From 1937 until 1999, West Nile virus (WNV) garnered
scant medical attention as the cause of febrile illness and
sporadic encephalitis in parts of Africa, Asia, and Europe.
After the surprising detection of WNV in New York City in
1999, the virus has spread dramatically westward across
the United States, southward into Central America and the
Caribbean, and northward into Canada, resulting in the
largest epidemics of neuroinvasive WNV disease ever
reported. From 1999 to 2004, >7,000 neuroinvasive WNV
disease cases were reported in the United States. In 2002,
WNV transmission through blood transfusion and organ
transplantation was described for the first time, intrauterine
transmission was first documented, and possible transmis-
sion through breastfeeding was reported. This review high-
lights new information regarding the epidemiology and
dynamics of WNV transmission, providing a new platform
for further research into preventing and controlling WNV
encephalitis in New York City. Over the next 5 years, the
virus spread across the continental United States as well as
north into Canada, and southward into the Caribbean
Islands and Latin America (1). This article highlights new
information about the epidemiology and transmission
dynamics of human WNV disease obtained over the past 5
years of intensified research.
est Nile virus (WNV) was first detected in the
Western Hemisphere in 1999 during an outbreak of
WNV is transmitted primarily by the bite of infected
mosquitoes that acquire the virus by feeding on infected
birds. The intensity of transmission to humans is dependent
on abundance and feeding patterns of infected mosquitoes
and on local ecology and behavior that influence human
exposure to mosquitoes. Although up to 55% of affected
populations became infected during epidemics in Africa,
more recent outbreaks in Europe and North America have
yielded much lower attack rates (1,2). In the area of most
intense WNV transmission in Queens, New York, in 1999,
≈2.6% of residents were infected (most of these were
asymptomatic infections), and similarly low prevalence of
infection has been seen in other areas of the United States
(3,4). WNV outbreaks in Europe and the Middle East since
1995 appear to have caused infection in <5% of affected
populations (1,5). These levels of infection are too low to
decrease the frequency of epidemics or modulate their
intensity through protective immunity.
Data on the incidence of WNV in most of the world are
not readily available. WNV transmission has been report-
ed in Europe, the Middle East, Africa, India, parts of Asia,
Australia (in the form of Kunjin virus, a subtype of WNV),
North America, and parts of Central America and the
Caribbean (1,6). In recent years human WNV disease in
the Eastern Hemisphere has been reported mostly from
areas in the Mediterranean Basin: in Algeria in 1994,
Morocco in 1996, Tunisia in 1997 and 2003, Romania in
1996 through 2000, the Czech Republic in 1997, Israel in
1999 and 2000, Russia in 1999 through 2001, and France
in 2003 (1,6,7). Enzootics involving horses were reported
in Morocco in 1996 and 2003, Italy in 1998, Israel in 2000,
and southern France in 2000, 2003, and 2004 (6–8).
In the Western Hemisphere, most human WNV disease
has occurred in the United States. Since the virus was
detected in New York from 1999 through 2004, 16,706
cases have been reported to the Centers for Disease
Control and Prevention (CDC); 7,096 of these were classi-
fied as neuroinvasive disease, 9,268 as West Nile fever
Epidemiology and Transmission
Dynamic s of West Nile V irus
Edward B. Hayes,* Nicholas Komar,* Roger S. Nasci,* Susan P. Montgomery,*
Daniel R. O’Leary,* and Grant L. Campbell*
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 8, August 20051167
*Centers for Disease Control and Prevention, Fort Collins,
(WNF), and 342 had other or unspecified clinical presen-
tation (reported through June 8, 2005; the proportion of
total cases reported that are neuroinvasive disease is artifi-
cially higher than what is believed to occur naturally since
neuroinvasive disease is more likely to be reported than
WNF or asymptomatic infection) (Table 1). Transmission
of WNV has spread dramatically from New York to the
north, south, and west (Figure 1). From 2002 to 2003, the
most intense transmission shifted from the Midwest and
south-central states to the western plains and Front Range
of the Rocky Mountains. In 2004, most WNV disease cases
were reported in California, Arizona, and western
Colorado, but foci of highest incidence were scattered
