TB and non-TB mycobaterium Oct18 M1 Flashcards
TB examples of symptoms
fever, cough, minimal sputum
TB CXR finding
- opaque -abnormality
- blunting of costophrenic angle
- straight line at bottom of lung (air-fluid interface)
what can counfound TB with
lung abcess
easy test for TB detection + gold standard
sputum analysis for acid-fast smear microscopy and culture
strongly positive smear for TB: what’s the diagnosis
active contagious pulmonary TB
TB level of contagion
highly contagious
2 evolving challenges with TB today
Global phenomenon (migration) Increasing antibiotic resistance
mycobacterium TB description
Aerobic slightly curved rod
mycobacterium TB: mechanism to survive certain conditions
survives in dormant state if adverse conditions (low oxygen, dry)
best conditions for TB growth and what it explains
high oxygen tension. explains why lung apices affected
TB physical protection it has
thick waxy outer layer (cell wall): protects from light, heat, dryning. + gives acid fast property
TB hosts known
humans only
TB transmission routes
airborne only
how to evaluate prob of inhaling TB
proportional to its conc. in air (essentially prob of inhaling a viable bacterium)
how to evaluate conc. of TB in air (2)
1) volume of air it’s diluted in (inside vs outisde, room size)
2) production vs elimination (ventilation. sunlight and drying kills it)
contagious TB CXR findings and smear findings
Cavities
AFB smear positivity
why TB prevalent in Inuit communities and northern Qc communities
Lot of people live in same house, no ventilation, isolation. higher TB conc. in air
primary infection def
when exposure to TB results in new infection
how good body responds to primary infection
initial immune response is highly ineffective
what determines if exposure results in new infection or no infection
innate immunity
1st phase of progression of TB and length
local alveolus (1-2 weeks)
2nd phase of progression of TB and length
TB drains/spreads to regional lymph nodes (2-4 weeks)
3rd phase of progression of TB and length
Hematogeneous dissemination (4+ weeks)
what kind of immunity against TB
cell mediated (not humoral) (T cells)
result of immune reaction to TB (on microscopy what we see)
hard shells called granulomas
what determines if disease will develop or become dormant after primary infection
the development of effective cell mediated immunity
who is most likely to get developing TB after primary infection
Young people, immunosuppressed, comorbidities, HIV
when effective cell mediated immunity to TB is developed
4-7 weeks after initial infection
if CMI defective, when TB becomes symptomatic
3-6 months after primary infection
TB risks 2 things to note if primary infection occured
1) More likely to get disease if young but less likely to get disease than not get it overall
2) infants vulnerable to severe TB (disseminated TB or TB meningitis)
what we mean by latent, dormant TB
contained in granulomas but keeps fighting to get out. Active immune response
how latent TB infection diagnosed LATENT
immune tests based on the cell immunity to TB
strongest risk factor for dev active TB
HIV/AIDS
risk factor of importance for active TB
time since infection. (greater risk in 1-2 years aftrer infection)
granuloma: what happens when active TB
hard shell breaks down and tubercle escapes and multiplies
when latent TB, risk for active TB if have no risk factor
10% over lifetime
when latent TB, risk for active TB if infected with HIV
7-10% per year
why younger children more at risk to progress to active TB
immature immune system
symptoms of active TB
fever, nigh sweats, cough, sputum, hemoptysis if advanced, lymph node,
3 tests for active TB
microscopy (look for acid fast org)
culture (gold standard)
nucleic acid amplification
what tests have no utility to detect latent TB
cultures, chest X ray, all routine tests (smear, nucleic acid amplif.)
2 tests for latent TB
immune based:
Tuberculin Skin Test (Purified protein derivative or PPD)
IF gama release assays (IGRAs)
TB treatment: what
2-4 drugs (if 1, TB develops resistance)
TB treatment: how long
minimum 6 months
3 TB drugs
isoniazid (INH), rifampin (RIF), pyrazinamide (PZA)
TB treatment if latent: what
1 drug: no risk of drug resistance
serious adverse effect to consider in TB treatment
liver toxicity
how TB incidence changing in Canada vs in Inuit communities precisely
decreasing overall
increasing in Inuit communities
why Inuit have high incidence of TB
housing conditions, smoking, diabetes, genetic factors, history of colonization and role of TB
most important causes of TB worlwide
HIV, smoking and alcohol, malnutrition, chronic illnesses (e.g. diabetes)
T-F: TB deaths started declined after first treatment
False, already in decline before
non-tuberculous mycobacteria definition
all mycobacteria except mycobacteria TB and mycobacteria leprae
T-F: TB infection must be reported toauthorities
True
main diff between TB and non-TB mycobacterium
non-TB mycobacterium is not contagious
non-TB myco that is most associated with human disease in Canada
mycobacterium avium
non-TB myco symptoms and chest X ray
symptoms: cough, sputum, weight loss
CXR: nodular infiltrates associated with bronchiectasis
cavitary lung disease (mimics TB)
non-TB myco treatment
No treatment if simply found in sputum
