This document summarizes childhood tuberculosis. It begins by defining tuberculosis and describing the portal of entry and primary infection. It then discusses the clinical states that can arise from TB infection in children versus adults. The rest of the document details various forms of TB based on organ system affected, along with their associated symptoms, presentations and complications. Radiological findings are also described. The diagnosis, treatment and policies for childhood TB are outlined.

1. CHILDHOOD
TUBERCULOSIS

2. Tuberculosis
 Tuberculosis is a chronic infectious disease caused by
Mycobacterium tuberculosis characterized by vague
constitutional symptoms and a protracted course of
illness with remissions and exacerbations.
 Tuberculosis is the reaction of tissues of the human
host to the presence and multiplication of Mycobacterium
tuberculosis.
 The clinical states arising from TB infection are the
outcome between the capacity of the host to contain
and eliminate the organism versus the capacity of the
organism to multiply and proliferate.

3. Portal of entry for tuberculosis
 Inhalation of Tubercle bacilli in >95% (M.TB)
 Ingestion of milk containing Bovine
Tubercle bacilli (M. bovis)
 Contamination of superficial skin or
mucous membrane lesion with tubercle
bacilli
 Congenital infection when mother has
lymphohematogenous spread during pregnancy
OR tuberculous endometritis

4. Primary tuberculous infection
Primary Focus (Ghon’s focus)
 at the site of first implantation
 usually single and Subpleural
 in most, - heals and disappears, or
 - fibroses or calcifies.
Primary Complex:
 primary focus + Hilar lymphnodes + draining
lymphatics
 complications arise more commonly from regional
adenitis than from the primary focus

5. Primary infection
Children vs. Adults
 In adults,
- regional lymphadenitis less marked
- bronchial erosion less frequent
- less risk of dissemination
 Thus, adult primary infection tends to be
more local and pulmonary.

6. Progressive primary tuberculosis
 Progression of TB depends on the age of
the child, number of tubercle bacilli, and
host resistance.
 Apparently healed focus or nodes may contain
viable organisms for many years.
 During 1st 4-8 weeks, organisms are disseminated
in the blood stream.

7. Progressive pulmonary disease
 Progressive primary infection: Progression of
recently acquired pulmonary primary
infection
 Endogenous exacerbation: reactivity of
organisms and breakdown of primary
lesions acquired > 5 years previously
 Exogenous exacerbation: Re-infection by newly
acquired bacilli in persons with healed primary
lesions

8. Symptoms of childhood
tuberculosis
1. Failure to thrive } &
2. Intermittent fever } are the commonest symptoms
3. Pleural effusion
4. Ascites
5. Abdominal mass (Painless)
6. Limp / Arthritis
7. Painless lymphadenopathy
8. Persistent skin ulcer
9. Sterile pyuria
10. Meningitis

9. Pulmonary lesions in tuberculosis
- the primary complex

10. Complications of the primary
focus
1. Rupture of focus into pleural space
causing serous effusion
2. Rupture of focus into bronchus
causing cavitation
3. Enlarged focus, sometimes laminated or “coin”
shadow

11. Complications of regional nodes
1. Incomplete (ball-valve) bronchial obstruction,
emphysema of middle & lower lobes
2. Complete bronchial obstruction, collapse
of right lower lobe
3. Erosion of node into bronchus &
segmental consolidation
4. Rupture of node into pericardium:
tuberculous pericardial effusion

12. Sequelae of bronchial complications
1. Stricture of bronchus at site of erosion
2. Cylindrical bronchiectasis in area of old
collapse
3. Wedge shadow: contracture & fibrosis
of segmental lesion
4. Linear scar of fibrosis following
segmental lesion

13. Symptoms
 Primary complex – mild fever, anorexia, weight
loss, decreased activity, cough
 Progressive primary complex – high grade fever,
cough. Expectoration and hemoptysis – usually
associated with cavity and ulceration of
bronchus.
Abnormal chest signs – decreased air entry,
dullness, creps

14.  Endobronchial tb – wheeze!!
Fever, troublesome cough, dyspnea, wheezing
and cyanosis
 Pleural effusion – follows a rupture of a
subpleural focus. Also by hematogenous spread
from primary focus. Occurs coz of
hypersensitivity to tuberculoproteins.
Fever, cough, dyspnea, pleuritic chest pain.

