A 25-year-old man, previously healthy, was initially admitted due to slowly progressive headache with blurry vision and fever for nine months. The patient recalls ingesting raw camel milk, which is a major risk factor for brucellosis. There was no previous contact with a tuberculosis case. The headache worsened one week before his admission and the patient lost vision in the left eye. His vital signs and cognitive function were normal. Pupils were reactive, but the patient was barely seeing the flash light with his left eye. Ophthalmologic examination revealed an atrophic optic disc mainly with decreased visual acuity bilaterally. Extraocular muscles were intact. The remaining neurological examination was unremarkable.
His diagnostic work up showed total white blood cell (WBC) count of 5.61 x 109 cells/mm3 and a C-reactive protein (CRP) level of 3.76 mg/L. His cerebrospinal fluid (CSF) acid fast bacilli (AFB) stain and Mycobacterium tuberculosis polymerase chain reaction (MTB-PCR) were both negative. Blood and CSF cultures were positive for Brucella spp. His serum serological test was positive for B. melitensis and B. abortus. Antibody titers were 1:640 for both strains, just at the cutoff level for the serological diagnosis of the infection. CSF analysis showed elevated WBC count (170 cells/mm3 with 34.9% lymphocytes) and decreased glucose level (34.2 mg/dL). Serum glucose level at that time was 99 mg/dL. CSF protein level was 1.5 g/L while red blood cell (RBC) count was 7 cells/mm3. A magnetic resonance imaging (MRI) of his brain showed multiple, bilateral small dural-based nodular enhancements in both upper frontal lobes (Image 1). The patient was diagnosed with neurobrucellosis. Unfortunately, the patient has completely lost his vision in the left eye with weakened vision in the right eye because of a late presentation and delayed diagnosis. As such, the patient was immediately started on ceftriaxone 2 g intravenously (IV) every 12 h, doxycycline 100 mg orally every 12 h and rifampin 900 mg orally once daily for six weeks along with amikacin 400 mg IV every 12 h for the first three weeks. Three weeks after treatment was initiated, both antibody titers remained at 1:640, which was expected as Brucella antibodies may persist for months after conclusion of therapy. His repeated blood and CSF cultures returned negative a few days after treatment. A repeated MRI of the brain showed interval decrease in the number of the previously reported bilateral frontal leptomeningeal enhancing foci. However, small residual abnormal enhancing foci were still noted. Fortunately, no interval development of new lesions was seen (Image 2).
Upon completion of the IV regimen (amikacin and ceftriaxone), the patient was discharged on oral doxycycline 100 mg every 12 h and rifampin 300 mg every 8 h to be taken for 6 months. In an outpatient follow up visit three months later, the patient's vision on the right side was slightly improving. While B. melitensis antibody titer slightly decreased to 1:320, B. abortus antibody titer remained at 1:640. Three months later (six months after discharge), a repeated lumbar puncture showed improved CSF analysis with WBC count of 6 cells/mm3, RBC count of 1 cell/mm3, protein level of 0.55 g/L and glucose level of 46.8 mg/dL (serum glucose level was not obtained at the time of this test). Brucella antibody titer in the serum declined from 1:640 to 1:40 for both strains. At this visit, the decision was made to extend the treatment to 3-6 more months to ensure full recovery. Three months later, a repeated brain MRI showed no more meningeal enhancement and CSF analysis was normal; therefore, antibiotic treatment for brucellosis was stopped.