This document provides an overview of tuberculosis in children. It defines TB, notes its global burden, and describes the etiology and pathogenesis of the disease. Key aspects of diagnosis are outlined, including presentations, investigations, and diagnostic criteria. Treatment recommendations are presented, including regimens for new and retreatment cases. The management of exposed children and important considerations like hospitalization and steroid therapy are also covered. Potential side effects of anti-TB drugs are reviewed.

1. TUBERCULOS
IS IN
CHILDREN
BY
J.TSOFWA
Lecturer MSA MTC,
department of medicine

2. Presentation outline
 Definition
 burden
 Etiology
 Pathogenesis
 Diagnosis
 Classifications
 Treatment
 Managing the PTB exposed child

3. Introduction/ burden
 Accounts to 15% of the 9million new cases of
TB worldwide
 75% of these childhood occur in the 22 high
TB burden countries, kenya is one of them.
 Its in the increase because of HIV,poverty,
drug resistance and immigration

4. definition
 Infection caused by mycobacterium
tuberculosis
 Mycobacterium bovis causes TB in cattle

5. pathology
 Myco. Bovis infects man after drinking non
sterilised milk from infected cows
 Myco. Tuberculosis is spread by droplet
infection
 In the lungs bacteria engulfed by
macrophages thus antigen reaction limiting
replication and spread of organisms(ghon
focus)-primary lesion

6. cont
 If the innate defense mechanism of the host fails
to eliminate this infection, the bacilli proliferate
inside alveolar macrophages and kill the cells.
 The infected macrophages produce cytokines and
chemokines that attract other phagocytic cells
including monocytes and other other alveolar
macrophages and neutrophils eventually form a
nodular granulomatous structure called tubercle.

7. Cont.. pathology
 Replication of the organisms occurs within the
macrophages, which carry some of the
organisms through the lymphatic to the
regional lymph nodes
 If the bacterial replication is not controlled, the
tubercles enlarges and the bacilli enter the
local draining lymph nodes leading to
lymphadenopathy, characteristic
manifestation of primary TB

8. cont
 The lesion produced by the expansion of the
tubercles into the lung parenchyma and lymph
node involvement is called ghon complex.
 The bacilli continue to proliferate until an effective
cell mediated immune response develops, usually
2-3weeks after initial infection.
 A CMI response terminates the unimpeded growth
of the m tuberculosis 2-3weeks after initial
infection

9. Cont..pathology
 Cd4 helper T cells activate the macrophages to kill
the intracellular bacteria with resultant epithelium
granuloma formation.
 Cd8 suppressor T cells lyse the macrophages
infected with bacteria, resulting in the formation of
caseating granulomas
 Progression of the primary complex may lead to
the enlargement of hilar and mediastinal lymph
nodes with resultant bronchial collapse

10. Cont..pathology
 Progressive primary TB may develop when the
primary focus cavitates and organisms spread
through contagious bronchi
 Failure by the host to mount an effective CMI
response and tissue repair leads to progressive
destruction of the lung.
 Bacterial products, tumor necrosis factor alpha,
reactive oxygen intermediates. Reactive nitrogen
intermediates all contribute to the development

11. cont
 All of these contribute to the development of
caseating necrosis that characterises a
tuberculous lesion
 If the bacterial growth remain unchecked, the
bacteria may spread haematogenously to
produce disseminated TB resembling millet seed.
 Bacilli can also spread mechanically by erosion of
the caseating lesions into the lung airways , it is at
this point that the host becomes infectious to
others

12. Cont..pathology
 Ghon focus is a mass of granulomas around a
caseation
 Ghon complex: primary lesion+regional
lymphnodes involvement
 If bacteria spreads before establishment of
immunity, a secondary foci is formed in other
organs. Eg bones, , kidney etc , but resolves after
immune response is established and bacteria may
remain latent for many years.

13. cont
 All above are subclinical in a health person
with a positive tuberculin test.

14. diagnosis
 Careful and thorough history
 Physical examination
 Relevant investigations eg sputum smear
microscopy, chest radiology, TST.

15. Clinical manifestation
 Latent(asymptomatic) infection
 Majority no symptoms at any time
 Occasionally: marked by several days of low
grade fever and mild cough
 Rarely: child experiences a clinically
significant disease with high fever, cough,
malaise and flu-like symptoms that resolve
within one week.

16. cont
 Positive tuberculin test
 symptomatic: non productive cough and mild
dyspnoea, wheezing esp. at night are most
common symptoms
 Systemic complaints such as fever, night sweats,
anorexia and decreased activity occur less often
 Some have failure to thrive that does not improve
significantly until after several months of
treatment.

17. History/symptoms
 Hx of contact, infancy, no BCG, recent
measles, cough for more than 2weeks, FTT or
weight loss, persistent unexplained fever,
malnutrition, night sweats, long duration
illness
 Signs: serous pleurisy, cold abscess, mottled
nodes, gibbus deformity, on CXR diffuse or
hilar shadows.

