1. PAEDIATRIC TUBERCULOSIS
DR (MRS) M.B. FETUGA

2. HISTORICAL FACTS 1882- Robert Kochs described the bacilli
1920- BCG was developed
1948- Use of Streptomycin in the treatment of TB was commenced
1952- Isoniazid (H) was introduced in the treatment of TB
DR (MRS) M.B. FETUGA

3. AETIOLOGY OF TB Mycobacterium tuberculosis-Genus M, sp. tb
-acid & alcohol fast bacilli (waxy outer capsule)
-non motile
-non sporulating
-aerobic
-produces no exotoxin or endotoxin
- causes disease by invoking immune reactions
Mycobacterium bovis
DR (MRS) M.B. FETUGA

4. EPIDEMIOLOGY OF TB About a third of the world population is infected
30% of those who develop the disease live in Africa
TB causes 25% of all preventable deaths in developing countries
95% of TB cases & 98% of TB deaths occur in the developing world
Exact incidence is unknown in Nigeria but 25,000 new cases are reported annually
Under-5 children & adolescents are more at risk
DR (MRS) M.B. FETUGA

5. RESURGENCE OF TB Civil wars, strife and conflicts
Increasing poverty, malnutrition and overcrowding
HIV pandemic
Collapse of the various National TB Control Programmes
Multi Drug Resistance
DR (MRS) M.B. FETUGA

6. TRANSMISSION TB is a vaccine-preventable killer disease
Source is usually an adult with smear pos. TB
Childhood TB is =5-15% of all TB cases
Children usually not infectious:
- often not smear pos.
. TB in children reflects the failure to control TB among adults
DR (MRS) M.B. FETUGA

7. TRANSMISSION C’ONTD
Inhalation of Infected droplets by sneezing, coughing and talking
Drinking milk infected by M. bovis (cattle TB)
Abrasions on the skin & mucous membranes
Perinatally acquired TB- very rare:
-TB bacillaemia can spread to the fetus
- Placental TB can spread to the fetus
- endocervical TB can spread by aspiration
- early neonatal exposure secondary to care by the infected mother
DR (MRS) M.B. FETUGA

8. COURSE OF TB
TB infection= presence of bacilli (mantoux pos.) but without clinical or radiological features
TB disease= presence of bacilli (mantoux pos.) + clinical and/or X-Ray features
Majority of children with TB infection do not develop TB disease
Chances of progression to disease is greatest shortly after infection & steadily decreases as time goes by
DR (MRS) M.B. FETUGA

9. COURSE OF TB C’ONTD
Risk factors for the progression of TB infection to disease:
-HIV infection
-Age->ter extent of glandular involvement
-Malnutrition especially, kwashiorkor
-Debilitating infections like Measles & Pertussis
-Diabetes mellitus
-Indiscriminate steroid use
-Malignancies & cyto-toxic therapy
-Physical & Emotional stress
DR (MRS) M.B. FETUGA

10. COURSE OF TB CONTD
Frequent intense exposure results in more severe infection
Overcrowding-more freq exposure
Poor vent- > conc of bacilli
Children usually acquire TB from an infectious parent or close contact
BCG vacc protects against severe forms of TB
DR (MRS) M.B. FETUGA

11. PATHOGENESIS OF TB
Primary TB is the first phase of infection with M.tuberculosis
It occurs mainly in the under-5 . The younger the child, the higher the severity of the local reactions
Lungs are the sites of Primary TB in >98%
Ghon focus is formed when the bacilli settles in the alveoli with inflammation
Histiocytes carry the multiplying bacilli through lymphatic channels to regional lymph nodes
DR (MRS) M.B. FETUGA

12. PATHOGENESIS C’ONTD
Ghon focus + Lymphatic channels + Nodes = Primary Complex or Ghon complex
Silent bacteraemia follows Primary Complex causing metastatic foci in the lung apices, vertebrae, meninges, kidneys
Development of Delayed Hypersensitivity (by T lymphocytes) follows in the next 2-8 weeks. Cell Mediated Immunity is formed & patient becomes mantoux positive
Ghon focus is usually subpleural in the mid-& lower lung lobes
DR (MRS) M.B. FETUGA

