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West Nile Virus Our courses fulfill continuing nursing education requirements in all 50 states. For more accreditation information, click here.
West Nile virus (WNV) is a mosquito-borne virus that was recently introduced into the temperate regions of North America and Europe. It is an arbovirus, meaning it is spread by an arthropod—in this case the Culex mosquito. Birds infected by a WNV-carrying mosquito inadvertently spread the virus when mosquitoes take a blood meal from the bird (Figure 1). Although most birds infected with WNV will not die, the occurrence of large numbers of bird deaths is a sentinel event and signals the presence of WNV in a particular geographic area. 
Figure 1 Mosquito feeding. Culex pipiens mosquitos carry West Nile virus. Photo courtesy of CDC. People and other animals, particularly horses, can be infected by a mosquito that has fed on an infected bird. Because the virus must enter the bloodstream to cause an infection, it is not likely for an individual to become infected by having casual contact with infected birds, animals, or people. There is no evidence that birds can directly infect other birds or animals. There are no reported cases of human-to-human infection. WNV can cause mild or severe symptoms. Most persons who become infected with WNV develop no clinical illness or symptoms. In previous outbreaks in the Northern Hemisphere, an estimated 80% of people who became infected never developed symptoms attributable to the infection. Of the approximately 20% of infected people who do develop symptoms, most develop what has been termed West Nile fever. The incubation period for WNV infection is thought to range from about 2 to 14 days, although longer incubation periods have been documented in immunosuppressed persons (CDC, 2004a). The most serious symptom is fatal encephalitis (inflammation of the brain) in humans and horses. Among humans with severe illness due to West Nile virus, case-fatality rates range from 3% to 15% and are highest among the elderly. Less than 1% of people who become infected with West Nile virus will develop severe illness—most people who get infected do not develop any disease at all (CDC, 2006a). GEOGRAPHIC DISTRIBUTIONWest Nile virus is present in Africa, Europe, the Middle East, west and central Asia, Oceania, and North America. In the United States from 1999 through 2005 WNV has been documented in every area except Alaska, Hawaii, and Puerto Rico (Figure 2). The discovery of virus-infected, overwintering mosquitoes during the winter of 1999–2000 in New York focused on identifying and documenting WNV infections in birds, mosquitoes and horses as sentinel animals that could predict the occurrence of human disease. By the end of the 2000 transmission season, WNV activity had been identified in a twelve-state area from Vermont and New Hampshire in the north to North Carolina in the south (CDC, 2003a). The 2002 WNV epidemic was the largest recognized arboviral meningoencephalitis epidemic in the Western Hemisphere and the largest WNV meningoencephalitis epidemic ever recorded. Significant human disease activity was recorded in Canada for the first time, and WNV activity was also documented in the Caribbean basin and Mexico (CDC, 2003a). By 2004 WNV had spread to the west coast of the United States; in early 2004 the first confirmed case of WNV was reported in California, including one death. By the end of 2005, WNV had spread to all areas of the country except Alaska, Hawaii, and Puerto Rico. 
Figure 2 2005 West Nile Virus Activity in the United States. This map reflects surveillance findings occurring between January 1, 2005 and December 31, 2005, as reported to CDC's ArboNET system for public distribution by state and local health departments. (CDC, 2006b) EPIDEMIOLOGYWest Nile virus is a member of the family Flaviridae (genus Flavivirus), part of the Japanese encephalitis virus complex that includes St. Louis encephalitis (SLE), Japanese encephalitis, dengue, tick-borne encephalitis, yellow fever, Kunjin, and Murray Valley encephalitis viruses, as well as others. For unknown reasons, deaths among birds from WNV infection have occurred only in the United States, Israel, Canada, and Mexico. Since 1999, very few genetic changes have occurred in the WNV strains circulating in the United States (CDC, 2004b). West Nile virus (WNV) was first isolated and identified in 1937 in a febrile person in the West Nile district of Uganda. Prior to 1999, the virus was found only in the Eastern Hemisphere, with wide distribution in Africa, Asia, the Middle East, and Europe. There were infrequent reports of human outbreaks, mainly associated with mild febrile illnesses, in Israel and Africa. These were mostly in groups of soldiers, children, and healthy adults. One notable outbreak in Israeli nursing homes in 1957 was associated with severe neurologic disease and death (CDC, 2004c). Since the mid-1990s, the frequency and apparent clinical severity of WNV outbreaks have increased. Outbreaks in Romania (1996), Russia (1999), and Israel (2000) involved hundreds of persons with severe neurologic disease. It is unclear if this apparent change in disease severity and frequency is due to differences in the circulating virus's virulence or to changes in the age structure, background immunity, or prevalence of other predisposing chronic conditions in the affected populations (CDC, 2004c). The first appearance of WNV in North America was in 1999, with encephalitis reported in humans and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus (CDC, 2003a). The spread of WNV in North America has been rapid. From 1999 through May 16, 2006 there were more than 19,000 confirmed cases of WNV human illness in the United States reported to CDC and 785 fatalities (Table 1).
