Paediatrics chapters
Tuberculosis in children
Childhood tuberculosis: how children catch it, the primary (Ghon) complex and its outcomes, pulmonary and extrapulmonary forms, the tuberculin test and other tests, first-line drug regimens and side effects, steroids, preventive therapy and BCG.
- Children catch TB from an infectious adult in the household; the first infection forms a primary (Ghon) complex (lung focus, lymphangitis and hilar nodes), and young children rarely infect others.
- Most infections heal, but infants and young children can progress to progressive primary disease, miliary TB or meningitis within months; lymph node TB is the commonest extrathoracic form, and Pott's disease the commonest skeletal form.
- Diagnosis rests on contact history, Mantoux test, chest X-ray and gastric aspirate or other samples for AFB; treatment is 2 months HRZE then 4 months HR under DOT (longer for bone and CNS disease), with isoniazid prophylaxis for exposed young children and BCG at birth.
On this page
Overview
Tuberculosis (TB) is caused by Mycobacterium tuberculosis. Pakistan carries one of the highest TB burdens in the world, and children are infected mainly by adults with lung TB in the same house. Childhood TB differs from adult TB: it is usually primary, paucibacillary (few organisms), hard to confirm and more likely to spread through the blood to the brain and other organs in infants and young children. TB meningitis is covered in its own chapter in the neurology section.
Aetiology
- M. tuberculosis: non-spore-forming, non-motile, weakly gram-positive curved rods; obligate aerobes.
- Acid-fast: the lipid-rich (mycolic acid) cell wall resists decolourisation by acid and protects the organism from antibody and complement.
- Slow growth: culture takes 3-6 weeks on solid media.
Epidemiology and transmission
- Spread by inhaled droplet nuclei from an adult with cavitary lung disease and sputum smear-positive TB; risk rises with close, prolonged contact and poor ventilation.
- Patients usually become non-infectious within about 2 weeks of effective treatment.
- Young children rarely infect others: they have few bacilli in their secretions and cannot cough forcefully enough. Adolescents with adult-type cavitary TB can spread it.
- Without treatment, infection progresses to disease in a minority of healthy adults; the risk is much higher in infants.
- Risk factors for disease: age under 5 years, malnutrition, measles and pertussis, HIV, steroids and other immunosuppression.
Pathogenesis: the primary complex
- Inhaled bacilli reach the alveoli; the lung is the portal of entry in about 98% of cases.
- Most are killed by macrophages; survivors are carried by lymphatics to the regional (hilar or paratracheal) nodes.
- The primary (Ghon) complex = Ghon focus in the lung + lymphangitis + enlarged regional nodes.
- During this phase bacilli spread silently through blood and lymph to many organs.
- Cell-mediated immunity and tuberculin sensitivity develop after about 4-8 weeks (Akbar: 3 weeks to 3 months). The complex then usually heals by fibrosis or calcification, but live bacilli may persist for years.
Possible outcomes
| Outcome | What happens |
|---|---|
| Healing | Calcified focus and nodes; positive tuberculin test; no disease (latent infection) |
| Node complications | Enlarging nodes compress a bronchus: partial block → obstructive emphysema (ball-valve); complete block → collapse-consolidation; caseous material can burst into a bronchus, causing tuberculous bronchopneumonia; later bronchiectasis |
| Progressive primary disease | The focus enlarges and caseates, forming a primary cavity |
| Pleural effusion | A caseous node or subpleural focus discharges into the pleura, usually 6-12 months after infection, in older children |
| Miliary TB and meningitis | Massive blood spread, usually within 3-6 months, mainly in infants and children under 5 |
| Reactivation (adult-type) | Years later, especially in adolescents: apical disease and cavities, little lymphadenopathy |
The hallmark of childhood pulmonary TB is prominent hilar or mediastinal lymphadenopathy; the adult picture of apical cavities appears mainly in adolescents.
Clinical forms
Pulmonary TB
- Often few symptoms; found by contact tracing with a positive tuberculin test and an abnormal X-ray.
- Symptoms: prolonged fever, cough for more than 2 weeks, poor appetite, irritability, fatigue, weight loss or failure to thrive, night sweats.
- Signs are few; there may be wheeze from bronchial compression, or signs of consolidation or effusion.
- Erythema nodosum may appear as delayed hypersensitivity develops (Nelson).
Miliary TB
- Massive blood spread affecting two or more organs (lungs, liver, spleen, marrow, brain).
- Fever, weight loss, malaise; after some weeks hepatosplenomegaly and generalised lymphadenopathy in about half.
- Chest X-ray: fine, evenly spread "millet seed" shadows in both lungs (may be normal early).
- Choroid tubercles on fundoscopy in a proportion; Akbar notes about 30% have a negative tuberculin test (anergy).
- Headache suggests meningitis; abdominal pain suggests peritonitis.
Superficial lymph node TB (scrofula)
- The commonest extrathoracic form; usually 6-9 months after infection.
- Cervical, supraclavicular and submandibular nodes: at first firm, discrete and non-tender, then enlarging and matted; the skin may break down to form a sinus.
- Diagnosis by fine-needle aspiration or excision biopsy; responds well to ATT.