13. PATHOGENESIS C’ONTD
Muco-cutaneous manifestations of Primary TB include:
-Erythema nodosum (painful, red patches in the inner side of leg & foreman)
-Phlyctenular conjuctivitis (small yellowish elevation of the conjuctiva at the edge of the cornea & surrounded by conjuctival vessels
Majority heals + calcifications
Some may be dormant & later re-activates
Some may be locally progressive
DR (MRS) M.B. FETUGA

14. PATHOGENESIS C’ONTD Acute dissemination may also follow
Risk of Primary TB progressing to active TB = 5-15%
Progression occurs when host resistance is poor, otherwise, the bacilli initially disseminated are killed or they remain dormant
When healing of the Primary Complex occurs, it is less in the nodes than in the lung parenchyma, hence the nodes are the sites of re-activation later in life.
DR (MRS) M.B. FETUGA

15. PATHOGENESIS CONTD
20 or adult type with cavitatn with reactivatn of dormant focus or re-attack-erosion into a bronchus- expectoratn of tubercle
20 dx spreads by local extensn & not thro LN or bld
Hypersensitivity accts for much of symptomatology of chidhood TB
DR (MRS) M.B. FETUGA

16. WALLGREN TIMETABLE 1.Incubation period: 3-8 weeks
2.Within 3 mo of primary TB:
-Miliary TB & TB Meningitis
3.Within 3-9 mo:
-TB of Lymph Glands
4.Within 1 year:
-TB Pleural Effusion
DR (MRS) M.B. FETUGA

17. WALLGREN TABLE C’ONTD TB of bones & joints 6.Within 5 years:
Progressive Pulmonary TB
7.After 5 years:
Urogenital TB
DR (MRS) M.B. FETUGA

18. PROGRESSION 1.Tuberculous pneumonia 2.Consolidation
3.TB Pleural Effusion
4.Atelectasis / Emphysema - pressure
5.Endobronchial TB
6.Bronchogenic spread =TB bronchopneumonia
7.Haematogenous spread =Disseminated TB
8.Cavitation from excessive caseation
DR (MRS) M.B. FETUGA

19. PROGRESSION
Healing occurs in most cases (fibrosis & calcification may occur)
Caseating hilar LNs may burst into pulm vein- miliary dx, TBM
Host factors determine response to infection; Overt & severe dx likely in malnourished, 20infectns like measles, HIV eg TBM, miliary or progressive I0 dx
DR (MRS) M.B. FETUGA

20. DIAGNOSIS OF TB 1.Tuberculin test:
-based on delayed hypersensitivity to tuberculin i.e. asseses cellular imm resp
-detects the presence of Mycobacterium either from vaccination or from natural infection -
-0.1 ml of 5 t.u PPD & read in hrs
-induration >10mm suggests infection
-induration >20mm suggests disease
DR (MRS) M.B. FETUGA

21. Intradermally, very small gauge needle (27G), too deep – false –ve
look for presence of wheal as fluid is injected
Read induration in 48-72hrs
BCG effect-most in 3-6/12, wanes by 2-3yrs
Heaf test- easier, < accurate-multiple puncture
DR (MRS) M.B. FETUGA

22. DIAGNOSIS C’ONTD - Pos. Tuberculin : >10mm in a child without BCG
-Tuberculin reaction to BCG is weaker & last shorter than that to natural infection
- Pos. Tuberculin : >10mm in a child without BCG
Pos. Tuberculin: >15mm in a child with BCG
Neg. Tuberculin: <10mm does not exclude TB (HIV, malnutrition, severeTB, viral infections, steroid use, malignancies)
DR (MRS) M.B. FETUGA