Among all reported cases in humans the median age is 55; 54% of cases are in men and 46% are in women. In 2002 the epidemic peaked during the week ending August 17 in the southern states and the week ending August 24 in the northern states. During 2002, Illinois, Michigan, and Ohio had the highest caseloads (CDC, 2003a).
ENTOMOLOGYMosquito Life CycleMosquitoes are insects. They go through four life stages (complete metamorphosis) and look completely different at each stage: egg, larva, pupa, and adult. The first three life stages are spent in water or wet places. Adults emerge from the pupal stage full size and able to fly. Adult females bite to get a blood meal that provides the nutrients they need to form each brood of eggs (CDC, 2004d). 
Figure 3 The mosquito life cycle. Courtesy of CDC. There are about 200 different species of mosquitoes in the United States, all of which live in specific habitats, exhibit unique behaviors, and bite different types of animals. Despite these differences, all mosquitoes share some common traits, such as a four-stage life cycle. After the female mosquito obtains a blood meal (male mosquitoes do not bite), she lays her eggs directly on the surface of stagnant water, in a depression, or on the edge of a container where rainwater may collect and flood the eggs (CDC, 2004d). 
Figure 4 A female mosquito laying her eggs in a stagnant body of water. Courtesy of CDC. The eggs hatch and a mosquito larva or "wriggler" emerges. The larva lives in the water, feeds and develops into a pupa or "tumbler." The pupa also lives in the water, but no longer feeds. Finally, the mosquito emerges from the pupal stage and the water as a fully developed adult, ready to bite (CDC, 2004d). Culex MosquitoesAlthough over 60 species of mosquitoes have tested positive for the West Nile virus, Culex pipiens (Northern house mosquitoes) are the species of mosquitoes most closely associated with transmitting WNV in the Northeast United States. These mosquitoes "prefer" to bite birds, but if breeding sites are available near homes and domestic animal enclosures, Culex pipiens may bite people and domestic animals. Culex pipiens are most active between dawn and dusk. Culex quinquefasciatus (Southern house mosquitoes) fill this niche in the southern United States (CDC, 2003b). Some other types of mosquitoes have been found to be WNV-positive in the United States. These include Culex salinarius and Aedes vexans, which are of potential concern because they feed more readily on mammals, including humans, than do other mosquito species associated with WNV. (Cx. Pipiens, Cx. restuans, and Culiseta melanura all prefer to feed on birds). Some of these species bite during the daytime. In all, 60 species of mosquitoes are known to be infected with WNV (CDC, 2003b). Transmission CycleIn 1999 WNV was transmitted principally by Culex species mosquitoes. In 2000 a total of fourteen WNV-infected mosquito species were identified, although 89% of positive mosquito pools were Culex. In contrast to Culex, many of these other species are daytime feeders and mammal feeders. The effect that this widened spectrum of WNV-infected mosquito species will have on WNV ecology in the United States is not known (CDC, 2003b). 
Figure 5 West Nile transmission cycle. Courtesy of CDC. Infectious mosquitoes carry virus particles in their salivary glands and infect susceptible bird species during blood-meal feeding. Birds will sustain an infectious viremia (virus circulating in the bloodstream) for 1 to 4 days after exposure, after which these hosts develop lifelong immunity. People, horses, and most other mammals are not known to develop infectious-level viremias very often, and thus are probably "dead-end" or incidental-hosts (CDC, 2003b). BirdsMortality in a wide variety of bird species has been a hallmark of WNV in the United States. The reasons for this are not known; however, public health officials were able to use bird mortality (particularly birds from the family Corvidae such as crows, blue jays, and ravens) to effectively track WNV expansion in 2000. Although WNV infection is fatal in a large percentage of Corvids, many other bird species survive WNV infection. It is not known if affected birds develop immunity or if they become chronically infected and susceptible to related illness during times of stress. Supportive treatment with antibiotics and nonsteroidal anti-inflammatories early in the illness appears to help. Migrating birds likely contribute to natural transmission cycles and dispersal of the virus (Cornell University, 2005a). Through May 2005 WNV had been detected in at least 285 bird species. The following bird species have been reported to CDC's West Nile Virus avian mortality database from 1999 to 2005 (CDC, 2005).
