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Table of Contents    
LETTER TO EDITOR
Year : 2017  |  Volume : 65  |  Issue : 5  |  Page : 1142-1144

Meningitis, polyradiculopathy, and optic nerve involvement in neurobrucellosis: A rare clinical presentation


Department of Internal Medicine, Shere Kashmir Institute of Medical Sciences, Soura, Jammu and Kashmir, India

Date of Web Publication6-Sep-2017

Correspondence Address:
Waseem Dar
Department of Internal Medicine, Shere Kashmir Institute of Medical Sciences, Soura, Jammu and Kashmir
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/neuroindia.NI_127_16

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How to cite this article:
Dar W, Latief M, Dar I, Sofi N. Meningitis, polyradiculopathy, and optic nerve involvement in neurobrucellosis: A rare clinical presentation. Neurol India 2017;65:1142-4

How to cite this URL:
Dar W, Latief M, Dar I, Sofi N. Meningitis, polyradiculopathy, and optic nerve involvement in neurobrucellosis: A rare clinical presentation. Neurol India [serial online] 2017 [cited 2019 Aug 17];65:1142-4. Available from: http://www.neurologyindia.com/text.asp?2017/65/5/1142/214038


Sir,

 Brucellosis More Details is a bacterial zoonosis transmitted directly or indirectly to humans from infected animals, predominantly domesticated ruminants and swine. The disease is colloquially known as undulant fever because of its remittent character. Its distribution is worldwide apart from few countries where it has been eradicated from the animal reservoir. Although brucellosis commonly presents as an acute febrile illness, its clinical manifestations vary widely, and definitive signs indicative of the diagnosis may be lacking. Neurologic involvement is common mostly in the form of depression and lethargy. A small proportion of patients develop lymphocytic meningoencephalitis, intracerebral abscess, a variety of cranial nerve deficits, or ruptured mycotic aneurysms. Polyradiculopathy is rare. Here, we present a case of meningitis, polyradiculopathy, and toxic optic neuropathy secondary to brucellosis. Such a clinical presentation has never been reported before.

A 20-year old female engineering student presented to the Neurology Department of our hospital with complaints of fever, headache, and weakness of lower limbs of 2 weeks duration. The patient had fever 2 weeks back that was low grade and intermittent, with no diurnal variation and had responded to antipyretics. The patient also developed headache that was global, moderate in intensity, and was associated with two episodes of projectile vomiting. She also reported weakness of bilateral lower limbs, which was insidious in onset, and started with difficulty in getting up and climbing stairs. The weakness progressed to difficulty in walking. This was associated with a mild pain in both the limbs. There was no significant past medical or travel history. However, there was history of contact with domestic animals at home. On examination, the patient was conscious and oriented. Her vital parameters were stable, and respiratory and cardiovascular examinations were normal. Central nervous examination (CNS) revealed normal higher mental functions, neck stiffness, normal cranial nerves, hypotonia, depressed reflexes in lower limbs, and grade 4 power in lower limbs, along with bilateral flexor plantar responses. Baseline investigations were normal. Magnetic resonance imaging (MRI) of the brain and spine were normal. Cerebrospinal fluid (CSF) examination was performed that revealed lymphocytic pleocytosis (total cell count 150/μL with 85% lymphocytes) with high protein (360 mg/dl) and low sugar (30 mg/dl). Gram stain, acid fast bacilli (AFB) stain, and fungal stain were negative. Adenosine deaminase (ADA) was 35 U/L. CSF culture was awaited. A diagnosis of chronic meningitis with polyradiculopathy was made and the patient was put on empirical antituberculous treatment.  Brucella More Details serology was negative. The patient initially showed mild improvement; however, a few days later, she again developed fever and diminution of vision in the left eye. Fundoscopic examination revealed left sided, superior ill-defined disc margins suggestive of optic neuritis. Rest of the cranial nerves were normal. Meanwhile, CSF culture grew Brucella melitensis. Hence, our complete diagnosis was neurobrucellosis presenting as meningitis with polyradiculopathy and optic nerve involvement. Antituberculous drugs were stopped and the patient was put on methylprednisolone 1 gram daily for 3 days followed by prednisolone 60 mg/day. In addition, the patient also received doxycycline 100 mg BD, rifampicin 600 mg OD, and ceftriaxone 1 g BD for 1 month. At present, the patient is on follow up; she is doing well, is afebrile, and is able to walk with minimal support. Her visual acuity has also improved. Repeat CSF also showed improvement (total cell count 80 cells/μL with 100% lymphocytes, protein 180 mg/dl, and glucose 40 mg/dl).

