Cryptogenic brain abscess mimicking brain tumor in an immunocompetent young adult

INTRODUCTION

Brain abscess represents a rare yet potentially fatal neuroinfection, occurring in 0.4–0.9/100,000 individuals, most frequently in adult males.^[1,2] Mortality has declined with modern imaging and antibiotics, yet morbidity persists. It arises through hematogenous spread, local extension, or trauma/surgery, with lesion location often indicating the source.^[3]

Clinical manifestations depend on lesion size and site, most often headache, seizures, focal deficits, and raised intracranial pressure (ICP), with the classic triad seen in only 15–20%. Neuroimaging may mimic intracranial neoplasms, as both present as space-occupying lesions with edema and mass effect. Absent systemic infection signs often delay diagnosis and favor misinterpretation as tumor.^[4,5] Moreover, 20–30% of cases are cryptogenic, further complicating management.^[3] We report a cryptogenic brain abscess in an immunocompetent 28yearold man that initially presented as an intracranial tumor.

CASE REPORT

A 28-year-old man was referred with a preliminary diagnosis of an intracranial space-occupying lesion after presenting with 4 days of headache, left-sided weakness, and two episodes of generalized seizures. He had no systemic symptoms, reported a history of metronidazole allergy, and his family history of malignancy was not known.

Neurological examination revealed left-side hemiparesis (MMRC grade 3/5) accompanied by facial and hypoglossal nerve palsy. Initial laboratory evaluation showed a normal leukocyte count (white blood cells 8.3 × 10³/µL) with neutrophil predominance (69%), mild lymphopenia (21%), and slightly elevated neutrophil-to-lymphocyte ratio (3.18). The erythrocyte sedimentation rate was elevated (38 mm/h).

Contrast-enhanced magnetic resonance imaging (MRI) [Figure 1] revealed a 2.2 × 2.3 × 3.0 cm ring-enhancing lesion in the right parietal lobe with extensive edema, midline shift, and hydrocephalus, suggestive of an abscess though neoplasm could not be excluded. Empirical antibiotic (ceftriaxone) and anticonvulsant (phenytoin) were initiated, and ear, nose, and throat/dental evaluations found no infection source. Due to mass effect, craniotomy with capsule excision and drainage was performed under general anesthesia for 3.5 h in the supine position. The procedure was uneventful, with ~150 mL blood loss, and histopathology confirmed necrosis, inflammatory infiltrates, and gliosis consistent with brain abscess. Pus and tissue cultures were negative for bacterial growth.

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Figure 1: Brain magnetic resonance imaging findings. (a) Axial contrast-enhanced T1-weighted image demonstrating a lobulated ring-enhancing lesion in the right parietal lobe with a central hypointense core. (b) Axial T2-fluid-attenuated inversion recovery image showing a hyperintense lesion with extensive surrounding vasogenic edema. The yellow arrows indicate the ring-enhancing lesion in the right parietal lobe with surrounding vasogenic edema and mass effect, representing the pathological focus of the brain abscess.

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Postoperatively, the patient received intravenous antibiotics (ceftriaxone) and anticonvulsants (phenytoin). He was discharged on day 14 and continued oral therapy (cefixime and co-trimoxazole). At 3 weeks, motor function improved markedly (Medical Research Council [MRC] grade 5/5). Six-week followup computed tomography (CT) [Figure 2] demonstrated a residual hypodense lesion in the right parietal lobe measuring 7.1 × 5.0 cm, without contrast enhancement, consistent with a resolving abscess. Clinical recovery was satisfactory, although the source of infection remained unidentified. The clinical timeline is summarized in Table 1.

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Figure 2: Post-operative contrast-enhanced computed tomography scan of the head showing a hypodense area in the right parietal lobe (yellow arrow) without contrast enhancement and midline shift.

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DISCUSSION

This case highlights a cryptogenic brain abscess in an immunocompetent 28-year-old man. Unlike typical abscesses associated with systemic infection or immunodeficiency, cryptogenic cases are rare and often manifest with non-specific symptoms such as headache, seizures, focal neurologic deficits, and signs of increased ICP.^[3,6] These features closely mimic intracranial neoplasms, often leading to an initial suspicion of brain tumor before an abscess is diagnosed.^[5,7]

Brain abscess in immunocompetent patients may present without systemic signs such as fever, leukocytosis, or a clear infectious source, making it easily mistaken for an intracranial neoplasm. Focal neurological deficits depend on lesion location, with the frontal lobe most frequently affected.^[8] In our case, left-sided weakness, headache, and seizures reinforced the impression of neoplasm, underscoring the importance of careful history and neurological examination to avoid delayed recognition.