There is no evidence that an individual can get WNV from handling live or dead infected birds. But people should avoid bare-handed contact when handling any dead animals, and use gloves or double plastic bags to place the bird carcass in a garbage bag or contact their local health department for guidance (CDC, 2003b). Dogs and CatsWest Nile virus does not appear to cause extensive illness in dogs or cats. There is a single published report of WNV isolated from a dog in southern Africa (Botswana) in 1982. West Nile virus was isolated from a single dead cat in 1999. A sero-survey in New York City of dogs in the 1999 epidemic area indicated that dogs are frequently infected. Nonetheless, disease from WNV infection in dogs has yet to be documented (CDC, 2003b). There is no documented evidence of person-to-person or animal-to-person transmission of WNV. Because WNV is transmitted by infectious mosquitoes, dogs or cats could be exposed to the virus in the same way humans become infected. Veterinarians should take normal infection-control precautions when caring for an animal suspected to have WNV infection. It is possible that dogs and cats could become infected by eating dead infected animals such as birds, but this is undocumented. There is no reason to destroy an animal just because it has been infected with WNV. Full recovery from the infection is likely. Treatment would be supportive and consistent with standard veterinary practices for animals infected with a viral agent (CDC, 2003b). HorsesHorses are affected by WNV more than other mammals, and cases of WNV disease in horses have been documented either by virus isolation or by detection of WN virus-neutralizing antibodies. Horses most likely became infected with WNV in the same way humans become infected, by the bite of infectious mosquitoes. Horses and humans are dead-end hosts and do not contribute to the transmission of the virus. Horses are not contagious and cannot infect other horses. Once a horse has been bitten by an infected mosquito, WNV multiplies in the horse's blood, crosses the blood-brain barrier, and infects the brain. The virus can interfere with normal central nervous system (CNS) functioning and cause inflammation of the brain. About 75% of horses that are bitten do not become seriously ill. Of the ones with a more serious illness, one-third of these will die or be euthanized (CDC, 2003b). 
Figure 6 Equine cases of West Nile virus during 2005, state by state. Courtesy of USDA, 2005. In locations where WNV is circulating, horses should be protected from mosquito bites as much as possible. Horses vaccinated against Eastern equine encephalitis (EEE), Western equine encephalitis (WEE), and Venezuelan equine encephalitis (VEE) are not protected against WNV infection. The mortality rate for horses exhibiting clinical signs of West Nile virus infection is approximately 33%. Data has supported that 40% of horses that survive the acute illness caused by WNV still exhibit residual effects, such as gait and behavioral abnormalities that were attributed to the illness by owners 6 months post diagnosis (American Association of Equine Practitioners, 2005). There is no reason to destroy a horse just because it has been infected with WNV. Data suggest that most horses recover from the infection. Treatment would be supportive and consistent with standard veterinary practices for animals infected with a viral agent (CDC, 2003b). Signs of severe WNV illness in horses may include ataxia (lack of coordination, stumbling, staggering), difficulty walking, knuckling over, head tilt, muscle twitches or tremors, inability to stand, circling, weakness or paralysis of limbs, apparent blindness, lip droop, grinding teeth, and death. However, these symptoms could also be caused by other diseases including rabies, eastern and western equine encephalitis virus infections, and equine herpes virus-1 infection. HORSE VACCINEIn November 2002 a vaccine (West Nile-Innovator) intended to aid in the prevention of WNV in horses was licensed by the Veterinary Services division of the U.S. Department of Agriculture's Animal and Plant Health Inspection Service. This is a killed vaccine product, and its use is restricted to licensed veterinarians. 