Skeletal TB
- Spine (Pott's disease): the commonest site; thoracic vertebrae are most often involved. Vertebral body destruction, disc space narrowing, wedging and gibbus (kyphosis); low-grade fever, back pain, abnormal posture or gait.
- The hip and dactylitis (fingers and toes) are next (Nelson).
Abdominal TB
- From swallowed sputum, infected milk or blood spread; ileum and jejunum near the Peyer's patches.
- Pain, diarrhoea or constipation, weight loss; ascites with a doughy abdomen and matted masses; intestinal obstruction.
Other forms
- Renal TB: rare in children (appears years after infection); sterile pyuria, haematuria.
- TB meningitis: most common under 5 years and within 6 months of infection (see the neurology chapter).
- Congenital TB: from a placental lesion or infected amniotic fluid; in the first weeks of life with respiratory distress, fever, hepatosplenomegaly, poor feeding and failure to thrive; high mortality if missed.
Diagnosis
Diagnosis in children usually combines several clues: contact history, tuberculin test, X-ray, microbiology and histology.
Contact history
Akbar counts as a contact any adult in the household or regular carer who has had anti-TB treatment within the last 2 years. Always look for the adult source.
Tuberculin skin test (Mantoux)
- A standard dose of purified protein derivative (PPD) is injected intradermally on the forearm to raise a small bleb.
- Read at 48-72 hours; measure induration across the forearm (not redness).
| Induration (Akbar) | Meaning |
|---|---|
| 10 mm or more | Positive: infection (current or past) |
| 5-9 mm | Doubtful: atypical mycobacteria or BCG; repeat on the other arm |
| Under 5 mm | Negative |
| 15 mm or more | Positive even after BCG |
Nelson uses lower cut-offs for high-risk children: 5 mm for close contacts, suspected disease or immunosuppression (including HIV); 10 mm for children under 4 years and other at-risk groups; 15 mm for older children with no risk factor.
| False negative | False positive |
|---|---|
| Severe malnutrition, measles, pertussis, other viral illness | BCG vaccination |
| Miliary TB or TB meningitis (overwhelming disease) | Atypical mycobacteria |
| Steroids, cytotoxic drugs, HIV and other immunodeficiency | Repeated tests (boosting) |
| Early infection (under about 6 weeks), poor technique | Reading error |
A positive Mantoux shows infection, not disease; a negative Mantoux does not exclude TB, especially in a sick, malnourished child.
In young children, use an early-morning gastric aspirate to look for AFB, because they swallow their sputum.
Interferon-gamma release assay (IGRA)
- A blood test measuring interferon-gamma from T cells exposed to TB-specific antigens.
- More specific than the Mantoux because it is not affected by BCG; like the Mantoux it cannot separate infection from disease.
Chest X-ray
- Hilar or paratracheal lymphadenopathy, with or without a parenchymal focus (primary complex).
- Obstructive emphysema, collapse-consolidation, bronchopneumonia, pleural effusion, miliary mottling, cavities in adolescents.
Microbiology
- Young children (under about 6 years) swallow sputum: use early-morning gastric aspirate by nasogastric tube on consecutive mornings (Akbar: positive in about 30-40%); induced sputum in older children.
- Acid-fast (AFB) stain, culture on Lowenstein-Jensen medium (4-6 weeks, plus 2-4 weeks for sensitivity); liquid (radiometric) culture gives results in about 7-10 days.
- PCR gives results within about 48 hours.
- Rapid molecular tests such as GeneXpert (which also detects rifampicin resistance) are used by Pakistan's national TB programme; check the current national guideline.
- Biopsy of lymph node or pleura; lumbar puncture if meningitis is possible; pleural or ascitic fluid shows lymphocytes and high protein.
Treatment
Principles
- Always a combination of drugs, correct dose, for the full duration.
- Directly observed treatment (DOT) ensures every dose is taken; irregular treatment breeds drug resistance.
- Treat the source and screen all household contacts.
- Hospital admission for TB meningitis, extensive pulmonary, bone, renal or miliary disease, young infants, and when surgery or steroids are needed.
Regimens (Akbar)
| Form | Intensive phase | Continuation phase | Total |
|---|---|---|---|
| Pulmonary, lymph node and most extrapulmonary TB | 2 months HRZE (isoniazid, rifampicin, pyrazinamide, ethambutol) daily | 4 months HR daily | 6 months |
| Bone and joint, disseminated (miliary) and CNS TB | 2 months HRZE | HR for longer | 9-12 months |
Nelson notes that hilar lymphadenopathy alone may be treated with 6 months of HR. Children are now treated with weight-band fixed-dose combinations; check the current national TB guideline (see WHO tuberculosis, checked 8 Nov 2026).