23. DIAGNOSIS C’ONTD
2. Sputum testing: difficult in children
- collection by gastric washing & bronchoalveolar lavage
- Ziehl- Neelsen stain (low yield on other body fluids)
- culture on Lowenstein Jensen medium for 6-8 weeks & sensitivity testing over another 2-4 wks
3.CXRay- no pathognomonic feature; widened superior mediastinum suggestive of TB
Cavitations unusual in children unless with HIV co-infection
4. Gastric washing is done by lavaging the gastic content every morning for three consecutive days before meal & the aaspirate is sent for Z-N stain
DR (MRS) M.B. FETUGA

24. DIAGNOSIS C’ONTD
5.Serology:More rapid, sensitive but expensive and not available for routine use eg. ELISA, PCR, DNA Probes
6. Accelerated BCG reaction:
- to be used when 100 t.u PPD fails
- induration in 48hrs, pustule on 3rd day, scab in 6 days & scar in 2 weeks unlike 6-8 weeks in a normal BCG reaction.
DR (MRS) M.B. FETUGA

25. DIAGNOSIS C’ONTD
7. Biopsies of tissues eg lymph nodes, peritoneum, pleura, bone usually for:
-microscopy (Z-N Stain)
-culture
-histology for tubercules & caseating lesions
. 8. Endoscopic examinations (peritoneoscopy, bronchoscopy etc)
DR (MRS) M.B. FETUGA

26. CATEGORIES OF DIAGNOSIS
1. Suspected TB- suspicious Chest X-Ray findings
2. Probable TB- suspicious CXR in addition to either : weight loss/ history of contact/ strongly positive tuberculin
3. Confirmed TB- Positive culture of M. tuberculosis
DR (MRS) M.B. FETUGA

27. PULMONARY TB
The commonest form of TB occurring alone or in combination in > 70% of cases.
PTB = Primary Complex + Direct Local Spread
Presents either as Consolidation, Pneumothorax, Atelectasis or Pleural Effusion.
DR (MRS) M.B. FETUGA

28. Pulmonary Tb c’ontd.
Effusion in TB may be due immune reaction to the of a sub-pleural focus into the pleural haemogenous TB Constrictive Pericarditis
Management of TB Effusion anti TB Steroids. TUBE DRAINAGE IS NOT DONE EXCEPT IN CASES OF SEVERE RESPIRATORY DISTRESS !!
TB Effusion is reportedly uncommon in Africa because the immune system is pre-occupied with many other antigenic stimulation.
DR (MRS) M.B. FETUGA

29. Pulmonary TB c’ontd.
Usually vague symptoms: fever, chronic cough, weight loss, anorexia, night sweat, dyspnea, localized wheezing.
Presentation with haemoptysis, which is common among adults is uncommon in children.
DR (MRS) M.B. FETUGA

30. Miliary TB Most severe form of disseminated TB
Common in under-5 usually within the first 3 months of infection.
Follows haematogenous dissemination of a large dose of the bacilli to many body tissues
Presentation is variable depending on the load of bacilli, immunity & the organ involved
May be insidious (with anorexia, weight loss, fever & generalized lymphadenopathy).
DR (MRS) M.B. FETUGA

31. Miliary TB May be fulminant with severe dyspnea & wheezing.
Choroidal Tubercules are pathognomonic
CXR = bilateral miliary mottling + infiltrations :
Differential Diagnosis-
mycotic pneumonia, chickenpox pneumonia, eosinophilic pneumonia, childhood histiocytosis, idiopathic pulmonary haemosiderosis, sarcoidosis, fibrolysing alveolitis.
DR (MRS) M.B. FETUGA

32. TB Meningitis
Gravest form of TB whose prognosis depends on the rapidity with which the diagnosis is made.
Metastatic cerebral foci may manifest immediately after Primary infection or may re-activate many years later.
The Riche’s focus at or near the surface of the brain enlarges, caseates, ruptures & discharges caseous materials into the subarachnoid space provoking hypersensitivity reactions.
DR (MRS) M.B. FETUGA

33. TB Meningitis c’ontd.
Cerebral vasculitis & cerebral infarcts.
Presentation in 3 stages:
I- Irritability, fever, lethargy
II- Features of cerebral involvement & raised Intracranial Pressure (vomiting, drowsiness, mental changes, seizures, meningeal signs)
III- Multiple CNS signs & coma.
DR (MRS) M.B. FETUGA

