Global invasive species database

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Common name
West Nile virus (English)
Synonym
Similar species
St. Louis encephalitis virus, Japanese encephalitis virus, Murray Valley encephalitis virus, Kunjin Virus
Summary
West Nile virus (WNV) is a mosquito-borne flavivirus native to Africa, Europe, and Western Asia. WNV is mostly transmitted by Culex mosquitoes in a cycle involving birds as amplifying hosts. However infected mosquitoes can also transmit the virus to other animals and humans. Most animals are “dead-end” hosts and do not contribute to virus spread or evolution in nature, because infection in non-avian species results in low virus levels that is insufficient for infection of mosquitoes.
Since its introduction into the United States in the New York City area in 1999 WNV has continued to expand its range across the United States and into Canada, Mexico and Central and South America. WNV causes severe disease humans, horses and other vertebrates. Most people infected with West Nile virus have only mild illness. However the virus can also cause severe neuroinvasive diseases, often leading to death. No specific medication exists to treat West Nile virus infection, and there is currently no vaccine available for humans. Control measures focus on reducing mosquito breeding habitat: standing water in urban areas, agricultural areas, and wetlands.
Species Description
According to Solomon et al. (2003), like other flaviviruses, West Nile virus is a small virus, with a single stranded, positive sense RNA genome comprising about 11,000 nucleotides wrapped in a nucleocapsid and surrounded by a lipid membrane. Under a microscope the virions appear roughly as spheres 40-65 nm in diameter.
Notes
Temperature and rainfall are important determinants of the activity of arboviruses. Recent West Nile virus epidemics have occurred during unusually hot and dry periods (e.g. Platonov et al. 2008; Paz 2006), thereby driving speculation that climate change could result in increased incidences of WNV and other vector-borne diseases (Epstein 2001; Lazar et al. 2002 in Torrence et al. 2006).
Lifecycle Stages
Enzootic Cycle: The natural WNV replication cycle involves culicine mosquitoes and different bird species. Wild bird species vary in their competence as hosts, depending on the duration and magnitude of infection and ability to transmit the virus to mosquitoes (Trevejo et al. 2008). It appears that only a small proportion of WNV-positive birds are competent (amplifying) hosts for the virus. Humans, horses and other mammalian species are so-called ‘‘dead-end’’ hosts characterised by WNV infections with potential clinical symptoms, but transient and low virus levels that are insufficient to establish a mosquito mammalian WNV replication cycle (Pfleiderer et al. 2008). “Although they are typically referred to as “dead-end” hosts (Komar 2000), occasional individuals, given sufficient numbers, may in fact be able to infect mosquitoes” (Castillo-Olivares and Wood 2004).

There is evidence that tree squirrels (Sciurus spp), eastern chipmunks (Tamias striatus), and eastern cottontail rabbits (Sylvilagus floridanus) may be sufficient to provide a source of infection for mosquitoes(Padgett et al. 2007; Platt et al. 2007; Tiawsirisup et al. 2005 in Trevejo et al. 2008). Alligators (Alligator mississippiensis) and in Russia the lake frog Rana ridibunda may be competent reservoirs (Hayes et al. 2005 in Trevejo et al. 2008). More studies are needed to determine how important these species are in WNV epidemiology.

Mosquito species vary in their vector competence. Culex quinquefasciatus, Culex pipiens, Culex restuans, Culex salinarius, and Culex tarsalis are the most significant vectors of WNV in the United States (CDC 2006; Hayes et al. 2005 in Trevejo et al. 2008), although Culex nigripalpus, Aedes albopictus, Aedes vexans, and Ochlerotatus triseriatus, may be important (CDC 2003 in Trevejo et al. 2008). Feeding preference of mosquitoes plays an important role in transmission and spread of WNV. While Culex spp. typically feed on birds, opportunistic feeding and transmission by secondary routes can cause mammalian hosts to become infected.

Allan et al (2009) tested the hypothesis that high bird diversity reduces WNV transmission because mosquito blood-meals are distributed across a wide range of bird species, many of which have low reservoir competence. A study in Saint Louis, MO determined that prevalence of WNV infection in mosquitoes and humans increased with decreasing bird diversity and with increasing reservoir competence of the bird community. The results suggest that “conservation of avian diversity might help ameliorate the current West Nile virus epidemic in the USA” (Allan et al. 2009).

