Childhood TB

Paediatric tuberculosis

1. CHILDHOOD CHILDHOOD
TUBERCULOSISTUBERCULOSIS
Arun GeorgeArun George

2. TuberculosisTuberculosis
Tuberculosis is a chronic infectious disease caused by Tuberculosis is a chronic infectious disease caused by
Mycobacterium tuberculosisMycobacterium tuberculosis characterized by vague characterized by vague
constitutional symptoms and a protracted course of constitutional symptoms and a protracted course of
illness with remissions and exacerbations.illness with remissions and exacerbations.
Tuberculosis is the reaction of tissues of the human Tuberculosis is the reaction of tissues of the human
host to the presence and multiplication of host to the presence and multiplication of Mycobacterium Mycobacterium
tuberculosistuberculosis..
The clinical states arising from TB infection are the The clinical states arising from TB infection are the
outcome between the capacity of the host to contain outcome between the capacity of the host to contain
and eliminate the organism versus the capacity of the and eliminate the organism versus the capacity of the
organism to multiply and proliferate. organism to multiply and proliferate.

3. MagnitudeMagnitude
1/31/3
rdrd
of the world’s population is or has been of the world’s population is or has been
infected with tubercle bacilli.infected with tubercle bacilli.
India accounts for one third of the word TB India accounts for one third of the word TB
burdenburden
Prevalence of the disease in IndiaPrevalence of the disease in India::
15-25 per 1000 population 15-25 per 1000 population
15 million infected, 25% sputum positive15 million infected, 25% sputum positive
3 to 4 million infected are children3 to 4 million infected are children

4. EpidemiologyEpidemiology
Agent : Mycobacterium tuberculosis, M. bovisAgent : Mycobacterium tuberculosis, M. bovis
Reservoir : Infected patientReservoir : Infected patient
Mode of infection : Droplet infection, dust, ingestion, Mode of infection : Droplet infection, dust, ingestion,
skin, mucous membrane, skinskin, mucous membrane, skin
Host FactorsHost Factors
Age : all ages affected, congenital is rareAge : all ages affected, congenital is rare
Sex : Girls > boys at PubertySex : Girls > boys at Puberty
Malnutrition : more succeptibleMalnutrition : more succeptible
Intercurrent infections : eg measles, whooping coughIntercurrent infections : eg measles, whooping cough
Environment : overcrowding, inadequate ventillation, Environment : overcrowding, inadequate ventillation,
damp, insanitary and unhygenic conditionsdamp, insanitary and unhygenic conditions

5. Portal of entry for tuberculosisPortal of entry for tuberculosis
Inhalation of Tubercle bacilli in >95% (M.TB)Inhalation of Tubercle bacilli in >95% (M.TB)
Ingestion of milk containing Bovine Tubercle Ingestion of milk containing Bovine Tubercle
bacilli (M. bovis)bacilli (M. bovis)
Contamination of superficial skin or mucous Contamination of superficial skin or mucous
membrane lesion with tubercle bacillimembrane lesion with tubercle bacilli
Congenital infection when mother has Congenital infection when mother has
lymphohematogenous spread during pregnancy lymphohematogenous spread during pregnancy
OROR tuberculous endometritis tuberculous endometritis

6. Primary tuberculous infectionPrimary tuberculous infection
Primary Focus (Ghon’s focus)Primary Focus (Ghon’s focus)
at the site of first implantationat the site of first implantation
usually single and Subpleuralusually single and Subpleural
in most, - heals and disappears, orin most, - heals and disappears, or
 - fibroses or calcifies.- fibroses or calcifies.
Primary Complex:Primary Complex:
primary focus + Hilar lymphnodes + draining primary focus + Hilar lymphnodes + draining
lymphaticslymphatics
complications arise more commonly from regional complications arise more commonly from regional
adenitis than from the primary focusadenitis than from the primary focus

7. Primary infectionPrimary infection
Children vs. AdultsChildren vs. Adults
In adults, In adults,
- regional lymphadenitis less marked- regional lymphadenitis less marked
- bronchial erosion less frequent- bronchial erosion less frequent
- less risk of dissemination- less risk of dissemination
Thus, adult primary infection tends to be Thus, adult primary infection tends to be
more local and pulmonary.more local and pulmonary.

