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West Nile Virus

West Nile Virus West Nile virus (WNV) first appeared in North America in the summer of 1999 in New York City causing 62 cases of human neurologic disease, 7 deaths, and leaving thousands of crows, other birds, and horses dead in its wake.1-3 At this time, there is no specific therapy available for WNV, which reappeared in 2000 and is expected to cause disease this year as well. Vaccines for WNV have been developed but still must undergo lengthy safety and efficacy testing. In this article, we will consider the epidemiology, clinical manifestations, diagnosis, and treatment of WNV infections and review currently available strategies for surveillance, prevention, and control of WNV. Epidemiology The WNV, an arbovirus (arthropod-borne virus) in the Flaviviridae family, was first isolated on the African continent and has since been found in the Middle East and Europe along major bird migration flyways (aerial routes that migratory birds usually follow on their annual north/south migrations) that connect Europe, Africa, and the Middle East. The strain of WNV currently active in the United States is most closely related to a strain that was recently circulating in Israel.4 The WNV is transmitted between the natural bird reservoir hosts primarily by mosquitoes.5 The primary mosquito vectors for WNV are in the Culex family.5 These mosquitoes prefer to feed on birds, but some will bite people as well. Humans are thought to be incidental or dead-end hosts, since they can become infected and may become ill as a result, but they do not develop a viremia that is sufficient for the continuation of a transmission cycle if bitten by another mosquito. The WNV produces a viremia that usually disappears with the onset of clinical symptoms, in contrast to the flaviviruses that cause yellow fever and dengue. In these illnesses, viremias persist into the early, acute stages of onset of symptoms.6,7 The WNV occasionally produces symptomatic infections in horses and other mammals that, like humans, act as dead-end hosts.5 In temperate climates, WNV is only active during the warmer months when mosquitoes can become infected from biting infected birds and transmit the virus. It is not known how the virus overwinters (is able to survive the cold temperatures that would ordinarily kill the mosquitoes harboring it), but this does appear to be possible. Evidence supporting both the presence of and a possible mechanism for local overwintering was obtained when New York City Department of Health and Centers for Disease Control and Prevention (CDC) investigators found, in February 2000, infected Culex pipiens mosquitoes that were overwintering in protected underground sites in New York.8 The WNV may also be reintroduced by migrating birds in subsequent years. Whether by overwintering or reintroduction, WNV did reappear again in 2000. The virus was discovered in a hawk in February in Connecticut and in another hawk in April in Suffolk County, New York. Later, there were cases of overt human encephalitis on Staten Island in Richmond County, New York and in New Jersey.9 Other foci of intense enzootic transmission occurred in other counties in New York and in several areas of Connecticut, Massachusetts, and Pennsylvania, although there were no reports of human cases of WNV encephalitis in these areas despite heightened publicity and active surveillance. Human serosurveys conducted in 3 of these areas in October and November 2000 showed very low overall infection rates compared with surveys in 1999, suggesting that conditions favoring epizootic transmission do not always place humans at risk. An additional explanation for the observed disparity between rates of infection in animals and humans may be the high ratio of inapparent infections to apparent cases of encephalitis produced by WNV. It has been estimated that there are as many as 120 to 160 inapparent infections for every overt infection.9,10 As the 2000 transmission season progressed, infection with WNV was found in 12 mosquito species. New control problems were posed by the recovery of the virus from the newly introduced species Ochlerotatus (Aedes) japonicus, which bites humans during the daylight hours and breeds in water containers that may be in the proximity of human households.11 In 2001, WNV–infected crows have been reported in Connecticut, Maryland, New Jersey, New York, Rhode Island, and Florida. As of early July 2001, no human cases have been documented (CDC, unpublished surveillance data, 2001). Clinical Considerations The vast majority of WNV infections are clinically silent. There is a low statistical likelihood of overt clinical disease, which does not always present as clinical encephalitis.9,10 Less than 1% of all infections (overt and clinically silent) will have a neurologic component.12 Milder infections are characterized by fever, malaise, lymphadenopathy, periocular pain, gastrointestinal symptoms, muscle pains, and possibly a headache. A fine maculopapular rash may be present; this occurs more frequently in children than in adults.13 Identification of these less severe cases may be difficult due to their resemblance to a mild viral syndrome. Elderly and young persons are at highest risk of developing severe clinical encephalitis.13,14 Fulminant encephalitis and death may occur. Among the cases seen in 1999, some patients had evidence of a transverse myelitis or Guillain-Barré syndrome; these patients exhibited symptoms ranging from