Other Routes of Transmission: Non-mosquito borne transmission of WNV to animals and humans can also occur. Transmission to fetuses can occur via the placenta during pregnancy, as was reported in a human infant born in 2002; although this is extremely rare (CDC 2002; O’Leary et al 2006 in Trevejo et al. 2008). Transmission via breastfeeding was reported in 2002 (CDC 2002), although further studies found no evidence of this, and suggest that this is also extremely rare (Hinckley et al. 2007). There have also been reports of WNV transmission in humans following blood transfusion, organ transplantation and dialysis (CDC 2002; Kotton 2007; CDC 2003 in Trevejo et al. 2008).

Birds with high levels of WNV can excrete large quantities of virus in oral and cloacal secretions and in feces (Komar et al. 2003; Nemeth et al. 2006 in Bowen and Nemeth 2007).

Theoretically companion animals such as dogs or cats could become infected through contact with or ingesting an infected bird or small mammal, but studies are needed to confirm such a route for transmission (Trevejo et al. 2008).

Habitat Description
WNV cycles enzootically between Culex mosquitoes and birds, although it also can infect and cause illness in a range of vertebrate species including humans and horses (Hayes et al. 2005a; Kile et al. 2005; Miller et al. 2003). These vertebrate animals act as dead-end hosts and generally do not contribute to virus spread or evolution in nature because infection in nonavian species results in a low-level, transient viremia that is generally insufficient for infection of mosquitoes (Hubalek et alCulex spp. of mosquito, which commonly breed in urban areas and prefer to feed on birds. Mosquitoes thrive wherever standing water exists, including wetland and agricultural areas. Mosquitoes also breed effectively in artificial containers and storm drain systems and thus often exhibit high abundance in urban areas (Allan et al. 2009).
Reproduction
West Nile virus can grow in a variety of cells from different tissues depending on the host species. These tissues include neurons, glial cells, and cells from spleen, liver, heart, lymph nodes and lung (Cantile et al. 2001 in Castillo-Olivares and Wood 2004). Virus replication takes place in the perinuclear region of the rough endoplasmic reticulum (ER) of cells. Newly synthesised E, NS1 and prM proteins are translocated to the ER lumen where prM and E heterodimerise. The immature virions are transported through the secretory pathway to the cell membrane where the final cleavage of the prM protein takes place (Castillo-Olivares and Wood 2004). It takes about 20-30 hours for the assembly and release of flaviviruses. The virions are finally released by exocytosis or by budding or when the cell lyses (Solomon et al. 2003).
Pathway
West Nile virus is introduced to new locations through infected birds (CDC, 2003).

Principal source: West Nile virus Basics (CDC, 2003)

Compiler: National Biological Information Infrastructure (NBII) & IUCN/SSC Invasive Species Specialist Group (ISSG)
Updates completed with support from the Ministry of Agriculture and Forestry (MAF)- Biosecurity New Zealand

Review: Michael Holbrook. Department of Pathology, Center for Biodefense and Emerging Infectious Diseases, and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston. USA

Publication date: 2006-03-31

Recommended citation: Global Invasive Species Database (2016) Species profile: West Nile virus. Downloaded from http://www.iucngisd.org/gisd/species.php?sc=304 on 27-09-2016.

General Impacts
According to the CDC (2003), most people infected with the West Nile virus will not display any symptoms. It is estimated that only 20% of the people who become infected will develop symptoms, which usually occur after an incubation period of 2-14 days. These are often flu-like including fever, headache, body aches, malaise, myalgia, fatigue, lymphadenopathy, vomiting, diarrhea and occasionally a skin rash. This relatively mild condition is known as West Nile fever (WNF), and most patients completely recover within days to months (Bode et al. 2003; Watson et al. 2004; Klee et al. 2004 in Kramer et al. 2007).

Please follow this link for detailed information on the impacts of the West Nile virus (WNV) on humans, horses and birds, compiled by the IUCN SSC Invasive Species Specialist Group.

Management Info
Because of the large impact of WNV on human and animal health, it is critical to develop effective methods to limit WNV transmission and prevent and/or treat WN disease.

Currently, control measures to curtail WNV transmission include reducing mosquito vector populations and limiting exposure to mosquito bites with protective clothing and repellents. Vector control agencies often use a combination of approaches (mosquito population monitoring, mosquito source reduction, larvicide and adulticide application, and public education) to reduce mosquito populations.

Please follow this link for detailed information on the control and management of the West Nile virus (WNV), compiled by the IUCN SSC Invasive Species Specialist Group.