8. Progressive primary tuberculosisProgressive primary tuberculosis
Progression of TB depends on the age of the Progression of TB depends on the age of the
child, number of tubercle bacilli, and host child, number of tubercle bacilli, and host
resistance.resistance.
Apparently healed focus or nodes may contain Apparently healed focus or nodes may contain
viable organisms for many years.viable organisms for many years.
During 1During 1
stst
4-8 weeks, organisms are disseminated 4-8 weeks, organisms are disseminated
in the blood stream.in the blood stream.

9. Progressive pulmonary diseaseProgressive pulmonary disease
Progressive primary infectionProgressive primary infection: Progression of : Progression of
recently acquired pulmonary primary infection recently acquired pulmonary primary infection
Endogenous exacerbationEndogenous exacerbation: reactivity of : reactivity of
organisms and breakdown of primary lesions organisms and breakdown of primary lesions
acquired > 5 years previouslyacquired > 5 years previously
Exogenous exacerbationExogenous exacerbation: Re-infection by newly : Re-infection by newly
acquired bacilli in persons with healed primary acquired bacilli in persons with healed primary
lesionslesions

10. Symptoms of childhood Symptoms of childhood
tuberculosistuberculosis
1.1.Failure to thrive } &Failure to thrive } &
2.2.Intermittent fever } are the commonest symptoms Intermittent fever } are the commonest symptoms
3.3.Pleural effusionPleural effusion
4.4.AscitesAscites
5.5.Abdominal mass (Painless)Abdominal mass (Painless)
6.6.Limp / ArthritisLimp / Arthritis
7.7.Painless lymphadenopathyPainless lymphadenopathy
8.8.Persistent skin ulcerPersistent skin ulcer
9.9.Sterile pyuriaSterile pyuria
10.10.MeningitisMeningitis

11. Pulmonary lesions in tuberculosisPulmonary lesions in tuberculosis
- the primary complex- the primary complex

12. Complications of the primary Complications of the primary
focusfocus
1. Rupture of focus into pleural space causing
serous effusion
2. Rupture of focus into bronchus causing
cavitation
3. Enlarged focus, sometimes laminated or “coin”
shadow

13. Complications of regional nodesComplications of regional nodes
1. Incomplete (ball-valve) bronchial obstruction,
emphysema of middle & lower lobes
2. Complete bronchial obstruction, collapse of
right lower lobe
3. Erosion of node into bronchus & segmental
consolidation
4. Rupture of node into pericardium: tuberculous
pericardial effusion

14. Sequelae of bronchial complicationsSequelae of bronchial complications
1. Stricture of bronchus at site of erosion
2. Cylindrical bronchiectasis in area of old collapse
3. Wedge shadow: contracture & fibrosis of
segmental lesion
4. Linear scar of fibrosis following segmental
lesion

15. SymptomsSymptoms
Primary complex – mild fever, anorexia, weight Primary complex – mild fever, anorexia, weight
loss, decreased activity, coughloss, decreased activity, cough
Progressive primary complex – high grade fever, Progressive primary complex – high grade fever,
cough. Expectoration and hemoptysis – usually cough. Expectoration and hemoptysis – usually
associated with cavity and ulceration of associated with cavity and ulceration of
bronchus. bronchus.
Abnormal chest signs – decreased air entry, Abnormal chest signs – decreased air entry,
dullness, crepsdullness, creps

16. Endobronchial tb – wheeze!! Endobronchial tb – wheeze!!
Fever, troublesome cough, dyspnea, wheezing Fever, troublesome cough, dyspnea, wheezing
and cyanosisand cyanosis
Pleural effusion – follows a rupture of a Pleural effusion – follows a rupture of a
subpleural focus. Also by hematogenous spread subpleural focus. Also by hematogenous spread
from primary focus. Occurs coz of from primary focus. Occurs coz of
hypersensitivity to tuberculoproteins. hypersensitivity to tuberculoproteins.
Fever, cough, dyspnea, pleuritic chest pain. Fever, cough, dyspnea, pleuritic chest pain.