across the United States (Figure 1). In the East, WNVtrans-
mission recurred for 6 consecutive years with the highest
number of human disease cases reported in 2003, indicating
that WNV disease has become seasonally endemic. In
Canada, transmission of WNV to humans has been docu-
mented in Quebec, Ontario, Manitoba, Saskatchewan, and
Alberta, and WNV-infected birds have also been found in
New Brunswick and Nova Scotia (http://www.phac-
aspc.gc.ca/wnv-vwn). Evidence of WNV transmission has
been reported from the Cayman Islands, Jamaica,
Dominican Republic, Mexico, Guadeloupe, El Salvador,
Belize, Puerto Rico, and Cuba, but only 1 human case has
been reported from Mexico and 1 from the Cayman Islands
m; www.paho.org/English/AD/DPC/CD/wnv.htm; http://
edu/labs/avian/wnv.jsp) (1). The paucity of human cases
thus far in Latin America and the Caribbean is surprising,
considering the ecologic conditions that favor arbovirus
transmission in these areas. WNV isolated from a bird in
Mexico in 2003 appeared to be attenuated, but whether
viral mutation accounts for the scarcity of human disease
remains to be seen (9).
The incidence of WNV disease is seasonal in the tem-
perate zones of North America, Europe, and the
Mediterranean Basin, with peak activity from July through
October (6,10). In the United States, the transmission sea-
son has lengthened as the virus has moved south; in 2003,
onset of human illness began as late as December, and in
2004 as early as April (CDC, unpub. data). Transmission
of WNV in southern Africa and of Kunjin virus in
Australia increases in the early months of the year after
heavy spring and summer rainfall (2,11).
In the United States, persons of all ages appear to be
equally susceptible to WNV infection, but the incidence of
neuroinvasive WNV disease and death increases with age,
especially among those 60 to 89 years of age, and is slight-
ly higher among male patients (Figure 2) (10). During
2002, the median age among neuroinvasive disease cases
was 64 years (range 1 month to 99 years), compared to a
median age of 49 years (range 1–97 years) for WNF cases
(10). Of the 2,942 neuroinvasive disease cases, 276 (9%)
were fatal (10). Although severe disease occurs primarily
in adults, neuroinvasive disease in children has been
reported. From 2002 through 2004, 1,051 WNV disease
cases among children <19 years of age were reported in the
United States; 317 (30%) had neuroinvasive disease; and
1168Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 8, August 2005
Figure 1. Reported incidence of neuroinvasive West Nile virus dis-
ease by county, United States, 1999–2004. Reported to Centers for
Disease Control and Prevention by states through April 21, 2005.
106 (34%) of these were <10 years (CDC, unpub. data;
reported through June 8, 2005). Two (0.6%) pediatric
patients with neuroinvasive WNV disease died: an infant
with underlying lissencephaly and a 14-year-old boy with
The most important risk factor for acquiring WNV
infection is exposure to infected mosquitoes. In Romania
the risk for WNVinfection was higher among persons with
mosquitoes in their homes and with flooded basements
(12). An analysis of the locations of WNV disease cases
during the 1999 outbreak in New York found that cases
were clustered in an area with higher vegetation cover,
indicating favorable mosquito habitat (13). A study of the
outbreak in Chicago in 2002 indicated that human disease
cases tended to occur in areas with more vegetation, older
housing, lower population density, predominance of older
Caucasian residents, and proximity to dead birds, but the
effects of these variables were influenced by differences in
mosquito abatement efforts (14). Risk factors for infection
not related to mosquito exposure include receiving blood
transfusions or organ donations, maternal infection during
pregnancy or breastfeeding, and occupational exposure to
the virus (15–17).
Apart from older age and immunosuppression after
organ transplantation, the risk factors for the development
of severe neuroinvasive WNV disease have yet to be deter-
mined (10,16). Underlying hypertension, cerebrovascular
disease, and diabetes have been considered as possible pre-
disposing factors; further study may elucidate the role of
these or other host factors that might modify the risk for
severe disease or death (12). Genetic predisposition for
severe disease has been described in mice but has not yet
been elucidated in humans (18). The role of innate and
adaptive immune responses in determining outcome
deserves further study.