Countries (or multi-country features) with distribution records for West Nile virus
Informations on West Nile virus has been recorded for the following locations. Click on the name for additional informations.
Lorem Ipsum
Location Status Invasiveness Occurrence Source
Details of West Nile virus in information
Status
Invasiveness
Arrival date
Occurrence
Source
Introduction
Species notes for this location
Location note
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Impact
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Ecosystem services:
Impact information
According to the CDC (2003), most people infected with the West Nile virus will not display any symptoms. It is estimated that only 20% of the people who become infected will develop symptoms, which usually occur after an incubation period of 2-14 days. These are often flu-like including fever, headache, body aches, malaise, myalgia, fatigue, lymphadenopathy, vomiting, diarrhea and occasionally a skin rash. This relatively mild condition is known as West Nile fever (WNF), and most patients completely recover within days to months (Bode et al. 2003; Watson et al. 2004; Klee et al. 2004 in Kramer et al. 2007).

Please follow this link for detailed information on the impacts of the West Nile virus (WNV) on humans, horses and birds, compiled by the IUCN SSC Invasive Species Specialist Group.

Red List assessed species 9: EW = 1; CR = 1; EN = 2; VU = 2; NT = 2; LC = 1;
Mechanism
[7] Disease transmission
Outcomes
[4] Environmental Species - Population
  • [4] Plant/animal health
[4] Socio-Economic
  • [1] Reduce/damage livestock and products
  • [3] Human health
Management information
Because of the large impact of WNV on human and animal health, it is critical to develop effective methods to limit WNV transmission and prevent and/or treat WN disease.

Currently, control measures to curtail WNV transmission include reducing mosquito vector populations and limiting exposure to mosquito bites with protective clothing and repellents. Vector control agencies often use a combination of approaches (mosquito population monitoring, mosquito source reduction, larvicide and adulticide application, and public education) to reduce mosquito populations.

Please follow this link for detailed information on the control and management of the West Nile virus (WNV), compiled by the IUCN SSC Invasive Species Specialist Group.

Locations
Management Category
Control
Monitoring
Bibliography
42 references found for West Nile virus

