A child can be infected with TB bacteria and not have active disease. The most common symptoms of active TB include fever, cough, weight loss, and chills. TB is diagnosed with a TB skin or blood test, chest X-ray, sputum tests, and possibly other testing or biopsies. TB treatment requires medicines for a few months.

1. 7/11/2021
1
CHILDHOOD TUBERCULOSIS

2. Outline
2
 Epidemiology
 Etiology
 Transmission
 Pathogenesis
 Clinical manifestations
 Diagnosis
 Management
 Prevention

3. Epidemiology
3
 One third of the world population is infected with M.TB
 In 2012, an estimated 8.6 million people developedTB
and 12 million prevalent cases ofTB globally
 1.3 million died from the disease (including 320 000
deaths among HIV-positive people)
 Globally in 2012, an estimated 450 000 people
developed MDR-TB and there were an estimated 170
000 deaths from MDR-TB
 The number ofTB deaths is unacceptably large given that
most are preventable

4. 4
 There were an estimated 0.5million TB cases among
children (under 15 years of age) and 74 000TB deaths
(among HIV-negative children) in 2012 (6% and 8%) of
the global totals, respectively
 The 22 High Burden Countries (HBCs) accounted for
82% of all estimated cases worldwide
 In Ethiopia according toWHO 2012:
 Prevalence was estimated to be 210,000( 224 per
100,000 population )
 Incidence was estimated to be 230,000( 247
per100,000 population)

5. Estimated TB incidence WHO 2012
5

6. 6
 The global burden ofTB remains enormous:
oHIV epidemics
o Poverty
o Crowding
o InefficientTB control programs
o Inadequate health coverage & poor access to
health services

7. Latent TB infection(LTBI)
7
 LatentTB infection(LTBI)-occurs after inhalation
of infected droplet nuclei with M.TB
This stage is characterized by:
ReactiveTuberculin skin test
Absence of clinical and
Absence of Radiological evidence of activeTB

8. 8
TB(Disease)-refers to apparent signs and symptoms
or radiologic changes of activeTB
Untreated infants with LTBI have 40% liklihood of
developing disease compared with only 5-10% in
adults
The greatest risk of progression occurs during the 1st
2yr after infection.

9. High risk of infection
9
 Close contacts of person withTB
 Foreign born persons from high risk countries
 High risk congregate settings
 Low socio-economic status
 Injection drug users

10. 10
 Risk for progression toTB disease from
LTBI increases in:
Infants & children below 5yrs of age (esp.<2yrs)
Co-infected with HIV
Persons with skin conversion in the past 1-2yr
Immunocompromization (malignancy,
drugs,DM,malnutrition)

11. 11
 Key risk factors forTB:
Strong contact with newly diagnosed smear +ve case
Age below 5yrs
HIV infection
Severe malnutrition

12. Etiology
12
 MycobacteriumTuberculous complex:
 M.Tuberculosis
 M.Bovis
 M.Africanum
 M.Microti
 M.Canetti
 All belong to the orderActinomycetales and
family Mycobacteriaceae

13. 13
M.TB
o Most important tuberculosis disease in humans
o Non-spore forming, Non-motile, Obligate aerobe
o Slow-growing, Grow best at 37-41o
C
o Cell wall with high lipid content which gives
“acid-fast” staining properties (resistance to
decolorization with acid alcohol)

14. Transmission & Pathogenesis
14
 Incubation period from infection to
development of +ve tuberculin test is 2-
6wks
 Transmission is person to person (usually by air
borne mucus droplet nuclei)
 Rarely occurs by direct contact with an infected
discharge or a contaminated fomite

15.  Risk of transmission is increase with
index case:
Smear positiveTB
Extensive upper lobe infiltrate & cavity
Copious production of sputum
Severe & forceful cough
Not treated
15

16. 16
 Environment:
Poor ventilation
Overcrowding
Intimacy
 Young children (<7yrs) rarely infect others b/c:
Sparse bacilli in the endobronchial secretions
Cough is often absent or lacks the tussive force
to suspend infectious particles of correct size
 M.bovis may penetrate the GI mucosa or invade
the lymphatic tissue of oropharynx when large
numbers are ingested

17. 17
 The risk of infection of a susceptible individual is high
with close,prolonged,indoor exposure to a
person with sputum smear-positive
pulmonaryTB.