Nonmosquitoborne WNV Transmission
In 2002, intrauterine WNV transmission was docu-
mented for the first time (15). A 20-year-old woman had
onset of WNV disease in week 27 of gestation. Her infant
was born at term with chorioretinitis and cystic damage of
cerebral tissue. Intensified surveillance identified 4 other
mothers who had WNV illness during pregnancy, 3 of
whom delivered infants with no evidence of WNV infec-
tion; all 3 infants appeared normal at birth and at 6 months
of age (15). The fourth woman delivered prematurely; her
infant had neonatal respiratory distress but was not tested
for WNV infection. In 2003, CDC received reports of 74
women infected with WNV during pregnancy; most of
these women followed up to date have delivered apparent-
ly healthy infants (CDC, unpub. data).
Probable WNV transmission through breast milk was
also reported in 2002 (15). A 40-year-old woman acquired
WNV infection from blood transfused shortly after she
delivered a healthy infant. WNV nucleic acid was detected
in her breast milk, and immunoglobulin (Ig) M antibody
was found in her infant, who remained healthy. No other
instances of possible WNV transmission through breast
milk have been reported. Until more data are available, and
because the benefits of breastfeeding are well documented,
mothers should be encouraged to breastfeed even in areas
of ongoing WNV transmission.
Transmission of WNV through blood transfusion was
first documented during the 2002 WNV epidemic in North
America (15). In June 2003, blood collection agencies in
the United States and Canada enhanced donor deferral and
began screening blood donations with experimental nucle-
ic acid amplification tests. During 2003 and 2004, >1,000
potentially WNV-viremic blood donations were identified,
and the corresponding blood components were sequestered.
Nevertheless, 6 WNV cases due to transfusion were docu-
mented in 2003, and at least 1 was documented in 2004,
indicating that infectious blood components with low con-
centrations of WNV may escape current screening tests
(19). One instance of possible WNV transmission through
dialysis has been reported (20).
WNV transmission through organ transplantation was
also first described during the 2002 epidemic (15).
Chronically immunosuppressed organ transplant patients
appear to have an increased risk for severe WNV disease,
even after mosquito-acquired infection (16). During 2002,
the estimated risk of neuroinvasive WNV disease in solid
organ transplant patients in Toronto, Canada, was approx-
imately 40 times greater than in the general population
(16). Whether other immunosuppressed or immunocom-
promised patients are at increased risk for severe WNV
West Nile Virus Epidemiology and Ecology
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 8, August 20051169
Figure 2. Reported incidence of neuroinvasive West Nile virus dis-
ease by age group and sex, United States, 1999–2004. Reported
to the Centers for Disease Control and Prevention by states
through April 14, 2005.
disease is uncertain, but severe WNV disease has been
described among immunocompromised patients.
WNV infection has been occupationally acquired by
laboratory workers through percutaneous inoculation and
possibly through aerosol exposure (21,22). An outbreak of
WNV disease among turkey handlers at a turkey farm
raised the possibility of aerosol exposure (17).
Dynamics of Transmission: Vectors
WNV is transmitted primarily by Culex mosquitoes,
but other genera may also be vectors (23). In Europe and
Africa, the principal vectors are Cx. pipiens, Cx. univitta-
tus, and Cx. antennatus, and in India, species of the Cx.
vishnui complex (6,24). In Australia, Kunjin virus is trans-
mitted primarily by Cx. annulirostris (11). In North
America, WNV has been found in 59 different mosquito
species with diverse ecology and behavior; however, <10
of these are considered to be principal WNV vectors
(CDC, unpub. data) (23,25,26). In 2001, 57% of the posi-
tive mosquito pools in the Northeast were Cx. pipiens, the
northern house mosquito, a moderately efficient vector
that feeds on birds and mammals (Table 2). In 2002, Cx.
pipiens made up more than half of the WNV-positive
pools, but Cx. quinquefasciatus, the southern house mos-
quito, generally considered a moderate- to low-efficiency
vector, appeared to be the predominant vector in the South.
