Isolated Tuberculous Brain Abscess in a 7-Year-Old Child: A Rare Presentation of CNS Tuberculosis: A Case Report

Abstract

Background. Tuberculous brain abscess (TBA) is a rare and often overlooked manifestation of central nervous system tuberculosis (CNS TB), particularly in children. The occurrence of isolated TBAs, where there is no clinical or radiological evidence of tuberculosis elsewhere in the body, is exceedingly uncommon in pediatric patients. Case presentation. A 7-year-old girl presented with a two-week history of persistent headaches and progressive left-sided weakness. Initially diagnosed and treated for pyogenic brain abscesses. However, microbiological and histopathological analysis of the drained abscess revealed the presence of acid-fast bacilli (AFB) and a positive CBNAAT for Mycobacterium tuberculosis, confirming TBA. The patient was successfully treated with surgical drainage and a course of anti-tubercular therapy (ATT). Conclusion. Isolated TBA, though rare, is a critical diagnostic consideration in pediatric CNS TB, especially in tuberculosis-endemic regions. This case emphasizes the need to consider Mycobacterium tuberculosis in the differential diagnosis of pediatric brain abscesses, particularly in regions with a high tuberculosis burden. It also highlights the need for routine tuberculosis testing, including CBNAAT, on all pus samples from intracranial abscesses to ensure timely and accurate diagnosis.

Introduction

Tuberculosis (TB) continues to be a significant global health issue, with central nervous system tuberculosis (CNS TB) representing a severe form of extrapulmonary TB, accounting for approximately 1% of all TB cases. This form of TB is especially prevalent in developing countries, where it can lead to high mortality rates and severe neurological complications, despite advances in imaging and treatment. CNS TB commonly manifests as meningitis, arachnoiditis, or tuberculomas, with tuberculous brain abscess being a rare occurrence.^{1 -3}

Tuberculous brain abscess (TBA) is a rare manifestation of CNS TB, affecting only 4% to 8% of patients with CNS TB who are not HIV-positive. TBA is infrequently reported, particularly in regions where TB remains a major public health issue. ⁴ While TB brain abscesses are more commonly seen in immunocompromised individuals, the incidence of TBA has increased with the rise of HIV infections. However, TBA remains rare in immunocompetent patients.^{4 -7} Clinically and radiologically, TBA closely resembles pyogenic abscesses, which makes differentiation challenging, especially in developing countries where TB remains endemic, posing diagnostic and treatment challenges.^5,6,8

Typically, TBAs are associated with a history of active tuberculosis, and isolated TBA in immunocompetent individuals without evidence of active pulmonary tuberculosis is uncommon.^{9 -11} In this report, we present a rare case of isolated TBA in a 7-year-old child with no clinical or radiological signs of tuberculosis elsewhere in the body. The patient initially exhibited clinical and radiological features consistent with a pyogenic brain abscess. The diagnosis of TBA was confirmed through microbiological and histopathological testing. The patient was successfully treated with neurosurgical drainage and antitubercular therapy.

Case Presentation

A 7-year-old female child from Ethiopia, previously in good nutritional health, presented with a 2-month history of headaches and high-grade fever. Over the past month, she also experienced excessive drowsiness, reduced appetite, subjective weight loss, and intermittent non-projectile vomiting. Initially, she was treated by her primary care physician with a 10-day course of daily intramuscular ceftriaxone and a 5-day course of oral azithromycin, but there was no significant improvement. Her headaches persisted, occasionally relieved by Ibuprofen. In the last 2 weeks, she developed progressive left-sided weakness, though there were no reports of abnormal body movements, loss of consciousness, trauma, respiratory or abdominal complaints, night sweats, or ear discharge. Her developmental milestones were appropriate for her age. She was born to a non-consanguineous couple and had 3 healthy older siblings. Her medical history was unremarkable, and she had received all routine immunizations. There was no known contact with a tuberculosis (TB) patient.

On examination, the patient was conscious, oriented, and febrile (axillary temperature of 38.1°C). Her pulse was 104/min, respiratory rate 32/min, and blood pressure 100/70 mmHg (within normal range for her age). The anthropometric assessment revealed moderate acute malnutrition with a weight of 20 kg, height of 116 cm, and BMI-for-age between −2 and −3 standard deviation (SD) Z-scores. However, height-for-age and mid-upper arm circumference (MUAC) were normal for her age. She exhibited conjunctival pallor but no cyanosis. Lymphadenopathy was absent, and a BCG scar was present. An otoscopic examination revealed normal findings and bilateral good air entry was noted in the chest without adventitious sounds. A cardiac examination showed no abnormalities, and the abdomen was soft with no tenderness or palpable masses. Neurological examination revealed a Glasgow Coma Scale (GCS) of 15/15. There was marked neck stiffness, a positive Kernig’s sign, and left-sided hemiparesis. Increased muscle tone was observed on the left side, with strength graded 2/5 in both the left upper and lower limbs. Reflexes were brisk, and abnormal plantar responses were noted in the left foot. Pupillary size and reaction were normal, as confirmed by fundal examination. All cranial nerves were intact, and the rest of the systemic examination was unremarkable.

