LETTER TO THE EDITOR
Year : 2021 | Volume
: 12 | Issue : 1 | Page : 46--47
Neurobrucellosis presenting as guillain–Barre syndrome
Abhishek Juneja1, Kuljeet Singh Anand1, Ritu Yadav2, Jyoti Garg1,
1 Department of Neurology, Dr. RML Hospital, New Delhi, India
2 Department of Pulmonary Medicine, Dr. RML Hospital, New Delhi, India
Dr. Abhishek Juneja
Department of Neurology, Dr. RML Hospital, New Delhi - 110 001
|How to cite this article:|
Juneja A, Anand KS, Yadav R, Garg J. Neurobrucellosis presenting as guillain–Barre syndrome.Indian J Med Spec 2021;12:46-47
|How to cite this URL:|
Juneja A, Anand KS, Yadav R, Garg J. Neurobrucellosis presenting as guillain–Barre syndrome. Indian J Med Spec [serial online] 2021 [cited 2022 Jan 18 ];12:46-47
Available from: http://www.ijms.in/text.asp?2021/12/1/46/306247
We report a case of a 38-year-old male patient, farmer by occupation, presenting with fever, chills, myalgia, and headache for 10 days and yellowish discoloration of urine for 4 days. There was a history of consuming unpasteurized raw milk for the past many years. On examination, the supine blood pressure was 106/62 mmHg, heart rate 104/min, and axillary temperature 102.2°F; mild icterus and conjunctival injection were present. The routine blood investigations revealed hemoglobin 12.6 g/dL, total leukocyte count 9600/mm3, bilirubin total 2.8 mg/dL, direct bilirubin 1.5 mg/dL, and serum glutamic oxaloacetic transaminase/serum glutamic pyruvic transaminase 76/54 IU/L. Serum lactic dehydrogenase, creatine kinase, and creatinine levels were normal. Viral testing for dengue, hepatitis B, hepatitis C, and human immunodeficiency virus were negative. Malarial antigen, typhidot, leptospiral, scrub typhus, and treponemal serology were also negative. Brucella IgM antibody titers were raised (1:1280; N < 1:40) by enzyme-linked immunosorbent assay. He was treated with intravenous (IV) ceftriaxone (2 g daily), oral rifampicin (600 mg once daily), and oral doxycycline (100 mg twice daily). Fever responded within 2 weeks of antibiotic therapy, but subsequently, he developed symmetric ascending flaccid quadriparesis with bilateral facial weakness. The deep tendon reflexes were absent, with bilateral flexor plantar response. Nerve conduction studies suggested demyelinating polyneuropathy involving the motor nerves. Cerebrospinal fluid (CSF) examination showed albuminocytological dissociation (2 mononuclear cells, protein –92 mg/dL) and normal glucose. The patient was treated with IV immunoglobulin at a dose of 2 g/kg body weight over 5 days. The patient regained complete motor strength over the next 4 weeks. He was advised to take oral rifampicin and doxycycline for the next 8 weeks to complete the antibiotic therapy.
Brucellosis is a common bacterial zoonotic disease with widespread geographical distribution; however, there are only few reports on neurobrucellosis.[1-3] Neurological complications in brucellosis are infrequent (2'–5') with variable presentation involving both central and peripheral nervous systems. Central nervous system involvement usually presents as acute meningoencephalitis, whereas the involvement of the peripheral nervous system usually presents as polyradiculopathy and less commonly as cauda equine-like syndromes and peripheral mononeuritis. The occurrence of polyradiculopathy during the acute phase of illness may be due to the immunologic and inflammatory reactions of the host to the bacteria. Brucella infection may trigger an immune-mediated demyelination such as Guillain–Barre syndrome (GBS). GBS is an acute inflammatory polyradiculoneuropathy characterized by rapidly progressive, ascending, symmetric weakness and areflexia. It is preceded, in most of the cases, by a gastrointestinal or respiratory infection such as Campylobacter jejuni, Chlamydia, or Mycoplasma. The pathogenesis of GBS is still not entirely clear; molecular mimicry has been suggested as a possible underlying mechanism, through the synthesis of autoantibodies against myelin gangliosides. Our case presented with symptoms consistent with neurobrucellosis and subsequently developed acute progressive, ascending, symmetric weakness and areflexia that were compatible with a diagnosis of GBS. The electrodiagnostic findings of demyelinating polyneuropathy involving the motor nerves and the albuminocytologic dissociation in the CSF supported our diagnosis. In our case, Brucella-induced GBS resolved with proper and early management.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
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