18. Suggestive CXR
 Tracheobronchial adenitis with/without
parenchymal involvement
 Persistent segmental lesion with mediastinal
adenopathy...central compartment of thoracic
cavity, containing heart, lungs, trachea,
esophagus, great vessels)
 Milliary mottling... Innumerable, small 1-4mm
pulmonary nodules scattered throughout the lungs

19. Suggestive physical findings
 Serous pleurisy
 Papulonecrotic skin lesions
 Cold abscess
 Large matted lymph nodes
 History of measles infection in previous 1-3months
followed by cough more than 2weeks with wt loss
 Gibbus deformity...due to collapse of vertebral
bodies( upper lumbar and lower thoracic
vertebrae)

20. cont
 Phlyctenular keratoconjuctivitis: nodular inflammation
of cornea or conjuctiva that results from a
hypersensitivity reaction to foreign body.
 Erythema nodosum: tender bumps under skin, painful.
Non specific x ray findings
 Diffuse/bizzare pulmonary shadows( untypical,
unusual)
 Hilar shadows
 Bone defects

21. Nonspecific signs and symptoms
 Persistent cough
 Measles or whooping cough infection (recent
past)
 Weight loss/FTT
 PEM
 Prolonged unresolving pneumonia
 Recurrent respiratory infection
 Prolonged unexplained fever

22. cont
 Increased ESR
 Meningeal syndrome
 hepatosplenomegally

23. investigations
 CXR
 Hemogram, ESR
 TST
 Biopsy
 Gastric aspirate, sputum, CXR, pleural fluid,
AFBs, culture, (PCR, DNA)
 Blood culture
 HIV serology/markers

24. Key elements to successful
diagnosis of PTB in children
1:Careful history taking( including TB contact
and symptoms consistent with TB)
2:Clinical examination(especially growth
monitoring)
3:Bacteriological diagnosis
 Microscopy for acid fast bacilli
 TB culture and drug suceptibility testing where
possible

25. cont
 Histopathology depending on specimen: tissue pathology
 Xpert MTB/RIF; detects DNA sequence specific to TB and
rifampicin
 Line probe assays (LIPA)
4: chest radiology:
 Persistent lung opacification
 Diffuse micronodular infiltrates(milliary pattern)
 Pleural effusions with apical infiltrates and cavities
especially in adolescents
 The findings of marked abnormality on CXR in a child with
no signs of respiratory distress(no fast breathing or chest
indrawing) highly supportive of TB

26. cont
5: HIV testing
6: TST : a positive TST is evidence that one is
infected with MTB, but does not necessarily
indicate disease

27. Score charts/diagnostic criteria
 Presence of 2 or more of the following
symptoms
 Cough more than 2weeks
 Weight loss or poor weight gain
 Persistent fever and /or night sweats more
than 2weeks
 Fatigue, reduced playfullness, less active
 Plus:

28. cont.
 Presence of 2 or more of the following
 Positive contact history
 Respiratory signs
 CXR suggestive of PTB (where available)
 Positive mantoux test( where available)
Then PTB is likely, and treatment is justified

29. RECOMMENDED TREATMENT
REGIMEN
 Changes
1: use of four drugs during intensive phase for
all children living in HIV endemic areas such as
kenya, adding ethambutol as a forth drug for all
children of all ages.
2: treatment of TB meningitis and TB bone to be
extended to a total of 12months (2months
intensive phase, 10months continuation phase)

30. cont
3: in TB meningitis, ethambutol to replace
streptomycin during intensive phase (RHZE)
due to poor penetration of streptomycin across
the blood brain barrier as well as toxicity.

31. New WHO recommended
treatment regimen
NEW cases
 Intensive phase(2months)
 RHZ:
 ETHAMBUTOL
• 4months of continuation phase
 RH

32. Cont.: treatment
Retreatment cases
Intensive phase: 3months (RHZE)
Continuation phase: 5months (RHE)
R: rifampcin
H: Isoniazid
E: ethambutol
Z: pyrazinamide
Note: ethambutol is safe and can be used in children
in doses not exceediing 20mg/kg/day

33. cont.
 NB: all children must be on pyridoxine 1-
2mg/kg/day
Additional management decisions
 Hospitalization: severe forms of PTB,
EPTB(e,g spinal TB)
 TB meningitis
 Severe malnutrition for nutritional
rehabilitation

34. cont.
 Signs of severe pneumonia (ie chest
indrawing)
 Other co-morbidities e,g severe anaemia
 Social or logistic reasons to ensure
adherence
 Severe adverse reactions such as
hepatoxicity

35. Steroid therapy
 Indications
 TB meningitis
 PTB with respiratory distress
 PTB with airway obstruction by hilar
lymphadenopathy
 Severe milliary TB
 Pericardial effusion

36. Side effects of anti. Tuberculosis
drugs
 Isoniazid:
 Peripheral neuritis( principal side effects)
 This results from competitive inhibition of
pyridoxine metabolism
 dose; 10mg/kg
o Rifampicin
 Its relatively non toxic, the principal side
effects is hepatitis, occurs with a frequency of
1%

37. Cont..
 GI disturbances, rashes, reversible
leukopenia, thrombocytopenia and blood urea
and nitrogen
 Rifampicin potentiates the action of
anticoagulants such as dicumarol
 Changes color of body fluids like feces, urine,
sputum, saliva, tears and sweat to orange-red
color

38. cont
 Rifampicin should be included in the
treatment of all serious tuberculosis infections
 Dosage: 10-20mg/kg/day

39. pyrazinamide
 It should be used in treating myco. With
multiple drug resistance, as well as in
meningeal and milliary infections
 In doses of 20-40mg/kg/day it is well tolerated
by children.

40. ethambutol
 Its bacteriostatic at the usual dose of 15mg/kg/day
 Most important toxic effect is a retrobulbur neuritis
that infrequently results in loss of visual acuity,
defects in visual fields and inability to distinguish
between red and green; the visual changes are
completely reversible.
 The inability to monitor the toxic effect of
retrobulbar neuritis by the required visual
examinations limits its use in young children.

41. streptomycin
 It is given intramuscularly and is rapidly
absorbed into the blood stream
 The principal toxic effect is eighth nerve
damage, mainly of the vestibular branch,
resulting in vertigo and ataxia that is usually
permanent.