Recurrent transverse myelitis following neurobrucellosis: Immunologic features and beneficial response to immunosuppression

Chitra Krishnan, Adam I. Kaplin, Jerome S. Graber, Jessica S. Darman, Douglas A. Kerr

Research output: Contribution to journalArticlepeer-review

37 Scopus citations

Abstract

The authors report the clinical course and immune system response of a patient with disease-associated recurrent transverse myelitis (TM) following cerebral infection with Brucellosis melitensis. The patient suffered four recurrences of his TM (each at a distinct spinal cord level) over the course of 2 years following his initial presentation, which ultimately progressed to quadriplegia. He had progressively declining cerebrospinal fluid (CSF) brucella antibody titers, suggesting a postinfectious, rather than an infectious, etiology. The authors simultaneously examined the expression of multiple cytokines in the CSF of this patient using cytokine antibody arrays and found a marked elevation of interleukin (IL)-6, IL-8, and macrophage chemoattractant protein (MCP)-1 levels relative to controls. Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of the CSF confirmed a 1700-fold elevation of IL-6 and more modest elevations of IL-8 and MCP-1. IL-6 levels returned to baseline following treatment of the patient with intravenous cyclophosphamide and plasma exchange and the patient experienced a significant and sustained recovery of function.

Original languageEnglish (US)
Pages (from-to)225-231
Number of pages7
JournalJournal of NeuroVirology
Volume11
Issue number2
DOIs
StatePublished - Apr 2005
Externally publishedYes

Keywords

  • Cytokine
  • IL-6
  • Immunosuppression
  • Neurobrucella
  • Plasma exchange
  • Recurrent
  • Transverse myelitis

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Virology

Fingerprint

Dive into the research topics of 'Recurrent transverse myelitis following neurobrucellosis: Immunologic features and beneficial response to immunosuppression'. Together they form a unique fingerprint.

Cite this