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PEDIATRIC
TUBERCULOSIS
DR.V.ANU REKHA
ASSISTANT PROFESSOR
INTRODUCTION
 Causative agent- Mycobacterium tuberculosis
 Less common- Mycobacterium bovis, M. Avium
intra cellulare
 Acid fast bacilli, non motile
 Obligate aerobe
 Discovered by Dr. Robert Koch, 1882
 White plague of 18 th century
 Mode of infection- droplet spread, air borne
infection
 Primary site of infection- lung
 May remain dormant- latentTB infection
(LTBI)
 May get activated – disease
 Affects almost all organs of the body
HOST FACTORS
 Age: no exemption for any age. Infants >>
more vulnerable
 Sex: adolescent girls; around puberty
 Malnutrition: undernourished >> more
susceptible; depressed immunological
reaction. SAM child who doesn’t respond to
nutritional therapy should be evaluated for
TB
 Immunodeficiency: both primary and
secondary- HIV, DM, immuno suppressives
 Inter-current infections: post viral
Incubation period: 4 to 8 weeks
How prevalent is TB in
children?
 In India, 3.42 lakh children getTB every year
 Male= female
 31% global burden
 6 % of cases reported to NTEP
 PulmonaryTB most common
 Extra pulmonary is common compared to adult
PATHOGENESIS
Primary complex (Ghon`s
complex)
EXTRA PULMONARY TB
 Lymph nodeTB
 Pleural effusion
 Meningitis
 DisseminatedTB
 Renal
 Bone
 GenitourinaryTB
CLINICAL FEATURES
 Primary infection:
 Asymptomatic
 Mild fever, anorexia, weight loss, decreased
activity
 Cough – inconsistent
 Diagnosed incidentally
 LatentTB(LTBI)- no symptoms/disease ;but
shows only hypersensitivity toTB;
 Progressive primary complex:
 High grade fever, cough- consolidation
 Endo-bronchial:
 troublesome cough, dyspnea, wheezing
 Miliary:
 Hematogenous spread ; infants
 Innumerable small foci
 Acute onset, high grade fever
 Pleural effusion:
 Rupture of sub-pleural focus
 Occurs due to the hypersensitivity to
tubercular proteins
 > 5years of age
 Insidious onset fever, cough , dyspnea,
pleuritic chest pain (pleural rub) initially
 Lymphadenitis:
 Extension of the primary
lesions of the lung
 mainly cervical nodes;
painless, matted
 Advances to caseating
necrosis (cold abscess),
rupture, draining sinus
 CNS tuberculosis:
 Rich focus in the brain- lympho hematogenous
spread
 Infants and children <4 years- vulnerable
 Infants- rapid progression- hydrocephalus, raised
ICT, seizures
 Older child- sub acute course
 Headache, irritability, drowsiness, vomiting,
focal signs
 AbdominalTB:
 Hematogenous spread
 Non specific abdominal pain
 Doughy abdomen- omental involvement
 Rolled up omentum , mesenteric adenitis,
thickened ileum- irregular nodular mass
 Ascites
 Hepato splenomegaly
DIAGNOSIS
 Clinical signs and symptoms
 CXR
 Tuberculin skin testing
 History of contact
 Microbiological confirmation- gold standard
Contact :
 Any child who lives in a household with an
adult taking ATT or has taken in the past 2
years.
COLLECTION OF SPECIMEN
 Gastric aspirate:
 In children who cant expectorate
 Early morning- after 4 to 6 hours fasting
 Pooled sample of swallowed sputum
 Induced sputum:
 Salbutamol nebulisation – hypertonic saline
nebulisation- nasopharyngeal aspirate with
suction
 Expectorated sputum
 Bronchio-alveolar lavage fluid
 FNAC of lymph node
 Biopsy of the node
 CSF
 Pleural fluid
 Ascitic fluid
MICROBIOLOGICAL DIAGNOSIS
 Ziehl –Neelson technique
 Auramine Rhodamine staining
 Cartridge based Nucleic acid amplification
technique (CB-NAAT)- 2 hours; identifies
rifampicin (rif) sensitivity
 Tru- NAT- 45 minutes
Culture:
 Lowenstein Jensen medium- conventional-
6weeks
 Mycobacterial growth indicator tube(MGIT)-
liquid culture- 2 weeks
 Line probe assay (LPA)- for detecting the drug
sensitivity
 Interferon gamma release assay(IGRA)-
alternative to Mantoux
 CopenhagenTB (CTb ) test- yet to come
MANTOUX TEST
 Demonstrate delayed type hypersensitivity
 2TU of tuberculin PPDRT23 0r 5TU of PPD-S
 0.1 ml of PPD ; intradermal; volar aspect of
forearm
 Read after 48-72 hours
 Induration (not erythema) to be measured
 > 10 mm & >5 – in immuno compromised
significant
 False positive- Atypical mycobacteria infection
 False negative- immuno compromised
RADIOLOGICAL DIAGNOSIS
CHEST X RAY:
 Highly suggestive:
 Hilar or para tracheal lymph adenopathy
 Miliary
 Cavitary
 Non specific shadows
 Broncho pneumonia, consolidation, collapse,
emphysematous change ,pleural effusion etc
DIAGNOSTIC ALGORITHM
PRESUMPTIVETB DIAGNOSIS
 Persistent fever >2wk, without a known cause
and/or
 Unremitting cough for >2wk and/or
 Weight loss of 5%; or, no weight gain in past 3
mo despite adequate nutrition; or, failure of
nutritional rehabilitation in babies with
severe acute malnutrition
 With or without contact with patient with
pulmonaryTB in past 2 years
DIAGNOSTIC ALGORITHM FOR DRTB
