• Print ISSN: 2395 - 1400, Online ISSN: 2455 - 8923

Case Report

Neurobrucellosis - A Case Report

S.Mohammad Ali1; *A.Satya Srinivas2; U.Gangaram3M; S.Srinivas Aditya3

1Assistant professor, Department of Pathology, Kamineni Institute of Medical Sciences, NKP, Telangana, 2Associate professor, Department of Pathology, Sri Devaraj Urs Medical College, Kolar, Karnataka, 3 Professor and HOD, Department of Pathology, Sri Devaraj Urs Medical College, Kolar, Karnataka

*Corresponding Author :

Dr. U. Gangaram,
Post Graduate Department of Medicine
Kamineni Institute of Medical Sciences Narketpally, Nalgonda Dist 508 254, Telangana


Background: :Brucellosis is rare in A.P and high degree of suspicion is necessary to identify this disease.

Patient: A 23 years old male farmer, presented with headache, vomiting, and paresthesias. Severe occipital headache.On physical exam illness, weakness, fever, wet skin, soft spleenomegaly were detected. He had positive Wright test (1/1250) and lymphocytic pleocytosis in CSF. Three drug regimen and steroid (1st month) were administered for 2 months and he responded well to this therapy.

Conclusion: Our patient showed progressive improvement in neurological manifestations under steroid and 3 antibiotic regimen treatment over a period of 2 months which along with history of goat milk consumption confirmed our diagnosis of Neurobrucellosis.

Keywords: Neurobrucellosis.


Brucellosis is a common zoonotic and an important occupational disease in our country1 .Animals are most exclusively source of infection for people.The major reservoirs include goats and sheep (B.melitensis), cattle (B.abortus), swine (B.suis), and dogs (B.canis). Infection occours through consumption of infected raw milk and their products or raw meat also.It is transmitted by direct contac with infected animals or abortive material. It presents as acute, subacute and chronic courses by involving different systems with varied manifestations. CNS involvement is important clinically and occurs in 2-12% of cases2,3,4. Brucellosis and neurobrucellosis are more common in second to forth decades5.Involvement of entire central and peripheral nervous system and also psychologic disturbancescan occur. Every patient with neurologic manifestations in endemic areas should be ruled out for brucellosis. For susceptible cases, travel history, occupation, and similar symptoms in other family members should be sought. Isolation of organism from blood,cerebrospinal fluid (CSF), and bone marrow; and serum antibody detection could establish the diagnosis2,5.


A 23 years old farmer was admitted because of Illness,weakness and paresthesias. Disease had begun 1month ago by weakness, fever, chills and orchitis which regressed after he received 1 week treatment. One month later, orchitis resolved but severe headache in occipital region, blurred vision, epigastric pain and vomiting were added. His past medical history was unremarkable.He is a shepherd by occupation. History of regular contact with sheep and consumption of its milk is present His brother had brucellosis one year ago. His sheep experienced abortion and death. On physical examination he was conscious, very ill, afebrile with soft spleenomegaly epigastric tenderness, bilateral papillary edema with direct and indirect light reflex,visual field is normal, visual acuity of 6/10, no meningeal and cerebellar signs. Paraclinical findings included normal complete blood count, urine analysis,chest-x ray,

echocardiography, electroencephalography, brain CT, abdominopelvic sonography, and erythrocyte sedimentation rate=15. megaloblastic anemia is present. Abnormal findings were: standard tube agglutination (STA)=3/1280. Treatment was commenced with streptomycin, rifampin, doxycycline, omeperazole and dexamethasone. CSF analysis for chronic meningitis was negative for biochemical abnormalities. At the end of the first month, prednisolone and streptomycin were discontinued and treatment was continued with 3 drugs (doxycycline, rifampin and ceftriaxone). Two months later, he was discharged with good health and was followed up. Three drugs were used for 2months with no side effect. All signs and symptoms were resolved. Although DNA-PCR was not done in our patient due to unavailability with the above history of consumption of goat milk, severe occipital head ache, paresthesias, diplopia, examination finding of soft spleenomegaly and positive STA in CSF, the patient was diagnosed to be having Neurobrucellosis.


Brucellosis could present with multiple clinical manifestations in different systems and may occur in different courses like peripheral neuropathy,lymphocytic meningoencephalitis,en docarditis and motor weakness2.Our patient was visited many times with physician with no attention to brucellosis in his brother and history of death and abortion in his sheep, therefore diagnosis and treatment was delayed for 1 month. It is demonstrated that antiplasmic protein antibody against Brucella spp. by ELISA, Western Blot of CSF in brain involvement7 , and imaging may not have correlation with clinical manifestations8. Our patient has normal brain CT and positive SAT (1/40) in CSF analysis. Meanwhile, paresthesias that was presented in our patient is a consequence of peripheral neuropathy which is seen in in brucellosis9, however, sporadic cases with brucellosis were also reported since 198610. This patient had second nerve involvement as papillary edema and blurred vision for 1month, and meningeal signs (headache, vomiting) resolved at the end of the first week. Early treatment resulted in complete papillary edema resolution5

  1. Saebi E, editor. Infectious diseases in Iran. 1st edition. Tehran: Arjmand Publication; 1994.
  2. Mandell GL, Bennet JE, Dolin R, editors. Principle and practice of infectious disease. 6th edition. Philadelphia: Churchill Livingstone, 2005.
  3. Bodur H, Erbay A, Akinci E, et al. Neurobrucellosis in an endemic area of brucellosis. Scand J Infect Dis 2003;35(2):94-7.
  4. Hajabdolbaghi M, Hasibi M. A significant case ofneurobrucellosis and review of literature. National Iranian Congress on Brucellosis. Shahid Beheshti Medical University, Tehran, Iran. 5-6 July, 2005.
  5. http://www.emedicine.come/neuro/tropic42htm.
  6. Kochar DK. Meningoencephalitis in brucellosis. Neurology India 2000;48(2):170-3.
  7. Baldi PC, Araj GF, Racaro GC, et al. Detection of antibodies to brucella cytoplasmic proteins in CSF of patients with neurobrucellosis. Clin Diag Lab Immunol 1999;6(5):756-9.
  8. Al-Sous MW, Boheleqa S, Al-Kawi MZ, et al. Neurobrucellosis: clinical and neuroimaging correlation. Am J Neuroradiol 2004;25(3):395-401.
  9. Bradley WG, Daroff RB, editors. Neurology in clinical practice. 4th edition. Philadelphia: Butter Worth Heinemann, 2004.
  10. Mousa AR. Brucella meningitis: presentation, diagnosis and treatment. Q J Med 1986;60(233):573-85.
  11. Ropper AH, Brown RH, editors. Adams and Victor's principles of neurology. 8th edition. New York: Mc Graw Hill, 2005.
  12. Marcos SF, Ucelay JF, Sanchez J, et al. Tremor as initial manifestation of neurobrucellosis. Ann Med Intern 1990;7(10):540-50.
  13. Koussa S. Neurobrucellosis: clinical features and therapeutic responses in 15 patients. Rev Neurol 2003;159(12):1148-55.