17. Miliary tuberculosisMiliary tuberculosis
most common within 1most common within 1
stst
3 to 6 months after 3 to 6 months after
infectioninfection
due to heavy hematogenous spread of tubercle due to heavy hematogenous spread of tubercle
bacillibacilli
Onset: Insidious, with Onset: Insidious, with
Fever and weight lossFever and weight loss
Palpable liver and/or spleenPalpable liver and/or spleen
Tachypnoea with normal chest findingsTachypnoea with normal chest findings

18. Miliary tuberculosisMiliary tuberculosis
Hematogenous dissemination leads to progressive Hematogenous dissemination leads to progressive
development of small lesions throughout the body, development of small lesions throughout the body,
with tubercles in the with tubercles in the
lung, spleen, liver, lung, spleen, liver,
bone marrow, heart, pancreasbone marrow, heart, pancreas
brain, choroid, skinbrain, choroid, skin
Radiologic diagnosisRadiologic diagnosis::
““Snow stormSnow storm”” appearance appearance
(Multiple small lung nodules 1mm size and above in (Multiple small lung nodules 1mm size and above in
both lung fields).both lung fields).

19. Miliary TBMiliary TB

20. Cutaneous TuberculosisCutaneous Tuberculosis
1.1.Associated with primary complexAssociated with primary complex
(Direct inoculation into Traumatized Area)(Direct inoculation into Traumatized Area)
- Painless nodule, leading to non healing ulcer with regional - Painless nodule, leading to non healing ulcer with regional
lymphadenitislymphadenitis
- Scrofuloderma over ruptured caseous lymph node- Scrofuloderma over ruptured caseous lymph node
2.2.Associated with Hematogenous disseminationAssociated with Hematogenous dissemination
- Papulonecrotic tuberculids- Papulonecrotic tuberculids
papules with soft centers on trunk, thighs and facepapules with soft centers on trunk, thighs and face
 - Tuberculosis verrucosa cutis- Tuberculosis verrucosa cutis
Large tuberculids on arms and legsLarge tuberculids on arms and legs
3.3.Associated with hypersensitivity to tuberculinAssociated with hypersensitivity to tuberculin
- Erythema nodosum- Erythema nodosum
painful indurated nodules on shins, elbows, forearms thatpainful indurated nodules on shins, elbows, forearms that
subside in 2-3 weekssubside in 2-3 weeks

21. TB verrucosa cutis TB verrucosa cutis

22. Erythema nodosumErythema nodosum

23. Tuberculosis of superficial Tuberculosis of superficial
lymph nodes (scrofula)lymph nodes (scrofula)
Tonsillar / submandibular Tonsillar / submandibular
(Spread from paratracheal nodes)(Spread from paratracheal nodes)
Supraclavicular Supraclavicular
(From primary lesion in upper lobe)(From primary lesion in upper lobe)
Axillary / epitrochlear Axillary / epitrochlear
(From skin lesion on hand)(From skin lesion on hand)
Inguinal Inguinal
(From ulcer on sole of foot)(From ulcer on sole of foot)

24. Ocular TuberculosisOcular Tuberculosis
Primary tuberculous conjunctivitisPrimary tuberculous conjunctivitis (after trauma) (after trauma)
Yellowish – gray nodules on palpebral conjunctiva Yellowish – gray nodules on palpebral conjunctiva
with preauricular adenopathywith preauricular adenopathy
Phlyctenular conjunctivitisPhlyctenular conjunctivitis (Hypersensitivity) (Hypersensitivity)
Nodules on limbus recurring in crops for weeksNodules on limbus recurring in crops for weeks
Tubercles of choroidTubercles of choroid (with miliary TB) (with miliary TB)

25. Choroidal tuberclesChoroidal tubercles

26. Tuberculous otitis mediaTuberculous otitis media
Primary with Preauricular adenitisPrimary with Preauricular adenitis
Metastatic spread with primary elsewhereMetastatic spread with primary elsewhere
 SymptomsSymptoms: Painless otorrhea, may be blood-: Painless otorrhea, may be blood-
stainedstained
 ComplicationsComplications: Secondary infection: Secondary infection
 DeafnessDeafness
 TB meningitisTB meningitis