Cx. tarsalis, 1 of the most efficient WNV vectors evaluat-
ed in laboratory studies, was the predominant vector west
of the Mississippi River (CDC, unpub. data) (26).
During 2003, as WNV activity progressed westward,
Cx. tarsalis became the most commonly reported WNV-
positive mosquito species, making up 32% of the positive
pools reported, followed by Cx. pipiens, Cx. quinquefas-
ciatus, and Cx. restuans (Table 2). Cx. salinarius and Cx.
nigripalpus may be important vectors in areas where they
are abundant (26). During 2004, when large epidemics
occurred in the southwestern United States, the most
commonly reported WNV-positive species was Cx. quin-
quefasciatus, which made up over half of the positive
pools, followed by Cx. tarsalis and Cx. pipiens (Table 2).
The intensity of WNV transmission is determined pri-
marily by the abundance of competent mosquitoes and the
prevalence of infection in mosquitoes. The estimated
prevalence of infection, measured as the minimum infec-
tion rate (MIR), that is needed to produce epidemics is
uncertain. Toward the end of the 1999 New York epidem-
ic, the WNV MIR for all Culex mosquitoes sampled in the
area was 0.3% with MIRs of individual collections, rang-
ing from 0.07% to 5.7% (27). During the 2000 Staten
Island epidemic, the MIRs in mixed Cx. pipiens/restuans
pools ranged from 0.5% to 1.6% and the MIR in Cx. sali-
narius from 0.3% to 1.2% (28). Relatively low MIRs in
Cx. restuans (0.2%), Cx. pipiens (0.1%) and Cx. salinarius
(0.1%) in Connecticut during 2000 were associated with
an intense epizootic, but apparently a low risk for humans
(29). In 2001, moderate to high MIRs in Cx. quinquefas-
ciatus (0.5%) and Cx. nigripalpus (1.1%) were associated
with epizootic and epidemic transmission in Florida (30).
In some North American outbreaks, MIRs as high as 15%
have been observed (CDC, unpub. data). Vertical transmis-
sion of WNV has been experimentally demonstrated in Cx.
pipiens, Cx. quinquefasciatus, and Cx. tarsalis, and the
virus has been isolated from hibernating female mosqui-
toes, which may provide a mechanism for persistence of
the virus in colder latitudes through the winter and reemer-
gence of transmission in the spring (31,32).
Although both soft and hard ticks can become infected
with WNV, they are unlikely to play a substantial role in
WNV transmission. In the laboratory, Argas arboreus ticks
transmitted WNV to chickens, and Ornithodoros savignyi,
O. maritimus, O. erraticus, and O. moubata transmitted
WNV to mice (33). However, of the hard ticks
Amblyomma americanum, Ixodes scapularis, I. ricinus,
Dermacentor variabilis, and D. andersoni, the last 4
1170Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 8, August 2005
species became infected with WNV, but none transmitted
the virus by subsequent bite (33,34).
Dynamics of Transmission: Vertebrate Hosts
Laboratory studies have demonstrated that 74%–100%
of Cx. tarsalis mosquitoes become infected after consum-
ing blood meals with WNV concentrations of 107.1plaque-
forming units (PFU)/mL, while only 0%–36% become
infected after consuming a meal containing 104.9PFU/mL
(35). The maximum estimated concentration of WNV in
human blood tested during screening of blood donors in
2002 was approximately 103.2PFU/mL (S. Stramer, M.
Busch, M. Strong, pers. comm.). Thus, it appears unlikely
that humans exhibit WNV viremia levels of sufficient
magnitude to infect mosquitoes.