Clinically, the possibility of tubercular meningitis with an intracranial space-occupying lesion was considered. Laboratory results showed elevated white blood cell count, an erythrocyte sedimentation rate (ESR) of 105 mm/hour, and microcytic hypochromic anemia. Other biochemical investigations, including liver and kidney function tests, were within normal limits. Lumbar puncture was deferred due to focal neurological deficits. Imaging studies, including chest X-ray and abdominopelvic ultrasound, showed no abnormalities. Gene X-pert testing of an early morning gastric aspirate was negative for tuberculosis, and the HIV test was also negative (Table 1). Unfortunately, the tuberculin skin test (TST) and T-cell interferon-γ (IFN-γ) release assays (IGRAs) were unavailable in the current healthcare setting. Family screening for tuberculosis contacts using chest X-ray and sputum Gene X-pert also returned negative results.

Table 1.

Clinical and Laboratory Follow-Up Summary of a 7-Year-Old with Isolated Tubercular Brain Abscess During Inpatient Care, 2023.

Parameters	Days during in-hospital stay
	Day 1	Day 3	Day 5	Day 7	Day 9	Day 11	Day 13	Day 15
BP (mmHg)	100/70	99/67	101/71	105/70	98/69	110/75	112/74	108/72
T (°C)	38.1	38.7	37.9	37.5	37.1	37.4	37.3	36.9
PR (rate/min)	104	108	102	98	92	94	96	90
RR (rate/min)	32	30	36	32	28	30	26	24
GCS	15/15	15/15	15/15	15/15	15/15	15/15	15/15	15/15
Pupil size & Rxn	N	N	N	N	N	N	N	N
Headache	Yes	Yes	Yes	Yes	No	No	Yes	No
Seizure	No		No	No	No	No	No	No
Power	LE–2/5	LE–2/5	LE–2/5	LE–2/5	LE–3/5	LE–3/5	LE–3/5	LE–4/5
	RE–5/5	RE–5/5	RE–5/5	RE–5/5	RE–5/5	RE–5/5	RE–5/5	RE–5/5
Meningeal signs	+ve	+ve	+ve	+ve	+ve	+ve	−ve	−ve
UAO (ml/hr)	0.9	1.1	1.4	1.2	0.8	1.3	1.6	1.4
Serum electrolyte	N	—	N	—	N	—	—	—
Urinalysis	Unremarkable		N
Treatment given	IV antibiotics	IV antibiotics	IV antibiotics	IV antibiotics	IV antibiotics	ATT steroid	ATT steroid	ATT steroid

Abbreviations: ATT, anti-tuberculous treatment; BP, blood pressure; GCS, Glasgow coma score; LE/RE, left/right extremities; PR: pulse rate; RR, respiratory rate; N, normal; T, temperature; R, reactive; UAO, urine output; +/−ve, positive/negative.

Contrast-enhanced brain CT revealed a ring-enhancing lesion with moderately thick walls in the right frontotemporal region (9.7 × 4 cm), with significant perilesional hypodensity. There was an adjacent leptomeningeal enhancement, effacement of the ipsilateral ventricle, and a dilated left lateral ventricle with significant left midline shift (Figure 1). The initial imaging findings were consistent with a pyogenic brain abscess and left-sided hydrocephalus. The patient was initially treated with intravenous antibiotics, including ceftriaxone, vancomycin, and metronidazole for 1 week, along with supportive care. Due to the large size of the abscess and the worsening neurological condition, neurosurgical consultation was sought. A surgical procedure was performed, resulting in the drainage of approximately 50 ml of thick, yellowish pus, with partial removal of surrounding tissue after careful dissection to separate the abscess from the brain (Figure 2). The pus sample was sent for several diagnostic tests, including gram staining, acid-fast bacilli (AFB) testing, fungal culture, and Gene X-pert MTB/RIF. Aerobic and anaerobic cultures showed no growth, but the AFB smear revealed a significant number of acid-fast bacilli. The Gene X-pert MTB/RIF test identified Mycobacterium tuberculosis in the aspirated pus, with the strain found to be rifampicin-sensitive. Histopathology of the abscess wall revealed granulation tissue with chronic inflammatory infiltration but no caseating granulomas or fungal elements.

