Tuberculosis.pptx by chairman itcc andhrapradesh

tuberculosis in asian countries

1. Tuberculosis Presenter : Dr Sugima Moderator: Dr Srihari Alapati

2. Epidemiology of Childhood TB TB continues to be an important cause of morbidity and mortality among children worldwide. The burden of childhood TB reflects the measure of TB control in a community as it reflects recent transmission. Childhood TB constitutes approximately 10- 40% of all TB in low and middle income countries and 2-7% in industrialized countries. 99% of children with TB who receive treatment survive. Without treatment - 22% of infected children under 15 die . 44% of those under 5 years die.

3. In March 2017, Lancet published the world’s first systemic review of risk of death suffering from TB. According to this review: One million children fall sick to TB each year. Only 1 in 3 children with TB is diagnosed . Nearly half of children under 5 who gets TB and are not treated die.

4. Percentage distribution of notified cases in 5-14 years of age group The top three regions of WHO which contributed to disease burden in children are Southeast asia(40%), African region (30%), Western pacific region(14%).

5. Natural History of Disease

6. Phase 5: More than 3 years after primary infection. Highest risk period has passed. Delayed onset adult type TB may present in adolescents.

7. Diagnosis of TB in Children

8. Presumptive TB Children with following symptoms, with OR without history of contact with an active TB case within last 2 years are suspected to have TB and are referred to as children with presumptive TB. Persistent and documented fever for 2 weeks or more without a known cause , Persistent cough for >2 weeks. Significant weight loss of > 5% body weight as compared to highest weight recorded in last 3 months. Non tender peripheral lymphadenopathy Chronic meningitis with or without neurological deficits.

9. Imaging in TB Chest X-ray shall be done upfront in cases who are suspected to have TB. It is an important imaging modality for pulmonary TB diagnosis in children. Radiology needs to be correlated with clinical findings. Radiological findings can help differentiate between primary vs progressive vs reactivation TB. Primary TB: Mediastinal lymphadenopathy, Right upper lobe consolidation. Progressive primary TB : Collapse consolidation, necrotic lymph nodes with pressure effects . Reactivation TB : Cavitation lesions , Endobronchial TB.

10. Imaging in TB cont’d….. Usg is also very useful for performing guided lymph node biopsies. Contrast CT scan chest is more accurate in detecting cavitation , bronchial wall thickening , collapse, centrilobular nodules, vertebral access, tree in bud appearance. Essential tool for evaluating children with persistent pneumonia or persistent fever without apparent focus.

11. Sample collection in TB suspect Good sputum sample consists of: Recently discharged material from bronchial tree Presence of mucoid or mucopurulent material Should be 2-5 ml in volume. Self expectorant sputum sample is the standard microbiological sample for older children. In young children who are unable to produce a good quality sputum specimen, either an induced sputum with 3% hypertonic saline or gastric lavage .

12. Tests for Bacteriological Confirmation Demonstration of AFB on smear microscopy or culture or by molecular tests is the gold standard of TB diagnosis. Rapid nucleic acid amplification tests like Xpert Rif/ True nat have much higher sensitivity as compared to smear and faster than culture ( turnaround time is 2 hours) Xpert Rif / Truenat have become point of care tests for TB diagnosis and detection of rifampicin resistance which is a surrogate marker for MDR-B . Liquid cultures for MTB using the BACTEC/Mycobacterium growth indicator tube ( MGIT 960) using special liquid ET tubes are preferred over the solid media. In addition , NTEP also recommends LPA – which are multiplex NAAT – to test for resistance to rifampicin, isoniazid and other second line drugs . LPA has longer turnaround time (3-4 days) due to its batch testing as compared to individually tested RAPID NAAT.

13. NAAT vs LPA NTEP approved NAAT shall be preferred over smear examination in all children . If a specimen is positive by any NAAT methods , the case is labeled as microbiologically confirmed TB. AT the initial step, if self expectorant sputum is available and imaging / NTEP approved NAAT is not available or delayed , smear may be done . Whenever smear is used for diagnosis, atleast 2 samples should be tested , while a single sample is sufficient for NAAT.

14. Skin test for TB Tuberculin Skin test Intradermal injection of Purified Protien Derivative (PPD ) Current recommendation is to use 2TU PPD RT23 for all diagnostic purposes. Considered positive if the induration is 10 mm or more. In HIV co infected cases, 5mm may be taken as the cutoff. Elicits delayed type Hypersensitivity Positive test indicates present or past infection with M.TB but cannot distinguish infection from disease.

