West Nile Virus
Renee R. Anderson and Laura C. Harrington
Numerous mosquito-borne viral diseases causing encephalitis (inflammation of the brain) occur throughout the United States. The virus responsible for West Nile virus (WNV) is the most recent addition. West Nile virus appeared during the summer of 1999 in the New York City area causing the hospitalization of 62 people and resulting in 7 deaths.1-3,8,10
West Nile virus, known since the late 1930s, is widely distributed throughout the world. It has been found in parts of Africa, the Middle East, Europe, Western Asia, and North and South America. It was not until this century that epidemics began to occur more frequently with subsequent increases in human fatality rates similar to rates observed when the virus was introduced into North America.5,6 As of September 2004, West Nile virus activity had been detected in all of the contiguous 48 states and is now considered endemic.
Infection with WNV may cause no symptoms or mild flu-like illness in humans. Clinical disease can progress to a lethal inflammation of the brain (encephalitis) and spinal cord (meningitis). Centers for Disease Control and Prevention scientists have recently alerted physicians of other possible neurological symptoms associated with WNV.4 These symptoms mimic those associated with strokes, polio, and Parkinson's disease. The incubation period of WNV in humans is typically 3-14 days. According to the Centers for Disease Control and Prevention, an estimated twenty percent of people infected will develop symptoms. The severe form of West Nile fever occurs in 1 in 150 people showing symptoms.
Currently no specific treatment exists for WNV infection in humans other than supportive therapy. Two antiviral drugs administered in high doses have shown some activity in vitro, but controlled case studies have not been completed. Early stage clinical trails are in progress to assess safety and effectiveness of treating patients with immunoglobulin G antibodies. Development of a protective vaccine for humans is underway and is not yet available.
The ecology of most arthropod-borne viruses is complicated, and WNV is no exception. It is currently thought that West Nile virus is maintained primarily in the bird population by mosquitoes. Birds are the natural host for the virus, although viral infection has been fatal to many native and exotic bird species in the United States. The most important birds involved in virus amplification have not been identified, although recent studies have demonstrated that perching birds (Passeriformes), certain gulls (Charadriiformes), and two birds of prey species (Falconiformes and Strigiformes) had a greater ability to pass on the virus to a mosquito host than other bird groups tested.7 Mosquito species that help maintain the bird cycle of transmission are called maintenance vectors.
Mosquito transmission of the virus from birds to humans also occur. These mosquitoes are referred to as bridge vectors and are species that readily feed on both birds and humans. Humans and horses are considered "dead-end hosts" because the virus does not circulate in the blood at high enough levels to be infectious to mosquitoes.
At least 62 known mosquito species occur in New York state, and at least 16 of these species have tested positive for WNV infection by virus isolation, detection of viral nucleic acids, or detection of viral antigen.9 One must be careful not to interpret this as evidence that all of these mosquitoes are involved in virus transmission. It simply means that these mosquitoes have fed upon an infected host at least once. Some mosquitoes can be infected with the virus but are not capable of transmitting it to birds or humans.
Several criteria must be met before incriminating a mosquito species as a vector. These established standards involve careful scientific scrutiny. Conditions for incrimination of a vector species can be summarized into four broad categories: 1) there must be repeated virus isolations from field-caught mosquitoes; 2) the alleged mosquito species must be susceptible to virus infection in a carefully controlled laboratory setting and be able to transmit the virus to a susceptible host; 3) the mosquito species must feed on vulnerable hosts in nature; and 4) an association between mosquito activity and virus transmission must exist in nature.
Based on the number of positive field-collected mosquito pools and our limited knowledge of mosquito host feeding preferences, a few mosquito species appear to be more important for virus maintenance in birds, while others are more likely to be involved in transmission of virus to humans, horses, and other animals as bridge vectors.9,11,12 Many suspected vectors are species that breed in discarded tires and similar habitats. Of the suspected mosquito vectors the following species occur in New York state and are known to breed in artificial containers: Culex p. pipiens, Culex restuans, Culex salinarius, Ochlerotatus j. japonicus, Ochlerotatus triseriatus, Ochlerotatus atropalpus, and Aedes albopictus.