18. Pathogenesis
18
 The 1o complex ofTB includes local infection at the portal
of entry & regional LNs.
 Lung is portal of entry in more than 98% of cases.
 Bacilli multiply initially within alveoli & alveolar ducts.
 Most are killed, some survive within non activated
macrophages; Macrophages carry the bacilli to regional LNs
by lymphatic vessels.
 If lung is portal of entry, hilar LNs are often involved but
paratracheal LNs may be involved(upper lobe).

19. 19
 Tissue reaction in the lung parenchyma & LNs intensifies over
the next 2-12wks
The parenchymal lesion of 1o complex often heals
completely by fibrosis or calcification.
Occasionally may continue to enlarge & result in focal
pneumonitis & pleuritis
If caseation is intense, center of the lesion liquefies & empties
into the bronchus leaving a residual cavity
The infection of regional LNS develop some fibrosis &
encapsulation, but healing is usually incomplete
Viable M.TB can persist for decades within parenchymal or LN
foci

20. 20
o If hilar & Para tracheal LNs enlarge(as part of host
inflammatory reaction), they may encroach on a regional
bronchus :
o Partial obstruction bronchus Distal hyperinflation
o Complete obstruction Atelectasis
Inflamed caseuos nodes can attach to the bronchial wall &
erode through it, causing endobronchialTB or a fistula tract
 A combination of pneumonitis and atelectasis
results in collapse-consolidation or segmental
lesion.

21. 21
Bacterial replication occurs in organs with conditions that
favor their growth:
Lung apices
Brain
Kidneys
Bones
 DisseminatedTB occurs if:
o Circulating number of bacilli is large and
o Host immune response is inadequate

22. 22
 The time b/n initial infection & clinically apparent
disease is variable:
o Disseminated & meningealTB are early manifestations
(2-6months after infection)
o TB LAP & endobronchialTB(3-9months)
o Bones & joints take several years
o RenalTB takes decades after infection
 PulmonaryTB that occurs more than a year after 1o infection is
usually due to endogenous regrowth of bacilli
persisting in partially encapsulated lesions.
 Common site of reactivation is the apex of upper lobes.

23. Immunity
23
 Cell-mediated immunity develops 2-12wk after infection ,
along with tissue hypersensitivity.
 After inhalation into the alveolus , bacillus is ingested by
macrophages but may not be killed
 Alveolar macrophages present the antigen to T-
lymphocytes, producing DTH, which together with newly
activated macrophages causes IC killing of bacilli &
granuloma formation.
 Development of specific cellular immunity prevents
progression of the initial infection in most persons.

24. 24
 The pathologic events in the initial tuberculous
infection depend on the balance between:
Mycobacterial antigen load
Cell-mediated immunity(enhance IC killing)
Tissue hypersensitivity(promotes extracellular killing)
 When Ag load is small & tissue hypersensitivity is high
 Granuloma formation (from organization of lymphocytes,
macrophages and fibroblasts)

25. 25
 When both (Ag & sensitivity) are high:
Granuloma is less organized
Tissue necrosis is incomplete
Results in formation of caseous material
 When degree of tissue sensitivity is low ( infants ,
low immunity)
Diffuse reaction
Infection is not well contained
Results in local tissue damage and dissemination

26. 26
 Factors that predispose to serious disease:
Young age
Genetic factors
Immunosuppresion (AIDS,malnutrition, measles,
pertussis, malignancy,steroids)

27. Tuberculin Skin Test (Mantoux Test)
27
 Id, 0.1ml, 5TU of PPD, volar surface of arms
 T-cells sensitized by prior infection are recruited to the skin;
release lymphokines that induce indurations through local
vasodilatation, edema, fibrin deposition and recruitment of
other inflammatory cells
 Amount of induration is measured 48-72hrs after
administration
 Tuberculin sensitivity develops 3 wk to 3 mo (most often
in 4-8 wk) after inhalation of organisms

28. Fig. TST induration
28

29. Positive TST
29
 >5 mm diameter of induration
oIn children who are immunosuppressed ( HIV-
positive children)
oSeverely malnourished child
 >10 mm diameter of induration
o In all other children (whether they have received a
BCG vaccination or not)

