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Central Nervous System Tuberculosis

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  • Author: John M. Leonard1
  • Editor: David Schlossberg2
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Medicine—Infectious Disease, Vanderbilt University Medical Center, Nashville, TN 37232; 2: Philadelphia Health Department, Philadelphia, PA
  • Source: microbiolspec March 2017 vol. 5 no. 2 doi:10.1128/microbiolspec.TNMI7-0044-2017
  • Received 30 September 2016 Accepted 23 January 2017 Published 10 March 2017
  • John M. Leonard, john.m.leonard@vanderbilt.edu
image of Central Nervous System Tuberculosis
  • Abstract:

    Central nervous system tuberculosis (CNS-TB) takes three clinical forms: meningitis (TBM), intracranial tuberculoma, and spinal arachnoiditis. TBM predominates in the western world and presents as a subacute to chronic meningitis syndrome with a prodrome of malaise, fever, and headache progressing to altered mentation and focal neurologic signs, followed by stupor, coma, and death within five to eight weeks of onset. The CSF formula typically shows a lymphocytic pleocytosis, and low glucose and high protein concentrations. Diagnosis rests on serial samples of CSF for smear and culture, combined with CSF PCR. Brain CT and MRI aid in diagnosis, assessment for complications, and monitoring of the clinical course. In a patient with compatible clinical features, the combination of meningeal enhancement and any degree of hydrocephalus is strongly suggestive of TBM. Vasculitis leading to infarcts in the basal ganglia occurs commonly and is a major determinant of morbidity and mortality. Treatment is most effective when started in the early stages of disease, and should be initiated promptly on the basis of strong clinical suspicion without waiting for laboratory confirmation. The initial 4 drug regimen (isoniazid, rifampin, pyrazinamide, ethambutol) covers the possibility of infection with a resistant strain, maximizes antimicrobial impact, and reduces the likelihood of emerging resistance on therapy. Adjunctive corticosteroid therapy has been shown to reduce morbidity and mortality in all but late stage disease.

  • Citation: Leonard J. 2017. Central Nervous System Tuberculosis. Microbiol Spectrum 5(2):TNMI7-0044-2017. doi:10.1128/microbiolspec.TNMI7-0044-2017.
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/content/journal/microbiolspec/10.1128/microbiolspec.TNMI7-0044-2017
2017-03-10
2018-07-15

Abstract:

Central nervous system tuberculosis (CNS-TB) takes three clinical forms: meningitis (TBM), intracranial tuberculoma, and spinal arachnoiditis. TBM predominates in the western world and presents as a subacute to chronic meningitis syndrome with a prodrome of malaise, fever, and headache progressing to altered mentation and focal neurologic signs, followed by stupor, coma, and death within five to eight weeks of onset. The CSF formula typically shows a lymphocytic pleocytosis, and low glucose and high protein concentrations. Diagnosis rests on serial samples of CSF for smear and culture, combined with CSF PCR. Brain CT and MRI aid in diagnosis, assessment for complications, and monitoring of the clinical course. In a patient with compatible clinical features, the combination of meningeal enhancement and any degree of hydrocephalus is strongly suggestive of TBM. Vasculitis leading to infarcts in the basal ganglia occurs commonly and is a major determinant of morbidity and mortality. Treatment is most effective when started in the early stages of disease, and should be initiated promptly on the basis of strong clinical suspicion without waiting for laboratory confirmation. The initial 4 drug regimen (isoniazid, rifampin, pyrazinamide, ethambutol) covers the possibility of infection with a resistant strain, maximizes antimicrobial impact, and reduces the likelihood of emerging resistance on therapy. Adjunctive corticosteroid therapy has been shown to reduce morbidity and mortality in all but late stage disease.

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Figures

Image of FIGURE 1
FIGURE 1

Computerized axial tomogram for a patient with TBM. Note the enlarged ventricles and effacement of sulci, indicating raised intracranial pressure.

Source: microbiolspec March 2017 vol. 5 no. 2 doi:10.1128/microbiolspec.TNMI7-0044-2017
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Image of FIGURE 2
FIGURE 2

MRI of the same patient as for Fig. 1 . After contrast enhancement, showing two dense, bilateral inflammatory masses (tuberculomas) in the region of the thalamus; T-2 weighted image showing inflammatory edema and possible ischemic changes of vasculitis in the basal region of the temporal lobe (arrowhead).

Source: microbiolspec March 2017 vol. 5 no. 2 doi:10.1128/microbiolspec.TNMI7-0044-2017
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Tables

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TABLE 1

Presenting symptoms and signs of TBM

Source: microbiolspec March 2017 vol. 5 no. 2 doi:10.1128/microbiolspec.TNMI7-0044-2017
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TABLE 2

Differential diagnosis of TBM

Source: microbiolspec March 2017 vol. 5 no. 2 doi:10.1128/microbiolspec.TNMI7-0044-2017

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