Figure 6 A horse being vaccinated against West Nile virus. Photo courtesy of CDC. The vaccine is administered to healthy horses in two (1-ml) intramuscular (IM) doses 3 to 6 weeks apart, followed by a yearly booster. Since the vaccine is not effective for five weeks after it is administered, the first dose should be given at least six weeks prior to expected mosquito activity in the area. Horses bitten by an infected mosquito before receiving the second dose of vaccine may become infected and ill. Booster shots should given yearly or every six months in warmer areas with large mosquito populations in order to maintain maximum immunity (USDA, 2005). Preliminary observations look promising: Of the 20,000 equines vaccinated during preliminary testing in Florida in 2001, only one developed WNV infection. It is possible that the much lower rate of WNV equine infections in East Coast states in 2003 compared with Midwest states is reflective of the efficacy of the equine virus (assuming that more East Coast horses were vaccinated than in states where WNV was not expected) (Cornell University, 2005b). A recombinant vaccine (RECOMBITEK Equine West Nile Virus vaccine) has also been licensed by the USDA for use in horses. The vaccine induces an immune response against WNV. In July 2005, the U.S. Department of Agriculture granted full licensure to Fort Dodge Laboratories, a division of Wyeth, for a DNA vaccine for horses. It is the first DNA vaccine to receive approval and represents a new generation of vaccine. DNA vaccines use a fragment of the organism's genetic material to stimulate an immune response in the host. The vaccine is expected to be available commercially sometime in 2006. Other VertebratesThe CDC has also received a small number of reports of WNV infection in bats, a chipmunk, a skunk, a squirrel, and a domestic rabbit (Cornell University, 2005a). CLINICAL FINDINGSSigns and SymptomsMost people who become infected with WNV do not get sick. If infection does occur, it may take 3 to 14 days to become ill. Older people are more likely to become very ill from WNV. It is estimated that about 20% of the people who become infected will develop West Nile fever: the symptoms include fever, headache, tiredness, and body aches, occasionally with a skin rash on the trunk of the body and swollen lymph glands (CDC, 2004a). Most WNV infections are mild and often clinically unapparent:
Severe infection (West Nile encephalitis or meningitis) is sometimes referred to as "neuro-invasive disease." It is estimated that approximately 1 in 150 persons infected with the WNV will develop a more severe form of disease (CDC, 2004a). The most significant risk factor for developing severe neurologic disease is advanced age. Encephalitis is more commonly reported than meningitis. Neurologic presentations included:
A minority of patients with severe disease developed a maculopapular or morbilliform rash involving the neck, trunk, arms, or legs. Several patients experienced severe muscle weakness and flaccid paralysis (CDC, March 2004). Although not observed in recent outbreaks, myocarditis, pancreatitis, and fulminant hepatitis have been described (CDC, 2004a ). In 1999 in New York, approximately 40% of laboratory-positive humans with encephalitis or meningitis had severe muscle weakness; 10% developed flaccid paralysis with electromyographic findings consistent with axonal neuropathy. Healthcare and Laboratory WorkersPeople working outdoors when mosquitoes are actively biting are at risk of infection and should be educated about this occupational health issue and available recommendations. Although WNV is most often transmitted by the bite of infected mosquitoes, the virus can also be transmitted through contact with infected animals, their blood, or other tissues. Thus laboratory, field, and clinical workers who handle tissues or fluids infected with WNV or who perform necropsies are at risk of WNV exposure (CDC NIOSH, 2005). These workers include laboratory diagnosticians and technicians, pathologists, researchers, veterinarians and their staff, wildlife rehabilitators, entomologists, ornithologists, wildlife biologists, zoo and aviary curators, health care workers, emergency response and public safety personnel, public health workers, and others in related occupations (CDC NIOSH, 2005). WNV may be present in blood, serum, tissues and CSF of infected humans, birds, mammals and reptiles. The virus has been found in the oral fluids and feces of birds. Parenteral inoculation with contaminated materials poses the greatest hazard for laboratory workers and contact exposure of broken skin is a possible risk. Sharps precautions should be strictly adhered to when handling potentially infectious materials. Workers performing necropsies on infected animals may be at high risk of infection (CDC, 2003b). CDC is currently developing commercial kits for human serological diagnosis of WNV