Managment information
CDC (Center for Disease Control and Prevention). 2003. West Nile Virus Basics. Fort Collins, Colorado.
Summary: A detailed report that describes all aspects of the ecology, biology, prevention and distribution of the West Nile Virus.
Available from: http://www.cdc.gov/ncidod/dvbid/westnile/#about [Accessed 13 May 2003].
CDC (Centers for Disease Control and Prevention. 2003b. Epidemic/Epizootic West Nile Virus in the United States: Guidelines for Surveillance, Prevention, and Control. Fort Collins, Colorado.
Summary: Available from: http://www.cdc.gov/ncidod/dvbid/westnile/resources/wnv-guidelines-apr-2001.pdf [Accessed 13 May 2003].
Davis, M.R., Langan, J.N., Johnson, Y.J., Ritchie, B.W. & Van Bonn, W. 2008. West Nile virus seroconversion in penguins after vaccination with a killed virus vaccine or a DNA vaccine. Journal of Zoo and Wildlife Medicine 39(4): 582-589.
Elnaiem, D.A., Kelley, K., Wright, S., Laffey, R., Yoshimura, G., Reed, M., Goodman, G., Theimann, T., Reimer, L., Reisen, W.K. & Brown, D. 2008. Impact of aerial spraying of pyrethrin insecticide on Culex pipiens and Culex tarsalis (Diptera: Culicidae) abundance and West Nile virus infection rates in an urban/suburban area of Sacramento County, California. Journal of Medical Entomology 45(4): 751-757.
Mehlhop, E. and Diamond, M.S. 2008. The molecular basis of antibody protection against West Nile virus.. Current Topics in Microbiology and Immunology 317: 125-153.
Reisen, W.K., Takahashi, R.M., Carroll, B.D. & Quiring, R. 2008. Delinquent mortgages, neglected swimming pools and West Nile virus, California. Emerging Infectious Diseases 14(11): 1747-1749.
Spurr, E.B., 2004. Preliminary risk assessment for the establishment of West Nile virus in New Zealand / Eric B. Spurr & Graham R. Sandlant. � Lincoln, N.Z. : Manaaki Whenua Press, 2004.
Summary: An assessment of the risk that West Nile virus (WNV) might establish in New Zealand was conducted by comparing the taxonomic relatedness of potential vectors and hosts in New Zealand to known WNV vectors and hosts overseas, and assessing whether WNV might survive and spread after arriving. Surveillance strategies currently used in North America to detect outbreaks of WNV were reviewed and assessed to establish whether they are relevant to New Zealand or whether other strategies should be used.
Available from: http://www.landcareresearch.co.nz/publications/scienceseries/downloads/lrsciseries25_spurr2004_4web.pdf [Accessed 9 September 2005]
Wilson, K. 2003, December 1. Endangered fish restore the balance. Arizona Daily Wildcat.
Summary: Available from: http://wc.arizona.edu/papers/97/67/03_3.html [Accessed 28 May 2009]
Zou, L., Miller, S.N. & Schmidtmann, E.T. 2007. A GIS tool to estimate West Nile Virus risk based on a degree-day model. Environmental Monitoring and Assessment 129: 413-420.
General information
Allan, B.F., Landerhans, B., Ryberg, W.A., Landesman, W.J., Griffin, N.W., Katz, R.S., Schutzenhofer, M.R., Smyth, K.N., de St. Maurice, A., Clark, L., Crooks, K.R., Hernandez, D.E., McLean, R.G., Ostfeld, R.S. & Chase, J.M. 2009. Ecological correlates of risk and incidence of West Nile virus in the United States. Oecologia 158: 699-708.
Almeida, A.P.G., Galao, R.P., Sousa, C.A., Novo, M.T., Parreira, R., Pinto, J., Piedade, J. & Esteves, A. 2008. Potential mosquito vectors of arboviruses in Portugal: species, distribution, abundance and West Nile infection. Transactions of the Royal Society of Tropical Medicine and Hygiene 102: 823-832.
BBC. 2004a. West Nile virus cases in Ireland
Summary: Available from: http://news.bbc.co.uk/2/hi/health/3927761.stm [Accessed January 28, 2009]
BBC. 2004b. West Nile virus strategy drawn up.
Summary: Available from: http://news.bbc.co.uk/2/hi/health/3757229.stm [Accessed January 28, 2009]
Bowen, R.A. & Nemeth, N.M. 2007. Experimental infections with West Nile virus. Current Opinion in Infectious Diseases 20: 293-297.
Burke, D. S. and Monath, T. P. 2001. Flaviviruses. In Field s Virology. Lippincott, William and Wilkin
Summary: A comprehensive text on all viruses.
Goddard, J. 2008. What is new with West Nile virus? Infections in Medicine 25(3).
Harasym, C.A. 2008. West Nile virus and hemoparasites in captive snowy owls (Bubo scandiacus) - Management strategies to optimize survival. Canadian Veterinary Journal 49(11): 1136-1138.
Hayes, C.G. 2001. West Nile virus: Uganda, 1937, to New York City, 1999. Annals of the New York Academy of Sciences 951: 25-37.
Hinckley, A.F., O�Leary, D.R. & Hayes, E.B. 2007. Transmission of West Nile virus through human breast milk seems to be rare. Pediatrics 119: 666-671.
Irwin, P., Arcari, C., Hausbeck, J. & Paskewitz. 2008. Urban wet environment as mosquito habitat in the upper Midwest. EcoHealth 5: 49-57.
Jacobson, E.R., Ginn, P.E., Troutman, J.M., Farina, L., Stark, L., Klenk, K., Burkhalter, K.L. & Komar, N. 2005. West Nile virus infection in farmed American alligators (Alligator mississippiensis) in Florida. Journal of Wildlife Diseases 41(1): 96-106.
