17. Childhood Tuberculosis lectureship .ppt

Tuberculosis

1. FentahunA
(MD, Asst. Professor of Pediatrics and
Child Health)
5/4/20241
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
developed TB and 12 million prevalent cases
of TB 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 of TB 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
74 000 TB 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 to WHO 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. Ethiopia: thousands per
1000,000
Prevalence: 210 224
Incidence 230 247
6

7. 7
The global burden of TB remains
enormous:
oHIV epidemics
oPoverty
oCrowding
oInefficient TB control programs
oInadequate health coverage & poor
access to health services

8. Latent TB infection(LTBI)
8
Latent TB infection(LTBI)-occurs after
inhalation of infected droplet nuclei with
M.TB
This stage is characterized by:
Reactive Tuberculin skin test
Absence of clinical and
Radiological evidence of active TB

9. 9
TB(Disease)-refers to apparent signs and
symptoms or radiologic changes of active
TB
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 1
st
2yr after infection

10. High risk of infection
10
Close contacts of person with TB
Foreign born persons from high risk
countries
High risk congregate settings
Low socio-economic status
Injection drug users

11. 11
Risk for progression to TB 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)

12. 12
Key risk factors for TB:
Strong contact with newly diagnosed
smear +ve case
Age below 5yrs
HIV infection
Severe malnutrition

13. Etiology
13
Mycobacterium Tuberculous complex:
M.Tuberculosis
M.Bovis
M.Africanum
M.Microti
M.Canetti
All belong to the order Actinomycetales
and family Mycobacteriaceae

14. 14
M.TB
oMost important tuberculosis disease in humans
oNon-spore forming, Non-motile, Obligate
aerobe
oSlow-growing, Grow best at 37-41
o
C
oCell wall with high lipid content which gives
“acid-fast” staining properties (resistance to
decolorization with acid alcohol)
Culture: solid media 3-4weeks, and in liquid media
it takes 1-3 weeks
In clinical specimen, can be detected with hours
using Nucleic acid amplification(NAA)tests

15. Transmission & Pathogenesis
15
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

16. Risk of transmission is increase with
index case:
Smear positive TB
Extensive upper lobe infiltrate & cavity
Copious production of sputum
Severe & forceful cough
Not treated
16

17. 17
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

18. 18
The risk of infection of a susceptible
individual is high with close, prolonged,
indoor exposure to a person with
sputum smear-positive pulmonary
TB.

19. Pathogenesis
19
The 1
o
complex of TB 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

20. 20
Tissue reaction in the lung parenchyma & LNs intensifies
over the next 2-12wks
The parenchymal lesion of 1
o
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
•2-12 weeks:
•Organism grow in number
•Tissue hypersensitivity develops

21. 21
oIf hilar & Para tracheal LNs enlarge(as part of host
inflammatory reaction), they may encroach on a regional
bronchus :
oPartial obstruction bronchus Distal hyperinflation
oComplete obstruction Atelectasis
Inflamed caseos nodes can attach to the bronchial wall &
erode through it, causing endobronchial TB or a fistula tract
A combination of pneumonitis and atelectasis results in
collapse-consolidationor segmental lesion
Primary complex( Ghon complex), During the
development of 1
o
complex, bacilli are carried to most
tissues of the body through the blood & lymphatic vessels;
common seeding is in the organs of Reticuloendothelial
System

22. 22
Bacterial replication occurs in organs with conditions
that favor their growth:
Lung apices
Brain
Kidneys
Bones
Disseminated TB occurs if:
oCirculating number of bacilli is large and
oHost immune response is inadequate
oMore often the number of bacilli is small, leading to
clinically inapparent metastatic foci in many organs

23. 23
The time b/n initial infection & clinically apparent
disease is variable:
oDisseminated & meningeal TB are early
manifestations(2-6mo after infection)
oTB LAP & endobronchial TB(3-9mo)
oBones & joints take several years
oRenal TB takes decades after infection
Pulmonary TB that occurs more than a year after
1
o
infection is usually due to endogenous regrowth
of bacilli persisting in partially encapsulated lesions
Common site of reactivation is the apex of upper
lobes(oxygen & blood flow good)

