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Letter
West Nile Poliomyelitis
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,* Nicole M. Monserrate,* Eric W. Czander,* and Elisabeth
J. Rushing†
*Virginia Hospital Center, Arlington, Virginia, USA; and †Armed Forces
Institute of Pathology, Walter Reed Army Medical Center, Washington, DC,
USA
Suggested citation
for this article:
Holman RP, Monserrate NM, Czander EW, Rushing EJ. West Nile poliomyelitis.
Emerg Infect Dis [serial online] 2004 Mar [date cited]. Available
from: http://www.cdc.gov/ncidod/EID/vol10no3/03-0593_03-0887.htm
References
- Sejvar JJ, Leis AA, Stokic DS, Van Gerpen JA, Marfin
AA, Webb R, et al. Acute
flaccid paralysis and West Nile virus infection. Emerg Infect Dis
2003;9:788–93.
- Kelley TW, Prayson RA, Isada CM. Spinal
cord disease in West Nile virus infection [letter]. N Engl J Med
2003;348:564–5.
- 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;119:749–53.
- Sampson BA, Ambrosi C, Charlot A, Reiber K, Veress JF, Armbrustmacher
V. The
pathology of human West Nile virus infection. Hum Pathol 2000;31:527–31.
- Jeha LE, Sila CA, Lederman RJ, Prayson RA, Isada CM, Gordon SM. West
Nile virus infection: a new acute paralytic illness. Neurology 2003;61:55–9.
- Glass JD, Samuels O, Rich MM. Poliomyelitis
due to West Nile virus [letter]. N Engl J Med 2002;347:1280–1.
Back to Top
In Reply: The letter by Holman, et al., (1)
in this edition of Emerging Infectious Diseases continues to broaden the
scope of illness attributable to West Nile virus (WNV) infection. However,
we would like to take the opportunity to clarify the conclusions drawn
from our article, “AFP and West Nile virus infection” (2).
In this article, we reported on seven patients, all of whom had asymmetric
weakness without sensory loss, which evolved acutely over the course of
several hours. Electrodiagnostic studies of all patients displayed markedly
reduced compound motor axon potentials with preserved sensory nerve action
potentials; the results were interpreted as consistent with a process
primarily localized to the motor axons or, far more likely, given the
clinical scenario and pathologic data from WNV-infected animals, the anterior
horn cells of the spinal cord. These findings were later substantiated
by Li et al. (3). Subsequently, Jeha et al. expanded
the scope of illness producing WNV-associated flaccid paralysis by describing
several patients with predominant myeloradiculitis (4).
The patient presented by Holman clearly seems to have a condition that,
as shown by electrodiagnostics and pathology, localizes to other areas,
in addition to spinal anterior horn cells. However, rather than suggesting
that a single case report “contradicts” the anterior horn cell hypothesis,
we suggest that WNV-associated flaccid paralysis be viewed as having a
spectrum of causes, one of which certainly is poliomyelitis like illness.
The neuropathologic findings in poliomyelitis (due to poliovirus, WNV,
or other viruses) are not restricted focally to the anterior horn cells
(5). Demonstrating pathologic changes as well as focal
anterior horn cell loss in the patient referenced by Holman is in keeping
with neuropathologic findings in poliomyelitis. Additionally, the presence
of a diffuse axonal polyneuropathy cannot be concluded from Holman’s data.
Reduced compound motor axon potentials and slowing of conduction velocity
could certainly be seen in pathologic conditions affecting anterior horn
cells or spinal nerve roots. In addition, reduced sensory nerve action
potentials in the median and ulnar nerves alone, without documentation
of neuropathy in additional nerves, cannot be used as evidence of a diffuse
axonal polyneuropathy, since both of these nerves are commonly prone to
entrapment neuropathies. Finally, the context in which the preservation
of this patient’s reflexes is observed remains unclear. Preserved “normal”
deep-tendon reflexes, in the setting of disease that interrupts the reflex
arc at any point, are incongruous with established physiologic and clinical
concepts.
The seven patients observed by our group clearly had a distinct clinical
syndrome with similar clinical findings and electrodiagnostic results.
However, as demonstrated by prior reports (3,5–7), multiple
mechanisms may lead to WNV-associated flaccid paralysis. In fact, we acknowledge
a spectrum of cord, root, and nerve involvement with WVN flaccid paralysis.
James J. Sejvar,* Arturo Leis,† Jay A. Van Gerpen,‡ Anthony A. Marfin,§
and Lyle R. Petersen§
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †Methodist
Rehabilitation Center, Jackson, Mississippi, USA; ‡Ochsner Clinic, New
Orleans, Louisiana, USA; and §Centers for Disease Control and Prevention,
Fort Collins, Colorado, USA
Suggested citation
for this article:
Sejvar JJ, Leis A, Van Gerpen JA, Marfin AA, Petersen LR. West Nile
poliomyelitis. Emerg Infect Dis [serial online] 2004 Mar [date cited].
Available from: http://www.cdc.gov/ncidod/EID/vol10no3/03-0593_03-0887.htm
References
- Holman RP, Monserrate NM, Czander EW, Rushing EJ.
West Nile poliomyelitis. Emerg Infect Dis 2004;10:547–8.
- Sejvar J, Stokic D, Van Gerpen J, Marfin A, Webb R, et al. AFP
and West Nile virus infection. Emerg Infect Dis 2003;9:788–93.
- Li J, Loeb J, Shy M, Shah A, Tselis A, Kupski W, et al. Asymmetric
flaccid paralysis: a neuromuscular presentation of West Nile virus infection.
Ann Neurol 2003;53:703–10.
- Jeha L, Sila C, Lederman R, Prayson R, Isada C, Gordon S. West
Nile virus infection: a new acute paralytic illness. Neurology 2003;61:55–9.
- Paul J. A history of poliomyelitis. New Haven (CT): Yale University
Press; 1971. p. 1–9.
- Ohry A, Karpin H, Yoeli D, Lazari A, Lerman Y. West
Nile virus myelitis. Spinal Cord 2001;39:662–3.
- Gadoth N, Weitzman S, Lehmann E. Acute
anterior myelitis complicating West Nile fever. Arch Neurol 1979;36:172–3.
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