15. Clinically diagnosed probable TB In a patient with high clinical suspicion of TB disease based on suggestive symptoms , radiology and supportive circumstances ( h/o exposure to TB case) or evidence of infection (Positive skin test for TB/ positive IGRA). But the rapid microbiological tests are negative. Such a case may be treated as Clinically diagnosed patient provided common alternative diagnosis have been ruled out . Where facilities exist, send one aliquot of the specimens liquid culture, if the NAAT is negative for MTB.

16. Diagnosis of Extrapulmonary TB

17. Presumptive Extrapulmonary TB Extrapulmonary TB: Microbiologically confirmed or clinically diagnosed case of TB involving organs than lungs. Eg : lymph nodes, pleura , bones, joints, intestine, genitourinary tract , meningitis of the brain. Presumptive Extrapulmonary TB Refers to the presence of organ specific symptoms and signs like swelling of lymph nodes, pain, and swelling in joints, neck stiffness, disorientation etc. Have constitutional symptoms like significant weight loss, persistent fever for more than 2 weeks , night sweats. Negative culture or NAAT cannot rule out TB due to the inadequate sensitivity of these tests I extrapulmonary specimen. Other test like histopathology , radiology, cytology etc , may be undertaken to reach a diagnosis.

18. Sensitivity of NAAT for MTB detection Pus, aspirate/biopsy specimen from lymph nodes , CSF - Low to moderately high. Pericardial, ascetic, and synovial fluid – Poor Pleural fluid - Poorer

19. TB Lymphadenitis Most common forms of EPTB Cervical lymph nodes particularly jugular, posterior triangle, and supraclavicular are affected . Usually occurs in 5- 9 years . Clinical correlated of diagnosis include progressive enlargement of lymphnode for more than 2 weeks , firm,minimally tender or non tender , with OR without fluctuation. Affected nodes get matted , turn into cold abscess , may rupture and develop chronic sinus.

20. TB Lymphadenitis Diagnosis Histopathology is the usual gold standard test. FNAC is the alternative test. Above test require a skilled pathologist to report on the specimen . Besides , needle aspirate from the node can be easily tested for the presence of AFB or NAAT to diagnose TB . USG – Helpful to identify affected non palpable or deep seated nodes for needle aspiration and testing . Central hypoechogenicity in the node on USG is considered suggestive of TB. DD of TB Lymphadenitis Lymphadenopathy is expected due to recurrent tonsillitis and upper respiratory tract infections. Reactive Lymphadenitis may clinically mimic tuberculosis but donot warrant anti-TB drugs.

21. TB Pleural Effusion Presents with high grade fever Clinical examination : Decreased air entry with dull percussion DIAGNOSIS Best diagnosed with USG. It’s benefit relates to establishing the presence and extent of PE . Pleural fluid aspiration should always be performed . Aspirate should be sent for biochemical, cytological, and smear examination by Ziehl Neelson (ZN) stain to confirm the diagnosis. Tubercular effusion fluid is straw colored, has large number of cells. (Predominantly mononuclear), with high protein (>3g/dl) . High protein cause the cobweb on standing Induced sputum / GA should always be tested for Mycobacterium TB. ESR has no role in establishing the aetiological diagnosis. ADA has been used extensively to diagnose TB effusion in adults . But it’s utility in children appears limited .

22. Diagnosis of TB pleural effusion cont’d… Pleural biopsy may be performed in unclear situations using Copes or Abraham’s pleural biopsy needle . Pleural tissue can be subjected to histopathology, ZN staining and MGIT cultures . Findings are granuloma with caseous necrotic tissue in the pleural biopsy . Yield of pleural biopsy is more than 80% .

23. Abdominal TB Present in the intestinal , Nodal, peritoneal, visceral and Disseminated forms , with almost one third of patients having involvement of more than one of these sites. Common symptoms Abdominal pain Fever Distension Weight loss Anorexia On examination Doughy abdomen Ascites Omental mass Organomegaly

24. Diagnosis of AbdominalTB DIAGNOSIS USG is recommended as the initial modality of choice , as it may pickup lymphadenopathy, peritoneal thickening, omental thickening , bowel wall thickening and ascites . Plain Xrays are not helpful for the diagnosis of Abdominal TB . Tissue diagnosis remains most reliable though it is often not feasible. Contrast enhanced CT and CT Enterography provide adequate cross sectional imaging in depicting various forms of abdominal TB . BARIUM STUDIES are gold standard in diagnosing strictures , fistula, erosion. Misleading features in USG abdomen Non Specific bowel wall thickening Small amount of fluid in the mesentry or dependant areas of abdomen Presence of non matted intraabdominal lymphadenopathy.

