from Epidemiological
Bulletin, Vol. 21 No. 4, December 2000
West Nile Virus in the Americas
West Nile Fever is a disease caused by the West Nile (WN) virus,
a flavivirus belonging taxonomically to the Japanese Encephalitis serocomplex.
It is a vector-borne disease that is transmitted to a wide range of vertebrates
by infected mosquitoes. Because of spatial and temporal proximity of avian and
human infections, epidemiologists have concluded that transmission follows an
enzootic cycle. Birds act as natural reservoir hosts infecting mosquitoes, which
in turn infect vertebrates (1).
In humans, the WN virus usually produces either asymptomatic
infection or mild febrile illness. Symptoms of infection include fever, headache,
and body aches, occasionally with skin rash and swollen lymph glands. More severe
infection may be marked by headache, high fever, neck stiffness, stupor, disorientation,
coma, tremors, convulsions, muscle weakness, paralysis and rarely death (2).
Meningoencephalitis is an occasional complication of this disease. Case definitions
of probable and confirmed cases have been developed by the United States Centers
of Disease Control and Prevention (CDC) (Table
1).
The WN virus was first isolated from an adult woman in the West
Nile District of Uganda in 1937. The first recorded epidemics of West Nile fever
occurred in Israel during the 1950’s. During this time, the virus became recognized
as a cause of severe human meningoencephalitis. Subsequently, its presence was
noted in Egypt, Israel, India and areas of Africa. In 1974, the largest known
epidemic caused by WN virus occurred in South Africa. Recent outbreaks of WN
viral encephalitis in humans have occurred in Algeria in 1994, Romania in 1996-1997,
the Czech Republic in 1997, the Democratic Republic of the Congo in 1998, Russia
in 1999, the United States in 1999-2000 and Israel in 2000 (2)
(Figure 1).
In the Americas, the first recorded epidemic of WN viral encephalitis
occurred in the New York metropolitan area during the late summer of 1999. A
total of 62 cases of neurological disease and 7 deaths were reported. In addition
to humans, concurrent epizootics occurred in birds and horses especially affecting
the American crow (3). During this epidemic/epizootic,
the virus was detected in 4 states, Connecticut, Maryland, New Jersey and New
York. In 2000, there were 18 cases with 1 death and epizootic activity in birds
and/or mosquitoes was recorded in 12 states (Connecticut, Delaware, Maryland,
Massachusetts, New Hampshire, New Jersey, New York, North Carolina, Pennsylvania,
Rhode Island, Vermont, Virginia) and the District of Columbia (4).
It has not been determined how WN virus was introduced into the
Western hemisphere. However, migratory birds are suspected as being principal
introductory hosts for several reasons (1): outbreaks of
the virus in temperate regions generally occur during late summer or early fall,
coinciding with the arrivals of large concentrations of migratory birds; outbreaks
often occur among humans living near wetlands where high concentrations of birds
come into contact with large numbers of mosquitoes; and antibodies to the virus
have been found in the blood of many migratory bird species of temperate regions.
In addition to migratory birds, international travel of infected persons to
New York, importation of infected birds or mosquitoes are other possible sources
of WN virus introduction.
As a result of the 1999 outbreak, U.S. public health officials
questioned the preparedness of the public health infrastructure to respond to
vector-borne diseases and recognized the ease with which emerging infectious
pathogens can move into new geographic areas. Furthermore, public health agencies
did not know how far the virus would spread and if it would sustain during the
winter season (5). To address these issues, guidelines
for an active surveillance system and prevention and control programs were established
by the CDC and U.S. Department of Agriculture (USDA)
(3).
An enhanced surveillance system is a priority for states along
the Atlantic Ocean and Gulf of Mexico. These states, from Massachusetts to Texas,
were selected to participate in WN virus surveillance on the basis of having
been affected by the 1999 outbreak and/or having high potential to become affected
because of bird migration patterns to the south. A major objective of WN virus
surveillance is to detect epizootic activity early so that intervention can
occur before severe human illnesses (4). From the 1999
outbreak epidemiological findings, WN virus-infected birds were identified before
human cases in their same county of residence suggesting that avian surveillance
data are sensitive indicators of epizootic transmission and may predict human
illness. The emphases on surveillance activities included: the monitoring of
arbovirus activity in wild birds, sentinel birds, and dead crows; surveillance
of mosquito populations to detect WN virus and other arbovirus activity; passive
surveillance for the presence of WN virus outside of the bird-mosquito cycles,
as in horses and other animals; and passive surveillance for cases of viral
encephalitis (3).
The success of the surveillance activities in the U.S. has depended
on the availability of laboratories that can provide diagnostic support. The
immunoglobulin M and G enzyme-linked immunosorbent assays (ELISA) are available
in public health and veterinary laboratories to provide the first-line testing
for human and animal serum and cerebrospinal fluid specimens. Selected public
health and reference laboratories have the capabilities to isolate and identify
the virus, perform neutralization tests to identify specific flavivirus antibody,
and perform immunohistochemistry to detect WN virus in autopsy tissues. All
laboratory investigations handling the virus is conducted under bio-safety level
3 containment.
The most effective method to prevent transmission of WN virus
or other arboviruses to humans is to reduce human exposure to mosquitoes. Public
health services should have capabilities to control mosquito populations by
larval control; control of adult mosquito populations by aerial application
of insecticides; and educating the public about vector-borne diseases, how they
are transmitted and how to prevent or reduce risk of exposure.