infection. Until these kits are available, CDC-defined immunoglobulin IgM and IgG enzyme-linked immunosorbent assay (ELISA) should be available for front-line testing. The hemagglutination inhibition (HI) and indirect immunofluorescent antibody (IFA) tests may also be used to screen samples for flavivirus antibodies (CDC, 2003b). TREATMENTThere is no specific treatment for WNV infection and care is supportive. Antiviral drugs may be effective against WNV because the infection is typically not chronic and antiviral drugs have been identified to be effective in vitro against other flaviviruses. More than 300 drugs have been screened for possible use against WNV infection, and twelve have shown promise for additional testing in animals. Immunotherapeutics (treatments that modify the body's immune response) are also being explored (NIAID, 2003). In severe cases, when WNV meningitis, encephalitis, or other neurologic symptoms are present, intravenous hydration and mechanical ventilation may be needed. The American College of Physicians recommends the following non-drug therapy in severe cases:
Drug therapy includes:
The National Institute of Allergy and Infectious Diseases (NIAID) currently funds a nationwide clinical trial to test whether antibodies from people who have recovered from WNV infection can be used to treat those with severe West Nile neurologic disease. Investigators are comparing this treatment to placebos to assess safety and to determine whether these antibodies help overcome the severe disease symptoms. More information on this clinical trial is available on the NIAID Collaborative Antiviral Study Group Web site at http://www.casg.uab.edu (NIAID, 2006). Because some drugs are effective against related viruses in laboratory tests, scientists are optimistic that they will be able to develop drugs to treat WNV disease. Over the past several years, NIAID has expanded its in vitro and in vivo antiviral screening program to screen chemical compounds for possible effectiveness against WNV. Promising antiviral drugs identified in vitro are subsequently tested in hamster or mouse models of the disease. Since October 2003, more than 2,500 drugs have been screened in vitro, and about 1% to 2% have shown promise for additional testing in animals (NIAID, 2006). NIAID clinicians are studying how WNV disease progresses in people who have or are at risk of developing its most serious complications. This research study, conducted through the Collaborative Antiviral Study Group and at the National Institutes of Health Clinical Center, measures the neurologic function of people hospitalized with WNV and will continue to monitor them as they recover. Data collected in this study will give doctors a better understanding of West Nile encephalitis and will assist in designing better treatments for this form of WNV disease (NIAID, 2006). PREVENTIONExposure to WNV can be prevented in two ways: (1) personal protective measures to reduce contact with mosquitoes, and (2) public health measures to reduce the population of infected mosquitoes in the environment. Personal protection measures include reducing time outdoors, particularly in early evening hours, wearing long pants and long-sleeved shirts, and applying mosquito repellent to exposed skin areas (CDC, 2003a). Public health measures include elimination of larval habitats or spraying of insecticides to kill juvenile (larvae) and adult mosquitoes. In emergency situations, wide-area aerial spraying is used to quickly reduce the number of adult mosquitoes. Precautions should continue until there have been two hard frosts (CDC, 2003a). A critical component of any prevention and control program for vector-borne diseases is public education about these diseases, how they are transmitted, and how to prevent or reduce risk of exposure (CDC, 2003a). As stated earlier, mosquitoes breed in wet areas, and Culex are found particularly where there is decaying organic matter (eg, leaves, grass clippings, animal wastes). There does not have to be much water and the water does not have to be left standing for very long. Thus, they can reproduce throughout the mosquito breeding season in your area (and especially after each rainstorm, drizzle, watering of the garden, or washing of the car). Follow these guidelines for eliminating potential mosquito breeding habitat:
RepellentsRepellents are an important tool to assist people in protecting themselves from mosquito-borne diseases. A wide variety of insect repellent products are available. The CDC recommends the use of products containing active ingredients that have been registered with the U.S. Environmental Protection Agency (EPA) for use as repellents applied to skin and clothing. EPA registration of repellent active ingredients indicates the materials have been reviewed and approved for efficacy and human safety when applied according to the instructions on the label (CDC, 2006e). Of the active ingredients registered with the EPA, two have demonstrated a higher degree of efficacy in the peer-reviewed literature. Products containing these active ingredients typically provide longer-lasting protection than others:
Repellents containing oil of lemon eucalyptus (p-menthane 3, 8-diol [PMD]), a plant-derived active ingredient, are also registered with EPA. In two recent scientific publications, when repellents containing oil of lemon eucalyptus were tested against mosquitoes found in the United States they provided protection similar to repellents with low concentrations of DEET. This recommendation refers to EPA-registered repellents containing the active ingredient oil of lemon eucalyptus (PMD). "Pure" oil of lemon eucalyptus (eg, essential oil) has not received similar, validated testing for safety and efficacy, is not registered with EPA as an insect repellent, and is not covered by this CDC recommendation (CDC, 2006e). VaccinesIn November 2003, Acambis, a biotechnology company with vaccine development laboratories in Cambridge, Massachusetts, started the first human clinical trial of a WNV vaccine. Scientists based the vaccine on one already licensed for preventing yellow fever, which is caused by another flavivirus (NIAID, 2006). Called a chimeric virus vaccine, the Acambis vaccine contains genes from two different viruses—yellow fever and West Nile. Researchers replaced some of the yellow fever virus genes with genes for a surface protein of WNV. They are also developing similar chimeric vaccines for dengue fever and for Japanese encephalitis. The Acambis West Nile vaccine performed well in hamsters, mice, monkeys, and horses, and has now entered human clinical trials (NIAID, 2006). NIAID scientists have developed a chimeric West Nile vaccine and tested it in monkeys with promising results. This experimental vaccine, which uses an attenuated dengue virus as a backbone to carry WNV protective antigens, is in an ongoing Phase I human trial (NIAID, 2006). Researchers at the NIAID Vaccine Research Center (VRC) have also developed an investigational vaccine for preventing WNV infection. In April 2005, VRC initiated a Phase I clinical trial to evaluate safety, tolerability, and immune responses of this recombinant-DNA vaccine in human volunteers. The Vaccine Research Center is currently developing a second-generation DNA vaccine using an improved expression vector that expresses the same WNV proteins. A Phase I clinical trial is planned for spring 2006 (NIAID, 2006). SURVEILLANCE AND CONTROLSurveillance is the organized monitoring of levels of virus activity, vector populations, infections in vertebrate hosts, human cases, weather, and other factors to detect or predict changes in the transmission dynamics of arboviruses. Optimal environmental conditions allow rapid increase of vectors and virus amplification in vertebrate hosts. It is urgent, therefore, that a well-organized surveillance program be in place well in advance of the virus transmission season (Moore et al, 1993). Surveillance is a high priority for states that are affected or that are at higher risk for being affected by WNV because of bird migration patterns and virus spread. Depending on the geographic location of the state, active surveillance should be implemented in the spring and continued until the late fall (for states where mosquito activity will cease because of cold weather) or through the winter months (for southern states where mosquito activity may be continuous throughout the year). In all states that face potential WNV activity, the following surveillance activities should be emphasized (CDC, 2003a):
Appropriate and timely response to surveillance data is the key to preventing human and animal disease associated with WNV and other arboviruses. If increasing levels of virus activity are detected in the birds or mosquitoes, the response must be effective mosquito control without delay. (For more information see CDC Guidelines for Arbovirus Surveillance Programs in the United States, available on the CDC home page at http://www.cdc.gov/ncidod/dvbid/arbor/arboguid.htm. CONCLUSIONAs we enter the 2006 mosquito season, the CDC has released more information about WNV—how it is transmitted, and how to prevent the virus from spreading to humans and other mammals. Many states have issued advisories with instructions on how to protect against mosquito bites. As WNV spreads across the United States and Canada, more is being learned about how the virus is transmitted. It is now known that, although rare, WNV can be transmitted via blood transfusion and transplanted organs. In at least one case, a mother contracted WNV from a blood transfusion and may have transmitted the virus to her baby through breast milk. Both the mother and the baby are healthy and have no symptoms of WNV. Most people who have WNV do not show symptoms, although some individuals develop minor