Neuroimaging is central to diagnosing brain abscess, particularly in cryptogenic cases where microbiological confirmation islimited.^[9] Brain MRI provides high diagnostic accuracy, though a false-negative rate of ~10% underscores the limitations of imaging alone.^[5] Current guidelines recommend contrast-enhanced MRI with diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) sequences to improve accuracy.^[10] In our case, only conventional MRI was available, and parietal lobe localization further complicated differentiation from a neoplasm. Unlike frontal or temporal lobe abscesses often linked to otogenic or sinus infections, parietal involvement is less specific.^[4] This highlights that expansive intracranial lesions with compatible clinical features should be managed as neurosurgical emergencies, whether abscess or tumor.

A solitary ring-enhancing lesion in a young immunocompetent patient necessitates a broad differential diagnosis beyond pyogenic abscess and neoplasm, including tumefactive demyelinating lesions (TDL), tuberculoma, and primary central nervous system lymphoma (PCNSL). TDL typically presents as large (>2 cm) demyelinating lesions associated with multiple sclerosis; however, the absence of prior demyelinating history and histopathological findings consistent with abscess excluded this possibility.^[11] Intracranial tuberculoma is also considered, mainly, in endemic regions due to its similar symptoms such as ring-enhancing mass lesion with seizures or focal deficits along with relevant risk factors or systemic features suggestive of infection. Tuberculoma typically exhibits well-defined boundaries, and there is necrotic caseation where tubercle bacilli can be found within the mass.^[12] Finally, PCNSL was also contemplated given its presentation as a solitary supratentorial mass in immunocompetent individuals.^[13] However, the identification of purulent material during surgery and histopathological confirmation of non-malignancy effectively ruled out lymphoma, rendering cryptogenic brain abscess the most plausible diagnosis.

The patient showed no clinical improvement despite empirical intravenous ceftriaxone and developed progressive neurological deterioration. Clinical and radiological findings remained inconclusive, and an underlying intracranial neoplasm could not be definitively excluded. Given this diagnostic uncertainty and worsening neurological status, surgical exploration was warranted. In cryptogenic brain abscess, surgical intervention serves both therapeutic and diagnostic purposes by relieving mass effect, reducing elevated ICP, and providing tissue for definitive histopathological confirmation.^[3] Current guidelines recommend neurosurgical aspiration or excision whenever feasible.^[10] In this case, craniotomy with excision and drainage was performed for radiological features suggestive of abscess, although neoplasm could not be excluded, and progressive neurological decline requiring decompression. Excision was preferred over stereotactic biopsy as it enabled immediate ICP control and definitive diagnosis, whereas biopsy alone would not have relieved the mass effect.^[5,10]

Empiric antimicrobial therapy was initiated without delay, although early treatment may decrease culture positivity.^[14] A third-generation cephalosporin plus metronidazole remains the standard regimen for immunocompetent adults. For culture-negative cases, empiric therapy should be continued based on clinical–radiological evolution and adjunct molecular diagnostics, with a total duration of 6–8 weeks and serial imaging follow-up.^[3,10] In this case, metronidazole allergy required modification of therapy, replacing intravenous ceftriaxone with cefixime and adding cotrimoxazole to broaden antimicrobial coverage.^[1]

This report has several limitations. Negative cultures from pus and tissue specimens may reflect the limited sensitivity of conventional microbiological methods, technical factors, or prior empirical antibiotic exposure.^[5] Advanced MRI sequences such as DWI and ADC were unavailable, and follow-up relied on CT imaging, which may reduce diagnostic specificity and sensitivity for detecting residual changes. In addition, molecular diagnostics, including metagenomic next-generation sequencing, were not accessible.^[9] Antibiotic selection and step-down strategy were also influenced by metronidazole allergy and local formulary constraints, necessitating modification of guideline-recommended empiric regimens.

CONCLUSION

Cryptogenic brain abscess should remain a key differential for intracranial tumors in young immunocompetent patients. Early recognition through multidisciplinary evaluation is critical to prevent delayed diagnosis and ensure good neurological outcomes.