Tuberculosis Pathogenesis and Clinical Features Flashcards
Mycypobacterium TB
Aerophilic
Slow growing
Acid-fast - mycolic acid
Humans are onyl reservoir
Active vs. latent
Active - has sx, CXR evidence and should be able to recover TB bacilli
Latent - immune sx controlled nad asymptomatic…may have G/R complex
Pathogenesis
TB inhaled…AM engulfs but cannot destroy…form early and small granuloma…then well-formed granuloma with central caseous necrosis - infected macrophjages killed (DTH) resulting in cessation of growth
If good immune sx, then healed granuloma
If not, then liqufactive necrosis occurs and the infection can spread
TST and IGRA
TST - Most pts control initial infection…get 5% lifetime risk of developing active dz
TST- positive indicates prior exposure and established DTH (5-7 weeks0
IGRA has same implicatiins
Mechs of spread
Erosion into bronchus (endobronchial spread)
Erosion into lymphatic - hematogenous sread (lungs)
Erosion in pulmonary vein (systemic spread)
Patho summary
INtracellular pahtogen that needs CMI for control
DTH is form of CMI manifested by caseous necrosis AND skin test reactivity
If poor, then active disease with negative TST and no DTH or cavity
If intermediate and active, then DTH positive and cavity forms
If latent, then positive DTH and no cavity
Bacillary load
Liaquefactive ncrosis leads to explosive extracellular growth
Higher loads mean more likely to show up in sputum and therefore more infedctvity
Radiography relationship to pathogenesis
Most have intiail infection leaving a nodule with associated adenopathy (middle and lower lobes…primary will also show up in these lobes)
Later, reactiviation may occur in upper areas
Poor CMI could lead to hematogenous dissemination
Ghon/Ranke complexes
Nodule representing the primary lesion of pulmonary TB with associated ipsilateral adenopathy
If both are calcified, then old and inactive dz
Other miliary patterns
Blastomycosis, histoplasmosis, TB