First-line drugs (Akbar)
| Drug | Daily dose | Key side effects and points |
|---|---|---|
| Isoniazid (H) | 10-15 mg/kg (max 300 mg) | Hepatotoxicity, peripheral neuropathy (pyridoxine for breastfed infants and children with poor diets), hypersensitivity rash; enters CSF well |
| Rifampicin (R) | 10-20 mg/kg (max 600 mg) | Orange-red urine, sweat and tears; hepatitis; flu-like illness, thrombocytopenia; take on an empty stomach |
| Pyrazinamide (Z) | 30-40 mg/kg | Hepatotoxicity, raised uric acid and joint pain; acts in acid pH inside macrophages |
| Ethambutol (E) | 20 mg/kg | Optic neuritis with loss of red-green colour vision; Akbar advises caution in young children whose vision cannot be tested |
| Streptomycin (S) | Injection | Eighth nerve damage (vertigo, ataxia, hearing loss); used as a third drug in severe or resistant disease |
Isoniazid 10-15 mg/kg × 15 = 150-225 mg
Rifampicin 10-20 mg/kg × 15 = 150-300 mg
Pyrazinamide 30-40 mg/kg × 15 = 450-600 mg
Ethambutol 20 mg/kg × 15 = 300 mg
Ethambutol causes optic neuritis (red-green colour loss); rifampicin only colours body fluids orange-red and is harmless in that respect.
Hepatotoxicity is more likely when isoniazid above 10 mg/kg is combined with rifampicin. Routine liver tests are not needed unless there is liver disease or symptoms.
Corticosteroids
- Used when inflammation is causing damage: TB meningitis, endobronchial disease with collapse or air trapping, miliary TB with alveolar-capillary block, pericarditis, peritonitis and large pleural effusion.
- Akbar: prednisolone 1-2 mg/kg/day for 4-6 weeks, then tapered.
Drug-resistant TB
Suspect it when the source case is resistant or the child fails to improve; second-line drugs (for example amikacin, kanamycin) are given through specialist programmes.
Prevention
Isoniazid preventive therapy
Akbar's indications:
- A positive tuberculin test with no clinical or X-ray evidence of disease.
- A negative tuberculin test but recent exposure to an infectious adult (young children).
- Recent conversion of the tuberculin test.
Active disease must be excluded first. Duration and regimen differ between sources (Akbar mentions 6 months and a 1-year course; Nelson gives 9 months of isoniazid); follow the current national guideline.
Newborn of a mother with infectious TB
- Do not separate the baby; continue breastfeeding.
- Baseline chest X-ray; give isoniazid for 3 months, then do a Mantoux test.
- If the test is positive, assess for disease and complete treatment; if negative, stop isoniazid and give BCG.
BCG vaccine
- Live attenuated M. bovis; given at birth, intradermally in the right deltoid (Akbar: 0.05 ml in infants).
- A papule forms, ulcerates and leaves a permanent scar in about 2 months.
- Protection against lung TB is variable (0-80%); its main value is preventing miliary TB and TB meningitis in young children.
- Not given to children known to have HIV infection (WHO, cited by Akbar).
"BCG saves the brain and blood": it mainly prevents meningitis and miliary spread.
Expect: the primary (Ghon) complex and its fate; lung as portal of entry in about 98%; why young children are not infectious; hilar lymphadenopathy as the hallmark; timing of miliary and meningeal TB; scrofula as the commonest extrathoracic form and Pott's as the commonest skeletal form; Mantoux technique, reading and cut-offs, false negatives (measles, malnutrition, miliary TB, steroids) and false positives (BCG, atypical mycobacteria); IGRA unaffected by BCG; gastric aspirate in young children; HRZE then HR for 6 months, 9-12 months for bone and CNS disease; drug side effects (orange urine, optic neuritis, neuropathy, hyperuricaemia, ototoxicity); steroid indications; isoniazid prophylaxis; newborn of a TB mother; BCG route and benefit.
Quick revision
- Source: sputum-positive adult; young children rarely infectious.
- Primary complex: Ghon focus + lymphangitis + hilar nodes; heals by calcification.
- Miliary and meningeal TB within 3-6 months, mostly under 5 years.
- Scrofula commonest extrathoracic; Pott's (thoracic spine) commonest skeletal.
- Mantoux: read at 48-72 hours; 10 mm positive (Akbar); infection not disease.
- Gastric aspirate in young children; culture slow; PCR or GeneXpert quick.
- 2HRZE + 4HR; 9-12 months for bone, miliary and CNS TB; DOT.
- H: neuropathy, liver. R: orange fluids. Z: urate. E: optic neuritis. S: eighth nerve.
- Isoniazid prophylaxis for exposed young children; BCG at birth protects against miliary TB and meningitis.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Why is childhood TB hard to confirm?
Children have few bacilli, cannot produce sputum, and often have mild symptoms, so diagnosis relies on contact history, the tuberculin test and X-ray as well as gastric aspirate culture.
Does a positive Mantoux test mean the child has active TB?
No. It means the child has been infected (or had BCG or atypical mycobacteria). Disease is shown by symptoms, X-ray or bacteriology.
Should a baby be separated from a mother with lung TB?
No. The baby stays with the mother and keeps breastfeeding, receives isoniazid preventive therapy, and gets BCG if later tests are negative.
Why is pyridoxine given with isoniazid to some children?
Isoniazid can cause peripheral neuropathy through vitamin B6 depletion. Breastfed infants and malnourished children have low stores and need it.