A 48-year-old African American female presented with a one-month history of headaches and nausea. Her only significant past medical history was diabetes. Her social history was negative for such risk factors as a high-risk profession in the healthcare field, recent incarceration, known contact with persons diagnosed with active tuberculosis or recent travel to areas in which tuberculosis is endemic. Her physical exam was unremarkable, and she had no focal neurological deficits. She was afebrile and hemodynamically stable. She presented to an outside facility where she had a computerized tomography (CT) scan of her head performed, which showed a posterior fossa mass with moderate hydrocephalus. This was followed by a magnetic resonance imaging (MRI) of the brain with and without contrast, which revealed a large right cerebellar ring-enhancing mass (Figures -). The primary concern at that time was that this mass could possibly be a primary brain glioma like a high-grade astrocytoma or a medulloblastoma. The patient was transferred to another hospital for neurosurgical evaluation and excision of the mass. She underwent an exploratory posterior fossa craniectomy, cerebellar exploration and decompression, but no mass was identified at that time. Due to persistent headaches, she then had a repeat exploration of posterior fossa 15 days later, and identification and excision of the cerebellar mass occurred. Histopathology from the procedure revealed necrotizing granulomas (Figure ), and stains specific for acid fast bacilli and fungus were both negative. Subsequently, the brain tissue grew Mycobacterium tuberculosis. The patient reported no prior knowledge of having tuberculosis, nor did she endorse exposure to patients with active tuberculosis. She previously had purified protein derivative (PPD) tests for employment, which had been negative. She was not immunocompromised and had recently been tested negative for human immunodeficiency virus (HIV) six months prior.
A 79-year-old African American male patient with a past medical history of prostate cancer presented with progressive weakness, headache, and confusion. Brain MRI with gadolinium contrast showed a 41 × 33 × 41 mm left frontal lesion at the surface of the left lateral ventricle with vasogenic edema and midline shift (). A stereotactic biopsy of the lesion presented the possibility of a non-caseating granuloma. Metastatic prostate cancer was ruled out. The free and total prostate specific antigen (PSA) level was within the normal limit. The patient had immigrated from Liberia but denied any constitutional symptoms such as fever, cough, night sweats, or weight loss. Quantiferon gold test was positive but active pulmonary tuberculosis was ruled out with chest imaging. The basic metabolic panel was unremarkable; complete blood count showed lymphocytosis only. HIV antibodies were negative. Subsequently, we proceeded with a lumbar puncture. Histoplasma, blastomycosis, and HIV antibodies in cerebrospinal fluid were negative. Serum Cryptococcus antigen, Bartonella Hensale, and Bartonella Quintana IgM and IgG and rapid plasma reagin (RPR) tests were negative. Bone marrow acid-fast bacteria (AFB) stain and culture, C-ANCA, and P-ANCA were negative. 1, 25 OH, 25 Oh vitamin D3, and angiotensin-converting enzyme level were within normal limits. He underwent a left-sided frontal open brain biopsy, and pathology results were compatible with non-caseous granulomatous inflammation (). Fungus tissue culture, sputum, and blood cultures were negative. He was empirically started on anti-tuberculous treatment with Ethambutol, Isoniazid (INH), Rifampin, Pyrazinamide, Pyridoxine, and dexamethasone. We were unable to achieve significant clinical improvement two weeks after anti-tuberculous treatment. Considering the possible diagnosis of neurosarcoidosis, methylprednisolone 1 g daily treatment was initiated for three days and gradually tapered. Later on, after six weeks, the culture of the brain biopsy result came positive for tuberculosis. Anti-tuberculosis (TB) medications were re-initiated, to be continued for 18 months. After two months of treatment, the control MRI brain with gadolinium contrast showed near resolution of the midline shift and a decrease in the left frontal lobe and bilateral parietal lobes edema ().