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Letter
“Acute” West Nile Virus Encephalitis
(Response to Krishnamoorthy et al.)
Read original letter,
http://www.cdc.gov/ncidod/EID/vol8no12/02-0532.htm
Read Krishnamoorthy's
letter, http://www.cdc.gov/ncidod/EID/vol9no5/03-0018.htm
Alexander Hindenburg* and Cinnia Huang†
*Winthrop University Hospital, Mineola, New York, USA; and †New York State
Department of Health, Albany, New York, USA
Suggested citation for this article: Hindenburg A, Huang
C. "Acute" West Nile virus encephalitis (response to Krishnamoorthy
et al.). Emerg Infect Dis [serial online] 2003 Apr [date cited]. Available
from: URL: http://www.cdc.gov/ncidod/EID/vol9no4/03-0128.htm
To the Editor: In a letter to the editor, Krishnamoorthy et al.
question the diagnosis of “acute West Nile encephalitis” in our case report.
We did not use the word “acute” in the paper, but the patient did in fact
have an acute illness. We believe that this case report, in which West
Nile virus (WNV) was isolated in cell culture, represents the best evidence
for a WNV infection in a human in the United States. The diagnosis of
West Nile encephalitis was based on clinical analysis (1);
not everyone with the diagnosis undergoes an autopsy. In many instances,
patients do recover. In our case, the patient had the clinical features
of encephalitis consisting of unremitting fever associated with a rapid
course of progressive confusion and lethargy followed by coma. In addition,
increased depression of respiratory drive existed, pointing to brain stem
involvement. We agree that the inflammatory changes in the brain were
limited as compared to such changes in other reported cases of WNV; however,
this limitation was attributable to the fact that the patient was both
immunocompromised and neutropenic at the time of acute infection. Therefore,
the usual inflammatory response cannot be expected. Even though the changes
were limited, they were consistent with the histologic findings in previously
published reports (1,2).
The second point by Krishnamoorthy et al. represents their hypothesis
about a human chronic carrier state for WNV. Although a chronic carrier
state is possible, the viremic period associated with arboviral infections
is typically short (3). While one cannot rule out persistent
infection with WNV, until our report attempts to recover the virus by
isolation in North America in humans have been uniformly unsuccessful.
Also, previous reports of successful WNV isolations by Israeli investigators
in immunocompetent hosts (4) have been from blood specimens
before seroconversion. These considerations indicate that the virus is
not routinely found in the blood in substantial amounts by the time clinical
symptoms consistent with WNV infection occur. We do not know, nor have
we speculated, about the timing of the infection as the patient had no
recollection of a mosquito bite. Tests for both immunoglobulin (Ig) G
and IgM antibodies to WNV were negative in our patient. Because the patient
was immunocompromised, a humoral response was not expected; therefore,
this information cannot be used as evidence that the patient had an acute
infection. However, observations that the patient had no manifestation
of encephalitis during a previous episode of neutropenia and that she
had an acute febrile illness associated with neurologic signs of encephalitis
point to an acute infection. The figure, in which WNV copy numbers are
correlated with leukocyte count, is not intended to pinpoint the time
of infection. However, as stated in the paper, this figure did show that
the virus was rapidly cleared after resolution of neutropenia.
A report by Camenga et al. (5) demonstrated that mice,
infected with WNV develop only an inapparent infection. These mice will
invariably die of fulminant encephalitis if only a single dose of cyclophosphamide
is given. However, mice treated with one dose of cyclophosphamide demonstrate
inflammatory changes in the brain. If a second dose of the drug is administered
5 days after infection, inflammation is completely suppressed in mice.
Although mice are immunologically different from humans, this work, done
almost 30 years ago, supports the argument for an acute infection in the
current case report. If the patient in our study was a chronic carrier,
she should have had manifestations of acute West Nile encephalitis immediately
following the first course of combination chemotherapy, which was much
more immunosuppressive than cyclophosphamide alone. This fact reemphasizes
our major point in the article that patients who are immunocompromized
and undergoing chemotherapy, which may cause neutropenia, should take
extra precautions against being exposed to WNV.
References
- Shieh WJ, Guarmer J, Layton M, Fine A, Miller J, Nash
D, et al. The
role of pathology in an investigation of an outbreak of West Nile encephalitis
in New York, 1999. Emerg Infect Dis 2000;6:370–2.
- Sampson BA, Armbrustmacher V. West Nile encephalitis. The
neuropathology of four fatalities. Ann NY Acad Sci 2001;951:172–8.
- Southam CM, Moore AE. Induced virus infections in man by the Egypt
isolates of West Nile virus. Am J Trop Med Hyg 1954;3:19–50.
- Hindiyeh M, Shulman LM, Mendelson E, Weiss L, Grossman Z, Bin H. Isolation
and characterization of West Nile virus from the blood of viremic patients
during the 2000 outbreak in Israel. Emerg Infect Dis 2001;7:748–50.
- Camenga DL, Nathanson N, Cole GA. Cyclophosphamide-potentiated
West Nile viral encephalitis: relative influence of cellular and humoral
factors. J Infect Dis 1974;130:634–41.
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