15. Miliary tuberculosis


most common within 1st3 to 6 months after
infection
due to heavy hematogenous spread of
tubercle

bacilli
Onset: Insidious, with
Fever and weight loss
Palpable liver and/or spleen
Tachypnoea with normal chest findings

16. Miliary tuberculosis
 Hematogenous dissemination leads to progressive
development of small lesions throughout the body,
with tubercles in the
 lung, spleen, liver,
 bone marrow, heart, pancreas
 brain, choroid, skin
 Radiologic diagnosis:
 “Snow storm” appearance
(Multiple small lung nodules 1mm size and above in
both lung fields).

17. Miliary TB

18. Cutaneous Tuberculosis
1. Associated with primary complex

(Direct inoculation into Traumatized Area)
- Painless nodule, leading to non healing ulcer with regional
lymphadenitis
 - Scrofuloderma over ruptured caseous lymph node
2. Associated with Hematogenous dissemination


- Papulonecrotic tuberculids
papules with soft centers on trunk, thighs and face
- Tuberculosis verrucosa cutis
Large tuberculids on arms and legs
3. Associated with hypersensitivity to tuberculin
 - Erythema nodosum
painful indurated nodules on shins, elbows, forearms that
subside in 2-3 weeks

19. TB verrucosa cutis

20. Erythema nodosum

21. Tuberculosis of superficial
lymph nodes (scrofula)
 Tonsillar / submandibular
(Spread from paratracheal nodes)
 Supraclavicular
(From primary lesion in upper lobe)
 Axillary / epitrochlear
(From skin lesion on hand)
 Inguinal
(From ulcer on sole of foot)

22. Ocular Tuberculosis
 Primary tuberculous conjunctivitis (after trauma)
Yellowish – gray nodules on palpebral conjunctiva
with preauricular adenopathy
 Phlyctenular conjunctivitis (Hypersensitivity)
Nodules on limbus recurring in crops for weeks
 Tubercles of choroid (with miliary TB)

23. Choroidal tubercles

24. Tuberculous otitis media
 Primary with Preauricular adenitis
 Metastatic spread with primary elsewhere
 Symptoms: Painless otorrhea, may be blood-
stained
Complications: Secondary infection



Deafness
TB meningitis

25. GI and Abdominal TB
 Hematogenous spread from lungs or swallowing
of infected sputum.
 Painless ulcer in gingivolabial sulcus with
submental or submandibular adenopathy
 Ulcer on tonsil
 Esophageal diverticulum secondary to rupture
of mediastinal nodes into lumen

26.  Tuberculous toxemia
 Present with colicky abdominal pain, vomiting and
constipation.
 Abdomen feels doughy.
 Rolled up omentum and enlarged lymph nodes may
appear as irregular nodular masses with ascites
 Tuberculous enteritis
Ulcers, mesenteric adenitis, peritonitis
Adhesions, subacute intestinal obstruction,
Hepatosplenomegaly

27. Renal tuberculosis
 Tubercles in glomeruli lead to shedding
of tubercle bacilli into tubules
 Caseous mass / Cavity between cortex and
pyramids
 TB of bladder (Tuberculous cystitis)
 Symptoms: dysuria, hematuria,
pyuria with TB bacilli

28. Caseous renal tuberculosis

29. Skeletal tuberculosis
 Bones involved in order of frequency:
Vertebrae > knee > hip > elbow
Upper extremities and non-weight-bearing bones
(skull, clavicle) rarely involved
 Tuberculous spondylitis most commonly
Thoracic / Lumbar / Both (Decreasing frequency)
 X-ray findings:
Narrowing of disc space, Collapse of
vertebral body
Extensive destruction with kyphosis (Pott disease)
 Complications:Para vertebral abscess (Pott abscess)
Psoas Abscess. Paraplegia, Quadriplegia (cervical)