30. 30
 False positive result:
o Cross-sensitization to Ags of
NTM(nontuberculous microbacterium)
(usually below 10mm)
o BCG
50% never develop the reaction.
Reactivity usually wanes in 2-3yrs
If > 10mm , it is taken as +ve
BCG is not a contraindication to PPD test

31. 31
 False Negative:
Young age(below 3months)
Malnutrition
Immunosupression
Viral infections (measles, mumps, varicella,
influenza)
Vaccination with live-viruses (within 6wks)
OverwhelmingTB

32. Interferon-γ Release Assays
32
 Two blood tests (T-SPOT.TB and Quanti FERON-TB)
 Detect IFN-γ generation by the patient'sT cells in
response to specific M.tuberculosis antigens
 Advantage overTST
 only one patient encounter,
 lack of cross reaction with BCG and most other
mycobacteria
 Should be interpreted with caution when used for children
<5 yr of age and immunocompromised

33. Clinical manifestations
33
1. Pulmonary
2. Extrapulmonary- occurs in 25-30% 0f children
-increases in HIV infection
Primary Pulmonary Disease
 70% of lung foci are subpleural & localized pleurisy is
common
 All lobar segments of the lung are at equal risk of initial
infection
 Enlarged LNs obstruction& compression of regional
bronchus
 Usual sequence: hilar LAP focal hyperinflation
atelectasis

34.  Subcarinal LAP may cause esophageal compression
& rarely bronchoesophageal fistula
 In children may have lobar pneumonia without
impressive hilar LAP
 Erosion of a parechymal lesion into blood or
lymphatic vessel may result in dissemination of
bacilli & a military pattern (small nodules
distributed on CXR)
34

35. 35
S/Sx of Primary Pulmonary Disease:
 Surprisingly minimal out of proportion of X-ray findings
 More than 50% with moderate –severe CXR findings have
no physical signs
 Infants are more likely to experience S/Sx
 Systemic (fever, night sweat, anorexia, decreased activity)
 Failure to thrive
 If bronchial obstruction, localized wheezes or decreased
breath sounds
 In young children (<3yr), milliaryTB may occur

36. 36
 Dx of primary pulmonaryTB:
Most specific is isolation of M.TB
• Sputum (>7yr) forAFB stainig & culture
• Early morning gastric aspirate (young age)
Yield is low (25-50% positive with 3cultures)
Negative culture never exclude pulmonaryTB
If positiveTST or IGRA,abnormal CXR &
contact Hx, adequate evidence

37. Progressive primary pulmonary TB
37
 Occurs when the primary infection is not contained
& produces bronchopneumonia or lobar pneumonia
(usually middle, lower) & cavitations
 High grade fever, severe cough with sputum,
weight loss, night sweats
 Reduced breath sounds, rales, dullness or egophony
over the cavity
 TST is reactive

38. Reactivation pulmonary TB
38
 Rare in children
 Most frequent site are the original parenchymal focus,LNS or
the apical segments (Simon foci) established during the
hematogenous phase of early infection
 Usually there is little/no LAP & no extathoracicTB b/c of
the established immune response preventing spread
S/Sx: related with cavitation & endobronchial spread
 Fever, night sweat, malaise, weight loss
 Productive cough, heomptysis
 CXR (commonly)- extensive infiltrates or thick-walled
cavities in the upper lobes

39. Upper Respiratory Tract TB
39
o LaryngealTB
 Croup-like cough, sore throat, hoarseness, dysphagia
 Most have extensive upper lobe pulmonary disease
 Occasionally primary laryngeal disease with normal CXR
o Middle earTB
 Painless unilateral otorrhea
 Tinnitus, decreased hearing, perforation of tympanic membrane
 Due to aspiration of infected pulmonary secretion or
hematogenous
 Preauricular & cervical LAP may be accompanied with it

40. Lymphohematogenous (Disseminated) Disease
40
MilliaryTB
 The most clinically significant form of disseminated
tuberculosis
 Occurs when massive numbers of tubercle bacilli are
released into the bloodstream
 Diagnosed when > 2organs are involved
 Commonly involved organs are: lungs, liver, spleen & BM
 Choroid tubercles are specific for Dx of milliaryTB
 Lesions are of roughly same size as that of a millet seed
 Development of disseminatedTB depends on:
 Number of bacilli released from primary focus
 Adequacy of immune response