NATIONAL TB ELIMINATION 2025
TREATMENT
 Only 1 category (4HRZE+ 2HRE); No class 2
 Total duration- 6 months; daily
 Neurological, bone, joint- continuation phase
extended up to 10 months
 Fixed dose combinations(FDC)
 Second line drugs: Quinolones, Injectable
aminoglycosides
 Newer- Bedaquiline; Delamanid
WEIGHT BANDS
MONITORING OF THERAPY
 Every 2-4 weeks initially; then every 4 -8 weeks
 Clinical resolution: maximum of 6 to 8 weeks
 Check for compliance
 Look for anthropometry, side effects of drugs
 If no response- think of DRTB
 Radiological- after 2weeks or based on clinical
response; clearance occurs late
 Microbiological- not routinely
 Notifiable disease
 Registered through NIKSHAY
NEONATES OF MOTHER WITH TB
CongenitalTB
 Hematogenous spread through umblical
vessels – primary foci- liver
 Ingestion of infected amniotic fluid- lung
 Post natal transmission possible
 Rule out active infection in neonate
 Mother can breast feed (if she had completed
1 month of intensive phase)
 Cough etiquette to be followed
 BCG can be given immediately
 Isoniazid prophylaxis ( INH 10 mg/kg/day
along with pyridoxine ) for 6 months
 Closely watch the baby for the development
of disease
ISONIAZID PREVENTIVE THERAPY
 Children < 5 years with Contact with adult
 Children 5 to 15 years who have tested for
LTBI
 Children with HIV
 Children on immunodeficiency or on
immunosuppressive drugs
 INH should be given 10 mg/kg/day for 6
months along with pyridoxine after ruling out
active disease
BACILLUS CALMITTE GUERIN (BCG)
VACCINE
 0.1 ml ; intra dermal; left arm; at the insertion
of deltoid
 Live attenuated vaccine
 Given at birth; Can be given up to 1 year
 Prevents serious extra pulmonary form ofTB
 Not for primary complex
 Efficacy- 20-80%
 Complication : BCG abscess, BCG adenitis,
THANK YOU

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Pediatric tuberculosis dr. anu

  • 2. INTRODUCTION  Causative agent- Mycobacterium tuberculosis  Less common- Mycobacterium bovis, M. Avium intra cellulare  Acid fast bacilli, non motile  Obligate aerobe  Discovered by Dr. Robert Koch, 1882  White plague of 18 th century
  • 3.  Mode of infection- droplet spread, air borne infection  Primary site of infection- lung  May remain dormant- latentTB infection (LTBI)  May get activated – disease  Affects almost all organs of the body
  • 4. HOST FACTORS  Age: no exemption for any age. Infants >> more vulnerable  Sex: adolescent girls; around puberty  Malnutrition: undernourished >> more susceptible; depressed immunological reaction. SAM child who doesn’t respond to nutritional therapy should be evaluated for TB
  • 5.  Immunodeficiency: both primary and secondary- HIV, DM, immuno suppressives  Inter-current infections: post viral Incubation period: 4 to 8 weeks
  • 6. How prevalent is TB in children?  In India, 3.42 lakh children getTB every year  Male= female  31% global burden  6 % of cases reported to NTEP  PulmonaryTB most common  Extra pulmonary is common compared to adult
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  • 11. EXTRA PULMONARY TB  Lymph nodeTB  Pleural effusion  Meningitis  DisseminatedTB  Renal  Bone  GenitourinaryTB
  • 12. CLINICAL FEATURES  Primary infection:  Asymptomatic  Mild fever, anorexia, weight loss, decreased activity  Cough – inconsistent  Diagnosed incidentally  LatentTB(LTBI)- no symptoms/disease ;but shows only hypersensitivity toTB;
  • 13.  Progressive primary complex:  High grade fever, cough- consolidation  Endo-bronchial:  troublesome cough, dyspnea, wheezing  Miliary:  Hematogenous spread ; infants  Innumerable small foci  Acute onset, high grade fever
  • 14.  Pleural effusion:  Rupture of sub-pleural focus  Occurs due to the hypersensitivity to tubercular proteins  > 5years of age  Insidious onset fever, cough , dyspnea, pleuritic chest pain (pleural rub) initially
  • 15.  Lymphadenitis:  Extension of the primary lesions of the lung  mainly cervical nodes; painless, matted  Advances to caseating necrosis (cold abscess), rupture, draining sinus
  • 16.  CNS tuberculosis:  Rich focus in the brain- lympho hematogenous spread  Infants and children <4 years- vulnerable  Infants- rapid progression- hydrocephalus, raised ICT, seizures  Older child- sub acute course  Headache, irritability, drowsiness, vomiting, focal signs
  • 17.  AbdominalTB:  Hematogenous spread  Non specific abdominal pain  Doughy abdomen- omental involvement  Rolled up omentum , mesenteric adenitis, thickened ileum- irregular nodular mass  Ascites  Hepato splenomegaly
  • 18. DIAGNOSIS  Clinical signs and symptoms  CXR  Tuberculin skin testing  History of contact  Microbiological confirmation- gold standard Contact :  Any child who lives in a household with an adult taking ATT or has taken in the past 2 years.
