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22y.o, housekeeper Inhaled droplet nuclei containing exposed to causative agents

low economic status Mycobacterium tuberculosis

lung tissue – lower two thirds usually peripheral

Multiplication of bacteria
hilar & paratracheal lymphadenopathy
Inflammation-activation of alveolar macrophages & neutrophils malaise
anorexia & weight loss
occasional hemoptysis
Acute Primary PTB

Localized (lung) infection Hematogenous spread (miliary TB)

Bronchopneumonia usually occurs 2-10 weeks after exposure

Granuloma formation

necrotic degeneration(caseation necrosis)

cavities filled w/ a cheese-like mass of tubercle bacilli, dead WBC,& necrotic lung tissue

lung lesions form calcified scar tissues – “Ghon tubercles”

dormant tubercle bacilli

Poor nutritional status

Presence of other diseases (e.g end-stage renal disease)
HIV infection impaired acquired immunity
prolonged corticosteroid therapy immune system
malabsorption syndromes
genetic predisposition inhibit further growth & development of active infection
low body weight
substance abuse
immunosupression Asymptomatic

Reactivation of TB (Secondary PTB/Post-primary)

active disease occurs

upper lobes of the lungs(high O2 concentration)

Softening & liquefaction occurs in the necrotic foci with

concomitant multiplication of tubercle bacilli

rupture of softened lesion

washed through previously unifected airways to normal lung tissues
necrotic degeneration(caseation necrosis-lungs)

cavities filled w/ a cheese-like mass of tubercle bacilli, dead WBC,& necrotic lung tissue

drains in tracheobronchial tree, reinfecting other normal lung tissue or spread to pleura (pleural effusion)
cough out sputum &/or blood(hemoptysis)

form scar tissues

(reduce lung vol.,gas exchange & function)

Symptomatic chronically untreated severe lung damage inability to breathe properly

Fatigue chest pain

weight loss anxiety Death
lethargy low-grade fever in the afternoons
night sweats productive cough
dyspnea Anorexia hemoptysis

Figure 2. Schematic Presentation of Patient’s Illness