41. 41
 S/Sx:
 Fever, weakness, malaise, anorexia,
 weight loss, LAP,
 night sweats & Hepatosplenomegally
 Diffuse bilateral pneumonitis & meningitis may
be noted
 Anemia, monocytosis, thrombocytopenia &
abnormal LFT are common
 Diagnosis can be difficult, needs high index of suspicion
and often presents with FUO
 TST is positive in only 60% of cases
Liver & BM Bx may be needed for DX

42. Extrapulmonary Tuberculosis (EPTB)
42
 Every organ can be affected by tuberculosis
 Common forms of extra pulmonaryTB in children:
TB Lymphadenitis
• TB of Superficial LNs (Scrofula) is most common form of
EPTB
• Tonsilar, anterior cervical, submandibular & supraclavicular
nodes are involved secondary to extension of lesions of
upper lung lobes & abdomen
• Inguinal, epitrochlear or axillary are associated with skin or
boneTB

43. TB Lymphadenitis…
Disease is usually unilateral, initially firm, discrete, non-
tender
when multiple nodes involved and mass of matted nodes will
be formed
Systemic symptoms (except fever) are rare
TST is usually reactive and CXR is normal in 70% of
cases
If untreated
 May resolve spontaneously
 Progress to caseation & necrosis (common)
Capsule will be ruptured & spread to adjacent nodes and
usually results in draining sinus tract
43

44. 44
 Dx ofTb lymphadenitis is
histiologic/bacteriologic confirmation
(FNA or excisional Bx).
 Culture yield is 50% of the cases.

45. Pleural disease
45
 TB effusion can be localized or generalized.
 May result from discharge of bacilli into the pleural space
from a subpleural pul. focus or caseated LN.
 Asymptomatic local pleural effusion is so frequent in primary
TB which is basically a component of the primary complex
 Large effusions occur months-yrs after primary infection
 TB effusion is infrequent in children below 6yrs and
rare < 2 years

46. 46
 Usually unilateral
 Rare in disseminatedTB
S/Sx:
 Radiologic finding is more extensive than physical findings
 Onset is usually sudden (fever, SOB, chest pain
during inspiration, reduced breath sounds)
 TST is positive in 70-80% of cases
 Prognosis is excellent

47. 47
Dx
 Pleural fluid & membrane examination
 Pleural tap (Thoracentesis)
- fluid is usually yellow (sometimes tinged with blood)
- Sp.gr is 1.02-1.025
- Glucose is low
- AFB is rarely positive
- culture is positive only in 30% of the cases
 Pleural membrane Bx
 has high yield of AFB & culture
 granuloma can be demonstrated

48. Pericardial TB
48
 Rare, 0.5- 4%
 Most common form of cardiacTB
 Usually arises from direct invasion or lymphatic
drainage from subcarinal LNs
 S/Sx:
 fever, malaise, wt.loss
 Chest pain (not common in children)
 Pericardial friction rub, Distant heart sounds,
Pulsus paradoxus

49. Pericardial TB….
 Pericardiocentesis:
 AFB staining is rarely positive
 culture is positive in 30-70% of cases
 pericardial Bx
 culture yield is higher
 granulomas are suggestive
49

50. CNS TB
50
 Most serious complication of dissemination (fatal if
no Rx)
TB meningitis
 complicates about 0.3% of untreated tuberculosis infections
in children
 Usually arises from the formation of a metastatic caseaus
lesions (cerebral cortex or meninges) that develop
during the lymphohematogenous spreed of primary
infection

51. 51

52. 52
Brain stem is often the site of greatest
involvement.
Commonly involved Cranial nerves are III,VI, and
VII
 The combination of vasculitis, infarction, cerebral
edema, and hydrocephalus results in severe damage
(gradual,rapid)
 Electrolyte abnormalities (abnormal metabolism, SIADH)
also contributes to the pathogenesis ofTB meningitis
 Most common b/n 6mo-4yrs

53. 53
 Clinical manifestation
 Rapid or slowly progressing
 Can be divided into 3 stages
Stage I (1-2wks):
 Non-specific symptoms
(fever, headache ,
irritability, malaise)
 Focal neurologic deficits
are rare
 Stagnation or loss of
developmental milestones
Stage II:
 Lethargy
 Nuchal rigidity
 Seizures
 Hypertonia
 Vomiting
 Cranial nerve palsies
 Positive Kerning &
Brudzinski sign

