Abstract
Tuberculous meningitis disproportionately affects young children. As the most devastating form of tuberculosis, it is associated with unacceptably high rates of mortality and morbidity even if treated. Challenging to diagnose and treat, tuberculous meningitis commonly causes long-term neurodisability in those who do survive. There remains an urgent need for strengthened surveillance, improved rapid diagnostics technology, optimised anti-tuberculosis drug therapy, investigation of new host-directed therapy, and further research on long-term functional and neurodevelopmental outcomes to allow targeted intervention. This review focuses on the neglected field of paediatric tuberculous meningitis and bridges current clinical gaps with research questions to improve outcomes from this crippling disease.
Highlights
Young children and individuals living with HIV are at high risk of progressing to tuberculosis (TB) disease following TB infection and are at elevated risk of progressing to severe forms of disease such as disseminated TB and tuberculous meningitis (TBM) [1]
In this article we review the natural history and pathogenesis of TBM in children, the epidemiology of the disease, approaches to diagnosis, developments in treatment and considerations for long-term prognosis
We propose a diagnostic algorithm for presumptive TBM in children which incorporates clinical, cerebrospinal fluid (CSF), neuroimaging features and rapid diagnostic results and provide guidance for possible clinical scenarios, including when diagnostic tools are negative or inconclusive for TBM and the clinician left to make a clinical judgement (Figure 2)
Summary
Young children and individuals living with HIV are at high risk of progressing to tuberculosis (TB) disease following TB infection and are at elevated risk of progressing to severe forms of disease such as disseminated TB and tuberculous meningitis (TBM) [1]. TBM can be diagnosed with reasonable confidence with clinical, laboratory, and Investigate the ability of MRI CSF flow imaging and thin slice CT to neuroimaging findings differentiate communicating and non-communicating hydrocephalus. MRI is superior to CT imaging for children being evaluated for TBM, both from Investigate utility of other modalities (e.g., 18F-PET/CT) to identify early small a diagnostic perspective and to delineate pathological and infarctions missed with conventional imaging prognostic features. Further investigate the utility of new omic technology, transcriptional and metabolomic biomarkers in diagnosing TBM from other non-TBM CNS infections, including in various populations, stages of TBM, and HIV-status. Morbidity and mortality from TBM remain unacceptably high, even if treated Establish validated and culturally appropriate tools to assess. TBM: tuberculous meningitis; TB: tuberculosis; BCG: bacille Calmette–Guérin; CSF: cerebrospinal fluid; MRI: magnetic resonance imaging; CT: computerised tomography; PET: positron emissions tomography; CNS: central nervous system; TNF: tumour necrosis factor
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