25. Peritoneal TB Diagnosis Peritoneoscopy has a very high sensitivity (93%) and specificity (98%). Findings Hyperemic peritoneal with ascites and whitish miliary nodules. Hyperemic peritoneal with ascites and adhesions Thickened parietal peritoneal with yellowish nodules.

26. Neurological TB

27. 1. TB meningitis Presents between 6 months to 4 years Most severe form of TB in children Leads to mortality if not treated timely and effectively

28. TB meningitis diagnosis CECT head is the initial modality of diagnosis. Have one or more of the following : Basal meningeal enhancement Hydrocephalus Tuberculoma Infarcts in different areas , especially the basl ganglia and precontrast basal hyperdensity. MRI is preferred when CT is inconclusive CSF tap : Mostly clear CSF leucocyte count 10 -500 cells/mm3 CSF glucose remains below 40mg/dl Protien is elevated .

29. TB meningitis diagnosis Differential Diagnosis: Cryptococcal meningitis Cytomegalovirus encephalitis Toxoplasmosis Sarcoidosis Meningeal metastasis Lymphoma Above conditions have similar radiological findings .

30. 2. Tuberculoma Intracranial space occupying lesion. Manifestation : Seizures Headache Focal neurological deficits Neurocysticercosis is an important differential diagnosis.

31. Bone and Joint TB Accounts for 5-15% of all EPTB Occurs due to reactivation of bacilli which had seeded the bones during the initial mycobacteremia . Typical presentation Potts spine Dactylitis Arthritis Osteomyelitis Uncommon presentation Reactive Arthritis ( Poncets arthritis) Tenosynovitis Bursitis

32. Dactylitis ( Spina ventosa ) Short tubular bones of the hands and feet are usually affected , typically involving the proximal phalanx of the index /middle fingers and middle /ring finger metacarpals . X-ray Involved bones show a diaphyseal expansile lesion. Healing is by sclerosis.

33. Spinal TB or Potts Spine Most common site : Thoracic followed by lumbar / cervical areas . CLINICAL FEATURES : Pain localized over the involved vertebral or referred to root pain. Neurological complication Paraparesis Cauda equina syndrome MRI is the most sensitive for picking up abnormalities (100%) Features of MRI Marrow edema Destruction of adjacent vertebral bodies and opposing endplates Destruction of the intervening disc Prevertebral, paravertebral or epidural abscess

34. Spinal TB or Potts Spine Plain X-ray of the spine is less sensitive in early disease as it does not reveal any abnormalities till about 30-50% of bone loss has occurred. X-ray findings Endplate erosion Decreased vertebral height Collapse and narrowing of discal space Paravertebral soft tissue shadow Microbiology should always be attempted for definitive diagnosis and to pickup MDR TB

35. TB Arthritis Involves weight bearing joint such as the hip and knee (90%) Pain is the first symptom followed by local tenderness and restriction of joint movement . Plain X-ray findings Soft tissue swelling Osteopenia Periarticular bone destruction Periosteal reaction

36. Diagnosis MRI is very sensitive Joint fluid aspiration or synovial biopsy should be carried out for a definitive diagnosis .which is further subjected to HPE or culture or CBNAAT .

37. Treatment of Rifamficin Sensitive TB TB treatment is biphasic with intensive phase followed by continuous phase. Intensive phase – Early and rapid killing of MTB thereby preventing death and reducing infectivity. Continuation phase- Eliminates the residual bacilli, thereby reducing the relapses and failures. Ethambutol is added as the fourth drug in IP and as a third drug in CP due to the high background resistance to Isoniazid upto 12-14% in our country.

38. Fixed Drug Combination for TB FDC s are preferred due to their safety, simplified treatment and avoiding errors in missing one or more of the drugs , thus reducing the risk of emergence of drug resistant strains. Pediatric FDC s are dispersible and flavored 3 Drug dispersible tablets for IP ( H50+ R75+ Z150) 2 Drug dispersible tablet for CP ( H50 + R 75) Ethambutol is added as a companion drug to both the phases and is available as 100 mg non dispersible tablet.