  • 19. COLLECTION OF SPECIMEN  Gastric aspirate:  In children who cant expectorate  Early morning- after 4 to 6 hours fasting  Pooled sample of swallowed sputum  Induced sputum:  Salbutamol nebulisation – hypertonic saline nebulisation- nasopharyngeal aspirate with suction  Expectorated sputum
  • 20.  Bronchio-alveolar lavage fluid  FNAC of lymph node  Biopsy of the node  CSF  Pleural fluid  Ascitic fluid
  • 21. MICROBIOLOGICAL DIAGNOSIS  Ziehl –Neelson technique  Auramine Rhodamine staining  Cartridge based Nucleic acid amplification technique (CB-NAAT)- 2 hours; identifies rifampicin (rif) sensitivity  Tru- NAT- 45 minutes
  • 22. Culture:  Lowenstein Jensen medium- conventional- 6weeks  Mycobacterial growth indicator tube(MGIT)- liquid culture- 2 weeks  Line probe assay (LPA)- for detecting the drug sensitivity  Interferon gamma release assay(IGRA)- alternative to Mantoux  CopenhagenTB (CTb ) test- yet to come
  • 23. MANTOUX TEST  Demonstrate delayed type hypersensitivity  2TU of tuberculin PPDRT23 0r 5TU of PPD-S  0.1 ml of PPD ; intradermal; volar aspect of forearm  Read after 48-72 hours  Induration (not erythema) to be measured  > 10 mm & >5 – in immuno compromised significant  False positive- Atypical mycobacteria infection  False negative- immuno compromised
  • 24. RADIOLOGICAL DIAGNOSIS CHEST X RAY:  Highly suggestive:  Hilar or para tracheal lymph adenopathy  Miliary  Cavitary  Non specific shadows  Broncho pneumonia, consolidation, collapse, emphysematous change ,pleural effusion etc
  • 25. DIAGNOSTIC ALGORITHM PRESUMPTIVETB DIAGNOSIS  Persistent fever >2wk, without a known cause and/or  Unremitting cough for >2wk and/or  Weight loss of 5%; or, no weight gain in past 3 mo despite adequate nutrition; or, failure of nutritional rehabilitation in babies with severe acute malnutrition  With or without contact with patient with pulmonaryTB in past 2 years
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  • 31.  Only 1 category (4HRZE+ 2HRE); No class 2  Total duration- 6 months; daily  Neurological, bone, joint- continuation phase extended up to 10 months  Fixed dose combinations(FDC)  Second line drugs: Quinolones, Injectable aminoglycosides  Newer- Bedaquiline; Delamanid
  • 33. MONITORING OF THERAPY  Every 2-4 weeks initially; then every 4 -8 weeks  Clinical resolution: maximum of 6 to 8 weeks  Check for compliance  Look for anthropometry, side effects of drugs  If no response- think of DRTB  Radiological- after 2weeks or based on clinical response; clearance occurs late  Microbiological- not routinely
  • 34.  Notifiable disease  Registered through NIKSHAY
  • 35. NEONATES OF MOTHER WITH TB CongenitalTB  Hematogenous spread through umblical vessels – primary foci- liver  Ingestion of infected amniotic fluid- lung  Post natal transmission possible  Rule out active infection in neonate
  • 36.  Mother can breast feed (if she had completed 1 month of intensive phase)  Cough etiquette to be followed  BCG can be given immediately  Isoniazid prophylaxis ( INH 10 mg/kg/day along with pyridoxine ) for 6 months  Closely watch the baby for the development of disease
  • 37. ISONIAZID PREVENTIVE THERAPY  Children < 5 years with Contact with adult  Children 5 to 15 years who have tested for LTBI  Children with HIV  Children on immunodeficiency or on immunosuppressive drugs  INH should be given 10 mg/kg/day for 6 months along with pyridoxine after ruling out active disease
  • 38. BACILLUS CALMITTE GUERIN (BCG) VACCINE  0.1 ml ; intra dermal; left arm; at the insertion of deltoid  Live attenuated vaccine  Given at birth; Can be given up to 1 year  Prevents serious extra pulmonary form ofTB  Not for primary complex  Efficacy- 20-80%  Complication : BCG abscess, BCG adenitis,
  • 39.