34. TB Meningitis c’ontd. Outcome: Stage I- mortality 3%, sequelae 13%
Stage II- mortality 14%, sequelae 26%
Stage III- mortality 30%,sequelae 42%
Investigation:
CSF chemistry- low glucose
CSF culture- positive in 75%
CSF microscopy - low yield (about 20%)
Prognosis depends on the stage of disease at commencement of therapy.
DR (MRS) M.B. FETUGA

35. Spinal TB Commonest & most important bone/joint TB.
Usually involves the mid & lower thoracic spinal segments. Rarely affects the lumbar & cervical areas.
Single or multiple vertebral involvement
The anterior part of the vertebral body is usually affected
Presentation: Back pain, difficulty in flexing the spine, abnormal gait (walking on eggs), Kyphosis, scoliosis, paraplegia (spastic or flaccid.)
DR (MRS) M.B. FETUGA

36. Spinal TB
Paralysis is spastic when there is cord compression & flaccid when there is cord infiltration and destruction. SPASTIC PARAPLEGIA CARRIES A BETTER PROGNOSIS THAN FLACCID PARALYSIS!
Psoas abscess follows lumbar segment TB while retropharyngeal abscess follows cervical segment TB.
Spinal TB X-Ray= reduced intervertebral spaces, destruction of vertebrae & paraspinal shadows. ***Immobilization in Meniever Spinal Jacket is no longer used.
DR (MRS) M.B. FETUGA

37. Abdominal TB May be part of the Primary disease or may follow PTB
Affects the mesentery & retroperitoneal glands, omentum & the intestine.
Different forms Hyperplastic TB TB mesenteric TB Mixed abdominal TB
Presents as abdominal mass, ascites, intestinal obstruction, enteritis & malabsorption.
Doughy abdomen due to the mass formed by the matted omentum & intestine , NOT to ascites.
DR (MRS) M.B. FETUGA

38. Lymphatic Gland TB
Primary focus may be in the tonsillar bed or other parts of the oro-pharynx.
Spreads to involve the cervical, submandibular & supraclavicular nodes.
May be unilateral or bilateral.
Glands are discrete, mobile, firm & non tender.
They become matted if there is periadenitis
May rupture through its capsule & leave a discharging sinus
Typically, no constitutional symptoms.
DR (MRS) M.B. FETUGA

39. Lymphatic Gland TB c’ontd.
Differrential Diagnosis of Lymphatic TB:
Pyogenic adenitis
Atypical Mycobacterium Complex (AMC) adenopathy
Hodgkins lymphoma
Leukaemia
Toxoplasmosis
DR (MRS) M.B. FETUGA

40. MANAGEMENT OF PAEDIATRIC TB
AIMS OF MANAGEMENT:
- To achieve cure
- To reduce transmission
- To prevent relapse.
DR (MRS) M.B. FETUGA

41. TB MANAGEMENT
New trends in the management of TB aimed at combating the resurgence in the prevalence of TB include :
CASE DEFINITION-
-for registration & notification
-for cohort analysis
-to prioritise treatment
DIRECTLY OBSERVED THERAPY-
-to achieve good drug compliance
-to reduce chances of resistance
-to increase the cure rate in TB.
DR (MRS) M.B. FETUGA

42. Components of DOT
Identify the source of infection i.e smear positive cases with good laboratory methods.
Observe the swallowing of the drugs especially during the initial phase.
Monitoring the progress of each case with monthly sputum microscopy.
Provision of the right drug in adequate quantity.
Supports from govt. agencies & NGOs.
DR (MRS) M.B. FETUGA

43. WHY DOT(S) DOT- Directly Observed Therapy
DOTS- Directly Observed Treatment Short Course.
Aim is to achieve adherence & prevent non-compliance.
Necessary to protect Rifampicin which is the only reliable sterilizing anti-TB drug without significant resistance.
IT IS COMPULSORY TO USE DOTS WHEN RIFAMPICIN IS PRESCRIBED.
DR (MRS) M.B. FETUGA

