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TB - Meningitis (1) .PPSX
TB - Meningitis (1) .PPSX
TB Meningitis
• Learning Objectives Figure 1: Estimated TB
• Introduction
incidence rates, 2010
• Global problem
• Aetiology and
pathogenesis
• Clinical Features
• Complications and
clinical outcome
• Diagnosis
• Microscopy and
Figure 2: Estimated
culture
HIV prevalence in new
• Imaging
TB cases, 2010
• Therapy
• Key points
• Summary
• References/Further
reading From: Global
• Self assessment Tuberculosis Control
2011, WHO, 2011.
Global Problem of Tuberculosis: Europe
and UK
TB Meningitis In the UK , there were 9040 cases of TB reported in 2009, the highest in 30
years. London had the highest rate of TB at 44.4/100,000. The majority of the
• Learning Objectives patients are non UK born (73%). Social risk factors of homelessness, drug or
alcohol excess and imprisonment have been associated with 1 in 10 patients
• Introduction
diagnosed with Tuberculosis.
• Global problem
• Aetiology and A report by Kruijshaar and Abubakar has demonstrated a rise in extra
pathogenesis pulmonary tuberculosis in the UK with the reported numbers of TB Meningitis
• Clinical Features cases exhibiting a steady increase
• Complications and
clinical outcome
• Diagnosis
• Microscopy and
culture
• Imaging
• Therapy
• Key points
• Summary
• References/Further
reading
• Self assessment
Aetiology and Pathogenesis of TB
Meningitis I
TB Meningitis Tuberculosis is caused by Mycobacterium
tuberculosis, an obligate aerobic bacterium.
• Learning Objectives
• Introduction After inhalation, the mycobacteria replicate in
the lung (in the alveolar macrophages – which
• Global problem
is why they are called facultative intracellular
• Aetiology and
pathogens). The mycobacteria then
pathogenesis disseminate to the regional lymph nodes
• Clinical Features forming the primary complex. Haematogenous
• Complications and dissemination also occurs throughout the body
clinical outcome and can result in seeding of M tuberculosis to
• Diagnosis other organs.
• Microscopy and
culture .
The next step depends on the host immune response. There may be
• Imaging complete elimination of the mycobacteria or the development of 'tubercles'.
• Therapy
• Key points Each tubercle has a caseous focus and is surrounded by a fibrous capsule.
• Summary If the host immunity wanes, viable bacteria can start proliferating in the
• References/Further tubercle which can then rupture resulting in the release of organisms and
reading their antigenic products.
• Self assessment
Aetiology and Pathogenesis of TB
Meningitis II
In the CNS, the tubercles are known as Rich foci. These are
TB Meningitis subependymal (in the sylvian fissure commonly) or sub pial.
• Learning Objectives
• Introduction Rupture of the Rich focus into the subarachnoid space results in TB
• Global problem Meningitis.
• Aetiology and
pathogenesis Rupture of a Rich focus located in the deeper parenchyma will result
• Clinical Features in a tuberculoma or abscess.
• Complications and
clinical outcome A robust inflammatory response occurs secondary to the rupture of
• Diagnosis the Rich focus. A thick gelatinous exudate infiltrating cortical and
• Microscopy and meningeal blood vessels is formed.
culture
• Imaging Adhesions due to the exudates can result in cranial nerve palsies.
• Therapy Adhesions in the Basal cisterns can result in hydrocephalus.
• Key points Vasculitis can cause strokes and encephalitis may result in
• Summary
increased intracranial pressure. CNS involvement is more likely to
• References/Further
occur in patients with miliary TB.
reading
• Self assessment
Clinical features
TB Meningitis
• Learning Objectives
• Introduction
• Global problem
• Aetiology and
pathogenesis
• Clinical Features
• Complications and
clinical outcome
• Diagnosis
• Microscopy and
culture
• Imaging
• Therapy
• Key points
• Summary
• References/Further
Left: Ring enhancing lesions
reading
• Self assessment
Right: Sulcal leptomeningeal enhancement
Therapeutic Options
Treatment may need to be started prior to a confirmatory
TB Meningitis diagnosis.
• Learning Objectives According to the NICE guidelines (March 2011), patients with
• Introduction active meningeal TB should be prescribed a treatment regime
• Global problem comprising four drugs for the first two months (isoniazid,
• Aetiology and pyrazinamide, rifampicin and a fourth drug such as ethambutol)
pathogenesis followed by isoniazid and rifampicin for the rest of the treatment
• Clinical Features
period.
• Complications and
clinical outcome
• Diagnosis
At present, the optimal drug regimen and duration is not
• Microscopy and established. Daily dosing and combination medications should be
culture considered.
• Imaging
• Therapy Aspects of possible drug resistance, poor compliance, disease
• Key points severity and variable CNS drug penetration should be borne in
• Summary mind while prescribing anti tubercular drugs.
• References/Further
reading
• Self assessment
Therapeutic Options
Adjunctive steroids are recommended in TBM.
TB Meningitis
Steroid doses should follow those used in proven trials. Tapering of
• Learning Objectives doses should be initiated within 2-3 weeks and done over 6-8 weeks.
• Introduction Glucocorticoid equivalent to 20 – 40 mg of Prednisolone for patients
• Global problem on rifampicin otherwise 10-20mg is recommended by NICE
• Aetiology and guidelines.
pathogenesis
• Clinical Features Benefits of steroid use in HIV positive individuals is not proven. In the
• Complications and case of multi-drug resistant TB (MDR-TB) experts should be involved
clinical outcome in the management. For advice email: mdrtbservice@lhch.nhs.uk.
• Diagnosis
• Microscopy and Complications of hydrocephalus
culture and tubercular abscess will need
• Imaging neurosurgical involvement.
• Therapy Ventriculoperitoneal shunts for
• Key points non communicating
• Summary hydrocephalus should be
• References/Further considered early rather than
reading later.
• Self assessment
Key Points
• Tuberculosis is a global emergency with very high morbidity and mortality
TB Meningitis
TB meningitis is a notifiable disease
• Learning Objectives
• Introduction
• Global problem
• Aetiology and
pathogenesis
• Clinical Features
• Complications and
clinical outcome
• Diagnosis True False
• Microscopy and
culture
• Imaging
• Therapy
• Key points
• Summary
• References/Further
reading
• Self assessment