consistent with TB
  • sputum stain/broth culture to detect acid fast bacteria
20
Q

describe Serial screening programs

A
  • Use purified MTB protein derivative (PPD) in tuberculin skin test (Mantoux skin test)
  • Small amount of antigen injected under the skin, size of induration measured after 48-72 hours
  • Boosters (persons with earlier infection with minimal reaction to PPD) are identified by quick second administration
21
Q

what can cause a false positive on TB skin test

A

BCG recipients and those infected with NTM may react as false positives

22
Q

length of treatment for active TB disease

A

extended duration (6-9 months), multi-drug regimen requiring patient compliance

23
Q

treament for latent TB

A

Isoniazid (9 months)

24
Q

Mycobacterium avium complex (MAC)

  • gram status
  • oxygen?
  • where is it found
A
  • gram positive
  • aerobic
  • ubiquitous
    • water, soil, plants
25
Mycobacterium avium complex (MAC) require what staining
acid fast
26
transmission of Mycobacterium avium complex (MAC)
* ingestion of contaminated water or food * \*\*NO person to person transmission * \*\*NO patient isolation required
27
Mycobacterium avium complex (MAC) are known to infect what patient populations
* **opportunistic human pathogens** * HIV
28
Mycobacterium avium complex (MAC) causes what in middle aged and older males with history of smoking
Cavitary lesions resemble TB
29
Mycobacterium avium complex (MAC) causes what in elderly female non-smokers
* Patchy or nodular on X-ray * Lady Windermere’s syndrome
30
MAC causes what in AIDS patients
**Disseminated disease**, no organ spared as immune system collapses
31
how is Non-tuberculous Mycobacterial Infections (NTM) – the Mycobacterium avium Complex (MAC) diagnosed
* clinical illness * **microscopy to reveal acid-fast bacteria and culture**
32
general rules for MAC treatment
* Both HIV positive and HIV negative patients use **combination therapy** * Take HIV infection status into account
33
MAC treatment length in HIV negative patients
Continue until sputum cultures are negative for 1 year
34
HIV positive patients take what prophylactically to prevent MAC infection
* Chemoprophylaxis with CD4 100 cell/µL * Can discontinue 3 months after CD4 \>100 cell/µL
35
Treatment In HIV+ patient with MAC infection
* Without immune reconstitution – lifelong * Or begin treatment for 2 weeks then anti-retroviral (HAART) therapy