Birds are presumed to be the most important amplify-
ing hosts of WNV. In laboratory studies, species in the
orders Passeriformes (song birds), Charadriiformes
(shorebirds), Strigiformes (owls), and Falconiformes
(hawks) developed viremia levels sufficient to infect most
feeding mosquitoes, whereas species of Columbiformes
(pigeons), Piciformes (woodpeckers), and Anseriformes
(ducks) did not (23,36). Certain passerines, including
common grackles (Quiscalus quiscula), various corvids
(crows, jays, magpies), house finches (Carpodacus mexi-
canus), and house sparrows (Passer domesticus) were
highly infectious to mosquitoes and had mortality rates
>40%. Field studies during and after WNV outbreaks in
several areas of the United States have confirmed that
house sparrows were abundant and frequently infected
with WNV, characteristics that would allow them to serve
as important amplifying hosts (23,25,37). The importance
of birds in dispersing WNV remains speculative. Local
movements of resident, nonmigratory birds and long-
range travel of migratory birds may both contribute to the
spread of WNV (38,39).
Although WNV was isolated from rodents in Nigeria
and a bat in India, most mammals do not appear to gener-
ate viremia levels of sufficient titer to contribute to trans-
mission (24,40–42). Three reptilian and 1 amphibian
species (red-ear slider, garter snake, green iguana, and
North American bullfrog) were found to be incompetent as
amplifying hosts of a North American WNV strain, and no
signs of illness developed in these animals (43). Viremia
levels of sufficient titer to infect mosquitoes were found
after experimental infection of young alligators (Alligator
mississippiensis) (44). In Russia, the lake frog (Rana ridi-
bunda) appears to be a competent reservoir (45).
Nonmosquitoborne WNV transmission has been
observed or strongly suspected among farmed alligators,
domestic turkeys in Wisconsin, and domestic geese in
Canada (17,46,47). Transmission through close contact has
been confirmed in both birds and alligators in laboratory
conditions but has yet to be documented in wild vertebrate
Control of WNV Transmission
Avoiding human exposure to WNV-infected mosqui-
toes remains the cornerstone for preventing WNV disease.
Source reduction, application of larvicides, and targeted
spraying of pesticides to kill adult mosquitoes can reduce
the abundance of mosquitoes, but demonstrating their
impact on the incidence of human WNV disease is chal-
lenging because of the difficulty in accounting for all
determinants of mosquito abundance and human exposure.
One study indicated that clustering of human WNV dis-
ease in Chicago varied between mosquito abatement dis-
tricts, suggesting that mosquito control may have some
impact on transmission to humans (14).
Persons in WNV-endemic areas should wear insect
repellent on skin and clothes when exposed to mosquitoes
and avoid being outdoors during dusk to dawn when mos-
quito vectors of WNV are abundant. Of insect repellents
recommended for use on skin, those containing N,N-
diethyl-m-toluamide (DEET), picaridin (KBR-3023), or
oil of lemon eucalyptus (p-menthane-3,8 diol) provide
long-lasting protection (48). Both DEET and permethrin
provide effective protection against mosquitoes when
applied to clothing. Persons’willingness to use DEET as a
repellent appears to be influenced primarily by their level
of concern about being bitten by mosquitoes and by their
concern that DEET may be harmful to health, despite its
good safety record (49).
To prevent transmission of WNV through blood trans-
fusion, blood donations in WNV-endemic areas should be
screened by using nucleic acid amplification tests.
Screening of organ donors for WNV infection has not
been universally implemented because of concern about
rejecting essential organs after false-positive screening
results (50). Pregnant women should avoid exposure to
mosquito bites to reduce the risk for intrauterine WNV
WNV disease will likely continue to be a public health
concern for the foreseeable future; the virus has become
established in a broad range of ecologic settings and is
transmitted by a relatively large number of mosquito
species. WNV will also likely continue to spread into
Central and South America, but the public health implica-
tions of this spread remain uncertain. Observations thus far
in North America indicate that circulation of other fla-
viviruses, such as dengue, viral mutation, and differing
ecologic conditions may yield different clinical manifesta-
tions and transmission dynamics. Over the next few years,
research efforts might well be focused in several areas.