symptoms of fever and headache. Blood banks and the organ donor networks need to be vigilant with those who may have minor illnesses, especially in areas where WNV is most active. Medical practitioners should be alert for symptoms that may be associated with WNV infection. Prompt reporting of these persons will help facilitate infection control procedures that will prevent the further spread of WNV in your area. Posted June 21, 2006 Expires July 1, 2008 Copyright © 2003, 2004, 2006 Wild Iris Medical Education. All rights reserved. REFERENCESAmerican Association of Equine Practitioners. (2005). West Nile Virus Vaccination Guidelines. Retrieved May 17, 2006 from http://www.aaep.org/pdfs/AAEP_WNV_Guidelines_2005.pdf. American College of Surgeons. (2006). Physicians' Information and Education Resource. West Nile Virus Disease: Non-Drug Therapy. Retrieved May 29, 2006 from http://pier.acponline.org/physicians/public/d951/nondrug.tx/d951-s6.html. CDC, Division of Vector-Borne Infectious Diseases. (2006a). West Nile Virus: Questions and Answers. Retrieved May 28, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/qa/cases.htm. CDC, Division of Vector-Borne Infectious Diseases. (2006b). West Nile Virus: Statistics, Surveillance, and Control. Final 2005 West Nile Virus Activity in the United States. Retrieved May 17, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/Mapsactivity/ CDC, Division of Vector-Borne Infectious Diseases. (2006c). West Nile Virus: Statistics, Surveillance, and Control. Maps and Data. Retrieved May 17, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/surv&control.htm. CDC, Division of Vector-Borne Infectious Diseases. (2006d). West Nile Virus: Statistics, Surveillance, and Control. 2005 West Nile Virus Activity in the United States. Retrieved May 17, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/ CDC, Division of Vector-Borne Infectious Diseases. (2006e). West Nile Virus. Updated Information regarding Insect Repellents. Retrieved May 29, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/RepellentUpdates.htm. CDC, Division of Vector-Borne Infectious Diseases. (2005). West Nile Virus. Vertebrate Ecology. Retrieved May 17, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/birdspecies.htm. CDC, Division of Vector-Borne Infectious Diseases. (2004a). West Nile Virus: Clinical Description. Retrieved May 28, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/clinicians/clindesc.htm. CDC, Division of Vector-Borne Infectious Diseases. (2004b). West Nile Virus: Epidemiologic Information for Clinicians. Retrieved May 17, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/clinicians/epi.htm. CDC, Division of Vector-Borne Infectious Diseases. (2004c). West Nile Virus: Background Information for Clinicians. Retrieved May 28, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/clinicians/background.htm. CDC, Division of Vector-Borne Diseases. (2004d). Entomology. Retrieved May 28, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/insects.htm. CDC, Division of Vector-Borne Diseases. (2003a). Epidemic/Epizootic West Nile Virus in the United States: Guidelines for Surveillance, Prevention, and Control. Retrieved May 28, 2006 from http://www.cdc.gov/ncidod/dvbid/westnile/resources/wnv-guidelines-aug-2003.pdf. CDC, Division of Vector-Borne Diseases. (2003b). Vertebrate Ecology Transmission Cycle. Retrieved July 12, 2004 from http://www.cdc.gov/ncidod/dvbid/westnile/birds&mammals.htm. CDC, National Institute for Occupational Safety and Health (NIOSH). (2005). NIOSH Safety and Health Topic: West Nile Virus Recommendations for Protecting Laboratory, Field, and Clinical Workers from West Nile Virus Exposure. Retrieved May 28, 2006 from http://www.cdc.gov/niosh/topics/westnile/reclab.html. Cornell University, Department of Communication. (2005a). Environmental Risk Analysis Program. West Nile Virus: Transmission, Infection, and Symptoms. Retrieved May 28, 2006 from http://environmentalrisk.cornell.edu/WNV/Summary2.php. Cornell University, Department of Communication. (2005b). Environmental Risk Analysis Program. West Nile Virus: Frequently Asked Questions. Retrieved May 18, 2006 from http://environmentalrisk.cornell.edu/WNV/FAQs.cfm#vaccine. Moore, CG, McLean RG, and Mitchell CJ et al. (1993) Guidelines for Arbovirus Surveillance Programs in the United States. Retrieved May 31, 2006 from http://www.cdc.gov/ncidod/dvbid/arbor/arboguid.pdf. National Institutes of Allergies and Infectious Diseases (NIAID). (2006.) NIAID Research on West Nile Virus. Retrieved May 29, 2006 from http://www.niaid.nih.gov/factsheets/westnile.htm. USDA, Animal and Plant Health Inspection Service. (2005). Disease Surveillance Information: West Nile Virus. Current Map: Equine West Nile Virus Cases in 2005. Retrieved May 18, 2006 from http://www.aphis.usda.gov/vs/ceah/ncahs/nsu/surveillance/wnv/wnv.htm. |
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