44. WHO SHOULD DO DOTS? Medical & Paramedical Personnels
Community Health Workers
Community Leaders
Relations of the patient
Important qualities include:
- must be concerned about the course
- must have influence on the patient
- must be accountable to the health system
DR (MRS) M.B. FETUGA

45. CASE DEFINITION Primary TB-involving lung parenchyma
Extra-pulmonary TB-involving other parts of the body apart from lung parenchyma
Intra-thoracic -TB adenopathy, TB pleural effusion are extra-pulmonary TB
Disseminated TB = Pulmonary TB + TB of at least one other organ-system + choroidal tubercules
DR (MRS) M.B. FETUGA

46. Case Definition c’ontd.
Severe Extra-pulmonary TB = Miliary TB, TB Meningitis, TB pericarditis, biilateral TB effusion, Tb peritonitis & spinal TB.
Non severe Extra-pulmonary TB = skin TB, Lymphatic TB, bone &joints TB
New Case = smear positive & never treated for more than one month.
Relapse = previously declared cured after full treatment for TB & later sputum positive.
DR (MRS) M.B. FETUGA

47. Case Definition c’ontd.
Failure: If still smear positive after 5months of treatment or becomes smear positive again after initial sero-conversion while still on treatment.
Chronic case: Remain or becomes smear positive again after a full course of re-treatment regimen.
DR (MRS) M.B. FETUGA

48. Indications for Hospitalization.
To initiate chemotherapy
For life threatening complications like severe haemoptysis
Severe forms of TB eg. TB meningitis
For investigations eg. Excisional biopsies
For surgical management eg. Lobectomy, laminectomy, I & D for abscesses.
Lack of social supports & possibility of poor compliance.
Defaulters.
DR (MRS) M.B. FETUGA

49. CHEMOTHERAPY
Mainstay is combination therapy to reduce the risk of drug resistance
HR for 6months is recommended worldwide for all pulmonary & extra-pulmonary TB.
Z must be added in the first 2 months.
For extra-pulmonary TB, when R cannot be used for more than 2 months, then treatment should be for at least 9 months with other drugs.
A fourth drug, E or S is used in places with resistance to that is greater than 10%.
DR (MRS) M.B. FETUGA

50. NTBLCP IN NIGERIA 2 phases of treatment:
- Initial phase usually 2 months to kill the largest proportion of the bacilli
- Continuation phase between 4 & 10 months to ensure cure & prevent relapse.
Short Course Chemotherapy:
-usually 8 months
-for new smear positive cases
-RHZS daily for 2 months (initial phase)
TH daily for 6 months(or RH daily for 4 months)
DR (MRS) M.B. FETUGA

51. NTBLCP IN NIGERIA C’ONTD.
Re-treatment regimen (8months):
-for relapses, defaults & failures
-SERZH daily for 3 months (skip only S in the third month)
-RHE thrice weekly for 5 months.
Standard regimen(12months):
-for smear negative cases & for those in whom compliance is likely to be poor.
-SHT daily for 2 months
-TH daily for 10 months.
DR (MRS) M.B. FETUGA

52. CLASSES OF DRUGS Bactericidal:
- H kills 90% of bacilli within a few days
- H active on metabolically active bacilli
- R kills semi-dormant bacilli which H cannot kill
- Z kills bacilli only in acid environment eg. in macrophages
Sterilizing drug:
- kills all population , active or dormant
- R is the most effective drug in this group.
DR (MRS) M.B. FETUGA

53. CLASSES OF DRUGS C’ONTD
Bacteriostatic:
TE are examples
Second generation anti-TB drugs:
-cycloserine
-para-amino salicylic acid
-quinolones
-kanamycin
-ethionamide
-capreomycin
DR (MRS) M.B. FETUGA

