Neurobrucellosis refers to central nervous system involvement by brucellosis and occurs secondary to ingestion or contact with gram-negative, facultative intracellular coccobacilli of the Brucella species. Up to 10% of infections are complicated by neurological involvement ¹. 

The remainder of this article is a discussion of CNS brucellosis. For a general discussion on systemic infection, please refer to the article on brucellosis.

Epidemiology

Brucella is found worldwide. High-risk areas include countries surrounding the Mediterranean Sea, Eastern Europe, Mexico, South and Central America, Africa, Asia, the Caribbean and the Middle East ². 

Clinical presentation

Onset is insidious; undulant, low-grade fever, headache, fatigue and malaise may precede any neurological findings by a number of months. A study of 128 patients with brucellosis found that central nervous symptom involvement is more likely if the following signs and symptoms are present ³:

• blurred vision

• sensorineural hearing loss

• disorientation

• recent behavioural change

• agitation

• muscle weakness

• neck stiffness

• deep tendon reflex change

• paraesthesia

• diplopia

• ataxia

• pseudotumour cerebri

• facial paralysis

Brucella may be isolated from blood cultures and/or cerebrospinous fluid (CSF). Additional CSF abnormalities include the presence of anti-Brucella antibodies, pleocytosis, high protein and low glucose levels ⁴.

Pathology

Transmission occurs secondary to direct contact with infected animals or the consumption of unpasteurised dairy products. In addition to the four main species causing brucellosis, ​B. ceti and B. pinnipediae have also been isolated in the context of neurobrucellosis ². 

Radiographic features

In just under half of brucellosis cases with neurological findings, imaging of the CNS is unremarkable ^5,6. Abnormal neuroimaging may involve the meninges, cranial nerves, white and grey matter, vasculature, and spinal nerve roots ^5,6. 

CT

Diffuse white matter changes, meningeal enhancement, lacunae and haemorrhages within the basal ganglia, hydrocephalus and cerebral oedema may be demonstrated.

MRI

• T1: arachnoiditis

• T2/FLAIR: ​arachnoiditis; diffuse, hyperintense lesions affecting the white matter, with an appearance of focal demyelination

• T1/T2 C+ (Gd): brain abscess or granuloma with ring enhancement; leptomeningeal, basal meningeal, perivascular and/or spinal root enhancement

Differential diagnosis

The heterogenous presentation and imaging findings of neurobrucellosis warrant a thorough history and risk-stratification. Clarification of recent travel and exposure to unpasteurised dairy is important, remembering that both acute and chronic presentations are possible.

Differentials are therefore numerous, but include:

• demyelinating disorders, such as

  • multiple sclerosis - note the possibility of blurred vision, weakness, ataxia, malaise, fatigue and persistent low-grade fever with evidence of demyelination on MRI as an easy misdiagnosis

  • acute disseminated encephalomyeltitis (ADEM) - fever, headache, cranial nerve palsies and behavioural change with imaging difficult to distinguish from multiple sclerosis again allowing for misdiagnosis

  • inherited vasculopathies

  • inflammatory vasculitides

• equine viral encephalomyelitis, secondary to infection with

  • epidemic Venezuelan equine encephalomyelitis

  • western equine encephalomyelitis

  • eastern equine encephalomyelitis

  • Japanese encephalitis

  • West Nile virus

• tuberculosis

• Murray Valley encephalitis

• histoplasmosis

• cryptococcal infection, which may present as

  • central nervous system cryptococcosis

  • cryptococcoma

• blastomycosis

• neurosarcoidosis