27. GI and Abdominal TBGI and Abdominal TB
Hematogenous spread from lungs or swallowing Hematogenous spread from lungs or swallowing
of infected sputum. of infected sputum.
Painless ulcer in gingivolabial sulcus with Painless ulcer in gingivolabial sulcus with
submental or submandibular adenopathysubmental or submandibular adenopathy
Ulcer on tonsilUlcer on tonsil
Esophageal diverticulum secondary to rupture of Esophageal diverticulum secondary to rupture of
mediastinal nodes into lumenmediastinal nodes into lumen

28. Tuberculous toxemiaTuberculous toxemia
Present with colicky abdominal pain, vomiting and Present with colicky abdominal pain, vomiting and
constipation. constipation.
Abdomen feels doughy. Abdomen feels doughy.
Rolled up omentum and enlarged lymph nodes may Rolled up omentum and enlarged lymph nodes may
appear as irregular nodular masses with ascitesappear as irregular nodular masses with ascites
Tuberculous enteritisTuberculous enteritis
Ulcers, mesenteric adenitis, peritonitisUlcers, mesenteric adenitis, peritonitis
Adhesions, subacute intestinal obstruction,Adhesions, subacute intestinal obstruction,
HepatosplenomegalyHepatosplenomegaly

29. Renal tuberculosisRenal tuberculosis
Tubercles in glomeruli lead to shedding of Tubercles in glomeruli lead to shedding of
tubercle bacilli into tubules tubercle bacilli into tubules
Caseous mass / Cavity between cortex and Caseous mass / Cavity between cortex and
pyramidspyramids
TB of bladder (Tuberculous cystitis)TB of bladder (Tuberculous cystitis)
SymptomsSymptoms: dysuria, hematuria, : dysuria, hematuria,

pyuria with TB bacillipyuria with TB bacilli

30. Caseous renal tuberculosisCaseous renal tuberculosis

31. Skeletal tuberculosisSkeletal tuberculosis
Bones involved in order of frequencyBones involved in order of frequency: :
Vertebrae > knee > hip > elbowVertebrae > knee > hip > elbow
Upper extremities and non-weight-bearing bonesUpper extremities and non-weight-bearing bones
(skull, clavicle) rarely involved(skull, clavicle) rarely involved
Tuberculous spondylitisTuberculous spondylitis most commonly most commonly
Thoracic / Lumbar / Both (Decreasing frequency)Thoracic / Lumbar / Both (Decreasing frequency)
X-ray findingsX-ray findings: :
Narrowing of disc space, Collapse of vertebral Narrowing of disc space, Collapse of vertebral
bodybody
Extensive destruction with kyphosis (Pott disease)Extensive destruction with kyphosis (Pott disease)
ComplicationsComplications:Para vertebral abscess (Pott abscess):Para vertebral abscess (Pott abscess)
Psoas Abscess. Paraplegia, Quadriplegia (cervical)Psoas Abscess. Paraplegia, Quadriplegia (cervical)

32. Genital tuberculosisGenital tuberculosis
Uncommon before pubertyUncommon before puberty
Usually due to lympho-hematogenous spreadUsually due to lympho-hematogenous spread
Occasionally by direct extension from Occasionally by direct extension from
adjacent lesion of bone, gut, or urinary tractadjacent lesion of bone, gut, or urinary tract

33. Genital tuberculosisGenital tuberculosis
SalpingitisSalpingitis
EndometritisEndometritis
OophoritisOophoritis
Cervicitis Cervicitis
Infertility is commonest sequel Infertility is commonest sequel
in malesin males::
Primary tuberculosis of penis after circumcision Primary tuberculosis of penis after circumcision
with inguinal adenopathywith inguinal adenopathy
Epididymitis / Epididymo – orchitis in early Epididymitis / Epididymo – orchitis in early
childhoodchildhood