Because WN virus is a zoonosis affecting mosquitoes and vertebrates,
a close coordination and data exchange between federal, state and local public
health, vector control, agriculture and wildlife departments is essential for
the success of addressing this vector-borne disease. A functional arbovirus
surveillance and response capability with an adequately equipped reference laboratory
with trained staff and veterinary/entomology health capacity is required (3).
The decrease in the number of cases of severe human illness from
1999 (62 cases) to 2000 (18 cases) in the U.S. may be attributed to prevention
and control measures taken by state and local public health departments. However,
previous experience in Europe has shown that incidence of human illness can
be variable and outbreaks sporadic. In spite of a decrease in cases, WN virus
activity has continued to expand to new locations and will persist. Research
of migratory bird patterns shows that “members of one or more avian species
that pass through New York and gather in wetlands in large, dense groups potentially
reach every part of the southeastern United States, Mexico and Central America,
the Caribbean Islands, and South America during their migration south to wintering
sites and nearly every part of North America during their migration north to
breeding sites” (1) (6) (7).
As noted by Blaskovic and Ernek (8), “the role of birds
in ecology of arboviruses depends upon whether the migrating vector finds favourable
conditions in the new environment and whether the local vectors are capable
of transmitting the appropriate virus. The presence of arbovirus antibody in
migratory birds indicates only a virus-host interaction but does not explain
when and where the infection occurred.” For these reasons, surveillance (mainly
of dead birds), prevention activities and mosquito control need to be well established
and maintained. Additionally, future research should define criteria for predicting
where the virus will go next (1).
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Table 1: Case definitions of West Nile Virus Encephalitis
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Confirmed Case
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Probable Case
|
Non-Case
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A confirmed case of WN encephalitis is defined as a
febrile illness associated with neurologic manifestations ranging from
headache to aseptic meningitis or encephalitis, plus at least one of
the following:
- Isolation of WNV from or demonstration of WN viral
antigen or genomic sequences in, tissue, blood, CSF, or other body fluid;
· Demonstration of IgM antibody to WN virus in CSF by IgM-capture EIA.
- A > 4-fold serial change in plaque-reduction neutralizing
(PRNT) antibody titer to WN virus in paired, appropriately timed serum
or CSF samples
- Demonstration of both WN virus-specific IgM (by EIA)
and IgG (screened by EIA or HI and confirmed by PRNT) antibody in a
single serum specimen.
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A probable case is defined as a compatible illness (as confirmed case)
that does not meet any of the above laboratory criteria, plus at least
one of the following:
- Demonstration of serum IgM antibody against WN virus
(by EIA);
- Demonstration of an elevated titer of WN virus-specific
IgG antibody in convalescent-phase serum (screened by EIA or HI and
confirmed by PRNT).
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A non-case is defined as an illness that doe not meet
any of the above laboratory criteria, plus:
- A negative test for IgM antibody to WNV (by EIA) in
serum or CSF collected 8-21 days after onset of illness; and/or
- A negative test for IgG antibody to WNV (by EIA, HI,
or PRNT) in serum collecteed > 22 days after onset of illness.
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| Note: Although tests of tissues or fluids
by PCR, antigen detection, or virus isolation can be used to confirm WN
encephalitis cases, they cannot be used to rule-out cases because the negative
predictive values of these test methods in this disease are unknown. |
References:
(1) Rappole, J., Derrickson, S., Hubalek, Z., Mirgratory Birds and Spread of
West Nile Virus in the Western Hemisphere. Emerging Infectious Diseases, 2000;
6:319-327.
(2) Centers for Disease Control and Prevention. West Nile Virus, Division of
Vector-Borne Infectious Diseases, 2000.
(3) Centers for Disease Control and Prevention. Epidemic/Epizootic West Nile
Virus in the United States: Guidelines for Surveillance, Prevention and Control,
1999.
(4) Centers for Disease Control and Prevention. Update: West Nile Virus Activity
- Eastern united States, 2000. Morbidity Mortality Weekly Report, 2000; 49;
1044-1047.
(5) Centers for Disease Control and Prevention. Guidelines for Surveillance,
Prevention, and Control of West Nile Virus Infection – United States, Morbidity
Mortality Weekly Report, 2000; 49;25-8.
(6) Bull J. Birds of New York State. Garden City (NY): Doubleday; 1974.
(7) Steele KE, Linn MJ., Schoepp RJ, Komar N., Geisbert TW, Manudca RM, et al.
Pathology of fatal West Nile virus infections in native and exotic birds during
the 1999 outbreak in New York City. Veterinary Pathology 2000; 37:208-24.
(8) Gubler, D.. Surveillance for West Nile Virus in the Americas, PAHO/WHO,
Third Meeting of the Surveillance Networks for Emerging Infectious Diseases
in the Amazon and Southern Cone Regions, 2000.
(9) Blaskovic D., Ernek E. Birds as hosts of arboviruses in connection of migratory
birds and their role in the distribution of arboviruses. Novosibirsk, Russia:
Nauka; 1972. p. 161-7.
(10) Centers for Disease Control and Prevention. http://www.cdc.gov/ncidod/dvbid/westnile/index.htm
, December 2000.
Source: PAHO. Division of Disease Prevention and Control.
Communicable Diseases Program (HCP/HCT)
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21 No. 4, December 2000
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