24. Immunity
24
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.

25. 25
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)

26. 26
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

27. 27
Factors that predispose to serious disease:
Young age
Geneticfactors
Immunosuppresion (AIDS,malnutrition,
measles, pertussis, malignancy,steroids)

28. Tuberculin Skin Test (Mantoux Test)
28
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 48-72hrsafter
administration
Tuberculin sensitivity develops 3 wk to 3 mo (most
often in 4-8 wk) after inhalation of organisms

29. Fig. TST induration
29

30. Positive TST
30
>5 mm diameter of induration
oIn children who are immunosuppressed (
HIV-positive children)
oSeverely malnourished child
>10 mm diameter of induration
oIn all other children (whether they have
received a BCG vaccination or not)

31. 31
False positive result:
oCross-sensitization to Ags of NTM
(usually below 10mm)
oBCG
50% never develop the raction
Reactivity usually wanes in 2-3yrs
If >10mm , it is taken as +ve
BCG is not a contraindication to PPD
test

32. 32
False Negative:
Young age(below 3months)
Malnutrition
Immunosupression
Viral infections (measles, mumps,
varicella, influenza)
Vaccination with live-viruses (within
6wks)
Overwhelming TB

33. Interferon-γ Release Assays
33
Two blood tests (T-SPOT.TB and Quanti
FERON-TB)
Detect IFN-γ generation by the patient's T cells
in response to specific M. tuberculosisantigens
Advantage over TST
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

34. Clinical manifestations
34
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: hilarLAP focal hyperinflation
atelectasis

35. SubcarinalLAP may cause esophageal
compression & rarely bronchoesophageal
fistula
In children may have lobar pneumonia
without impressive hilarLAP
Erosion of a parechymallesion into blood
or lymphatic vessel may result in
dissemination of bacilli & a military pattern
(small nodules distributed on CXR)
35

36. 36
S/Sxof 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

37. 37
Dx of primary pulmonary TB:
Most specific is isolation of M.TB
•Sputum (>7yr) for AFB stainig & culture
•Early morning gastric aspirate (young
age)
Yield is low (25-50% positive with
3cultures)
Negative culture never exclude
pulmonary TB
If positive TST or IGRA,abnormal CXR
& contact Hx, adequate evidence

38. Progressive primary pulmonary TB
38
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

39. Reactivation pulmonary TB
39
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 extathoracic TB 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
Children with a healed tuberculosis infection acquired at <2
yr of age rarely develop chronic reactivation pulmonary
disease, which is more common in those who acquire the
initial infection at >7 yr of age

40. Upper Respiratory Tract TB
40
oLaryngeal TB
Croup-like cough, sore throat, hoarseness,
dysphagia
Most have extensive upper lobe pulmonary disease
Occasionally primary laryngeal disease with normal
CXR
oMiddle ear TB
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

41. Lymphohematogenous (Disseminated)
Disease
41
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 Dxof milliaryTB
Lesions are of roughly same size as that of a millet seed
Development of disseminated TB depends on:
Number of bacilli released from primary focus
Adequacy of immune response
Tubercle bacilli are disseminated to distant sites,
including liver, spleen, skin, and lung apices, in all
cases of tuberculosis infection

42. 42
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
Choroid tubercles occur in 13-87% of patients
and are highly specific for the diagnosis of
miliary tuberculosis.

43. Extrapulmonary Tuberculosis
(EPTB)
43
Every organ can be affected by tuberculosis
Common forms of extra pulmonary TB in children:
TB Lymphadenitis
•TB of Superficial LNs (Scrofula) is most
common form of EPTB
•Tonsilar, anterior cervical, submandibular&
supraclavicularnodes are involved secondary to
extension of lesions of upper lung lobes &
abdomen
•Inguinal, epitrochlearor axillaryare associated
with skin or bone TB

44. 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
44

45. 45
Dx of Tb lymphadenitis is
histiologic/bacteriologic confirmation
(FNA or excisional Bx)
Culture yield is 50% of the cases

46. Pleural disease
46
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

47. 47
Usually unilateral
Rare in disseminated TB
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