54. 54
Stage III:
 Coma
 Hemi-or para-plegia
 Hyperetension
 Decerebration
 Deterioration of vital signs
Prognosis is dependent on stage ofTB
meningitis
 Stage I: almost all survive without sequelae
 Stage II: 10-20% mortality and sequelae
 Stage III: 50% mortality and almost all remain with
sequelae

55. 55
 Common permanent disabilities:
Blindness
Deafness
Paraplegia
Diabetes Insipides
Mental retardation
Prognosis is worse in infants

56. 56
Diagnosis:
o high degree of suspicion
o TST is positive in 50%
o CXR is normal in 20-50%
o CSF-WBC(10-500/mm3)
increased protein (400-5,000mg/dl)
glucose is usually < 40mg/dl
AFB & culture yield is dependent on volume of CSF
 (if 5-10ml:AFB is +ve in 30%, cultture –50-70%)
o CT/MRI of the brain
o Normal in early stages
o basilar enhancement, hydrocephalus ,cerebral
edema, focal ischemia

57. 57
Tubeculoma
 Presents as brain tumor
 In children most common infratentorial(base of the
brain near the cerebellum)
 Lesions are most often singular
 S/Sx:
 headache, seizure, fever and focal neurologic deficit
 TST is usually reactive
 CXR is usually normal
 Dx: CT/MRI- discrete lesions with significant
surrounding edema and ring enhancement

58. GI/Peritoneal TB
58
 GITB
 Oral cavity or pharynx is rare, most common lesion is
pain less ulcer
 EsophagealTb is rare (may be associated with
tracheoesophageal fistula)
 TB Enteritis
 Caused by hematogenous route or swallowing of bacilli
from their own lungs or ingestion of raw milk (M.bovis)
 Most common sites of involvement; ileum, jejunum
& appendix

59. 59
 Clinical manifestations
 Pain, diarrhea/constipation, wt.loss, fever due to
shallow ulcer
 Mesenteric adenitis is common
 Enlarged nodes may cause intestinal obstruction or
erode through the omentum to cause generalized
peritonitis

60. 60
Tuberculous peritonitis
 Common in adults, rare in children
 Generalized peritonitis :- from subclinical or miliary
hematogenous dissemination.
 Localized peritonitis:- direct extension from an
abdominal lymph node, intestinal focus, or genitourinary
tuberculosis
 Rarely a doughy irregular nontender mass
 Abdominal pain or tenderness, ascites, anorexia, and low-
grade fever
 TheTST is usually reactive
 Dx can be confirmed by paracentesis with appropriate
stains and cultures

61. Renal TB
61
 Rare in children (longer incubation period)
 Usually due to lymphohematogenous spread
 Disease is usually unilateral
 Bacilli are often seen from urine in case of milliaryTB
with out renal parenchyma disease
 Fistula into the renal pelvis and spread locally to ureters,
prostate, epididymis

62. 62
 Usually silent early being marked by Microscopic
Hematuria & sterile pyuria
 As diseases progresses, dysuria, flank/abdominal pain &
gross hematuria develop
 Urine culture is positive in 80-90% of cases
 AFB (large volume of urine) is cases+ve in 50-70% of
 IVP- may show mass lesion, dilatation of proximal
ureters, multiple small filling defects &
hydronephrosis

63. 63
Bone and JointTB
 Vertebrae is commonly involved with gibbus
deformity & kyphosis and paralysis
 The classic manifestation of tuberculous spondylitis is
progression to Pott disease
 Other sites: long & flat bones; hip, knee
CutaneousTB
Common with HIV, malnutrition and poor
hygiene
Sites of predilection: face, lower limbs & genitals

64. Perinatal TB
64
 Can be congenital , commonly acquired postnatal
 C/ms;
 similar to sepsis & other neonatal problems
 May manifest early but common time is 2-3wks of age
 RD, poor feeding, fever, HSM, FTT, abdominal
distension
 Many infants have an abnormal chest radiograph, most often
with a miliary pattern
 Hilar and mediastinal lymphadenopathy and lung infiltrates
 Generalized lymphadenopathy and meningitis occur in 30-
50% of cases

65. 65
Dx and Mx of PerinatalTB
If mother has activeTB:
Screen the newborn (S/Sx, gastric aspirate, CXR)
If positive, start antiTB
If negative for activeTB
Option one: INH for 6 months, followed by BCG
Option two: INH for 3 months
At 3months, PPD
o if +ve, continue an other 3 months, then BCG
o If non-reactive, give BCG and discontinue INH

