Recent transmission from infected adult • Measure of TB control in community, rarely transmit TB • Higher risk & more rapid progression to active disease • 95% of children who develop TB, w/in 12 mos (1ary infection) • Reflection of immature immune system • Innate (macrophages), DC (de...
Recent transmission from infected adult • Measure of TB control in community, rarely transmit TB • Higher risk & more rapid progression to active disease • 95% of children who develop TB, w/in 12 mos (1ary infection) • Reflection of immature immune system • Innate (macrophages), DC (dendritic cells) & acquired T-cell (CD4) immunity • EPTB more common • Infants: high morbidity and mortality • Disseminated TB/meningitis: 10-20% • Pulmonary TB: 30-40%. Diagnosis TB childhood difficult clinical presentation variable & nonspecific confirmation by culture < 40% absence productive cough , paucibacillary disease contact investigation of adults w/ infectious pulmonary TB 60-80% children infected when exposed to AFB + sputum 30-40% children infected when exposed to AFB - sputum most efficient method dx children w/ TB
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Tuberculosis in Children Sona Thesis Consultancy www.stc4medicos.com +91 9304786310
Introduction / Burden India carries a significant burden of childhood tuberculosis (TB), accounting for a substantial portion of the global pediatric TB cases. 3,30,000 children in the 0-14 age group: TB annually in India Representing a large share of the global burden.
Definition Infection caused by Mycobacterium tuberculosis Mycobacterium bovis causes TB in cattle
Pathology I
Pathology II
Pathology III Macrophages carry bacilli to lymph nodes Replication causes lymphadenopathy - Primary TB sign
Pathology IV Ghon complex = lung lesion + lymph node Cell-mediated immunity stops spread in 2-3 weeks
Pathology V CD4 T cells activate macrophages CD8 T cells lyse infected macrophages Caseating granuloma formation
Pathology VI
Pathology VII
Pathology VIII Ghon focus = granuloma with caseation Ghon complex includes regional lymph nodes Latent bacteria may remain in organs
Subclinical Course
Diagnosis Thorough history and physical exam Investigations: Sputum, Chest X-ray, TST
Clinical Manifestations Latent infection mostly asymptomatic Sometimes mild fever, cough, flu-like symptoms Productive or non-productive cough Dyspnea, wheezing, fever, night sweats Failure to thrive in some cases
History / Symptoms Contact history, no BCG, recent measles Persistent fever, FTT, malnutrition, long illness Suggestive CXR Tracheobronchial adenitis Segmental lesions, miliary mottling
Suggestive Physical Findings Serous pleurisy, lymphadenopathy, gibbus deformity Skin lesions, cold abscesses Phlyctenular keratoconjunctivitis Erythema nodosum Bone defects on X-ray
CXR, ESR, Hemogram TST, Biopsy, Culture, HIV serology
Successful Diagnosis History (contact, TB symptoms) Clinical examination Microscopy, TB culture Histopathology, Xpert MTB/RIF, LIPA Radiology: persistent opacification, miliary pattern CXR with no signs of distress is suggestive HIV testing TST - indicates infection, not disease
GHON COMPLEX PRIMARY TB
T1-Weighted MRI - Shows enlarged lateral ventricles with periventricular hypointensities , suggesting hydrocephalus . T2-Weighted MRI- Better shows the hyperintense CSF in the ventricles . DWI (Diffusion-Weighted Imaging ) -This sequence is sensitive for detecting restricted diffusion.The ventricles are clearly visualized, but no obvious areas of acute infarction or abscess are seen in this frame .
(A) Non-Contrast CT Scan (NCCT )- This is an axial section from a plain CT of the brain.Shows hypodensities in the basal ganglia and internal capsule regions bilaterally . ( B) Axial T2-Weighted MRI- This T2 image clearly shows hyperintense signals in the bilateral basal ganglia and thalamus, marked by arrows . ( C) – Diffusion-Weighted Imaging (DWI )- This sequence shows restricted diffusion in the bilateral basal ganglia . Areas appear bright, indicating acute infarction . ( D) – Apparent Diffusion Coefficient (ADC) Map- The ADC map complements DWI.Shows corresponding hypointensity in the same basal ganglia areas seen in (C ).
Treatment Regimen REGIMEN I Four drugs in intensive phase (HIV areas) 12-month treatment for TB meningitis, TB bones REGIMEN II Replace streptomycin with ethambutol in meningitis Intensive phase: RHZE
New WHO Treatment Regimen New cases: 2-month RHZ+E, 4-month RH Retreatment Cases Intensive: 3-month RHZE Continuation: 5-month RHE
Additional Management Pyridoxine 1–2 mg/kg/day Hospitalization for severe TB, meningitis STERIOD THERAPY Indicated for meningitis, airway obstruction, effusions Also for milliary TB and distress Hospitalization Indications Severe pneumonia Severe anemia, malnutrition, adverse reactions
Side effects Rifampicin Hepatitis, GI upset Orange-red body fluids Dosage: 10–20 mg/kg/day Isoniazid Peripheral neuritis Pyridoxine deficiency Dose: 10 mg/kg Pyrazinamide Used in drug-resistant TB Dose: 20–40 mg/kg/day Ethambutol Retrobulbar neuritis Visual field changes Used with caution in children Streptomycin Ototoxicity – vestibular nerve IM administration
Tuberculosis In Children : Diagnosis of a Case Involving Isolated Lymphadenitis
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