Culex p. pipiens prefers to feed on birds. Laboratory studies have demonstrated that this species is a moderately efficient vector of West Nile virus.11,12 Based on our knowledge of Culex p. pipiens bird-feeding habits, numerous field isolates, and laboratory demonstration of vector competence, this species is likely to be the most important vector in maintaining West Nile virus in birds in a peridomestic habitat. Culex restuans also shows potential for being involved in virus transmission between birds. Ochlerotatus j. japonicus, Ochlerotatus triseriatus, Ochlerotatus atropalpus, Aedes albopictus, and Culex salinarius are opportunistic feeders and have been shown to be competent vectors in the laboratory.11,12 Additional field and laboratory studies are essential to clarify what role these and other mosquito species play in virus transmission to humans, horses, and other animals.
Do your part to eliminate mosquito-breeding sites around your home, because many of the suspected vectors are those that utilize natural habitats and artificial containers found around residential areas. Control targeted at the larval stage is best both economically and ecologically because mosquitoes are confined to one space at this stage of their development. Please refer to the fact sheet "Mosquito Biology for the Homeowner" for information on controlling larvae.
Medical entomologists are often asked whether recent heavy rains will result in an increased activity level of West Nile virus. Another common question is what impact recent droughts will have on the transmission of West Nile virus. Other questions include what influence a recent cool spell or heat wave may have on virus transmission. These seemingly simple questions are very difficult to answer, and numerous researchers have conducted and are currently conducting studies in order to understand temperature and rainfall impacts on the ecology of West Nile virus. It has been shown that heavy rainfalls can at times be detrimental to container-breeding mosquitoes. Heavy and frequent rain can flush out egg rafts, larvae, and pupae from containers and can be detrimental to localized populations in the microhabitat.
Mosquitoes are cold-blooded animals, and their development depends upon ambient temperature. Generally, the warmer it is the more quickly the mosquito develops from egg to adult stage. Replication of the virus in the mosquito is also temperature-dependent. Cooler ambient temperatures slow virus replication, while warmer temperatures increase replication.
There is no way to visually determine whether a mosquito is infected, thus it is prudent to avoid any bites. Check with your county health department for reports on virus activity in your area. Protection from mosquito bites involves making individual choices. Please refer to the fact sheet, "Mosquito Biology for the Homeowner" for additional information on personal protection.
Centers for Disease Control and Prevention. 1999. Outbreak of West Nile-like viral encephalitis--New York, 1999. Morbidity and Mortality Weekly Report 48(38): 845-849.
Centers for Disease Control and Prevention. 1999. Outbreak of West Nile-like viral encephalitis--New York, 1999. Morbidity and Mortality Weekly Report 48(39): 890-892.
Centers for Disease Control and Prevention. 1999. Outbreak of West Nile-like viral encephalitis--New York, 1999. Morbidity and Mortality Weekly Report 48(41): 944-946.
Centers for Disease Control and Prevention. 2002. Acute flaccid paralysis syndrome associated with West Nile virus infection-Mississippi and Louisiana, July-August 2002. Morbidity and Mortality Weekly Report 51(37): 825-828.
Hubalek, Z. 2000. European experience with the West Nile virus ecology and epidemiology: could it be relevant for the new world? Viral Immunology 13(4): 415-426.
Hubalek, Z. and J. Halouzka. 1999. West Nile fever -- a reemerging mosquito-borne viral disease in Europe. Emerging Infectious Diseases 5(5): 643-650.
Komar, N., S. Langevin, S. Hinten, N. Nemeth, E. Edwards, D. Hettler, B. Davis, R. Bowen, and M. Bunning. 2003. Experimental infection of North American birds with the New York 1999 strain of West Nile virus. Emerging Infectious Diseases 9(3): 311-322.
Nash, D., F. Mostashari, A. Fine, J. Miller, D. O'Leary, K. Murray, A. Huang, A. Rosenberg, A. Greenberg, M. Sherman, S. Wong, and M. Layton. 2001. Outbreak of West Nile virus infection, New York City area, 1999. New England Journal of Medicine 344(24): 1807-1814.
New York State Department of Health. Accessed February 2004, at http://www.health.state.ny.us/
Novello, A. C. 2000. West Nile virus in New York State: The 1999 outbreak and response plan for 2000. Viral Immunology 13(4): 463-467.
Turell, M. J., M. L. O'Guinn, D. J. Dohm, and J. W. Jones. 2001. Vector competence of North American mosquitoes (Diptera: Culicidae) for West Nile virus. Journal of Medical Entomology 38(2): 130-234.
Turell, M. J., M. R. Sardelis, and D. J. Dohm. 2001. Potential North American vectors of West Nile virus. Annals New York Academy of Sciences 951: 317-324.
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