48. 48
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
granulomacan be demonstrated
Protein-2-4g/dl
Cell count—hundreds to thousands

49. Pericardial TB
49
Rare, 0.5-4%
Most common form of cardiac TB
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

50. Pericardial TB….
Pericardiocentesis:
AFB staining is rarely positive
culture is positive in 30-70% of cases
pericardial Bx
culture yield is higher
granulomasare suggestive
50

51. CNS TB
51
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

52. 52

53. 53
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 of
TB meningitis
Most common b/n 6mo-4yrs
Cerebral salt wasting appears to be the result of
hypersecretion of atrial natriuretic peptide and is

54. 54
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

55. 55
Stage III:
Coma
Hemi-or para-plegia
Hyperetension
Decerebration
Deterioration of vital signs
Prognosis is dependent on stage of TB
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

56. 56
Common permanent disabilities:
Blindness
Deafness
Paraplegia
Diabetes Insipides
Mental retardation
Prognosis is worse in infants

57. 57
Diagnosis:
ohigh degree of suspicion
oTST is positive in 50%
oCXR is normal in 20-50%
oCSF-WBC(10-500/mm
3
)
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%)
oCT/MRI of the brain
oNormal in early stages
obasilar enhancement, hydrocephalus
,cerebral edema, focal ischemia

58. 58
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

59. GI/Peritoneal TB
59
GI TB
Oral cavity or pharynx is rare, most common
lesion is pain less ulcer
Esophageal Tb 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

60. 60
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

61. 61
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
The TST is usually reactive
Dx can be confirmed by paracentesis with
appropriate stains and cultures

62. Renal TB
62
Rare in children (longer incubation period)
Usually due to lymphohematogenous spread
Disease is usually unilateral
Bacilli are often seen from urine in case of
milliary TB with out renal parenchyma disease
Fistula into the renal pelvis and spread locally
to ureters, prostate, epididymis

63. 63
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 +ve in 50-70%
of cases
IVP-may show mass lesion, dilatation of
proximal ureters, multiple small filling defects
& hydronephrosis

64. 64
Bone and Joint TB
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
Cutaneous TB
Common with HIV, malnutrition and poor
hygiene
Sites of predilection: face, lower limbs &
genitals

65. Perinatal TB
65
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

66. 66
Dx and Mx of Perinatal TB
If mother has active TB:
Screen the newborn (S/Sx, gastric aspirate,
CXR)
If positive, start antiTB
If negative for active TB
Option one: INH for 6 months, followed by
BCG
Option two: INH for 3 months
At 3months, PPD
oif +ve, continue an other 3 months, then BCG
oIf non-reactive, give BCG and discontinue INH

67. 67
Isolation of the newborn:
Seriously sick mother
Previous Rx for TB
Suspected drug resistant TB

68. Diagnosis of TB in Children
68
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 plussputum culture positive for M. tuberculosis.

69. 69
Smear -ve TB:
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.

70. 70
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

71. 71
If AFB is negative, Dx is based on:
Contact with patient(adult) with pulmonary
TB
S/Sx suggestive of TB
X-Ray finding consistent with TB
Positive TST
If 3 are fullfilled, TB is likely Dx
If severe malnutrition or immunosupresion,
2 criteria are enough

72. Recommended Approach to Diagnose TB
in Children
72
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

73. 73
D. Tuberculin Skin Test
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
An erythrocyte sedimentation rate (ESR) of >30mm/hr indicates
inflammation and the need for further evaluation for infectious,
autoimmune, or malignant diseases.
An ESR of >100mm/hr suggests Tuberculosis, Kawasaki
disease, Malignancy, or Autoimmune disease

74. G. Investigation for common forms of EPTB
74

75. 75

76. 76
The Presence of any one of the followings is
diagnostic of TB in a child:
Radiological picture of miliary pattern
Histopathologic findings compatible with TB
Culture positive
Isolation of organism by AFB

77. Management of of Childhood TB
77
Principles :
Chemotherapy/AntiTB drugs
Nutritional rehabilitation
Screening of the family(index case, other
contacts)
Follow up (Adherence, response, drug side effect)