Neurobrucellosis is a very serious complication of brucellosis. It can develop at any stage of brucellosis. The most frequent complication is meningitis.[1],[2],[3] Other CNS manifestations include encephalitis, meningoencephalitis, radiculitis, myelitis, peripheral and cranial neuropathies, subarachnoid hemorrhage, and psychiatric manifestations.[4] Yetkin et al., conducted a study on 305 patients of brucellosis. The rate of neurobrucellosis was 6.6%. Fever, headache, confusion, and gait disorders were the main complaints. Polyradiculopathy was seen in 2 patients.[5] A similar study was done by Kochar et al., in Bikaner, India. In a series of 175 patients, 33 (18.86%) patients were diagnosed with neurobrucellosis.

Cranial nerve involvement occurs in up to 25% of patients with neurobrucellosis, particularly the VIth and VIIIth cranial nerves. VIIIth cranial nerve palsy may be due to involvement of the central auditory pathways or ischemia of neural tissue owing to the reflex spasms caused by endotoxins. The VIth cranial nerve has the longest intracranial course, and is, therefore, susceptible to direct and indirect insults such as microvascular infarction or direct compression.[6],[7],[8] Involvement of the optic nerve in brucellosis is very rare.[9] Vinod et al., reported a patient of brucellosis who presented with extensive meningoencephalitis, retrobulbar neuritis, and pulmonary involvement. The diagnosis was made by increasing the antibody titre and the patient was successfully managed with triple drug therapy.

Clinical-radiologic correlation in neurobrucellosis varies from a normal imaging study despite positive clinical findings, to a variety of imaging abnormalities that reflect an inflammatory process, an immune-mediated process, or a vascular insult. The gold standard for the treatment of brucellosis in adults is intramuscular streptomycin (0.75–1 g daily for 14–21 days) together with doxycycline (100 mg twice daily for 6 weeks). In both clinical trials and observational studies, relapse follows such treatment in 5–10% of cases. The usual alternative regimen (and the current World Health Organization recommendation) is rifampicin (600–900 mg/d) plus doxycycline (100 mg twice daily) for 6 weeks. Significant neurologic disease due to brucella requires prolonged treatment (i.e., for 3–6 months), usually with ceftriaxone supplementation. The duration of therapy is generally individualized according to the clinical signs and symptoms and continues until CSF parameters return to normal.

Brucellosis is a common disease in cattle rearing areas of the world. Signs and symptoms are usually nonspecific and nonfocal. Neurobrucellosis is an important complication and needs a high index of suspicion because diagnostic modalities may not reveal anything. Polyradiculopathy and optic nerve involvement are rare. Treatment is prolonged, and the prognosis is usually good.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Young EJ. Brucella species. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 7th ed. Philadelphia: Churchill Livingstone; 2010. p. 2921-5.  Back to cited text no. 1
    
2.
Pappas G, Akritidis N, Bosilkovski M, Tsianos E. Brucellosis. N Engl J Med 2005;352:2325-36.  Back to cited text no. 2
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3.
McLean DR, Russell N, Khan MY. Neurobrucellosis: Clinical and therapeutic features. Clin Infect Dis 1992;15:582-90.  Back to cited text no. 3
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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
    
5.
Kochar DK, Gupta BK, Gupta A, Kalla A, Nayak KC, Purohit SK. Hospital-based case series of 175 cases of serologically confirmed brucellosis in Bikaner. J Assoc Physicians India 2007;55:271-5.  Back to cited text no. 5
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6.
Karakurum Goksel B1, Yerdelen D, Karatas M, Pelit A, Demiroglu YZ, Kizilkilic O, et al. Abducens nerve palsy and optic neuritis as initial manifestation in brucellosis. Scand J Infect Dis 2006;38:721-5.  Back to cited text no. 6
    
7.
Abd Elrazak M. Brucella optic neuritis. Arch Intern Med 1991;151:776-8.  Back to cited text no. 7
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8.
Romero M, Sãnchez F, Fernãndez-Bolaños R, Jiménez MD. Optic neuritis as a clinical manifestation of neurobrucellosis. Rev Neurol 1999;28:438.  Back to cited text no. 8
    
9.
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. 9
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