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MLSCI 242 > LECTURE - Mycobacterium tuberculosis > Flashcards

LECTURE - Mycobacterium tuberculosis Flashcards

1
Q

TB was on its way to being controlled in the 80s so what happened in the 80s?

A
  • immigration

- crowding and substance abuse leading to HIV = in homeless shelters and prisons

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2
Q

what are NTM?

A
  • also known as mycobacteria other than tuberculosis (MOTT) or ‘atypical mycobacteria’
  • normally inhabit the environment, but some can cause tuberculosis-like disease in humans
  • HIV-AIDS HAS GREATLY increased awareness of disease caused by these organisms
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3
Q

preferred medium to grow NTM

A

Lowenstein-Jensen medium

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4
Q

Runyon Classification

A

useful distinctions observed among NTM species based on three key features:

  • growth RATE on LJ medium (slow growers >7 days; rapid 3-7 days)
  • optimal growth temp (30-32 C, 35-37 C, 42 C)
  • photoreactivity =
    > photochromogens: produce pigment on exposure to light
    > scotochromogens produce pigment in the light or dark
    > nonchromogenic produce no pigments (buff colour)
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5
Q

slow growers

A

Mycobacterium tuberculosis

Mycobacterium avium complex

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6
Q

Mycobacterium leprae

A
  • acid-fast Fite stain for this anaerobic rod
  • does NOT grow in vitro; grow in footpads of mice or armadillos
  • AKA Hansen’s disease (leprosy); rare here but still a challenge worldwide
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7
Q

how is leprosy transmitted?

A

droplets from nose and mouth of untreated patients with severe disease BUT not highly infectious
- left untreated = cause nerve damage = muscle weakness, atrophy, and permanent disabilities

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8
Q

treatment of leprosy

A

MDT = multidrug therapy

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9
Q

leprosy can occur in two polar forms:

A
  • tuberculoid (TT)
  • lepromatous (LL)
    with 3 intermediate (borderline) forms, depending no state of cell-mediated immunity (CMI)
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10
Q

WHO only makes a distinction for leprosy between these two

A
  • PB paucibacillary = no bacilli present

- MB multibacillary = bacilli present

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11
Q

TB causes death in ___% of untreated cases

A

50%

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12
Q

W strain of TB

A

extremely drug resistant!!! (XDR-TB)

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13
Q

one of the top ten causes of death worldwide

A

tB

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14
Q

worldwide, TB is the ___th leading cause of death and the _____ leading infectious killer (after COVI-19 and above HIV/AIDS)

A

13th; secind leading

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15
Q

T or F. TB is not curable

A

F! it is!

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16
Q

TB characteristics

A
  • acid-fast aerobic gram pos rod ; much extra lipid and an outer, mycomembrane, akin to that of gram negs
  • very slow growth
  • spread by aerosols
  • fever, cough (often w blood sputum); irreversible lung damage; can disseminate throughout body
  • skin test pos confirms exposure (1% of those exposed develop TB IF healthy!) (40% if HIV-positive)
17
Q

steps in migration of M. tb across the alveolar barrier

A
  1. adheres to, invades, and replicates in alveolar epithelial cells
  2. penetrates the BM and endothelial cells
  3. exits the ECs to enter circulation
  4. infects extra-pulmonary EC to establish latent TB infection (LTBI) in EP sites
  5. ‘Trojan Horse’ mechanism by which M. tb crosses the barrier via infected alveolar macrophages
18
Q

KEY to beating TB

A

efficient production of CD4+ and CD8+ cells and the activation of macrophages that can kill M. tb

antibodies = minimal effect

19
Q

latency in TB

A
  • ability of organisms to survive in body for many decades; hypotheses:
    1. organism stops replacing in a quasi-sporelike state; sigF is known to regulate spore formation in Streptomyces sp.
    2. organism still metabolically active but barely; antibiotics reduce likelihood of reactivation of TB so bacteria must be metabolizing at least a little
20
Q

presumptive diagnosis of TB using this stain

A

Ziehl-Neelsen (acid-fast)

- reveals M. tb as pink acid-fast bacilli in sputum

21
Q

secretion system unique to mycobacteria

A

type VII (ESX) secretion system

22
Q

t kill M. tb, special antibiotics are required…

A
  • exceptions are rifampin and streptomycin
  • Ethambutol appears to be, and isoniazid is, an inhibitor of the mycolic acid synthesis
  • mechanism of pyrazinamide appears to be disruption of membrane transport and energetics
23
Q

resistance to anti-TB drugs

A
  • resistance to rifampin and isoniazid occurs at high frequency, so using both drugs together reduces this chance; most common therapy for TB!
  • many TB drugs = daily pills for six months+ and it’s hard to comply= resistance! (ep. if drugs make you nauseated)
  • high mutation rates as well
24
Q

targets for new TB drugs

A
  • isocitrate lyase in the glyoxylate cycle of M.tb metabolism that is linked to latency
  • Or enzymes that make up the antigen 85 complex = transferring mycolic acids onto trehalose residues in cell walls
25
Q

how to diagnose TB?

A
  • sputum and detection of FB (presumptive)
  • skin test (Mantoux); uses purified protein derivative to detect prior exposure based on previously primed CD4+ T cells
  • radiography (chest x-ray)
  • WHO recommends rapid test based on PCR (detects TB and resistance to rifampin); Xpert MTB/RIF test; nucleic acid amplification test
26
Q

1 virulence characteristic of M. tb

A

ability to grow in resting macrophages (mediated by ESX-1 genes)

27
Q

how does TB trigger a destructive immune response

A
  • muramyl dipeptide stimulates cytokine secretion
  • TNNF-alpha is produced in response to various cell wall components and triggers lung damage; Abs to TNF-alpha can prevent this
  • release of lysosomal components of macs and PMNs
28
Q

host susceptibility to TB depends on: (4)

A
  • dose of organisms
  • exposure time to inoculum
  • health of individual
  • genetic factors of host and of bacterium
29
Q

treatment for leprosy today

A
  • early to avert disability!

- MDT (multidrug therapy) = dapsone, rifampicin, and clofazimine ; kills pathogen and cures patient

30
Q

T or F. immunological manifestations can everse upon antibiotic therapy (Leprosy)

A

T! have to keep immune system dampened so that CMI doesn’t go nuts with MB leprosy and MDT

MLSCI 242 (39 decks)

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