78. Chemotherapy/Anti TB drugs
78
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.

79. 79
TB patient categories and how to select the
correct treatment regimen
Before you put patients on anti TB drugs:
Determine the type of TB: 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

80. 80
Phases of chemotherapy
A. Intensive (initial) phase
oFour drugs(RHZE) for the first 8 weeks for
new cases
oIt renders the patient non-infectious by rapidly
reducing the load of bacilli in the sputum,
usually within 2-3 weeks
B. Continuation phase
oEnsure cure or completion of treatment
oTwo drugs, to be taken for 4 months for new
cases
oThree drugs for re-treatment cases for
5months.
New case: A patient who never had treatment

81. 81

82. 82
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) for Two months
Two drug ( RH) for Ten months
Relapse: patient declared cured or treatment completed of
any form of TB in the past, but who reports back to the
health service and is now found to be AFB smear-positive
or culture positive
Treatment after Failure (F):
A patient who, while on treatment, is smear or culture positive
at the end of the fifth month or later, after commencing.

83. 83
Second line antiTBdrugs for treatment of MDRTBin
children
Ethionamideor prothionamide
Fluoroquinolones
Ofloxacin
Levofloxacin
Moxifloxacin
Gatifloxacin
Ciprofloxacin
Aminoglycosides
Kanamycin
Amikacin
Capreomycin
Cycloserineor terizidone
paraAminosalicylicacid
Return after default (D):
A patient previously recorded as defaulted from treatment
and returns to the health facility with smear-positive sputum.

84. 84
Steroids in TB indications:
Meningitis
Pericarditis
Adrenal insufficiency
Airway obstruction (LAP, laryngeal TB)
Bilateral pleural effusion with respiratory problem
Indications for prescribing steroids in renal TB:
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
oThere is convincing evidence that corticosteroids decrease mortality
rates and long-term neurologic sequelae in some patients with
tuberculous meningitis
oSeveral randomized clinical trials have shown that corticosteroids can
help relieve symptoms and constriction associated with acute
tuberculous pericardial effusion

85. 85
Pyridoxine
Indications:
Breast feeding infants
Severely malnourished children
Symptomatic HIV-infected children
Dose: Pyridoxine 5-10 mg/day

86. Monitoring TB treatment
86
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:
osymptom assessment
oreview of treatment adherence,
oenquiry about any adverse events
oweight measurement.
oAdherence should be assessed by reviewing
the treatment card

87. Adverse Reactions to TB Drugs in
Children
87
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

88. 88
Side effects of anti TB drugs
INH
oHepatotoxicity, peripheral neuropathy
Rifampicin
oGI upset with cramps, nausea, vomiting, and
anorexia
oHepatotoxicity ( transient elevation of liver
enzymes)
oheadache; dizziness; and immunologically
mediated fever and flulike symptoms.
oThrombocytopenia and hemolytic anemias
oOrange/Red urine *
oInduce cytochrome P450 *

89. 89
Pyrazinamide
oGI upset (e.g., nausea, vomiting, poor appetite)
oHepatotoxicity
oElevated serum uric acid levels
oarthralgias, fatigue
Ethambutol
oOptic neuritis
oheadache, dizziness, confusion,
ohyperuricemia, GI upset, peripheral neuropathy,
ohepatotoxicity, and cytopenias, especially
neutropenia and thrombocytopenia

90. Contact Screening and Management
90
Young children living in close contact with a
source case of smear-positive pulmonary TB are
at particular risk of TB
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

91. 91

92. Drug resistant TB in children
92
Drug-resistant TB 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 from
TB;
A child with TB is not responding to first-
line therapy despite adherence;
A child previously treated for TB
presents with recurrence of disease

93. Prevention of childhood TB
93
Tuberculosis control, case finding and treatment
IPT for asymptomatic children age < 5 years
exposed to close contacts
BCG vaccine
Efficacy is 50% in preventing pulmonary TB in
children and adults, and 50 –80% for disseminated
and meningeal tuberculosis
A GOOD TB CONTROL PROGRAMME IS THE
BEST WAY TO PREVENT TB IN CHILDREN

94. 94