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 Table of Contents  
Year : 2022  |  Volume : 11  |  Issue : 2  |  Page : 214-216

Central nervous system tubercular abscess masquerading as intracranial space-occupying lesion

1 Department of Microbiology, Tirunelveli Medical College, Tirunelveli, Tamil Nadu, India
2 Department of Neurosurgery, Tirunelveli Medical College, Tirunelveli, Tamil Nadu, India
3 Department of General Medicine, Shifa Hospitals, Tirunelveli, Tamil Nadu, India

Date of Submission30-Mar-2022
Date of Decision05-Apr-2022
Date of Acceptance13-Apr-2022
Date of Web Publication14-Jun-2022
Date of Print Publicaton14-Jun-2022

Correspondence Address:
Poongodi Santhana Kumarasamy
Department of Microbiology, Tirunelveli Medical College, Highgrounds, Tirunelveli - 627 011, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijmy.ijmy_52_22

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This is a case report of patient suffering from multiple central nervous system tuberculoma which progressed to tubercular abscess. Patient developed signs and symptoms of mass effect and compression. Computed tomography of brain and magnetic resonance spectroscopy confirmed the diagnosis. Patient underwent left temporal craniotomy with evacuation of pus. The abscess wall and the pus sent for histopathological and microbiological examination which confirmed the etiological agent – Mycobacterium tuberculosis. Appropriate treatment was started and discharged. Hence, early diagnosis and treatment of intracranial tuberculoma are pivotal in preventing morbidity and mortality of the condition.

Keywords: Central nervous system abscess, multiple, tuberculoma

How to cite this article:
Kumarasamy PS, Stuart JD, Mohamed MA, Sundararajan P. Central nervous system tubercular abscess masquerading as intracranial space-occupying lesion. Int J Mycobacteriol 2022;11:214-6

How to cite this URL:
Kumarasamy PS, Stuart JD, Mohamed MA, Sundararajan P. Central nervous system tubercular abscess masquerading as intracranial space-occupying lesion. Int J Mycobacteriol [serial online] 2022 [cited 2022 Jul 6];11:214-6. Available from: https://www.ijmyco.org/text.asp?2022/11/2/214/347517

  Introduction Top

Tuberculosis (TB) is caused by Mycobacterium tuberculosis which is a major cause of death worldwide. This disease primarily affects lungs, and extrapulomonary involvement is noted in 20% and its incidence increasing.[1] Central nervous system (CNS) tuberculosis is a devastating manifestation presenting as meningitis, cerebritis, and tuberculous abscesses or tuberculomas. Intracranial tuberculomas are the least common presentation of CNS TB, found in 1% of cases.[2] They are multiple in 15%–33% of the cases.[3] Miserably, clinical manifestations of CNS tuberculosis are nonspecific and definite evidence of systemic tuberculosis may be absent in up to 70% of cases.[4] Here, we report a case of multiple CNS tuberculoma with cerebral abscess.

  Case Report Top

Day 1

A 37-year-old female presented with complaints of headache for 1 week. She had one episode of giddiness, became restless, and brought for further evaluation and management. She is not a known diabetic, hypertensive, or asthmatic. She had a history of spinal tuberculosis 4 months back, with irregular antituberculous therapy. On examination, Glasgow Coma Scale was 11/15 (eyeopening – 2, verbal response – 4, motor response – 5), bilateral pupils – equal and reacting to light, vitals – stable, CNS – higher mental function was within the normal limits, able to move all four limbs, other systems – normal, laboratory investigations – total cell count of 8800 with neutrophilic predominance, hemoglobin – 11 g/dL, erythrocyte sedimentation rate – 10 mm in half an hour and 21 mm in 1 h, INR – 1.08, liver and renal profile – within the normal limits. HIV, hepatitis B, hepatitis C – negative, reverse transcription-polymerase chain reaction (RT-PCR) for COVID-19 was negative.

Computed tomography - Brain (plain)

  • Well-defined hypodense lesion noted in left temporal lobe with minimal mass effect and edema.