West Nile Virus Epidemiology and Ecology
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 8, August 2005 1171
Research into new methods to reduce human exposure to
mosquitoes is crucial and can help prevent other mosquito-
borne illnesses. This should include development of new
methods to reduce mosquito abundance, development of
new repellents, and behavioral research to enhance the use
of existing effective repellents and other personal protec-
tive measures against mosquito bites. A better understand-
ing of the dynamics of nonmosquitoborne transmission is
essential to prevent disease among infants of infected
mothers and recipients of blood transfusions and trans-
planted organs. Currently available prevention strategies
such as the dissemination of knowledge and products for
personal protection from mosquito exposure and the appli-
cation of existing techniques for reducing mosquito abun-
dance in communities at risk of WNV transmission need to
be vigorously implemented. National and international
surveillance for WNV transmission will be important to
monitor spread of the virus and the effect of control strate-
gies. Finally, further research into the ecologic determi-
nants of WNV transmission, including climatic factors and
dynamics of reservoir and vector populations, could help
in determining geographic areas of higher risk for WNV
We thank Krista Kniss for her assistance in preparing
Table 1 and the figures.
Dr. Hayes is a medical epidemiologist and pediatrician with
CDC’s Division of Vector-Borne Infectious Diseases. His current
research is focused on the epidemiology of arboviral and other
vectorborne infectious diseases.
1. Dauphin G, Zientara S, Zeller H, Murgue B. West Nile: worldwide
current situation in animals and humans. Comp Immunol Microbiol
Infect Dis. 2004;27:343–55.
2. McIntosh BM, Jupp PG, Dos Santos I, Meenehan GM. Epidemics of
West Nile and Sindbis viruses in South Africa with Culex (Culex) uni-
vittatus Theobald as vector. S Afr J Sci. 1976;72:295–300.
3. Mostashari F, Bunning ML, Kitsutani PT, Singer DA, Nash D,
Cooper MJ, et al. Epidemic West Nile encephalitis, New York, 1999:
results of a household-based seroepidemiological survey. Lancet.
4. Centers for Disease Control and Prevention. Serosurveys for West
Nile virus infection—New York and Connecticut counties, 2000.
MMWR Morb Mortal Wkly Rep. 2001;50:37–9.
5. Campbell GL, Ceianu CS, Savage HM. Epidemic West Nile
encephalitis in Romania: waiting for history to repeat itself. Ann N Y
Acad Sci. 2001;951:94–101.
6. Zeller HG, Schuffenecker I. West Nile virus: an overview of its spread
in Europe and the Mediterranean basin in contrast to its spread in the
Americas. Eur J Clin Microbiol Infect Dis. 2004;23:147–56.
7. Schuffenecker I, Peyrefitte CN, el Harrak M, Murri S, Leblond A,
Zeller HG. West Nile virus in Morocco, 2003. Emerg Infect Dis.
8. Zeller H, Zientara S, Hars J, Languille J, Mailles A, Tolou H, et al.
West Nile outbreak in horses in southern France: September 2004.
Eurosurveillance Weekly. 2004:8:Oct 7, 2004.
9. Beasley DW. Genome sequence and attenuating mutations in West
Nile virus isolate from Mexico. Emerg Infect Dis. 2004;10:2221–4.
10. O’Leary DR, Marfin AA, Montgomery SP, Kipp AM, Lehman JA,
Biggerstaff BJ, et al. The epidemic of West Nile virus in the United
States, 2002. Vector Borne Zoonotic Dis. 2004;4:61–70.
11. Hall RA, Broom AK, Smith DW, Mackenzie JS. The ecology and epi-
demiology of Kunjin virus. Curr Top Microbiol Immunol.
12. Han LL, Popovici F, Alexander Jr JP, Laurentia V, Tengelsen LA,
Cernescu C, et al. Risk factors for West Nile virus infection and
meningoencephalitis, Romania, 1996. J Infect Dis. 1999;179:230–3.
13. Brownstein JS, Rosen H, Purdy D, Miller JR, Merlino M, Mostashari
F, et al. Spatial analysis of West Nile virus: rapid risk assessment of
an introduced vector-borne zoonosis. Vector Borne Zoonotic Dis.
14. Ruiz MO, Tedesco C, McTighe TJ, Austin C, Kitron U.
Environmental and social determinants of human risk during a West
Nile virus outbreak in the greater Chicago area, 2002. Int J Health
15. Hayes EB, O’Leary DR. West Nile virus infection: a pediatric per-
spective. Pediatrics. 2004; 113:1375–81.
