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Year : 2012  |  Volume : 55  |  Issue : 1  |  Page : 128-130
Dementia, peripheral neuropathy, and chronic meningitis in Neurobrucellosis


1 Department of Neurology, National Institute of Mental Health and Neuro Science, Hosur Road, Bengaluru, India
2 Department of Neuromicrobiology, National Institute of Mental Health and Neuro Science, Hosur Road, Bengaluru, India
3 Project Directorate on Animal Disease Monitoring and Surveillance, (PD-ADMAS), Hebbal, Bengaluru, India
4 Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neuro Science, Hosur Road, Bengaluru, India

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Date of Web Publication11-Apr-2012
 

How to cite this article:
Nalini A, Nagarathna S, Rajeshwari S, Rose D, Veena Kumari H B, Nagalingam M. Dementia, peripheral neuropathy, and chronic meningitis in Neurobrucellosis. Indian J Pathol Microbiol 2012;55:128-30

How to cite this URL:
Nalini A, Nagarathna S, Rajeshwari S, Rose D, Veena Kumari H B, Nagalingam M. Dementia, peripheral neuropathy, and chronic meningitis in Neurobrucellosis. Indian J Pathol Microbiol [serial online] 2012 [cited 2019 Dec 12];55:128-30. Available from: http://www.ijpmonline.org/text.asp?2012/55/1/128/94896


Sir,

 Brucellosis More Details, a zoonotic infection of human beings is due to direct or indirect exposure to animals and their products like consumption of raw milk or milk products and meat. [1] The disease commonly affects the gastrointestinal tract, hepatobiliary and the skeletal systems. However, nervous system involvement is seen in 5% to 7% of the cases of brucellosis, both in acute and chronic stages of the disease. [2] Neurobrucellosis has protean clinical manifestations like meningitis, encephalitis, myelitis-radiculoneuritis, brain abscess, epidural abscess, peripheral neuropathy, and psychosis. [1],[3]

An adult male, farmer and a Hindu priest, associated with cattle rearing and consumption of unpasteurized raw cattle milk, presented with distal symmetrical paraesthesia of lower limbs gradually extending upward, pyrexia, joint pain, unsteadiness of gait, decreased cognitive ability, and memory disturbances over a period of 6 months. Urinary, fecal incontinence, and progressive painless visual loss in right eye, dependent for day-to-day activities during the later stages of illness, were the additional findings. Prior to reporting to our Institute, the treatment with Vitamin B 12 injections, antibiotics was instituted with other supportive medications.

Preliminary examination revealed disorientation to time and place with spastic ataxic gait. The visual acuity was 6/60 and 6/36 in right and left eye, respectively, with reactive pupils. He had spasticity of all the limbs, weakness of the distal muscles, and pinprick and fine touch sensations impairment in glove and stocking distribution. Deep tendon reflexes were normal in upper limbs and exaggerated in lower limbs with ankle clonus and extensor plantar response. Neuropsychological assessment revealed involvement of premotor area, dorsolateral, prefrontal cortex, and left anterior temporal lobes.

The hematological profile, liver and renal function tests were within normal limits. Rheumatoid arthritis factor and antinuclear antibody tests were negative. Serum and cerebrospinal fluid (CSF) VDRL and HIV were non-reactive. CSF analysis showed 20 lymphocytes/dl, with 45 mg/dl and 120 mg/dl of protein and glucose, respectively. Contrast magnetic resonance imaging (MRI) of brain and spine revealed multiple discrete and confluent white matter lesions involving the periventricular and the subcortical areas with multiphasic, multifocal morphology similar to multiple sclerosis plaques with the involvement of hypothalamus. It also revealed fine perivenular and ring-like enhancement of the lesions.

The cervical spine imaging revealed multiple discrete short segment lesions sparing the posterior surface of the cord.

The above radiological findings initiated our search for multiple sclerosis-like lesions and a differential diagnosis of Neurobrucellosis [Figure 1].
Figure 1: MR Images of the Brain and spine reveals multiple discrete and confluent white matter lesions involving the periventricular and the subcortical white matter. In Flair Axial (Fig 1A) and the T2 weighted coronal images (Fig 1B) the hyperintense lesions are seen having the classic multiphasic, multifocal morphology similar to the Multiple sclerosis plaques. Involvement of the hypothalamus seen in fig B is however rare in MS. Post contrast T1 axial (1C) and coronal (1D) images reveals fine perivenular enhancement along with ring like enhancement of the lesions. Prominent perivenular enhancement is not a striking feature of MS lesions though the lesions are known to be perivenular. The T2 Weighted Sagittal image of the cervical spine (E) reveals multiple discrete MS like lesions sparing the posterior surface of the cord. Typical MS lesions are known to involve the posterior surface of the cord. The suspicious imaging features along with the clinical history helped us in clinching the diagnosis.

