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Presentation on theme: "PAEDIATRIC TUBERCULOSIS"— Presentation transcript:


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

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

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

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

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

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

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


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