30. Genital tuberculosis
 Uncommon before puberty
 Usually due to lympho-hematogenous spread
 Occasionally by direct extension from
adjacent lesion of bone, gut, or urinary
tract

31. Genital tuberculosis
 Salpingitis
 Endometritis
 Oophoritis
 Cervicitis
 Infertility is commonest sequel
 in males:
 Primary tuberculosis of penis after
circumcision with inguinal adenopathy
 Epididymitis / Epididymo – orchitis in early
childhood

32. Tuberculous meningitis
TB meningitis seen in 1/300 Primary infections
Pathophysiology:
Rupture of a subcortical caseous focus (Rich’s) into the
subarachnoid space.
Inflammatory exudates form about base of brain and
along cerebral vessels as they pass over hemispheres.
Raised intracranial pressure due to increased secretion
of CSF
Adhesions along base and roof of 4thventricles lead to
obstruction to CSF flow and hydrocephalus,
involvement of cranial nerves III VI VII and optic chiasma.
Cerebral endarteritis narrows lumen, reduces blood flow,
leads to cerebral thrombosis and infarction.

33. Stages of TB meningitis
Stage I Irritability, anorexia, personality change
Stage II
Occasional vomiting, fever
Poor school performance
Focal neurological signs, cranial nerve palsies,
Seizures, hemiplegia, squint
Stage III Loss of consciousness, Coma, Papilloedema
Decerebrate rigidity

34. Complications of TB meningitis
Hydrocephalus
Subdural effusion
Late: Hemiplegia / Paraplegia
Intellectual impairment
Blindness
Deafness
Intracranial calcifications leading to
hypothalamic and pituitary dysfunction
- Growth failure
- Diabetes insipidus
- Failure of development of secondary
sexual characteristics

35. Diagnosis of TB meningitis
 Signs of meningeal irritation
 X-ray chest
 CT scan – basal exudates, inflammatory granulomas etc
 Tuberculin testing
 Retinoscopy for choroidal tubercles
 Lumbar puncture
Elevated CSF pressure(30 – 40cm h2o)
Cobweb Coagulum/ pellicle on standing
100 – 500 WBCs / cu.mm
>40 mg% protein
Low / Normal sugar
AFB smear & culture

36. Prognosis in TB meningitis
100% mortality in 3-4 weeks without treatment
100% survival with treatment started in Stage I
75% survival with treatment started in Stage II
Stage III – variable survival, all will have sequelae

37. Direct tests for tuberculosis
 Ziehl-Neelsen staining for AFB in clinical specimens
(sputum, gastric juice, biopsy)
 AFB culture on Lowenstein-Jensen solid medium (4
weeks)
 PCR amplification of targeted mycobacterial DNA
sequences
 DNA probes: fluorescence in situ hybridization assays

38. Culture
 LJ medium
 BACTEC radiometric assay
 Septichek AFB system
 MGIT – mycobacterial growth indicator tube
system

39.  PCR – rapid results
 Serodiagnosis – ELISA
 QuantiFERON- TB test (QFT) – for diagnosing
latent TB. Based on IFN-gamma released from
sensitized lymphocytes.
ELISPOT

40. Positive Mantoux

41. Mantoux Test
 MC used test for establishing diagnosis of TB
in children
 Delayed type hypersensitivity reaction
 0.1 ml of 5 TU PPD is injected intradermally
into the volar aspect of the forearm (or 2 TU
of PPD RT 23)
 A weal of 5 mm should be raised
 Reaction is read after 48 – 72 hrs
 Look for induration and erythema

