Primary Tuberculosis (Ghon Complex): Symptoms & Why Cough May Be Absent
Primary TB (Ghon complex) is the initial infection with Mycobacterium tuberculosis, typically in children or recent exposures. It differs significantly from reactivation (post-primary) TB.
Pathogenesis
- Inhaled droplet nuclei → alveolar deposition.
- Alveolar macrophages ingest but fail to kill → bacilli replicate.
- Bacilli drain to hilar lymph nodes → Ghon focus (lung) + hilar lymphadenopathy = Ghon complex.
- Cell-mediated immunity develops (2–8 weeks) → caseation, containment → calcification (Ranke complex).
Clinical Presentation
- Most (90–95%): Asymptomatic; diagnosed by TST/IGRA conversion.
- Symptomatic minority: Low-grade fever, night sweats, fatigue, weight loss, anorexia.
- Cough: Present in ~50%; usually mild, non-productive. Absence of cough does not exclude primary TB.
- Complications: Pleural effusion, pericarditis, bronchial compression from nodes → wheeze/stridor.
Diagnosis
- TST (Mantoux) / IGRA (QuantiFERON/T-SPOT): Detects infection; cannot distinguish latent vs. active.
- CXR: Ghon focus (small peripheral opacity), hilar/mediastinal lymphadenopathy (key sign), pleural effusion.
- Sputum/Gastric aspirate: AFB smear/culture/PCR; low yield in primary TB (paucibacillary).
Treatment
- Latent TB infection (LTBI): Positive TST/IGRA, no symptoms, normal CXR → 3HP (isoniazid+rifapentine weekly×12), 4R (rifampin daily×4mo), or 9H.
- Active primary TB: Standard 2HRZE/4HR (isoniazid, rifampin, pyrazinamide, ethambutol).
- Corticosteroids: Adjunct for bronchial compression, pericarditis, meningitis.
Key Distinction from Reactivation TB
| Feature | Primary TB | Reactivation TB |
|---|---|---|
| Typical age | Children, recent exposure | Adults, remote infection |
| Site | Lower/mid lung zones | Apical/posterior upper lobes |
| Cavitation | Rare | Common |
| Sputum AFB | Rarely positive | Often positive |
| Contagiousness | Low | High |