Computed tomography - Abdomen

  • Right obturator internus, right piriformis, and iliacus muscle appear bulky and show internal hypodense collection. Hypodense presacral collection – infective/granulomatous lesion.

Computed tomography – Whole spine

  • Lytic area involving the ala of sacrum on the right side associated with hypodense collection along the presacral space suggestive of spondylitis and right sacroiliitis.


Magnetic resonance imaging of the brain with magnetic resonance spectroscopy

  • Well-defined, capsulated, T1-hypointense, T2-hyperintense lesion measuring 2.4 cm × cm 2.4 × 2.5 cm noted in left temporal lobe with minimal mass effect and surrounding edema noted suggestive of cerebral abscess
  • The lesion shows diffusion restriction and on contrast administration, multiple nodules show peripheral enhancement suggestive of multiple tuberculoma [Figure 1]
  • Magnetic resonance (MR) spectroscopy shows elevated lipid/lactate peak [Figure 2].
Figure 1: Magnetic resonance imaging of the brain showing ring-enhancing lesion with tuberculomas

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Figure 2: Magnetic resonance spectroscopy showing lipid lactate peak

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Day 3

Left temporal craniotomy and evacuation of cerebral abscess were done. Thick yellowish-green pus was aspirated, and abscess wall was excised and sent for histopathological, which revealed proliferating vascularized inflammatory granulation tissue with dense chronic inflammatory cell infiltration and areas of congestion suggestive of an organizing abscess. Pus sent for AFB staining was positive [Figure 3]. RT-PCR revealed Mycobacterium tuberculosis (2.5 × 108 cfu/ml). The patient was started on antituberculous therapy (ATT) and antiepileptics. After symptomatic improvement, she was discharged.
Figure 3: Acid–fast bacilli in pus from cerebral abscess

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  Discussion Top

Intracranial tuberculomas are rare, confused with intracranial neoplasm whenever presented without signs and symptoms of tuberculosis.[5] Risk factors for CNS TB include children, malnutrition, alcoholism, malignancies, and immunosuppressed states.[6] Microglial cells are the principal target cells in CNS TB.[7] This occurs mainly by hematogenous spread from other sites or through cervical lymph nodes. Tuberculous lesions (Rich's focus) develop in the brain during the stage of bacteremia. The stimulus needed for rupture or growth of these lesions is known to be immunological in nature.[8] There will be central caseation, liquefaction, and formation of an abscess which commonly occurs in patients with abnormal cell-mediated immunity.[9]

The lesions more frequently arise as solitary, but multiple tuberculomas are also seen. Tuberculoma of the brain exhibit granulomatous reaction consisting central caseating necrosis sourrounded by epitheloid cells, giant cells and lymphocytes. On liquefaction, it contains clear or straw colored fluid, unlike pus in abscess.[4]

Clinical presentation includes headache, seizures, papilledema, or other signs of increased intracranial pressure. The manifestation of TB brain abscess is more acute (1 week to 3 months) than tuberculoma but slower in onset than pyogenic brain abscesses.[10]

Microscopic examination and culture of cerebrospinal fluid to detect AFB remain the most important and widely available method to diagnose CNS TB. CSF analysis may not always be possible due to raised intracranial pressure. Contrast-enhanced magnetic resonance imaging (MRI) is commonly considered superior than computed tomography in detecting and assessing CNS TB.[11]

MR spectroscopy and magnetization transfer MR imaging may distinguish tuberculous from pyogenic abscesses.[12] Molecular methods are used in the diagnosis of tuberculosis from paucibacillary specimens like pus, in which conventional methods may show low sensitivity.[13] The absence of multiplet of amino acids-lipids at 0.9 ppm seems to be a hallmark of TB abscess in MR spectroscopy.[12]

ATT for tuberculoma is given for 9–18 months; based on the radiological response, it may extend up to 30 months. Paradoxical development or enlargement of tuberculoma during ATT has also been documented and is possibly due to immunological mechanisms.[14] Follow-up with the radiological examination (preferably MRI) is a must. Steroids can be added in patients with large lesions, raised intracranial pressure, or associated meningitis.[15] Surgical treatment is required for isolated cases only.