54. Drug Resistance
Natural : a wild strain which has never been in contact with the drug
Acquired/Secondary : resistance develops after initial sensitivity to the drug
Primary : bacilli with acquired resistance infecting a new host
Multi-drug resistance – resistance to multiple drugs including H & R
DR (MRS) M.B. FETUGA

55. Indications for Adjuvant Steroid Therapy in TB
TB Meningitis
TB Pericarditis
TB Pleural Effusion
TB Laryngitis
Endobronchial TB
Severe hypersensitivity reactions to drugs
Massive TB lymphadenopathy causing pressure symptoms
Renal Tract TB (to prevent ureteric scarring)
Miliary TB
DR (MRS) M.B. FETUGA

56. TB in Special Situations
Therapeutic trial with H, Z, PAS when diagnosis is not obvious & TB is strongly suspected.
Chronic renal failure:
-use only HRZ & avoid SET
Chronic liver diseases:
-use only HSE & avoid RZ
Drug-induced hepatitis:
-stop all the drugs
-after resolution, start all over again with 2SHE + 10HE
DR (MRS) M.B. FETUGA

57. Special Situations in TB c’ontd
Infant of a mother with TB:
-Start the baby on H as soon as positive
-When mother is smear negative for 3 consecutive months, do mantoux test for baby
-If mantoux is negative, stop H & give BCG
-If mantoux is positive, do CXR
-If CXR is normal, give H for total of 9 months
-If CXR is abnormal, treat baby as a TB case.
-Allow breastfeeding & rooming-in.
DR (MRS) M.B. FETUGA

58. Prevention of TB Case finding & effective treatment
Contact tracing & H chemoprophylaxis
- all contacts with positive mantoux but no clinical or CXR feature should have H for 6 months
-under-5 contacts with negative mantoux should have H after 3 months. If repeat mantoux is negative, stop H; if positive, give H for the total of 6 months
BCG vaccination
DR (MRS) M.B. FETUGA

59. Prevention of TB c’ontd.
BCG vaccination:
- give as soon in the first week of life as possible
-no scientific basis for multiple vaccination
- 0-80% efficacy (50% on the average)
-protects against the severe forms of TB like TB Meningitis
-give to HIV infected children in Africa but avoid it if they are symptomatic.
DR (MRS) M.B. FETUGA

60. HIV/AIDS & TB HIV increases the burden of TB
Exact picture in children is unknown
Among adults:
- 70% of TB/HIV dually infected people live in Sub-Saharan Africa,
- HIV is the most potent factor aiding the progression of tuberculosis infection to disease
% of TB patients in Sub Saharan Africa are positive.
DR (MRS) M.B. FETUGA

61. HOW HIV AFFECTS CLINICAL PICTURE OF TB
In children, the natural history of TB depends on the stage of HIV disease
Early in HIV, TB is similar to that in children without HIV
Late in HIV, TB tends to be severe & disseminated
Early in HIV, it resembles Post Primary TB, smear positive & CXR shows cavities
Late in HIV, it resembles Primary TB, smear negative & CXR shows infiltrates
Avoid T in TB therapy & replace it with E or S
DR (MRS) M.B. FETUGA

62. HIV & CLINICAL TB C’ONTD.
Increased chances of progression to active disease
Accelerated progression
Death occurs earlier without treatment
More cases of extra-pulmonary involvement
Formidable diagnostic difficulties
Increased rate of MDR & difficulty with achieving cure.
DR (MRS) M.B. FETUGA

63. How HIV affects TB control
Over diagnosis of smear negative TB
Under diagnosis of smear positive TB
Low cure rate
High Case Fatality Ratio
High default rate from adverse drug effects eg. Dermatitis from T therapy
Increased emergence of MDR
DR (MRS) M.B. FETUGA

64. Differential Diagnosis of PTB in HIV-infected children
Bacterial Pneumonia
Viral Pneumonia (Cytomegalovirus)
Fungal Pneumonia (Cryptococcus)
Pneumocystis carinii pneumonia
Lymphocytic Interstitial pneumonia
Pulmonary Lymphoma
DR (MRS) M.B. FETUGA