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CSF and fresh blood cultures were sterile. Serological tests such as Rose Bengal Plate Test (RBPT), Standard Tube Agglutination Test (STAT), and indirect IgG ELISA (iELISA) were carried out. PCR was performed using published genus-specific primers for amplification of  Brucella More Details bcsp31 primer pair, the amplified PCR product being sequenced by double pass analysis (Chromous Biotech Pvt. Ltd. Bangalore) subsequently submitted to the Genbank.

Central nervous system involvement is a serious complication and neurologic findings may be the only sign of brucellosis. [1] The diagnosis of neurobrucellosis requires direct or indirect evidence of Brucellae in the CSF. [1],[4] In Brucellosis, low recovery of organisms (<20%) is well known, hence not ideal for diagnosis of neurobrucellosis. [5]

Serum and CSF were positive for anti-Brucella antibodies by RBPT, iELISA with STAT titers of 1:160. Brucella-specific antibodies in the CSF is indicative of neurobrucellosis. In plasma and CSF samples, Brucella genus-specific 223bp amplicon was observed by PCR, which confirmed the presence of Brucella DNA [[Figure 2] and Accession no. HM030804]. The bcsp 31 primer-based PCR was selected owing to its high sensitivity in detection of Brucella DNA directly in the clinical specimens. [6]
Figure 2: PCR amplification of 223 bp product of partial bcsp31 gene of Brucella sp. Lane 2 and 3: 223 bp PCR amplified product from plasma and CSF of the patient; Lane M : 100 bp molecular marker; Lane 4 : Positive control B. abortus S99 strain; Lane 1 and 5: Non-template control

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Based on the clinical features, exposure to animals, image findings, antibody detection, PCR assay, and neuropsychological evaluation, it was possible to arrive at the diagnosis, thus detection of complications.

Specific treatment with doxycycline, rifampicin, and streptomycin was instituted as per recommendations. Into the follow-up, significant improvement in cognition and gait was observed with no features of peripheral neuropathy.

Neurobrucellosis, a subtle disease, is uncommon with heterogeneous clinical profile. Hence, high degree of suspicion and recognition is prudent and fundamental for accurate diagnosis and management.

 
   References Top

1.Mahboubeh HA, Mehrnaz RN, Sirous J, Mehrdad H, Abdolreza S. Clinical and laboratory findings in neurobrucellosis: Review of 31 Cases. Arch Iranian Med 2008;11:21-5.  Back to cited text no. 1
    
2.Mantur BG, Amarnath SK, Shinde RS. Review of clinical and laboratory features of human Brucellosis. Indian J Med Microbiol 2007;25:188-202.  Back to cited text no. 2
[PUBMED]  Medknow Journal  
3.Vinod P, Singh MK, Garg RK, Agarwal A. Extensive meningoencephalitis, retrobulbar neuritis, and pulmonary involvement in a patient of neurobrucellosis. Neurol India 2007;55:157-9.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
4.Yetkin MA, Bulut C, Erdinc FS, Oral B, Tulek N. Evaluation of the clinical presentations in Neurobrucellosis. Int J Infect Dis 2006;10:446-52.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Kochar DK, Agarwal N, Jain N, Sharma BV, Rastogi A, Meena CB. Clinical profile of neurobrucellosis- A report on 12 cases from Bikaner (North-West India). J Assoc Physicians India 2000;48:376-80.  Back to cited text no. 5
[PUBMED]    
6.Baily GC, Kraahn JB, Drasar BS, Stokeer NG. Detection of Brucella melitensis and Brucella abortus by DNA amplification. J Trop Med Hyg 1992;95:271-5.  Back to cited text no. 6
    

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Correspondence Address:
S Nagarathna
Department of Neuromicrobiology NIMHANS Hosur Road, Bengaluru - 560 029
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.94896

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