16. Kumar D, Prasad GV, Zaltzman J, Levy GA, Humar A. Community-
acquired West Nile virus infection in solid-organ transplant recipi-
ents. Transplantation. 2004;77:399–402.
17. Centers for Disease Control and Prevention. West Nile virus infection
among turkey breeder farm workers—Wisconsin, 2002. MMWR
Morb Mortal Wkly Rep. 2003;52:1017–9.
18. Ceccaldi PE, Lucas M, Despres P. New insights on the neuropathol-
ogy of West Nile virus. FEMS Microbiol Lett. 2004;233:1–6.
19. Centers for Disease Control and Prevention. Transfusion-associated
transmission of West Nile virus—Arizona, 2004. MMWR Morb
Mortal Wkly Rep. 2004;53:842–4.
20. Centers for Disease Control and Prevention. Possible dialysis-related
West Nile virus transmission—Georgia, 2003. MMWR Morb Mortal
Wkly Rep. 2004;53:738–9.
21. Nir Y, Beemer A, Goldwasser RA. West Nile virus infection in mice
following exposure to a viral aerosol. Br J Exp Pathol. 1965;46:
22. Centers for Disease Control and Prevention. Laboratory-acquired
West Nile virus infections—United States, 2002. MMWR Morb
Mortal Wkly Rep. 2002;51:1133–5.
23. Komar N. West Nile virus: epidemiology and ecology in North
America. Adv Virus Res. 2003;61:185–234.
24. Hayes CG. West Nile fever. In: Monath TP, editor. The arboviruses:
epidemiology and ecology, vol. V. Boca Raton (FL): CRC Press;
1989. p. 59–88.
25. Godsey MS, Blackmore MS, Panella NA, Burkhalter K, Gottfried K,
Halsey LA, et al. West Nile virus epizootiology in the southeastern
United States, 2001. Vector Borne Zoonotic Dis. 2005;5:82–9.
26. Turell MJ, Dohm DJ, Sardelis MR, Oguinn ML, Andreadis TG, Blow
JA. An update on the potential of north American mosquitoes
(Diptera: Culicidae) to transmit West Nile virus. J Med Entomol.
27. Nasci RS, White DJ, Stirling H, Daniels TJ, Falco RC, Campbell S,
et al. West Nile virus isolates from mosquitoes in New York and New
Jersey, 1999. Emerg Infect Dis. 2001;7:626–30.
28. Nasci RS, Gottfried KL, Burkhalter KL, Kulasekera VL, Lambert AJ,
Lanciotti RS, et al. Comparison of vero cell plaque assay, TaqMan
reverse transcriptase polymerase chain reaction RNA assay, and
VecTest antigen assay for detection of West Nile virus in field-collect-
ed mosquitoes. J Am Mosq Control Assoc. 2002;18:294–300.
1172Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 8, August 2005
29. Hadler J, Nelson R, McCarthy T, Andreadis T, Lis MJ, French R, et Download full-text
al. West Nile virus surveillance in Connecticut in 2000: an intense
epizootic without high risk for severe human disease. Emerg Infect
30. Blackmore CG, Stark LM, Jeter WC, Oliveri RL, Brooks RG, Conti
LA, et al. Surveillance results from the first West Nile virus transmis-
sion season in Florida, 2001. Am J Trop Med Hyg. 2003;69:141–50.
31. Goddard LB, Roth AE, Reisen WK, Scott TW. Vertical transmission
of West Nile Virus by three California Culex (Diptera: Culicidae)
species. J Med Entomol. 2003;40:743–6.
32. Nasci RS, Savage HM, White DJ, Miller JR, Cropp BC, Godsey MS,
et al. West Nile virus in overwintering Culex mosquitoes, New York
City, 2000. Emerg Infect Dis. 2001;7:742–4.
33. Lawrie CH, Uzcategui NY, Gould EA, Nuttall PA. Ixodid and argasid
tick species and West Nile virus. Emerg Infect Dis. 2004;10:653–7.