39. Adjunctive therapy along with Anti TB drugs Pyridoxine therapy : Supplementation with 10mg/day is recommended for all patients receiving INH containing regimens . Steroids in TB : Steroids decrease inflammation related injury and shown to reduce morbidity ( sequelae ) and even mortality in cases of TB when given for appropriate indications .

40. Adjuctive therapy with Anti TB drugs cont’d….. Definite indications for use of steroids in TB : TB meningitis Pericarditis Addisons disease Miliary TB with alveocapillary block TB uveitis Prednisolone 1-2mg/ kg/day or dexamethasone 0.6 mg/kg/day or it’s equivalent are used for 2-4 weeks and then tapered over the next 4 weeks.

41. Adjunctive therapy with Anti TB drugs cont’d…. Additional indications where steroids maybe used: Endobronchial TB Bronchial compression Mediastinal compression syndrome Pleurisy with severe respiratory distress Laryngeal TB TB immune reconstitution inflammatory syndrome (IRIS)

42. Monitoring by Investigation Microbiological : Respiratory specimens if available are tested at the end of IP and completion of treatment with smear and culture for bacterial negativity. MGIT culture: To be performed if the child is not responding even after 4 weeks of therapy . However as most young children are unable to produce sputum or may have complete resolution of symptoms , then the response to treatment may need to be clinically assessed with the help of radiological testing.

43. Monitoring by investigation cont’d….. 3.Follow up chest radiographs: To be done only at the end of therapy Done earlier if clinically indicated due to nonimprovement , deterioration or emerging complications. 4. Other imaging : Ultrasonography, echocardiography, CT/MRI of the affected organ system Advised at the end of the therapy or when the patient is clinically not improving , deterioration or emerging complications.

44. Monitoring by investigation cont’d….. 5. Liver function tests( LFT) LFT are done if any child shows symptoms or signs of liver dysfunction.

45. Non response to therapy Clinical or radiological no response or deterioration during follow-up could be due to : Incorrect diagnosis ( particularly in a clinically diagnosed case of TB) Lack of adherence to therapy Incorrect dosages or drugs taken Inability to retain drugs : Due to vomiting Secondary infection or untreated comorbidity Drug resistance Paradoxical upgrading reactions (TB-IRIS)

46. Paradoxical Upgrading reactions Enlargement of existing lesions or unexpected appearance of new lesions during apparently adequate ATT. Occurs 3-12 weeks after beginning of therapy Lasts for approximately 2 months. It is a self limiting condition, regres without change of initial drug regimen . Occurs post treatment (as late as 2 years) in case of lymph node TB.

47. Suspected drug resistance Children with any of the following should be suspected to have drug resistance : Non or poor response to first line therapy Treatment after lost to follow up (defaulter) Recurrent TB (relapse) Contact of MDR patients and /or CLHA and /or with history of TB death in the household

48. Confirmed Drug resistant TB cases A patient is confirmed to have drug resistant TB only when the results suggest drug resistance are from an NTEP quality assured Culture and DST laboratory, and an NTEP endorsed testing method ( NAAT/LPA/Culture).

49. Approach to the diagnosis of DRTB Epidemiological markers: History of contact with suspect MDR Details of previous poor treatment and lack of adherence Patient not responding to therapy or those with recurrence of disease after previous treatment. Paradoxical upgrading reactions , Other untreated coexisting or inter current co infections. TB among chilren

50. Methods for Drug Susceptibility/ Drug Resistance Testing 1. DRUG RESISTANCE TEST USING MOLECULAR METHODS These methods are PCR based and cannot be used for determining response to treatment, unlike a smear . Nucleic Acid Amplification Test (NAAT) NTEP approved cartridge /Chip based NAATs Can be performed on smear positive, smear negative and Extrapulmonary specimens as they can detect DNA even with few copies. Detect M.TB as well as resistance to Rifampicin in the MTB. Test time is about 2 hours.

51. Line Probe assay Used for detection of MTB complex and rapid diagnosis of R and H resistance. Used to detect resistance to class FQ and Class SLID Needs many DNA copies thus can be used directly only on smear positive specimens . Processing time is 72 hours each for both first line and second line LPA . LPA canberra used for genotypes drug sensitivity on an isolated from culture from any specimen , including smear negative samples. This mixed method approach could decrease turnover .