Jansen, C.C., Webb, C.E. Northill, J.A., Ritchie, S.A., Russell, R.C. & Van Den Hurk, A.F. 2008. Vector competence of Australian mosquito species for a North American strain of West Nile virus. Vector-Borne and Zoonotic Diseases 8(6): 805-811.
Komar, N. & Clark, G.G. 2006. West Nile virus activity in Latin America and the Carribean. Pan American Journal of Public Health 19(2): 112-117.
Kramer, L.D., Li, J. & S. P.Y. 2007. West Nile virus. Lancet Neurology 6: 171-181.
Kramer, L.D., Styer, L.M. & Ebel, G.D. 2008. A global perspective on the epidemiology of West Nile Virus. Annual Review of Entomology 53: 61-81.
LaDeau, S., Marra, P.P., Kilpatrick, A.M., Calder, C.A. 2008. West Nile virus revisited: consequences of North American ecology. Bioscience 58(10): 937-946.
Lindsey, N.P., Kuhn, S., Campbell, G.L. & Hayes, E.b. 2008. West Nile virus neuroinvasive disease incidence in the United States, 2002-2006. Vector-Borne and Zoonotic Diseases 8(1): 35-39.
Lvov, D.K., Shchelkanov, M.Yu., Kolobukhina, L.V., Lvov, D.N., Galkina, I.V., Aristova, V.A., Morozova, T.N., Proshina, Ye.S., Kulikov, A.G., Kogdenko, N.V., Andronova, O.V., Pronin, N.I., Shevkoplyas, V.N., Fontanetsky, A.S., Vlasov, N.A. & Nepoklonov, Ye.A. 2008. Serological monitoring of arbovirus infections in the estuary of the Kuban River (the 2006-2007 data). Voprosy Virusologii 53(4): 30-35.
Mackay, A.J., Roy, A., Yates, M.M. & Foil, L.D. 2008. West Nile virus detection in mosquitoes in East Baton Rouge Parish, Louisiana, from November 2002 to October 2004. Journal of the American Mosquito Control Association 24(1): 28-35.
Moskvitina, N.S., Romanenko, V.N., Ternovoi, V.A., Ivanova, N.V., Protopopova, E.V., Kravchenko, L.B., Kononova, Y.V., Kuranova, V.N., Chausov, E.A., Moskvitin, S.S., Pershikova, N.L., Gashkov, S.I., Konovalova, S.N., Bolshakova, N.P. & Loktev, V.B. 2008. Detection of the West Nile virus and its genetic typing in ixodid ticks (Parasitiformes: Ixodidae) in Tomsk City and its suburbs. Parazitologiya 42(3): 210-225.
Murray, K.O., Baraniuk, S., Resnick, M., Arafat, R., Kilborn, C., Shallenberger, R., York, T.L., Martinez, D., Malkoff, M., Elgawley, N., McNeely, W., Khuwaja, S.A. 2008. Clinical investigation of hospitalized human cases of West Nile virus infection in Houston, Texas, 2002-2004. Vector-Borne and Zoonotic Diseases 8(2).
New Jersey Department of Agriculture 2001. West Nile Virus in New Jersey Equine.
Summary: A report on the economic impact of West Nile Virus on the equine community.
Available from: http://www.state.nj.us/agriculture/wnveq0001.htm [Accessed 15 May 2003]
Paramasivan, R., Mishra, A.C. & Mourya, D.T. 2003. West Nile virus: the Indian scenario. Indian Journal of Medical Research 118: 101-108.
Paz, S. 2006. The West Hile virus outbreak in Israel (2000) from a new perspective: the regional impact of climate change. International Journal of Environmental Health Research 16(1): 1-13.
Petersen, L.R. & Hayes, E.B. 2008. West Nile virus in the Americas. Medical Clinics of North America 92: 1307-1322.
Pfleiderer, C., Blumel, J., Schmidt, M., Roth, K., Houfar, M.K., Eckert, J., Chudy, M., Menichetti, E., Lechner, S. & Nubling, C.M. West Nile virus and blood product safety in Germany. Journal of Medical Virology 80: 557-563.
Platonov, A.E., Fedorova, M.V., Karan, L.S., Shopenskaya, T.A., Platonova, O.V. & Zhurayle, V.I. 2008. Epidemiology of West Nile infection in Volgograd, Russia, in relation to climate change and mosquito (Diptera: Culicidae) bionomics. Parasitology Research 103: 45-53.
Puig-Basagoiti, F., Tilgner, M., Forshey, B.M., Philpott, S.M., Espina, N.G., Wenworth, D.E., Goebel, S.J., Masters, P.S., Falgout, B., Ren, P., Ferguson, D.M. & Shi, P.Y. 2006. Triaryl pyrazoline compound inhibits flavivirus RNA replication. Antimicrobial Agents and Chemotherapy 50(4): 1320-1329.
Solomon, T., M. H. Ooi, D. W. C. Beasley, and M. Mallewa. 2002. West Nile encephalitis. BMJ Publishing Group Ltd. 326:865-869.
Summary: A clinical review on information about all aspects of the West Nile Virus.
Available from: http://bmj.com/cgi/content/full/326/7394/865 [Accessed 13 May 2003].
Sovada, M.A., Pietz, P.J., Converse, K.A., King, T., Hofmeister, E.K., Scherr, P. & Ip, H.S. 2008. Impact of West Nile virus and other mortality factors on American white pelicans at breeding colonies in the northern plains of North America. Biological Conservation 141: 1021-1031.
Trevejo, R.T. 2008. West Nile Virus. Journal of the American Veterinary Medical Association 232(9): 1302-1309.
Wolf, T.M., Gandolf, A.R., Dooley, J.L., Atkinson, M.W. & Wolfe, B.A. 2008. Serologic responser to West Nile virus vaccination in the greater one-horned rhinoceros (Rhinoceros unicornis). Journal of Zoo and Wildlife Medicine 39(4): 537-541.
Contact
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