2. INTRODUCTIONChildhood tuberculosis is reflection of ongoing transmission of
Mycobacterium tuberculosis in a community.
Udani has discribed tb in children as a pyramid as follows.
Group 1. pt admitted in hospital and constitute 6 to 10 percent of total
admission in hospital ,majority of them have serious disease like
meningitis,miliary disease,or severe pulmonary involvement.they
constitute apex of pyramid.
Group 2.Majority of pt in this group have nonspecific symptoms,some may
have characterisitic symptom .they are either undiagnosed,untreated or
inadequately treated.
Group 3.it constitute base .the children are either asymptomatic or have
nonspecific symptoms ,hence are usually undiagnosed and
untreated.They constitute the reservoir of primary infection from which
various post primary complication devlop.these are forerunner of large
percentage of 1.adult type of tb disease among adolescent children.and
2.chronic pulmonary tb in adults.
3. Natural history of tuberculosis
infection
Time table of clinical disease after pulmonary infection in
childhood.
Phase 1- 3 to 8 wks after primary infection initial incubation
period is usually asymptomatic but at times may have
fever,erythema nodosum ,a positive tuberculin test .on
CXR there is formation of primary complex.
Phase 2 1 to 3 months after primary infection.this period
follows occult hematogenous spread occuring during
incubation period.it is the period of development of TBM
and miliary tb.
Phase 3 3 to 7 mth after primary infection .period for pl.
effusion > 5 yr children and bronchial disease in < 5 yr
children
4. Phase 4. 1 to 3 yr after primary infection and continues
until the primary complex calcified.this is the period
of osteoarticular tb in children < 5 yr.
Phase 5.it occurs more than 3 yrs after primary infection
.This represents the period in which late manifestation
of tb including pulmonary reactivation disease
devlops.
5. Childhood tuberculosis can be classified in to two broad category –
1.Intrathoracic tuberculosis
2.Extrathoracic tuberculosis
INTRATHORACIC TUBERCULOSIS
It includes 1.Primary pulmonary complex (PPC) 2.Progressive primary disease
(PPD) 3.Fibrocavitory tuberculosis 4.Bronchiectasis 5.Pleural involvement
1.Primary complex – The usual sites of primary tuberculos implantation in
lungs are the lower segment of middle lobe and upper segment of lower
lobe.Initially polymorph response later replaced by macrophage or
mononuclear response . Mycobacteria engulfed by macrophage multiplies
intracelluraly together with lymphocyte , giant cell forming a granuloma
called tubercle . The primary focus( Ghon focus) ,the draining lymphatics
and the involved regional LN are collectively called primary complex.
primary infection passes off unrecognized .Asymptomatic infection is
defined as infection associated with tuberculin hypersensitivity and a
positive tuberculin test but no striking clinical or radiological manifestation
.Most symptoms in children with primary complex are constitutional in the
form of mild fever ,anorexia , wt loss , decreased activity, Irritating dry
caugh can be a symptom of bronchial and tracheal compression due to
enlarged lymph nodes .
6. 2. PPD – Sometimes the ghon focus or its draining lymph
nodes enlarge and develop central caseous necrosis
and liquefication . Liquefication is generally associated
with the development of clinical disease. Pt may
present with moderate to high grade fever with caugh
.Expectoration and hemoptysis are usually a/w
advanced disease and development of cavitation an
ulceration of the bronchus.
3. Fibrocavitory TB – Repeated reactivation or reinfectn.
Especially in older children.
4.Bronchectasis – It may develop due to active tb or
sequalae of healed disease and may be caused
persistent atelactasis due to enlarged mediastinal LN
.C/F Caugh with copious faul smelling sputum.
7. Pleural disease – a.Allergic reaction to subleural focus
results in acute onset large pl. effusion in
previouslywell nourished child.
b. Tubercle bacilli directly spill over due to bursting of
subpleural foci
Empyema neccesitans rarely and dry pleuritis also occur.
11. Specimenfor demonstrationof M.tuberculosis
1.Sputum – It is difficult to collect sputum in young children
.Therefore gastric aspirate is used .for induction of sputum
child is nebulised with salbutamol 200 to prevent
bronchoconstriction.A jet nebuliserattached to oxygen @ 5
l/min or compressor can be used to deliver 5 ml of 3 % saline
for induction.If expectoration is difficult as usaully in children
suctioning nasopharynx or oropharynx using mucus extractor
size 6 can be done to obtain sample.
2.Gastric lavage – the best specimen in children.Early morning
gastric aspirate obtained by using NG tube before the child
wakes up and peristalsis empties the stomach of the
respiratory secretions over night.
3.Bronchoscopy and bronchoalveolar lavage – Bronchoscopy is
cnsidered when diagnosis is doubtful or resistant tb is
considered
12. Method for identification of M.Tuberculosis
A.Smear - ZN stain , auramine o stain (needs fluroscopy)
B.Culture – LJ Media(8 wks approx),BACTEC(9 to 14
days),Septicheck AFB system( 3 wks),Mycobacterial growth
indicator tube system(MGIT)
C.PCR
D.Gas liquid chromatography (GLC) or High performance liquid
chromatography – Analysis of long chain fatty acid.fatty acid is
species specific
Method for identification of M.tuberculosis exposure through
host response
1.Tuberculin skin test – Using 2tu PPD with RT23 and tween 80
2.PCR based cytokine detection in tuberculosis
3.Circulating immunecomplexes glycolipid LOS ,DAT,and PGL tb1
4.Radiology
13. Method to diagnose latent tuberculosis infection
Recently ,New in vitro diagnostic aid that measure a
component of cell mediated immune activity in response
to infection, and is based on IFN gamma released from
sensitised lymphocyte in whole bld incubated over night
with different antigen from M tuberculosis .initially
Antigen used were PPD,Now a days more specific antigen
like ESAT-6,CFP 10,TB 7.7 (Rv 2654). Commercialy
available test for it QFT -IT,and T-SPOT.TB .
14. Basis of treatment – Children with primary tb and EPTB
are infected with less number of tubercle bacilli and
expected bacillary load is paucibacillary .although
paucibacillary another consideration is primary
resistance (naturally occuring resistance even before
chemotherapy).The occurrence of chance resistance is
unrelated to that of other ATT drug so Combination
therapy decreases the chance of resistance.As the
organism to be naturally resistant to two drug the
population size would have to be 10 11 to 10 17 which is
comperatively rare in clinical practice.