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Infectious Diseases

Tuberculous Meningitis (TB Meningitis)

Meningitis caused by Mycobacterium tuberculosis, resulting from haematogenous spread from a primary site (usually lungs) or rupture of a Rich focus in the brain/meninges. Typically has a subacute onset.

Also known as: TBM

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Referral and warning signs

When to refer

IMMEDIATE URGENT REFERRAL/ADMISSION to Hospital (H/RR) for ALL suspected cases of TB meningitis for LP, initiation of ATT +/- steroids, and management of complications.

Red flags

  • Subacute onset neurological symptoms (headache, confusion, cranial nerve palsy).
  • Signs of meningitis + risk factors for TB (HIV, known TB contact).
  • CSF findings suggestive of TBM (lymphocytes, low glucose, high protein).
  • Hydrocephalus or basal enhancement on imaging.

Signs and symptoms

  • Gradual onset over days to weeks (subacute).
  • Prodromal phase: Malaise, fatigue, low-grade fever, headache, anorexia, weight loss, personality changes, irritability.
  • Meningitic phase: Worsening headache, vomiting, neck stiffness (may be mild initially), confusion, lethargy, drowsiness progressing to stupor/coma.
  • Cranial nerve palsies (especially CN VI - abducens nerve, causing diplopia).
  • Focal neurological deficits (hemiparesis).
  • Seizures.
  • Signs of raised intracranial pressure (papilloedema).
  • May have signs of TB elsewhere (cough, night sweats, lymphadenopathy).

Risk factors

  • Active pulmonary or disseminated TB.
  • HIV co-infection (major risk factor).
  • Immunosuppression (other causes).
  • Malnutrition.
  • Young age (<5 years).
  • Incomplete TB treatment.
  • Close contact with active TB case.

Diagnosis

Clinical assessment

Suspicion based on subacute onset of meningitis symptoms, especially in patient with risk factors (HIV, known TB). Presence of cranial nerve palsies or focal deficits increases suspicion. Differentiate from other subacute/chronic meningitis causes.

Differential diagnosis

  • Cryptococcal meningitis.
  • Partially treated bacterial meningitis.
  • Viral encephalitis.
  • Cerebral malaria (if acute).
  • Brain abscess / Tuberculoma.
  • CNS lymphoma.
  • Neurosyphilis.
  • Fungal meningitis (other).
  • Carcinomatous meningitis.

Investigations

  • Lumbar Puncture (LP) and CSF Analysis: Essential.
  • - CSF Appearance: Often clear or slightly opalescent, may form fibrin web/pellicle on standing.
  • - CSF Opening Pressure: Usually elevated.
  • - CSF Cell Count: Elevated WBC (typically 50-500 cells/µL), predominantly Lymphocytes (early on may have neutrophils).
  • - CSF Glucose: Low (<40% of serum glucose).
  • - CSF Protein: Markedly elevated (often >100-500 mg/dL).
  • - CSF AFB Smear (Ziehl-Neelsen): Low sensitivity (<10-30%), but diagnostic if positive.
  • - CSF GeneXpert MTB/RIF: Rapid molecular test, higher sensitivity than smear (~50-80%), detects MTB DNA and Rifampicin resistance. Recommended test.
  • - CSF TB Culture: Gold standard, but takes weeks (liquid culture faster).
  • - CSF Adenosine Deaminase (ADA): May be elevated (non-specific marker of inflammation).
  • Chest X-ray: Look for evidence of pulmonary TB (present in ~50%).
  • HIV Testing. CD4 Count.
  • Sputum AFB/GeneXpert: If respiratory symptoms present.
  • Consider CT/MRI Brain: May show basal enhancement, hydrocephalus, tuberculomas, infarcts.

Diagnostic criteria

Clinical suspicion + Characteristic CSF findings (lymphocytic pleocytosis, low glucose, high protein) +/- Positive AFB smear/GeneXpert/Culture from CSF or other site +/- suggestive imaging.