34. Tuberculous meningitisTuberculous meningitis
TB meningitis seen in 1/300 Primary infectionsTB meningitis seen in 1/300 Primary infections
Pathophysiology:Pathophysiology:
Rupture of a subcortical caseous focus (Rich’s) into the Rupture of a subcortical caseous focus (Rich’s) into the
subarachnoid space.subarachnoid space.
Inflammatory exudates form about base of brain and along Inflammatory exudates form about base of brain and along
cerebral vessels as they pass over hemispheres.cerebral vessels as they pass over hemispheres.
Raised intracranial pressure due to increased secretion of Raised intracranial pressure due to increased secretion of
CSF CSF
Adhesions along base and roof of 4Adhesions along base and roof of 4
thth
ventricles lead to ventricles lead to
obstruction to CSF flow and hydrocephalus,obstruction to CSF flow and hydrocephalus,
involvement of cranial nerves III VI VII and optic chiasma.involvement of cranial nerves III VI VII and optic chiasma.
Cerebral endarteritis narrows lumen, reduces blood flow, Cerebral endarteritis narrows lumen, reduces blood flow,
leads to cerebral thrombosis and infarction. leads to cerebral thrombosis and infarction.

35. Stages of TB meningitisStages of TB meningitis
Stage I Irritability, anorexia, personality changeStage I Irritability, anorexia, personality change
Occasional vomiting, feverOccasional vomiting, fever
Poor school performancePoor school performance
Stage II Focal neurological signs, cranial nerve palsies,Stage II Focal neurological signs, cranial nerve palsies,
Seizures, hemiplegia, squintSeizures, hemiplegia, squint
Stage III Loss of consciousness, Coma, Papilloedema Stage III Loss of consciousness, Coma, Papilloedema
Decerebrate rigidityDecerebrate rigidity

36. Complications of TB meningitisComplications of TB meningitis
HydrocephalusHydrocephalus
Subdural effusionSubdural effusion
Late: Hemiplegia / ParaplegiaLate: Hemiplegia / Paraplegia
Intellectual impairmentIntellectual impairment
BlindnessBlindness
DeafnessDeafness
Intracranial calcifications leading to Intracranial calcifications leading to
hypothalamic and pituitary dysfunctionhypothalamic and pituitary dysfunction
- Growth failure- Growth failure
- Diabetes insipidus- Diabetes insipidus
- Failure of development of secondary sexual - Failure of development of secondary sexual
characteristicscharacteristics

37. Diagnosis of TB meningitisDiagnosis of TB meningitis
Signs of meningeal irritationSigns of meningeal irritation
X-ray chestX-ray chest
CT scan – basal exudates, inflammatory granulomas etcCT scan – basal exudates, inflammatory granulomas etc
Tuberculin testingTuberculin testing
Retinoscopy for choroidal tuberclesRetinoscopy for choroidal tubercles
Lumbar punctureLumbar puncture
Elevated CSF pressure(30 – 40cm h2o)Elevated CSF pressure(30 – 40cm h2o)
Cobweb Coagulum/ pellicle on standing Cobweb Coagulum/ pellicle on standing
100 – 500 WBCs / cu.mm100 – 500 WBCs / cu.mm
>40 mg% protein>40 mg% protein
Low / Normal sugarLow / Normal sugar
AFB smear & cultureAFB smear & culture

38. Prognosis in TB meningitisPrognosis in TB meningitis
100% mortality in 3-4 weeks without treatment100% mortality in 3-4 weeks without treatment
100% survival with treatment started in Stage I100% survival with treatment started in Stage I
75% survival with treatment started in Stage II75% survival with treatment started in Stage II
Stage III – variable survival, all will have sequelaeStage III – variable survival, all will have sequelae

39. Direct tests for tuberculosisDirect tests for tuberculosis
Ziehl-Neelsen staining for AFB in clinical specimens Ziehl-Neelsen staining for AFB in clinical specimens
(sputum, gastric juice, biopsy)(sputum, gastric juice, biopsy)
AFB culture on Lowenstein-Jensen solid medium (4 AFB culture on Lowenstein-Jensen solid medium (4
weeks)weeks)
PCR amplification of targeted mycobacterial DNA PCR amplification of targeted mycobacterial DNA
sequences sequences
DNA probes: fluorescence DNA probes: fluorescence in situin situ hybridization assays hybridization assays

40. CultureCulture
LJ mediumLJ medium
BACTEC radiometric assayBACTEC radiometric assay
Septichek AFB systemSeptichek AFB system
MGIT – mycobacterial growth indicator tube MGIT – mycobacterial growth indicator tube
systemsystem