52. Xpert M.TB / XDR Newer version of Catridge Based NAAT Can detect mutation associated with resistance towards H,FQ, SLI and Eto in a single test using a semi quantitative nested PCR followed by high resolution melt technology. Requires GeneXpert platforms equipped with 10 colour modules Processing time is about 90 minutes .

53. 2. GROWTH BASED PHENOTYPIC DRUG SUSCEPTIBILITY TESTING Highly sensitive and specific method . Requires 2-8 weeks to yield results and g Hence does not allow rapid confirmation. Needs to be used for long term follow up and he.ps detect early recurrence in both drug sensitive and drug resistant TB . Growth based phenotypic culture methods include automated Liquid culture systems . Eg : BACTEC MGIT 960, BacTAlert , solid(Lowenstein Jensen ) media.

54. MGIT (Mycobacteria growth indicator tube ) Currently the preferred method for DST under NTEP Both first and second line anti TB drugs sensitivity can be tested . Following drugs can be tested for susceptibility by liquid culture, First line drugs : R,H,E,Z Second line drugs : S, Lfx , Mfx , Km, Cm, Lzd , Cfz , Bdq , Dlm etc.

55. Probable MDR TB among Children This term is applied to children where DR TB is clinically suspected strongly , but bacteriological confirmation is not technically feasible / negative, and the Nodal DR-TB committee takes the decision regarding diagnosis and initiation of treatment.

56. Treatment of Rifampicin resistant TB in children RR-TB treatment regimens are longer in duration and have higher pill burden and toxicity profiles as compared to regimen for RS-TB. Short regimen : Who have limited disease No risk of resistance due to prior prolonged exposure to fluoroquinolones Not having combined InhA and KatG mutations. All other patients are prescribed longer regimens.

57. ADVERSE EVENTS FOLLOWING ANTI TB DRUGS

58. 1. QT Prolongation Suspected agents are Bdq, FQs,Cfz Among FQs, Mfx and Gfx cause the most remarkable QTcF prolongation. Low serum levels of potassium, calcium and magnesium are associated with QTc prolongation. QT prolongation can result in ventricular arrhythmia (Torsades de Pointes) and sudden death. ECG must be used to mentor the QT interval regularly.

59. 2. Hepatitis Suspected agents : Z,H,R,Eto , PAS, Bdq

60. 3. Hearing loss Suspected agents : Aminoglycosides

61. TB with HIV Coinfection

62. People living with HI (PLHIV) are nearly 18 time more likely to develop Tb . HIV and TB make for a fatal combination with extremely high death rates(15-18%). Serious drug interactions between some Antiretroviral drugs and drugs used for TB treatment leads to changes in treating confection. At all ART centre’s , National AIDS Control Organisation ensures strengthening of 3Is strategy, Intensive case finding (ICF) Airborne Infection Control (AIC) Isoniazid preventive therapy ( IPT) Along with the provision of ATT for PLHIV

63. TB screening among PLHIV

64. Problems in diagnosing TB in Children infected with HIV

65. Diagnostic Algorithm of TB in CLHIV

66. ART regimens for in CLHIV on First line ART with TB Coinfection

67. TB diagnosed in PLHIV already receiving ART NACO recommends the following guiding principles If TB occurs within 6 months of initiation of ART, it should not be considered a failure of treatment .ART regimen should be adjusted for co administration with rifampicin / bedaquilline containing regimens. If TB develops more than 6 months after initiation of ART, and data on the CD4 count are available, the decision on whether the diagnosis of TB represents ART failure should be based on the CD4 count and viral load data.

68. The development of an episode of pulmonary TB after 6 months of ART without other clinical and immunological evidence of disease progression , should not be regarded as representing ART failure. Extrapulmonary TB should be indicative of ART failure .Close monitoring is needed, and adherence support should be reinforced.

69. ART among CLHIV with DR TB Coinfection Second line ant TB drugs should be initiated first followedby ART as soon as second-in-command anti TB drugs are tolerated . Ideally ART should be started within first 2 weeks of initiating DR TB treatment. Undue delay in starting ART could result in a significant risk of HIV related death among DR TB patients. Patients who are already on RT during DR-TB diagnosis can be continued on ART when DR TB therapy is initiated.