66. 66
Isolation of the newborn:
 Seriously sick mother
 Previous Rx forTB
 Suspected drug resistantTB

67. Diagnosis of TB in Children
67
 Acid Fast Staining/culture (sputum, gastric aspirate, LN,
fluid) is definitive
Smear +veTB:
The criteria are:
 Two or more initial sputum smear examinations positive
for acid fast bacilli; or
 One sputum smear examination positive for acidfast
bacilli plus
 CXR abnormalities consistent with active pulmonary TB,
as determined by a clinician; or
 One sputum smear examination positive for acid fast
bacilli plus sputum culture positive for M. tuberculosis.

68. 68
Smear -veTB:
 Pulmonary TB, sputum smear negative
A case of pulmonary TB that does not meet the
definition for smear positive pulmonary TB; Such
cases include :
 cases without smear results, which should be
exceptional in adults but relatively more frequent in
children.

69. 69
 In keeping with good clinical and public health practice,
diagnostic criteria for sputum smear negative pulmonary
TB should include:
 At least three sputum specimens negative for acid fast
bacilli; and
 Radiological abnormalities consistent with active
pulmonary TB; and
 No response to a course of broad spectrum antibiotics;
and
 Decision by a clinician to treat with a full course of
antiTB chemotherapy

70. 70
 If AFB is negative, Dx is based on:
Contact with patient(adult) with pulmonaryTB
S/Sx suggestive ofTB
X-Ray finding consistent withTB
PositiveTST
 If 3 are fullfilled,TB is likely Dx
 If severe malnutrition or immunosupresion, 2
criteria are enough

71. Recommended Approach to Diagnose TB in
Children
71
A.Typical symptoms
 Cough, especially persistent and non-improving
 Weight loss or failure to gain weight
 Fever and/or night sweats
 Fatigue, reduced playfulness, inactivity
B. History of contact
C. Clinical Examination
 Conduct thorough physical examination
 special emphasis on weight measurement (look for weight
loss or poor weight gain), fever, signs of respiratory distress
and chest finding.
 Can present with acute severe pneumonia

72. 72
D.Tuberculin SkinTest
E. Bacteriological Confirmation
 All attempts must be made to confirm diagnosis of
TB in a child using whatever specimens
 sputum, gastric aspirates and lymph node, fine-
needle aspiration or other tissue biopsy
F. Chest X-Ray
 Enlarged hilar lymph nodes and opacification in the
lung tissue
 Miliary mottling in lung tissue
 Cavitation (common with older children)
 Pleural or pericardial effusion

73. G. Investigation for common forms of EPTB
73

74. 74

75. 75
 The Presence of any one of the followings is diagnostic of
TB in a child:
 Radiological picture of miliary pattern
 Histopathologic findings compatible withTB
 Culture positive
 Isolation of organism byAFB

76. Management of Childhood TB
76
 Principles :
Chemotherapy/AntiTB drugs
Nutritional rehabilitation
Screening of the family(index case, other contacts)
Follow up (Adherence, response, drug side effect)

77. Chemotherapy/Anti TB drugs
77
The main objectives of antiTB treatment are to:
1. cure the patient (by rapidly eliminating most of
the bacilli);
2. prevent death from active TB or its late effects;
3. prevent relapse of TB (by eliminating the
dormant bacilli);
4. prevent the development of drug resistance (by
using a combination of drugs);
5. decrease TB transmission to others.

78. 78
 TB patient categories and how to select the correct
treatment regimen
 Before you put patients on antiTB drugs:
 Determine the type ofTB: PTB+, PTB- and EPTB
 Determine previous treatment history: New patient,
Previously treated
 Select based on the three standard treatment
regimens:
i. New patient regimen
ii. Previously treated patient regimen
iii. MDR-TB regimen

79. 79
Phases of chemotherapy
A. Intensive (initial) phase
o Four drugs(RHZE) for the first 8 weeks for new cases
o It renders the patient non-infectious by rapidly reducing
the load of bacilli in the sputum, usually within 2-3
weeks
B. Continuation phase
o Ensure cure or completion of treatment
o Two drugs, to be taken for 4 months for new cases
o Three drugs for re-treatment cases for 5months.