Figure 1.

(A) Pre-contrast and (B) post-contrast enhanced CT scans show a large “ring enhancing” lesion in the right frontotemporal region with significant perilesional hypodensity. Additionally, the ipsilateral ventricle has an adjacent leptomeningeal enhancement and effacement. A dilated left lateral ventricle and significant left midline shift are also noted.

Figure 2.

Intraoperative gross appearance of the mass after circumferential debulking, revealing a grayish wall approximately 10 mm thick, surrounding a central core of yellowish, friable pus.

Following abscess drainage, the patient began a 12-month course of antituberculosis therapy. During the intensive phase, she received a combination of isoniazid, rifampicin, pyrazinamide, and ethambutol, along with steroids for the first 2 months. In the continuation phase, she continued with isoniazid and rifampicin for the remaining 10 months. Within a week of starting treatment, her fever and headache subsided (Table 1). After 2 months of intensive treatment, the patient’s symptoms resolved, her neurological condition improved, and her muscle strength increased to 4/5. She also gained weight appropriately. The patient adhered to her anti-tuberculosis therapy (ATT) and attended regular follow-up visits. By the sixth month of treatment, there were no signs of neurological deficits. However, due to financial constraints, follow-up neuroimaging was not conducted.

Discussion

Central nervous system tuberculosis (CNS TB) typically manifests as meningitis or tuberculoma. Tuberculous brain abscess (TBA), however, is a rare form of CNS TB, most commonly seen in immunocompromised individuals who cannot mount an effective immune response against the infection. In developing countries, TBA has been reported in 4% to 7.5% of patients with CNS tuberculosis. TBA is observed in 4% to 8% of non-HIV patients and 20% of patients with AIDS. Unlike tuberculoma, a tuberculous abscess is encapsulated, containing abundant viable tubercle bacilli, and is surrounded by a dense capsule of vascular granulation tissue without evidence of tubercular granulomas. Additionally, the walls of the abscess lack the epithelioid and giant cells characteristic of tuberculomas. The factors influencing the development of abscesses instead of tuberculomas remain unclear but are thought to involve host immunity, the dose of the infecting pathogen, the nature of the affected tissue, and antitubercular therapy (ATT).^3,6,12

Pyogenic brain abscesses often present with clinical features similar to those of tuberculous brain abscesses (TBA). Both conditions typically have an acute onset with overlapping signs and symptoms, frequently leading to a diagnostic challenge.^12,13 Both pyogenic brain abscesses (PBA) typically have a rapid onset (days to weeks) and are associated with risk factors like otitis media, CHD, sinusitis, or trauma, alongside systemic sepsis signs. In contrast, TBA presents sub-acutely or chronically (weeks to months) with meningeal signs and systemic TB evidence, such as weight loss or lymphadenopathy.^14,15 The presence of extracranial evidence of tuberculosis is a key differentiating factor in patients with TBA. ⁶ In our patient, there was initially no evidence of extracranial tuberculosis. The Gene X-pert test from gastric aspirate was negative, and there were no radiological findings suggestive of pulmonary TB. This absence of risk factors or indicative findings made it difficult to suspect TB, resulting in initial empirical treatment for pyogenic brain abscesses. Additionally, the radiological features of TBA closely mimic those of pyogenic brain abscesses, further complicating the diagnosis. ⁵ Given this overlap, it is crucial to include TBA as a differential diagnosis when evaluating cases of brain abscesses. In 1978, Whitner established criteria for diagnosing TBA, which remains a valuable tool for identifying this rare manifestation of CNS TB. These criteria are: (I) Macroscopic evidence of a true abscess formation within the brain as confirmed during surgery or autopsy. (II) Histological proof of the presence of inflammatory cells in the abscess wall. (III) Demonstration of AFB in the pus or abscess wall. ⁶

Tuberculous brain abscesses (TBAs) typically originate from the bloodstream, with the infection spreading to the brain from active tuberculosis in other parts of the body. Individuals with compromised immune systems, such as HIV-positive patients and malnourished children, are particularly susceptible to central nervous system (CNS) tuberculosis, including TBAs. Diagnosis is often considered in immunocompromised patients, regardless of HIV status, or in healthy individuals from regions where tuberculosis is endemic, especially when a pulmonary source of infection is suspected. However, a pulmonary source is identified in only about one-third of cases. ³ In this case, the patient was HIV-negative and showed no evidence of pulmonary infection, highlighting an unusual and atypical presentation of the condition.

