Tuberculosis in children — formative SAQs

SAQ 1 \u2014 The contact, the spectrum and the decision (10 marks)

A four-year-old boy is brought to your clinic because his uncle was diagnosed with smear-positive pulmonary tuberculosis two weeks ago. The boy is thin, has had a cough and intermittent fever for six weeks, and his chest radiograph shows right paratracheal lymph-node enlargement with no cavitation. [1] [3]

Questions

1. Classify this child on the exposure \u2192 TB infection \u2192 TB disease spectrum, and outline the investigations that confirm the diagnosis. (4 marks) [1] [5]

2. Describe the pathophysiology that explains why young children progress rapidly to severe disease, and how that applies to this child's risk. (3 marks) [2]

3. Outline the definitive management and the public-health actions you must take. (3 marks) [7] [1]

Model answer

Classification and investigations (4). This child has TB disease, not merely exposure or TB infection, because he has both symptoms (six weeks of cough and fever with thinness) and a compatible radiograph (paratracheal lymph-node enlargement). I classify the disease by site as intrathoracic and by severity as non-severe (lymph-node, non-cavitary, smear-negative pattern). To confirm, I collect two to three early-morning gastric aspirates (or induced sputum) for Xpert MTB/RIF Ultra plus culture and phenotypic susceptibility, take a tuberculin skin test or IGRA to support infection, and test for HIV. A chest radiograph is already diagnostic in pattern. I treat empirically even if samples are negative, because childhood TB is paucibacillary and a negative Xpert does not exclude disease. [1] [5] [3]

Pathophysiology (3). Inhaled droplet nuclei reach the terminal airway and are taken up by alveolar macrophages to form the primary (Ghon) focus, which drains to the regional node to form the primary complex. Outcome hinges on cell-mediated containment: if it holds the child has TB infection, but young children (especially under five) have immature cell-mediated immunity and fail to contain the bacilli, so they progress rapidly to disseminated and meningeal disease. This child's risk of progression to severe disease is therefore elevated by his age, and his paratracheal lymph-node pattern is the intrathoracic signature of recent primary infection. [2]

Management and public health (3). Because his disease is non-severe, I treat with the weight-based 4-month regimen (intensive phase then continuation) validated by the SHINE trial for minimal, lymph-node or non-cavitary disease, using child-friendly fixed-dose combinations and adjusting the dose to his weight at every visit. I build adherence support and follow-up to cure. As public health, I notify the case, trace and screen household and close contacts (symptom review, TST/IGRA, chest radiograph as indicated), give tuberculosis preventive treatment to under-five and immunocompromised contacts, and find and treat the infectious source adult \u2014 here the uncle \u2014 to close the transmission loop. [7] [1]

SAQ 2 \u2014 Tuberculous meningitis and the asymptomatic contact (10 marks)

A two-year-old girl whose mother is being treated for pulmonary tuberculosis presents with a one-week history of irritability, vomiting and drowsiness. Separately, an eight-month-old well sibling of another newly diagnosed smear-positive case is brought for contact screening. [6] [1]

Questions

1. Describe your immediate assessment and management of the two-year-old, including the key diagnosis to exclude. (4 marks) [6]

2. Outline the management of the asymptomatic eight-month-old contact and justify the approach. (3 marks) [1]

3. Discuss the role of immune-based tests (TST and IGRA) and the principal pitfalls in the diagnosis of childhood TB. (3 marks) [8] [5]

Model answer

Tuberculous meningitis (4). The two-year-old has a TB contact and a subacute neurological prodrome (irritability, vomiting, drowsiness), so I presume tuberculous meningitis until proven otherwise. I assess airway, breathing and circulation and conscious level, arrange urgent brain imaging (basal exudate, hydrocephalus, infarct), perform a lumbar puncture with CSF sent for cell count, protein, glucose, acid-fast bacilli, Xpert MTB/RIF and culture, and start an extended intensive anti-TB regimen with corticosteroids empirically without waiting for confirmation, because outcome depends on treating in the prodrome rather than in coma. I manage raised intracranial pressure with neurosurgical input for hydrocephalus. The key diagnosis to exclude is TBM itself; the differentials are partially treated bacterial meningitis, viral encephalitis and fungal meningitis, but I do not delay empirical therapy for them. [6]

The asymptomatic contact (3). The eight-month-old is a well household contact of a smear-positive case, so after excluding disease with symptom screen and chest radiograph I give presumptive tuberculosis preventive therapy, because under-five contacts have the highest risk of rapid progression to severe, disseminated and meningeal disease and the benefit of preventive therapy outweighs its small cost. I re-screen at 8\u201312 weeks with TST/IGRA, complete the preventive course if infection is confirmed, and ensure the source case is on effective therapy. I notify and trace the wider household. [1]

Immune-based tests and pitfalls (3). The TST (Mantoux) and IGRA indicate TB infection, not disease; they support a disease diagnosis and screen contacts but cannot rule TB in or out alone, and a single negative test must not delay treatment of compatible disease. IGRA does not cross-react with BCG and needs one visit, which suits older children, while the TST remains useful especially in young children; a systematic review shows IGRA performs better than a single TST but is interpreted with the clinical picture. The principal pitfalls are withholding treatment while waiting for microbiology in paucibacillary disease, missing TBM in its prodrome, under-dosing across months of therapy, and failing to notify, trace contacts and find the source case. [8] [5]