42. Observation and Inference
 48-72 hours later  diameter of induration
is measured transversely to the long axis of
the forearm.
 Induration > 10mm is suggestive of
natural infection.
 5-10 mm  borderline; considered positive in
immunocompromised host
 <5mm  Negative mantoux test does not rule
out TB

43. False Negatives
 Test done in incubation period of TB
 For several weeks following measles
 During Corticosteroid therapy
 Overwhelming TB infection (milliary, meningits)
 Severe Malnutrition
 If given Sub Cutaneous instead of Intra dermal
 Inactive Tuberculin

44. False positive
 Atypical mycobacteria
 BCG vaccine
 Infection at site of test

45. Guidelines for presumptive diagnosis
of tuberculosis
Pediatr Infect Dis J 1993;12: 499-504)
 A combination of at least 3 of the following:
 Symptoms/signs s/o TB:
(fever > 1 mo., cough, weight loss)
 History of close contact with TB
 Positive tuberculin skin test (Mantoux > 10 mm)


sputum / gastric juice AFB +ve
lymph node / tissue biopsy positivity
 Radiologic features suggestive of TB
 Response to Anti TB Therapy

46.  History of contact = any child who lives in a
household with an adult taking ATT or has
taken therapy in the past 2 years

47. Radiology
 In extra pulmonary tb, presence of lesions on chest
radiograph supports diagnosis.
 Enlarged lymph nodes in hila, right paratracheal region
 Consolidation in progressive primary disease –
heterogenous, poorly marginated with predilection to
apical or posterior segments of upper lobe or
superior segments of lower lobe.
 Bronchiectasis
 Pleural effusion
 Miliary tb – millet sized lesions

48. Treatment for TB
1stline anti-tuberculous drugs
 Isoniazid (INAH)
Rifampicin
 Pyrazinamide
Ethambutol
 Streptomycin
5 mg/kg/day H
10 mg/kg/day R
25 mg/kg/day Z
20 mg/kg/day E
20mg/kg/day S

49.  2ndLine drugs
 Drug resistant cases or when first line drugs cant be used
 Eg. Cycloserine, ethionamaide, PAS, kanamycin
 Other drugs
 Strictly for drug resistant cases
 Eg. Quinolones, rifamycin, amikacin, imipenem,
ampicillin

50. Phases of Treatment
 Intensive Phase
 Eliminate bacterial load
 Prevent emergence of drug resistant strains
 Atleast 3 Bactericidal Drugs used
 Continuation Phase
 Continue and complete therapy
 Atleast 2 Bactericidal drugs used
 Steroids
 Anti inflammatory effect – millary, peritonitis, pericarditis
 TB meningitis

51. RNTCP Treatment

52. Treatment policies in children
with tuberculosis (IAP)
 Preventive Therapy In Mantoux Positive : 6 HR
 Primary complex
 Isolated LNE
}
} 2 HRZ + 4 HR
 Pleural Effusion }
 Progressive Pulmonary Tuberculosis }
 Multiple LNE } 2 HRZE + 4 HR
 Miliary, Bone, Renal, Pericardial }
 TB Meningitis }
2 HRZE + 7HR
2 HRZE + 10 HRE +
Prednisolone / Dexamethasone

53. The 5 components of DOTS
Political & administrative commitment
Diagnosis by good quality sputum microscopy
Adequate supply of good quality drugs
Directly observed treatment
Systematic monitoring & Accountability

54. Drug Resistance
 Natural or Primary
 Acquired
 Initial
 Multidrug resistance (MDR)

55. Treatment of resistant
tuberculosis
 INH-resistant TB: 18 RZE
 Rifampicin-resistant TB: 18 – 24 HZE
 Multidrug-resistant TB:
 Treat for 24 mo. after culture conversion
with regimen containing 3 second-line
drugs, including IM aminoglycoside/ SM,
one fluoroquinolone and one oral 2ndline
drug.

57. References
 Nelson’s textbook of paediatrics
 OP Ghai – Essential Paediatrics
 Preventive and Social Medicine – Park & Park
 The Internet…