70. Drug Interactions of second line Anti TB Drugs with ART Bdq should be used with caution in PLHIV infection treated with ARV , which exhibit drug-drug reaction with ef irenz or prolong QT interval with lopinavir / Ritonavir. Dolutegravir can be used safely with new TB drugs Bedaquilline and Delamanid . PLHIV already on NRTI+DTG regimen may be continued with Bedaquilline / Dela and containing DRTB regimen . PLHIV on NNRTI/ PI based ART regimen need substitution of PI with DTG in the ARV regimen, when co prescription with BDQ/DLM containing DRTB regimen required. All Tb HIV co infected PLHIV diagnosed with drug resis5TB should be referred to the linked DR TB centre for starting treatment for DR /MDR TB.

71. Cotrimoxazole prophylaxis

72. Monitoring during treatment HIV infected children on ATT should have LFT s at baseline, day 5 , day 15 , month 1 and month 3. After 3 months , a symptom- directed approach is helpful. If symptoms of drug toxicity develops , a physical examination and liver enzymes measurement should be repeated .

73. TB Immune Reconstitution Inflammatory Syndrome

74. Types of IRIS

75. Treatment of IRIS ATT and ART should be continued in every case . Mild IRIS should be managed with symptomatic treatment , eg : aspiration of large fluctuant lymph nodes or subcutaneous abscess. Moderate to severe IRIS : short term therapy with corticosteroids can be given . ( Prednisolone in a dose of 1.5 mg/ kg orally for 2 weeks followed by 0.75 mg / kg orally for 2 weeks and then tapered off.

76. BCG in children with HIV BCG is useful in CLHIV born in TB endemic countries. BCG vaccination should be given at birth to all symptomatic HIV exposed infants . If BCG has not been given at birth, it should not be given in symptomatic HIV infected older infants and children.

77. Management of neonates born to a mother with TB

78. Safety of ATT during pregnancy Newborn can be exposed to TB with an absolute but variable risk of transmission of infection. Situations include Mother has active TB when the baby is born Mother has completed treatment for TB while carrying this baby or else neonates exposed to a Health care worker/ another contact with Pulmonary TB. ATT should be given to pregnant women having TB as most First Line Drugs are safe.

79. Preventive therapy to neonates It is recommended for neonates born to mothers with any form of active TB in pregnancy or after birth. Active disease should be ruled out in such a neonates before starting preventive therapy. INH preventive therapy is given in a dose of 10mg/kg for 6 months. If the neonate has been exposed to an MDR contact , then TB preventive therapy is not recommended. Modern chemotherapy is so efficacious in drug sensitive cases.

80. Separation of mother and infant is no longer considered mandatory, provided that mothers therapy is started , and infant is no longer considered mandatory, provided the mother therapy is started , and the baby is on IPT. Breastfeeding can continue and is safe . ATT excreted in small amounts in the milk has no therapeutic or adverse effect on the baby. Separation should be practiced only if the mother is ill enough to require hospitalization , or if she is infected with a drug resistant strain of M.Tuberculosis . All children born to mothers with TB should receive BCG at birth if they are isoniazid preventive therapy.

81. Perinatal TB There are 2 main infectious routes : Transplantal route Through aspiration or ingestion of infected amniotic fluid. Many parents die without a diagnosis, especially in conditions where the index of suspicion is low. Treatment regimen of Perinatal TB is similar to paediatric TB.

82. Management prevention of TB

83. BCG vaccination It is a weakened version of Mycobacterium bovis Routinely given at birth or as soon after that as an Intradermal injection. It is a single dose vaccine and can be given safely to older children too, where the dose at birth is missed. Efficacy is better in school age children with prior testing (74%) and neonatal vaccination (60%). For prevention of meningeal and miliary TB, overall protection by BCG is around 85% and with neonatal vaccination it is approximately 90%

84. Complication- BCG lymphadenitis Isolated axillary ( or supraclavicular/cervical) lymphnode enlargement with BCG history on the same arm. There is usually no tenderness or raise temperature over swelling and no fever or other constitutional symptoms.

85. Management of Lymphadenitis Non suppurative BCG lymphadenitis should be allowed to regress spontaneously. If already suppurated or suppration develops, needle aspiration may prevent rupture and subsequent large ulceration. Repeated aspiration on refilling maybe required, and gradually the pus starts thinning out and decreasing in volume . If the pus is thick, Incision and drainage maybe needed. Antibiotics and ATT are ineffective . However Immunosuppressed children can develop Disseminated BCGiosis , which will require therapy.

86. Thank you