A 25-years-old man who was previously healthy came to the hospital complaining of left lower limb pain that progressed to limb weakness with decreased ability to walk. Physical examination revealed moderate lower limb weakness with foot drop. It was worse on the left side with lower motor neuron lesion findings. He had normal sensory exam. He reported drinking raw camel milk three months before the first episode of pain with a family member who was diagnosed with brucellosis recently. There was no tuberculosis contact. Since the patient was suspected to have neurobrucellosis, lumbar puncture was done. CSF analysis showed a WBC count of 420 (polymorphonuclear cells of 4% and lymphocytes of 90%) cells/mm3, RBC count of 18 cells/mm3, elevated protein level at 2.45 g/L and glucose level of 21.6 mg/dL (serum glucose was 81 mg/dL). The CSF culture was positive for Brucella species. The acid fast bacilli stain and culture were negative, as well as the MTB-PCR. Other investigations including tests for hepatitis B and C viruses and human immunodeficiency virus (HIV) 1 and 2 were all negative. Serologically, antibody titers results from the CSF for B. melitensis and B. abortuswere 1:160 and 1:80, respectively. His serum titers were not obtained initially. His CRP level was within normal limits. The patient refused to have a tuberculin skin test. An MRI of lumbosacral spine revealed enhancement of cauda equina nerve roots and surface of thecal sac, as well as L5-S1 degenerative changes with central posterior disc bulge indenting the ventral aspect of the thecal sac with no significant neural compromise associated with intervertebral disc dehydration (Image 3). He was admitted as a case of cauda equina syndrome secondary to neurobrucellosis and was started on ceftriaxone 2 g IV every 12 h, amikacin 500 mg IV every 8 h, doxycycline 100 mg orally every 12 h and rifampin 900 mg orally once daily. The initial plan was to continue the antibiotics with daily physiotherapy then re-evaluate after 6 weeks. However, two weeks into the treatment, the patient's status deteriorated significantly, from difficulty walking to being completely bed bound. Repeated work up showed no other significant findings. Furthermore, after 4 weeks of treatment, the patient started complaining of decreased hearing and pain in both ears resulted in discontinuation of amikacin. Six weeks into therapy, a repeated lumbar puncture did not show a significant improvement with a CSF analysis showing a WBC count of 315 cells/mm3 (polymorphonuclear cells of 41% and lymphocytes of 45%), RBC count of 15 cells/mm3, protein of 3.73 g/L and glucose level of 23.4 mg/dL (serum glucose was 82 mg/dL). Serum antibody titers were 1:320 and 1:80 for B. melitensis and B. abortus, respectively. Since the CSF repeated culture returned negative for Brucella spp., prednisone 1 mg/kg tapering dose was added aiming to reduce further nerve impingement. Luckily, the patient started to show clinical improvement and the IV ceftriaxone was discontinued after completing six weeks of treatment. The patient continued to restore his lower limb power and he was able to transfer to the wheelchair independently. Hence, he was discharged on doxycycline 100 mg orally every 12 h and rifampin 900 mg orally once daily for one year. The patient was scheduled for follow up in both the infectious diseases and neurology clinics. On his outpatient visits, the patient showed remarkable improvement of his lower limb weakness and he restored the ability to walk again using a cane. Serum antibody titers for both Brucella strains were at 1:80 and CRP remained within the normal range.