34. Anderson JF, Main AJ, Andreadis TG, Wikel SK, Vossbrinck CR.
Transstadial transfer of West Nile virus by three species of ixodid
ticks (Acari: Ixodidae). J Med Entomol. 2003;40:528–33.
35. Goddard LB, Roth AE, Reisen WK, Scott TW. Vector competence of
California mosquitoes for West Nile virus. Emerg Infect Dis.
36. Komar N, Langevin S, Hinten S, Nemeth N, Edwards E, Hettler D, et
al. Experimental infection of North American birds with the New
York 1999 strain of West Nile virus. Emerg Infect Dis.
37. Komar N, Panella NA, Langevin SA, Brault AC, Amador M, Edwards
E, et al. Avian hosts for West Nile virus in St. Tammany Parish,
Louisiana 2002. Am J Trop Med Hyg. 2005. In press.
38. Rappole JH, Hubalek Z. Migratory birds and West Nile virus. J Appl
Microbiol. 2003;94 Suppl:47S–58S.
39. Peterson AT, Vieglais DA, Andreasen JK. Migratory birds modeled as
critical transport agents for West Nile virus in North America. Vector
Borne Zoonotic Dis. 2003;3:27–37.
40. Bunning ML, Bowen RA, Cropp CB, Sullivan KG, Davis BS, Komar
N, et al. Experimental infection of horses with West Nile virus.
Emerg Infect Dis. 2002;8:380–6.
41. Austgen LE, Bowen RA, Bunning ML, Davis BS, Mitchell CJ,
Chang GJ. Experimental infection of cats and dogs with West Nile
virus. Emerg Infect Dis. 2004;10:82–6.
42. Ratterree MS, Gutierrez RA, Travassos da Rosa AP, Dille BJ, Beasley
DW, Bohm RP, et al. Experimental infection of rhesus macaques with
West Nile virus: level and duration of viremia and kinetics of the anti-
body response after infection. J Infect Dis. 2004;189:669–76.
43. Klenk K, Komar N. Poor replication of West Nile virus (New York
1999 strain) in three reptilian and one amphibian species. Am J Trop
Med Hyg. 2003;69:260–2.
44. Klenk K, Snow J, Morgan K, Bowen R, Stephens M, Foster F, et al.
Alligators as west nile virus amplifiers. Emerg Infect Dis.
45. Kostiukov MA, Gordeeva ZE, Bulychev VP, Nemova NV, Daniiarov
OA. [The lake frog (Rana ridibunda)—one of the food hosts of
blood-sucking mosquitoes in Tadzhikistan—a reservoir of the West
Nile fever virus]. Med Parazitol (Mosk). 1985;49–50.
46. Austin RJ, Whiting TL, Anderson RA, Drebot MA. An outbreak of
West Nile virus-associated disease in domestic geese (Anser anser
domesticus) upon initial introduction to a geographic region, with
evidence of bird to bird transmission. Can Vet J. 2004;45:117–23.
47. Jacobson ER, Ginn PE, Troutman JM, Farina L, Stark L, Klenk K, et
al. West Nile virus infection in farmed American alligators (Alligator
mississippiensis) in Florida. J Wildl Dis. 2005;41:96–106.
48. Barnard DR, Xue RD. Laboratory evaluation of mosquito repellents
against Aedes albopictus, Culex nigripalpus, and Ochlerotatus trise-
riatus (Diptera: Culicidae). J Med Entomol. 2004:41:726–30.
49. Herrington JE Jr. Pre-West Nile virus outbreak: perceptions and prac-
tices to prevent mosquito bites and viral encephalitis in the United
States. Vector Borne Zoonotic Dis. 2003;3:157–73
50. Kiberd BA, Forward K. Screening for West Nile virus in organ trans-
plantation: a medical decision analysis. Am J Transplant.
Address for correspondence: Edward B. Hayes, Division of Vector-Borne
Infectious Diseases, Centers for Disease Control and Prevention, PO Box
2087, Fort Collins, Colorado 80526, USA; fax: 970-221-6476; email:
West Nile Virus Epidemiology and Ecology
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 8, August 2005 1173
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