41. PCR – rapid resultsPCR – rapid results
Serodiagnosis – ELISASerodiagnosis – ELISA
QuantiFERON- TB test (QFT) – for diagnosing QuantiFERON- TB test (QFT) – for diagnosing
latent TB. Based on IFN-gamma released from latent TB. Based on IFN-gamma released from
sensitized lymphocytes.sensitized lymphocytes.
ELISPOTELISPOT

42. Positive MantouxPositive Mantoux

43. Mantoux TestMantoux Test
MC used test for establishing diagnosis of TB in MC used test for establishing diagnosis of TB in
childrenchildren
Delayed type hypersensitivity reactionDelayed type hypersensitivity reaction
0.1 ml of 5 TU PPD is injected intradermally 0.1 ml of 5 TU PPD is injected intradermally
into the volar aspect of the forearm (or 2 TU of into the volar aspect of the forearm (or 2 TU of
PPD RT 23)PPD RT 23)
A weal of 5 mm should be raisedA weal of 5 mm should be raised
Reaction is read after 48 – 72 hrsReaction is read after 48 – 72 hrs
Look for induration and erythemaLook for induration and erythema

44. Observation and InferenceObservation and Inference
48-72 hours later 48-72 hours later  diameter of induration is diameter of induration is
measured transversely to the long axis of the measured transversely to the long axis of the
forearm. forearm.
Induration > 10mm is suggestive of natural Induration > 10mm is suggestive of natural
infection. infection.
5-10 mm 5-10 mm  borderline; considered positive in borderline; considered positive in
immunocompromised hostimmunocompromised host
<5mm <5mm  Negative mantoux test does not rule Negative mantoux test does not rule
out TBout TB

45. False NegativesFalse Negatives
Test done in incubation period of TBTest done in incubation period of TB
For several weeks following measlesFor several weeks following measles
During Corticosteroid therapyDuring Corticosteroid therapy
Overwhelming TB infection (milliary, meningits)Overwhelming TB infection (milliary, meningits)
Severe MalnutritionSevere Malnutrition
If given Sub Cutaneous instead of Intra dermalIf given Sub Cutaneous instead of Intra dermal
Inactive TuberculinInactive Tuberculin

46. False positiveFalse positive
Atypical mycobacteriaAtypical mycobacteria
BCG vaccineBCG vaccine
Infection at site of testInfection at site of test

47. Guidelines for presumptive diagnosis Guidelines for presumptive diagnosis
of tuberculosisof tuberculosis
Pediatr Infect Dis J 1993;12: 499-504)Pediatr Infect Dis J 1993;12: 499-504)
A combination of at least 3 of the following:A combination of at least 3 of the following:
Symptoms/signs s/o TB: Symptoms/signs s/o TB:
(fever > 1 mo., cough, weight loss) (fever > 1 mo., cough, weight loss)
History of close contact with TBHistory of close contact with TB
Positive tuberculin skin test (Mantoux > 10 mm)Positive tuberculin skin test (Mantoux > 10 mm)
 sputum / gastric juice AFB sputum / gastric juice AFB ++veve
 lymph node / tissue biopsy positivitylymph node / tissue biopsy positivity
Radiologic features suggestive of TBRadiologic features suggestive of TB
Response to Anti TB Therapy Response to Anti TB Therapy

48. History of contact = any child who lives in a History of contact = any child who lives in a
household with an adult taking ATT or has household with an adult taking ATT or has
taken therapy in the past 2 yearstaken therapy in the past 2 years

49. RadiologyRadiology
In extra pulmonary tb, presence of lesions on chest In extra pulmonary tb, presence of lesions on chest
radiograph supports diagnosis. radiograph supports diagnosis.
Enlarged lymph nodes in hila, right paratracheal regionEnlarged lymph nodes in hila, right paratracheal region
Consolidation in progressive primary disease – Consolidation in progressive primary disease –
heterogenous, poorly marginated with predilection to heterogenous, poorly marginated with predilection to
apical or posterior segments of upper lobe or superior apical or posterior segments of upper lobe or superior
segments of lower lobe. segments of lower lobe.
BronchiectasisBronchiectasis
Pleural effusionPleural effusion
Miliary tb – millet sized lesionsMiliary tb – millet sized lesions

