Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 10, Number 3—March 2004

West Nile Poliomyelitis

On This Page
Article Metrics
citations of this article
EID Journal Metrics on Scopus

Cite This Article

To the Editor: In the July 2003 article, “Acute Flaccid Paralysis and West Nile Virus Infection” (1), Sejvar et al. reported seven patients with acute onset of asymmetric weakness and areflexia but no sensory abnormalities. The authors also referenced three previously reported cases of West Nile virus (WNV)–associated flaccid paralysis and argued that all of these symptoms could be explained by anterior-horn cell loss. The two cases of spinal cord pathologic findings published to date demonstrated focal loss of anterior-horn neurons (2,3). We report a case of West Nile poliomyelitis with preserved deep-tendon reflexes, diminished sensory nerve action potentials, and pathologic findings which do not localize to the anterior horn.

An 83-year-old woman sought treatment at the hospital on September 12, 2002, with 3 days of fever, acute confusion, nausea, vomiting, and profound weakness. Computed tomography (CT) of the head was unremarkable. Her examination was notable for dysarthria, tremors, and global weakness with rightsided predominance. Cerebrospinal fluid contained 75 leukocytes/mm3 (84% neutrophils), glucose 88 mg/dL, and protein 97 mg/dL. On the second hospital day, respiratory failure developed, requiring mechanical ventilation. Electrodiagnostics performed on hospital day 7 demonstrated reduced motor and sensory amplitudes on right median and ulnar nerves, reduced motor amplitudes, and mildly reduced conduction velocities in the right peroneal nerve and right posterior tibial nerves. These findings suggested a predominantly axonal polyneuropathy involving both sensory and motor nerves. No myopathic process was demonstrated. Serum antibodies for WNV (immunoglobulin [Ig] M capture enzyme-linked immunosorbent assay [ELISA] 73.8; IgG capture ELISA 0.738) and cerebrospinal fluid antibody titer (IgM capture ELISA 200.5) were both positive. Weakness, respiratory failure, and preserved deep-tendon reflexes persisted.

On hospital day 15, the patient died after withdrawal of support. Sections from the postmortem medulla and spinal cord were positive for WNV RNA by reverse transcription–polymerase chain reaction testing at the state laboratory. The brain demonstrated characteristic microglial nodules and perivascular lymphocytic infiltrates (4). Spinal cord sections showed leptomeningeal and parenchymal chronic inflammatory infiltrates, often perivascular in location. Patchy cellular infiltration was found throughout the spinal cord, without a predilection for the anterior-horn. Spinal nerve roots demonstrated focal lymphocytic inflammation within the endoneurial compartment. No evidence of a demyelinating process was found.

Our data contradict the thesis proposed by Sejvar et al. that West Nile poliomyelitis is restricted to the anterior-horn (1). The electrodiagnostics showing axonal polyneuropathy and the spinal cord pathologic findings, which did not demonstrate focal loss of anterior-horn neurons, suggest a broader spectrum of the clinical-pathological syndrome of West Nile poliomyelitis than previously described (2,3). Our findings conform to the hypothesis outlined by Jeha et al., which favors a more widespread myelitis (5). We also confirm the findings of preserved deep-tendon reflexes in West Nile poliomyelitis first reported by Glass et al. (6).


Robert P. Holman*Comments to Author , Nicole M. Monserrate*, Eric W. Czander*, and Elisabeth J. Rushing†

Author affiliations: *Virginia Hospital Center, Arlington, Virginia, USA; †Armed Forces Institute of Pathology, Walter Reed Army Medical Center, Washington, DC, USA



  1. Sejvar  JJ, Leis  AA, Stokic  DS, Van Gerpen  JA, Marfin  AA, Webb  R, Acute flaccid paralysis and West Nile virus infection. Emerg Infect Dis. 2003;9:78893.PubMed
  2. Kelley  TW, Prayson  RA, Isada  CM. Spinal cord disease in West Nile virus infection [letter]. N Engl J Med. 2003;348:5645. DOIPubMed
  3. Kelley  TW, Prayson  RA, Ruiz  AI, Isada  CM, Gordon  SM. The neuropathology of West Nile virus meningoencephalitis: a report of two cases and review of literature. Am J Clin Pathol. 2003;119:74953. DOIPubMed
  4. Sampson  BA, Ambrosi  C, Charlot  A, Reiber  K, Veress  JF, Armbrustmacher  V. The pathology of human West Nile virus infection. Hum Pathol. 2000;31:52731. DOIPubMed
  5. Jeha  LE, Sila  CA, Lederman  RJ, Prayson  RA, Isada  CM, Gordon  SM. West Nile virus infection: a new acute paralytic illness. Neurology. 2003;61:559.PubMed
  6. Glass  JD, Samuels  O, Rich  MM. Poliomyelitis due to West Nile virus [letter]. N Engl J Med. 2002;347:12801. DOIPubMed


Cite This Article

DOI: 10.3201/eid1003.030593

Related Links


Table of Contents – Volume 10, Number 3—March 2004


Please use the form below to submit correspondence to the authors or contact them at the following address:

Robert P. Holman, 1715 N. George Mason Dr., Suite 108, Arlington, VA 22205, USA; fax: 703-558-6657

James J. Sejvar, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop A39, 1600 Clifton Road, Atlanta, GA 30333, USA; fax: 404-639-3838

Send To

10000 character(s) remaining.


Page created: April 23, 2012
Page updated: April 23, 2012
Page reviewed: April 23, 2012
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.