Important Note First

Wallgren's Timetable of Primary Tuberculosis

Introduction

The Timetable - Sequential Events After Primary Infection

• Tubercle bacilli are inhaled and deposited in the lung periphery (middle zone - upper part of lower lobe or lower part of upper lobe)
• Bacilli are ingested by alveolar macrophages
• Local multiplication begins - the Ghon focus forms
• Bacilli travel via lymphatics to regional (tracheobronchial/hilar) lymph nodes
• Ghon complex = Ghon focus + draining lymphatics + hilar lymph nodes
• Bacillaemia (bacteremia) occurs silently - organisms are seeded to all organs of the body (especially lung apices, vertebrae, renal cortex, epiphyses of long bones, brain meninges)
• No symptoms at this stage; patient is tuberculin-negative
• 4-6 weeks after infection: Tuberculin hypersensitivity develops (tuberculin test converts from negative to positive) - this is the "tuberculin conversion" point
• Mild fever and malaise may appear

• Pleural effusion - rupture of subpleural Ghon focus into pleural space can cause TB pleurisy (one of the earliest complications)
• Segmental lesions - due to enlarged lymph node compressing adjacent bronchus, causing collapse or consolidation (epituberculosis)
• Miliary TB and TB meningitis can occur at this stage in infants and immunocompromised (due to the early bacillaemia)
• TB meningitis is most dangerous within the first 3-6 months

• Caseous lymph nodes may erode through bronchial walls (broncholymphatic fistula) - causing bronchogenic spread
• Endobronchial TB, obstructive emphysema (ball-valve obstruction), or segmental atelectasis
• Pericardial TB may develop from contiguous spread
• Erythema nodosum and phlyctenular conjunctivitis - hypersensitivity manifestations - appear around the time of tuberculin conversion

• Bone and joint TB (especially vertebrae - Pott's disease, hip, knee) begins to manifest
• These arise from the early hematogenous seeding of bones during primary bacillaemia
• Renal TB seeding also occurs at this stage (though clinical disease manifests much later)

• Radiologically visible calcification of the Ghon focus and lymph nodes begins to appear (microscopic calcification can start at 2 months but X-ray visible calcification takes 1 year or longer)
• This marks the healing phase of primary TB

• Clinical renal TB begins to manifest (from the seeded renal cortical foci)
• Usually occurs within 2 years in 90-95% of cases following primary TB

• Miliary TB can occasionally occur as a late complication (from breakdown of old foci)
• TB bronchiectasis from healed obstructive lesions

• Post-primary / reactivation TB - from dormant apical foci (Simon's foci) deposited during early bacillaemia
• Occurs in apical and posterior segments of upper lobes (>95% cases)
• Triggered by: old age, malnutrition, HIV infection, diabetes mellitus, immunosuppressive therapy, malignancy, chronic kidney disease
• 10% of infected individuals will develop active TB at some point in their lifetime (5% within 2 years, 5% later)
• Genital TB (especially in females - fallopian tubes) is also a late manifestation

Summary Table

Significance of Wallgren's Timetable

1. Predicts timing of complications - allows early screening and prophylaxis
2. Guides contact tracing - helps identify when tuberculin testing will be positive
3. Explains organ-specific TB timing - why renal TB is late and meningitis is early
4. Basis for chemoprophylaxis - preventive therapy in contacts timed appropriately
5. Epidemiological importance - explains disease patterns in endemic areas

Key Points for Exam

• Tuberculin conversion occurs at 4-6 weeks - critical timing
• TB meningitis is most feared early complication - peaks at 3-6 months (rare after 1 year in primary TB)
• Renal TB is one of the latest manifestations
• Calcification visible on X-ray only after 1 year
• 90% of primary TB heals spontaneously - only 10% progress
• The early silent bacillaemia is responsible for ALL extrapulmonary TB