Chattopadhyay and Kundu ¹⁰ reported a case of TBA in a young patient with no prior history of tuberculosis, where the diagnosis was confirmed using polymerase chain reaction (PCR). Notably, the patient did not present with any respiratory symptoms, suggesting a non-pulmonary route of infection. It was hypothesized that early exposure to maternal tuberculosis might have contributed to the condition, although a tuberculin skin test was not performed to evaluate latent TB. Diagnosing TBA is challenging in the absence of an extracranial infection source, as clinical presentation and routine CT scan findings are often nonspecific. Definitive diagnosis requires demonstrating mycobacteria through cartridge-based nucleic acid amplification testing (CBNAAT) of pus and excluding other pathogenic organisms. Histopathological examination of the abscess wall further supports the diagnosis.^6,16

Tuberculous brain abscesses (TBAs) are characterized by a thicker abscess wall compared to pyogenic brain abscesses, both visually and on imaging. Histopathological examination of tissue samples reveals that the abscess wall primarily consists of vascular granulation tissue containing acute and chronic inflammatory cells along with bacilli. Notably, there is no granulomatous reaction in the pus or abscess wall. Unlike tuberculomas, TBA walls lack epithelioid and giant cells. Unlike tuberculomas, abscess walls do not have epithelioid and giant cells. ⁵ In our case, the tubercular origin of the abscess was confirmed by microscopic examination of the pus smear, which demonstrated acid-fast bacilli. The Gene X-pert MTB/RIF test detected a high level of Mycobacterium tuberculosis in the pus, and the strain was sensitive to rifampicin. Histopathological analysis further supported the diagnosis, revealing chronic inflammatory infiltrates and necrosis without evidence of a granulomatous reaction.

In CT imaging, both pyogenic brain abscesses and TBAs are identified by a contrast-enhanced rim surrounding a low-density zone, with the entire lesion encased by low-density brain tissue indicative of surrounding edema. Radiological features alone often cannot distinguish between TBAs and pyogenic abscesses. However, TBAs tend to develop more gradually and have thicker walls compared to their pyogenic counterparts. Luthra et al highlighted the utility of in vivo MR spectroscopy, which is considered the gold standard for imaging-based differentiation. This technique identifies distinct metabolite profiles: amino acids, acetate, and succinate indicate pyogenic abscesses, whereas a lipid peak is characteristic of tuberculous abscesses. Unfortunately, this advanced diagnostic tool was unavailable in our patient’s treatment setting, adding to the diagnostic challenges. Additionally, benign pediatric cystic tumors, such as pilocytic astrocytomas, can mimic TBAs on CT imaging. In contrast, tuberculomas typically present as dense, solid masses with enhanced contrast and no central cystic component, clearly differentiating them from abscesses.^12,17

The primary treatment for TBAs involves a combination of surgical drainage and antitubercular therapy (ATT). Although research on TBA management is limited, most studies emphasize the importance of integrating both surgical and medical approaches.^18,19 The choice of surgical method depends on the size and complexity of the abscess, as well as the patient’s neurological condition. Burr hole drainage is typically sufficient for smaller abscesses, but larger lesions (over 3 cm) or more complex cases often require craniotomy. Smaller abscesses may resolve completely with standard ATT alone, supplemented by corticosteroid therapy, which is crucial for reducing inflammation and achieving an effective cure.^5,20 In this case, the patient underwent craniotomy and abscess drainage, followed by an extended course of ATT lasting 1 year, along with an 8-week course of corticosteroid therapy. An early surgical procedure can improve the efficacy of standard ATT and promote a better clinical response after the reduction of bacillary load. Long-term clinical and imaging follow-ups are essential in managing TBAs to monitor recovery and address potential complications. These may include adverse effects of ATT, recurrent lesions, or paradoxical reactions during treatment. Some patients may also require additional surgical interventions due to clinical deterioration or changes in imaging findings while on ATT.^4,19 Our patient followed this treatment protocol and has been monitored for over 1 year to ensure a successful outcome.

Conclusion

Isolated tuberculous brain abscess is an extremely rare form of CNS tuberculosis in children. However, in regions where tuberculosis is endemic, it should always be considered a possible cause of brain abscesses. Accurate and timely diagnosis requires a high index of suspicion along with thorough microbiological and histopathological evaluations. Routine testing of all pus samples from intracranial abscesses, including Ziehl–Neelsen staining and the Gene Xpert MTB/RIF assay (CBNAAT), is essential for identifying Mycobacterium tuberculosis. Additionally, a comprehensive assessment of the patient’s medical history and potential exposure to tuberculosis is crucial for guiding diagnosis and management. This case highlights the critical need for systematic tuberculosis screening in pediatric patients with brain abscesses, particularly in high-burden regions, to improve patient outcomes and prevent delays in the treatment of this life-threatening condition.