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 Recommended doses of first-line anti-TB drugs for
children
Drug Dose(mg/kg)
 Isoniazid 10 (10-15) ,max-300mg/day
 Rifampicin 15 (10-20) , max- 600mg/day
 Pyrazinamide 35 (30-40)
 Ethambutol 20 (15–25)
Suspected or confirmed tuberculous meningitis and
osteo-articularTB
Four drug( RHZE) forTwo months
Two drug ( RH) forTen months

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Second line antiTB drugs for treatment of MDRTBin
children
 Ethionamide or prothionamide
 Fluoroquinolones
 Ofloxacin
 Levofloxacin
 Moxifloxacin
 Gatifloxacin
 Ciprofloxacin
 Aminoglycosides
 Kanamycin
 Amikacin
 Capreomycin
 Cycloserine or terizidone
 paraAminosalicylic acid

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Steroids inTB indications:
Meningitis
Pericarditis
Adrenal insufficiency
Airway obstruction (LAP, laryngealTB)
Bilateral pleural effusion with respiratory problem
Indications for prescribing steroids in renalTB:
 Severe bladder symptoms
 Tubular structure involvement (eg, ureter, fallopian
tubes, spermatic cord)
Prednisone 2mg/kg daily( max 60mg/day) for 4
weeks, and then gradually tapered over 1-2 wks

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Pyridoxine
Indications:
 Breast feeding infants
Severely malnourished children
Symptomatic HIV-infected children
Dose: Pyridoxine 5-10 mg/day

85. Monitoring TB treatment
85
 Each child should be assessed
 2 weeks after Rx initiation
 At the end of intensive phase
 Every two months until completion of treatments
 The assessment should include:
o symptom assessment
o review of treatment adherence,
o enquiry about any adverse events
o weight measurement.
o Adherence should be assessed by reviewing the treatment
card

86. Adverse Reactions to TB Drugs in Children
86
 Adverse events are less common in children than in
adults
 The most common adverse reaction is the development of
hepatotoxicity,
 Caused by Isoniazid, Rifampicin or Pyrazinamide
 Isoniazid may cause symptomatic pyridoxine
deficiency, particularly in severely malnourished children

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 Side effects of antiTB drugs
 INH
o Hepatotoxicity, peripheral neuropathy
 Rifampicin
o GI upset with cramps, nausea, vomiting, and anorexia
o Hepatotoxicity ( transient elevation of liver enzymes)
o headache; dizziness; and immunologically mediated fever
and flulike symptoms.
o Thrombocytopenia and hemolytic anemias
o Orange/Red urine *
o Induce cytochrome P450 *

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 Pyrazinamide
o GI upset (e.g., nausea, vomiting, poor appetite)
o Hepatotoxicity
o Elevated serum uric acid levels
o arthralgias, fatigue
 Ethambutol
o Optic neuritis
o headache, dizziness, confusion,
o hyperuricemia, GI upset, peripheral neuropathy,
o hepatotoxicity, and cytopenias, especially
neutropenia and thrombocytopenia

89. Contact Screening and Management
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 Young children living in close contact with a source case of
smear-positive pulmonaryTB are at particular risk ofTB
 The risk of infection is greatest if the contact is close and
prolonged.
 The risk of developing disease after infection is much greater
for infants and young children under 5 years.
 If disease develops, it usually does so within 2 years of
infection
 INH 10mg/kg daily for 6months, and follow up
every month until completion for those < 5 years of
age

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91. Drug resistant TB in children
91
 Drug-resistantTB should be suspected if any of
the features below are present:
 There is contact with known DR-TB;
 There is contact with suspected DR-TB,i.e.source
case is a treatment failure or are treatment case or
recently died fromTB;
 A child withTB is not responding to first-line
therapy despite adherence;
 A child previously treated forTB presents with
recurrence of disease

92. Prevention of childhood TB
92
 Tuberculosis control, case finding and treatment
 IPT for asymptomatic children age < 5 years exposed to
close contacts
 BCG vaccine
 Efficacy is 50% in preventing pulmonaryTB in children and
adults, and 50 – 80% for disseminated and meningeal
tuberculosis
A GOODTB CONTROL PROGRAMME ISTHE BESTWAYTO
PREVENTTB IN CHILDREN

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Any Questions?