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)
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 1st 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
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)
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
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 1o 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
20. 20
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
• 2-12 weeks:
• Organism grow in number
21. 21
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 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-consolidation or segmental lesion
Primary complex( Ghon complex), During the
development of 1o complex, bacilli are carried to most
tissues of the body through the blood & lymphatic vessels;
common seeding is in the organs of Reticuloendothelial
22. 22
Bacterial replication occurs in organs with conditions
that favor their growth:
Lung apices
Brain
Kidneys
Bones
Disseminated TB occurs if:
o Circulating number of bacilli is large and
o Host immune response is inadequate
o More 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:
o Disseminated & meningeal TB are early
manifestations(2-6mo after infection)
o TB LAP & endobronchial TB(3-9mo)
o Bones & joints take several years
o Renal TB takes decades after infection
Pulmonary TB 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(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 48-72hrs after
administration
Tuberculin sensitivity develops 3 wk to 3 mo (most
often in 4-8 wk) after inhalation of organisms
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
o In all other children (whether they have
received a BCG vaccination or not)
31. 31
False positive result:
o Cross-sensitization to Ags of NTM
(usually below 10mm)
o BCG
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
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. tuberculosis antigens
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: hilar LAP focal hyperinflation
atelectasis
35. 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)
35
36. 36
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), milliary TB 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
40. Upper Respiratory Tract TB
40
o Laryngeal TB
Croup-like cough, sore throat, hoarseness,
dysphagia
Most have extensive upper lobe pulmonary disease
Occasionally primary laryngeal disease with normal
CXR
o Middle ear TB
Painless unilateral otorrhea
Tinnitus, decreased hearing, perforation of tympanic
membrane
Due to aspiration of infected pulmonary secretion or
hematogenous
41. Lymphohematogenous (Disseminated)
Disease
41
Milliary TB
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 milliary TB
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
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 &
supraclavicular nodes are involved secondary to
extension of lesions of upper lung lobes &
abdomen
• Inguinal, epitrochlear or axillary are 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
granuloma can 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
granulomas are 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
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
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:
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
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
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
o if +ve, continue an other 3 months, then BCG
o If 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 +ve TB:
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.
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 >30 mm/hr indicates
inflammation and the need for further evaluation for infectious,
autoimmune, or malignant diseases.
An ESR of >100 mm/hr suggests Tuberculosis, Kawasaki
disease, Malignancy, or Autoimmune disease
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
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.
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-
articular TB
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
83. 83
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
Return after default (D):
A patient previously recorded as defaulted from treatment
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
o There is convincing evidence that corticosteroids decrease mortality
rates and long-term neurologic sequelae in some patients with
tuberculous meningitis
o Several randomized clinical trials have shown that corticosteroids can
help relieve symptoms and constriction associated with acute
tuberculous pericardial effusion
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:
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
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
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 *
89. 89
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
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
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
