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| CASE REPORT |
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| Year : 2022 | Volume
: 11
| Issue : 2 | Page : 214-216 |
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Central nervous system tubercular abscess masquerading as intracranial space-occupying lesion
Poongodi Santhana Kumarasamy1, Joel Dhanapandian Stuart2, Mohamed Arafath Mohamed3, Priya Sundararajan1
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 Submission | 30-Mar-2022 |
| Date of Decision | 05-Apr-2022 |
| Date of Acceptance | 13-Apr-2022 |
| Date of Web Publication | 14-Jun-2022 |
| Date of Print Publicaton | 14-Jun-2022 |
Correspondence Address:
Poongodi Santhana Kumarasamy
Department of Microbiology, Tirunelveli Medical College, Highgrounds, Tirunelveli - 627 011, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijmy.ijmy_52_22
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 | |  |
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 | | |
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.
Day-2
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
Click here to view |
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.
| Discussion | | |
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 | | |
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.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]
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