50. Treatment for TBTreatment for TB
11
stst
line anti-tuberculous drugs line anti-tuberculous drugs
Isoniazid (INAH) 5 mg/kg/day H Isoniazid (INAH) 5 mg/kg/day H
Rifampicin 10 mg/kg/day RRifampicin 10 mg/kg/day R
Pyrazinamide 25 mg/kg/day Z Pyrazinamide 25 mg/kg/day Z
Ethambutol 20 mg/kg/day E Ethambutol 20 mg/kg/day E
Streptomycin 20mg/kg/day SStreptomycin 20mg/kg/day S

51. 22
ndnd
Line drugs Line drugs
Drug resistant cases or when first line drugs cant be usedDrug resistant cases or when first line drugs cant be used
Eg. Cycloserine, ethionamaide, PAS, kanamycinEg. Cycloserine, ethionamaide, PAS, kanamycin
Other drugsOther drugs
Strictly for drug resistant casesStrictly for drug resistant cases
Eg. Quinolones, rifamycin, amikacin, imipenem, Eg. Quinolones, rifamycin, amikacin, imipenem,
ampicillinampicillin

52. Phases of TreatmentPhases of Treatment
Intensive PhaseIntensive Phase
Eliminate bacterial loadEliminate bacterial load
Prevent emergence of drug resistant strainsPrevent emergence of drug resistant strains
Atleast 3 Bactericidal Drugs usedAtleast 3 Bactericidal Drugs used
Continuation PhaseContinuation Phase
Continue and complete therapyContinue and complete therapy
Atleast 2 Bactericidal drugs usedAtleast 2 Bactericidal drugs used
SteroidsSteroids
Anti inflammatory effect – millary, peritonitis, pericarditisAnti inflammatory effect – millary, peritonitis, pericarditis
TB meningitis TB meningitis

53. RNTCP TreatmentRNTCP Treatment

54. Treatment policies in children Treatment policies in children
with tuberculosis (IAP)with tuberculosis (IAP)
Preventive Therapy In Mantoux Positive : 6 HRPreventive Therapy In Mantoux Positive : 6 HR
Primary complex }Primary complex }
Isolated LNE } 2 HRZ + 4 HRIsolated LNE } 2 HRZ + 4 HR
Pleural Effusion }Pleural Effusion }
Progressive Pulmonary Tuberculosis }Progressive Pulmonary Tuberculosis }
Multiple LNE } 2 HRZE + 4 HRMultiple LNE } 2 HRZE + 4 HR
Miliary, Bone, Renal, Pericardial } 2 HRZE + 7HRMiliary, Bone, Renal, Pericardial } 2 HRZE + 7HR
TB Meningitis } 2 HRZE + 10 HRE +TB Meningitis } 2 HRZE + 10 HRE +
Prednisolone / DexamethasonePrednisolone / Dexamethasone

55. The 5 components of DOTS
Political & administrative commitment
Diagnosis by good quality sputum microscopy
Adequate supply of good quality drugs
Directly observed treatment
Systematic monitoring & Accountability

56. Drug ResistanceDrug Resistance
Natural or PrimaryNatural or Primary
AcquiredAcquired
InitialInitial
Multidrug resistance (MDR)Multidrug resistance (MDR)

57. Treatment of resistant Treatment of resistant
tuberculosistuberculosis
INH-resistant TB: 18 RZEINH-resistant TB: 18 RZE
Rifampicin-resistant TB: 18 – 24 HZERifampicin-resistant TB: 18 – 24 HZE
Multidrug-resistant TB:Multidrug-resistant TB:
Treat for 24 mo. after culture conversion Treat for 24 mo. after culture conversion
with regimen containing 3 second-line with regimen containing 3 second-line
drugs, including IM aminoglycoside/ SM, drugs, including IM aminoglycoside/ SM,
one fluoroquinolone and one oral 2one fluoroquinolone and one oral 2
ndnd
line line
drug.drug.

59. ReferencesReferences
Nelson’s textbook of paediatricsNelson’s textbook of paediatrics
OP Ghai – Essential PaediatricsOP Ghai – Essential Paediatrics
Preventive and Social Medicine – Park & ParkPreventive and Social Medicine – Park & Park
The Internet…The Internet…