  Conclusion Top

Tuberculoma can occur in immunocompetent patients without a history of TB with atypical manifestations. Despite novel molecular techniques, the diagnosis of CNS TB relies mostly on microbiological methods that are insensitive and possess a diagnostic challenge. Early diagnosis and treatment are pivotal in preventing morbidity and mortality of the condition.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Forssbohm M, Zwahlen M, Loddenkemper R, Rieder HL. Demographic characteristics of patients with extrapulmonary tuberculosis in Germany. Eur Respir J 2008;31:99-105.  Back to cited text no. 1
Rock RB, Olin M, Baker CA, Molitor TW, Peterson PK. Central nervous system tuberculosis: Pathogenesis and clinical aspects. Clin Microbiol Rev 2008;21:243-61.  Back to cited text no. 2
Mohammadian M, Butt S. Symptomatic central nervous system tuberculoma, a case report in the United States and literature review. IDCases 2019;17:e00582.  Back to cited text no. 3
Garg RK. Tuberculosis of the central nervous system. Postgrad Med J 1999;75:133-40.  Back to cited text no. 4
Sharma K, Kanaujia V, Jaiswal S, Jain A, Kumar S, Srivastava AK, et al. Brain stem tuberculoma presenting with isolated ocular motility abnormality: A series of two cases and review of literature. Oman J Ophthalmol 2012;5:61-3.  Back to cited text no. 5
[PUBMED]  [Full text]  
Yaramiş A, Gurkan F, Elevli M, Söker M, Haspolat K, Kirbaş G, et al. Central nervous system tuberculosis in children: A review of 214 cases. Pediatrics 1998;102:E49.  Back to cited text no. 6
Spanos JP, Hsu NJ, Jacobs M. Microglia are crucial regulators of neuro-immunity during central nervous system tuberculosis. Front Cell Neurosci 2015;9:182.  Back to cited text no. 7
van den Bos F, Terken M, Ypma L, Kimpen JL, Nel ED, Schaaf HS, et al. Tuberculous meningitis and miliary tuberculosis in young children. Trop Med Int Health 2004;9:309-13.  Back to cited text no. 8
Zhang Q, Sugawara I. Immunology of tuberculosis. World J Exp Med 2012;2:70-4.  Back to cited text no. 9
Shah IA, Asimi RP, Kawoos Y, Wani M, Sarmast AH. Tuberculomas of the brain with and without associated meningitis: A Cohort of 28 cases treated with anti-tuberculosis drugs at a tertiary care centre. Int J Contemp Med Res 2016;3:3484-7.  Back to cited text no. 10
Bernaerts A, Vanhoenacker FM, Parizel PM, Van Goethem JW, Van Altena R, Laridon A, et al. Tuberculosis of the central nervous system: Overview of neuroradiological findings. Eur Radiol 2003;13:1876-90.  Back to cited text no. 11
Gupta RK, Vatsal DK, Husain N, Chawla S, Prasad KN, Roy R, et al. Differentiation of tuberculous from pyogenic brain abscesses with in vivo proton MR spectroscopy and magnetization transfer MR imaging. AJNR Am J Neuroradiol 2001;22:1503-9.  Back to cited text no. 12
Lodha R, Kabra SK. Newer diagnostic modalities for tuberculosis. Indian J Pediatr 2004;71:221-7.  Back to cited text no. 13
Ng SK, Zhu XL, Poon WS. Paradoxical enlargement of tuberculous brain abscess during drug treatment: A case report. Singapore Med J 2001;42:325-7.  Back to cited text no. 14
Gundamraj S, Hasbun R. The use of adjunctive steroids in central nervous infections. Front Cell Infect Microbiol 2020;10:592017.  Back to cited text no. 15


  [Figure 1], [Figure 2], [Figure 3]


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