West Nile Virus:Preparing for the Sequel
abstract & commentary
In august 1999, a hospital in queens, new york, admitted five patients with fever, weakness, and confusion. Ultimately, four of the five developed flaccid paralysis and required mechanical ventilation. Shortly after, three less severe cases presented to the hospital’s emergency room. Concurrently, a pathologist at the Bronx Zoo noticed birds that were dying from a neurological disorder.1 Tissue samples resembled the St. Louis encephalitis virus. The Centers for Disease Control (CDC) in Atlanta confirmed that the New York City patients were infected by the same virus as the birds and proved to be 99.8% homologous to a West Nile virus (WNV). WNV was subsequently confirmed in several horses on the North Shore of Long Island and a domestic cat in New Jersey.2
How did the virus get to New York City? The summer had been unusually dry and hot, which may have contributed to the outbreak. One consideration was that an infected, incoming person was bitten by a mosquito here, which transmitted the virus through birds to other persons. Possibly, the virus was lurking in or around the city for years without detection.1 Other possible sources included an infected bird (either migrated or imported from an endemic region), infected mosquitoes, and least likely, a viremic person.3
Once infected with WNV, the incubation period generally lasts 5-15 days, at which time an abrupt, wide array of symptoms invariably affect different persons. Characteristically, WNV causes fever of up to 104°, which lasts from 3-5 days with or without chills. Other influenza-like symptoms may include frontal headache, sore throat, backache, myalgia, arthralgia, fatigue, conjunctivitis, and ocular pain. About half the cases develop maculopapular or roseolar rashes that spread from the trunk to the extremities and head. Lymphadenopathy, anorexia, nausea, abdominal pain, diarrhea, and respiratory symptoms are frequent. Rarely, WNV can cause acute aseptic meningitis, encephalitis, and/or signs of increased intracranial pressure. Hepatosplenomegaly, hepatitis, pancreatitis, and myocarditis have occurred. Infected birds show no symptoms, but horses may show fever, staggering gait, weakness, and hind leg paralysis.
Among the eight initial New York City patients, seven had fever higher than 101°, four had frontal headache, and two had stiff neck. Among six with mental status abnormalities, three proceeded to coma and death. One had a maculopapular rash across her back, seven had either abdominal pain and/or diarrhea, and four developed severe muscle weakness.3 Lumbar puncture in all eight cases showed cerebrospinal fluid (CSF) pleocytosis, with lymphocytic predominance and normal protein and glucose typical of a viral meningitis. A disturbing finding in the New York patients was that three of the eight patients were thought to have Guillain-Barré syndrome (GBS) prior to WNV diagnosis.3 Two of the three died, and the other now walks with a quad cane, has left-sided weakness, and episodic memory loss. GBS-like symptoms have been rarely associated with other Flaviviruses such as Japanese encephalitis and dengue fever, but not with WNV.3 Lumbar puncture in all eight cases showed CSF pleocytosis, with lymphocytic predominance and normal protein and glucose typical of a viral meningitis, but not of GBS.
All three of the eight fatalities were elderly, with ages older than 75 years. Two had a history of cancer. During the 1996-1997 Romanian outbreak, 17 died, all older than 50 years. Gender was similar.
Following the above, the New York City Department of Health (NYCDOH) alerted all nearby hospitals to report anyone with the following: 1) a clinical syndrome of fever plus altered mental status, CSF pleocytosis, and muscle weakness; 2) presumed viral encephalitis; 3) fever and presumed GBS; and 4) aseptic meningitis. After the alert, hospitals reported many suspected cases, confirming the infection in 61 patients, with seven deaths. Treatment was symptomatic and included a varying combination of IV ampicillin, ceftriaxone, acyclovir, plasmapheresis, or IV immunoglobulin. None induced a definitive response. The NYCDOH also recommends that public health agencies take preparatory action at the first signs of danger. Four approaches are suggested: 1) education; 2) larval habitat source reduction; 3) larval mosquito control; and 4) adult mosquito control. Mosquito activity begins in the spring and lasts until several weeks after the first frost.
The CDC confirms the WNV diagnosis by any of the following:
• A fourfold rise in serum antibody titer.
• Isolation of WNV from tissue, blood, CSF, or other body fluids, which demonstrate the viral genome sequence.
• Capture of IgM antibody in CSF or serum by use of ELISA.4 —emt & rrt
References
1. Enserink M. New York’s lethal virus came from Middle East, DNA suggests. Science 1999;286:1450-1451.
2. New York State Department of Health. 2000. Draft for New York State West Nile virus response plan. Online. Available: http://www.health.state.ny.us/nysdoh/westnile/intro.htm and http://www.health.state.ny.us/nysdoh/westnile/prevresp.htm.
3. Asnis DS, et al. The West Nile virus outbreak of 1999 in New York: The Flushing Hospital experience. Clin Infect Dis 2000;30:413-418.
4. CDC. 1999. MMWR Morb Mortal Wkly Rep 1999;48: 845-849; MMWR Morb Mortal Wkly Rep 1997;46:1-55.
5. Hubalek Z, Halouzka J. West Nile fever—A reemerging mosquito-borne viral disease in Europe. Emerg Infect Dis 1999;5:643-650.
Which of the following is true regarding the 1999 New York City epidemic of West Nile-like viral encephalitis?
a. Most infected patients were febrile.
b. Mortality is approximately 10%.
c. Some patients were initially suspected to have Guillain-Barré syndrome.
d. Symptoms of the New York City cases may be different from other worldwide epidemics.
e. All of the above
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