VL18b: tuberculosis Flashcards

1
Q

Why do TB rates reduce over time?

A

better sanitation and housing situations

treatments did not make a huge difference

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2
Q

How is TB spread?

A

-person to person
-through air via droplet nuclei
(Cough, sneeze, speak, sing)

-probability of transmissiosn depends on
infectioousness of person with tb
length of exposure
viulence of tubercule bacili

hardly any genetic variation in TB, little to no horizontal genetransfer so no more or less virulent strains

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3
Q

4 different TB drugs

A

Isoniazid (INH)
Rifampicin (RIF)
Pyrazinamide (PZA)
Ethambutol (EMB)

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4
Q

What’s the difference between primary and secondary resistance?

A

primary: caused by transmission of drug-resistant prganism
secondary: develops during drug treatment
- patient was not given appropriate treatment regimen
- patient did not follow treatment as prescribed

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5
Q

What different kinds of resistance are there?

A

Mono-resistant: resistant to any 1 of drugs
Poly-resistant: resistant to any 2 drugs (but not INH or RIF)
Multidrug resistant (MDR TB): resistant to at least INH and RIF
Extensively drug resistant (XDR TB): INH and RIF + resistant to any fluoroquinolone + at least 1 of 3 second-line drugs

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6
Q

What is DOTS, DOTS Plus strategy therapy?

A

Directly observed therapy short course
(patients are monitored, cocktail of different drugs)

DOTS Plus strategy
monthly monitoring for presence of resistant strains, changing drug regimen as resistance occurs

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7
Q

What are the differences between treatment of latent infection and acute disease?

A

Treatment of LTBI
- daily INH for 9 months
or RIF for 4 months

Treatment of TB Disease
Include INH, RIF, PZA, EMB, adjust regimen when susceptibility
New patients: 2 months: INH, RIF; PZA, EMB +4 months: INH, RIF
old patients: longer, more, (9months)
MDR TB 18-24 months 4-6 drugs, greater risk of death

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8
Q

What is a latent TB infection? vs TB disease?

A

LTBI: immune system keeps bacilli under control, not infectious
TBdisease: immune system can*t keep it under control, soon, or years after infection, 10% of people with normal immune system develop disease in their lives, infectious

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9
Q

Describe the development of TB

A
  1. droplet nuclei with tubercle bacilli are inhaled, travel to alveoli in lungs
  2. multiply in alveoli
  3. small number of bacilli enter bloodstream, spread throught body
  4. within 2-8 weeks, immune system produces macriphages that surround the tubercle bacilli, keep them contained (in alveoli)
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10
Q

How can TB be diagnosed?

A

chest X-ray (calcified tubercles can be seen)

TB skin test: injection of M. tuberculosis proteins, positive test leads to red area at injection site

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11
Q

How does latent TB progress to TB disease?

A
  1. tubercle bacilli in alevoli, most digested by macrophage, others survive, no symptoms
  2. bacili multiply, more macrophages come, formation of early tubercle, immune response cause lung damaging inlfammation
  3. after a few weeks, disease symptoms appear, many macriphages die, tubercle bacilli are released, form a caseous center in tubercle, bacili grow slowly, many remain dormant for later reactivation, diasease may arrst at this stage and lesions become calcified
  4. in some individuals: mature tubercle is formed -> disease symptomsm caseous center enlarges during liquefaction, air filled tuberculous cavity, aerobic bacili multiply
  5. liquefaction continues, tubercle ruptures,bacilli spill into bronchiole, disseminated throughout lungs, then circulatory ad lymphatic system
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12
Q

At what locations, in whom occurs TB?

A

Pulmonary TB -> lungs -> most cases
extrapulomnary-> larynx, lympha nodes, kidney, brain -> young children or immunosuppresed people
Miliary TB-> all parts body (through bloodstream) -> rare

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13
Q

Are there any good animal models, vaccines for TB?

A

no, for different parts of infection cycle different models,

(includig mice guinepigs cow, monkey

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14
Q

Where is TB most prevalent?

A

africa, asia,

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