Management

Non-pharmacological management

  • Hospital Admission.
  • Supportive care (nutrition, hydration, fever control).
  • Management of raised ICP (may require therapeutic LPs or shunt).
  • Manage seizures.
  • Physiotherapy for neurological deficits.

Pharmacological treatment

  • Anti-Tuberculosis Therapy (ATT): Start promptly based on high clinical suspicion, DO NOT wait for culture confirmation. Use standard 4-drug regimen.
  • - Intensive Phase (2 months): Rifampicin (R), Isoniazid (H), Pyrazinamide (Z), Ethambutol (E). Dosed daily based on weight. (LOC: H)
  • - Continuation Phase (Prolonged - 7 to 10 months minimum, total 9-12 months): Rifampicin (R), Isoniazid (H). Dosed daily. Longer duration needed for CNS penetration.
  • - Pyridoxine (Vitamin B6): Give concurrently with Isoniazid (10-25mg daily) to prevent peripheral neuropathy.
  • - Adjust regimen if Rifampicin resistance detected (GeneXpert) - specialist consultation needed.
  • Adjunctive Corticosteroids: Generally recommended (especially if no HIV or high CD4). Reduce inflammation, oedema, mortality, possibly neurological sequelae.
  • - Dexamethasone IV/PO (or Prednisolone PO) for 4-8 weeks with gradual taper.
  • - Example: Dexamethasone 0.3-0.4mg/kg/day initially, tapering over 6-8 weeks.
  • - Use with caution or modified regimen in HIV co-infection, balancing risk of IRIS and other infections (specialist guidance/refer to HIV guidelines).
  • Management of Complications: Anticonvulsants for seizures. Mannitol/hypertonic saline for acute raised ICP. Shunt surgery for hydrocephalus.
  • ART Initiation (in HIV+): Start ART as soon as possible, ideally within 2-8 weeks of starting ATT (balancing TBM treatment and IRIS risk - refer to HIV guidelines).

Monitoring

Monitor clinical response (consciousness, fever, neurological signs). Monitor for drug side effects (hepatotoxicity, neuropathy, optic neuritis). Monitor for complications (hydrocephalus, IRIS). Repeat LP may be needed if poor response.

Complications

  • Hydrocephalus.
  • Cranial nerve palsies.
  • Stroke / Vasculitis / Infarcts.
  • Seizures / Epilepsy.
  • Cognitive impairment.
  • Motor deficits.
  • Visual loss.
  • Endocrine dysfunction (SIADH).
  • Death.

Prevention

  • BCG vaccination at birth (reduces risk of severe disseminated TB, including TBM, in children).
  • Treatment of latent TB infection (LTBI) in high-risk individuals (e.g., contacts, HIV+).
  • Effective treatment of pulmonary TB to prevent dissemination.
  • Airborne infection control measures for pulmonary TB.

Patient education

  • Explanation of serious TB infection of the brain lining.
  • Need for hospitalization and LP.
  • Importance of prolonged multi-drug anti-TB treatment (9-12 months) and adherence.
  • Role of steroids if prescribed.
  • Potential neurological complications and need for rehabilitation.
  • Information about TB transmission and contact screening if appropriate.

Uganda-specific notes

TBM is a severe form of TB, often associated with HIV co-infection. Diagnosis relies on clinical suspicion, CSF analysis (lymphocytes, low glucose, high protein), and ideally GeneXpert on CSF. Treatment follows standard national TB guidelines but with prolonged continuation phase (10 months). Adjunctive steroids commonly used but require careful consideration in HIV.

References

  • Uganda Clinical Guidelines (UCG) 2023

    Chapter 2, Section 2.1.5.3

  • Uganda Clinical Guidelines (UCG) 2023

    Chapter 5 (Tuberculosis)

  • National Tuberculosis and Leprosy Programme (NTLP) Guidelines, MOH Uganda

    (Specific TB treatment protocols)

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