pronounced proximal muscle weakness to flaccid paralysis of their extremities. While not universal, this presentation may be a useful additional clinical sign pointing toward a WNV etiology. The other hallmarks of encephalitis—fever, confusion, disorientation, and/or coma—may also be present.13,14 Of 62 case-patients identified in the 1999 New York outbreak, there were 7 deaths for a case fatality rate of 12%.15 Diagnosis and Treatment Diagnostic tests for WNV are available in state health department laboratories in the northeastern United States and most other states. Testing is also available from the CDC, although the CDC recommends that specimens be submitted through state health departments so that these departments are aware of potential human cases of WNV infection. Serologic diagnosis of WNV infection may be misleading because of cross-reactivity among flaviviruses; the diagnosis may remain unclear until the arboviral agent is actually isolated and identified.16-19 False-positive results for WNV may be obtained when the infecting virus is St Louis encephalitis, dengue, and several others, or when the patient has been immunized with yellow fever or Japanese encephalitis vaccines. When WNV appeared in North America in 1999, human cases of encephalitis were initially diagnosed as St Louis encephalitis due to cross-reactivity between these related members of the Flavivirus genus. The serologic screening test of choice is the WNV enzyme-linked immunosorbent assay (ELISA).17,18 If positive, the ELISA results should be verified by the much more specific plaque reduction neutralization test, which takes 7 to 10 days to complete.19 Separate ELISA tests are performed for IgM and IgG antibodies.20 In some cases, IgM antibodies will persist for up to a year, occasionally causing confusion as to whether the antibodies reflect a current or previous infection. For patients with encephalitis, cerebrospinal fluid (CSF) should be tested by ELISA for IgM antibodies and analyzed by polymerase chain reaction (PCR) for the detection of viral nucleic acid.21 Detection of IgM antibodies against WNV in CSF from a patient with encephalitis is considered to be strong evidence of a WNV etiology. Postmortem specimens of brain tissue are useful for detection of viral nucleic acid by PCR or for detection of viral antigens by immunohistochemical (IHC) staining techniques using polyclonal or monoclonal antibodies.22 Detection of WNV by either technique is considered to be definitive evidence of WNV infection, although negative PCR results on CSF or tissue or negative IHC results on tissue do not rule out WNV infection. In a recent study, PCR testing of CSF specimens from patients with clinically evident and serologically confirmed WNV infection was positive only 50% to 60% of the time.21 Clinical outcome was not associated with PCR results. Negative PCR results on CSF may be due to the WNV having been cleared by the time diagnostic lumbar puncture was performed or could reflect a sensitivity threshold for PCR. There is no specific therapy for WNV encephalitis. Ribavirin has been shown to inhibit the virus in neural cell cultures23 and has also been administered to a small number of patients. Well-controlled clinical trials of ribavirin therapy are needed. Supportive care is the currently accepted mode of therapy. Surveillance in Nature Surveillance of WNV has been established to monitor prevalence of infection in birds, horses, and adult mosquitoes.24 Since WNV is new in North America, its normal avian hosts will be susceptible to it as an infecting virus and some will also be susceptible to disease and death when infected. Crows and blue jays are particularly susceptible to WNV and large numbers of them become ill and die when infected.2 Examination of fresh bird carcasses by traditional virus isolation techniques or by the newer, less labor intensive TaqMan PCR technology (PE Applied Biosystems, Foster City, Calif) can detect the presence of WNV and thus the general geographic location of WNV–infected mosquitoes.21,25 Because WNV has been shown to cause disease in a wide variety of wild and domestic animals, vigilance by the veterinary community is important. Another surveillance method involves using domestic chickens as sentinel animals. Maintained in outdoor cages where they can be fed upon by local mosquitoes, chickens can be periodically tested for WNV antibody seroconversion. Such seroconversion should alert officials to virus activity. This technique has apparently been less successful for WNV surveillance in the northeastern United States than it has been for surveillance of other arboviruses.24 Surveillance for infected mosquitoes is also a useful technique.24 Placement of traps near sewage treatment plants or irrigated fields will capture Culex mosquitoes that are common vectors for WNV. Clinically apparent encephalitis cases in horses have been used as sentinel events to monitor arboviruses in nature.24 The occurrence of equine cases has been thought to represent an increased risk for the surrounding human population. However, many equine cases in the 2000 epidemic season occurred after the incidence of WNV infection in humans peaked, suggesting that equine encephalitis cases due to WNV are not always useful for predicting human risk, although they are good indicators of the geographic location of virus activity. Personal and Community Protective Measures Mosquito surveillance, public education programs, and application of pesticides are the main components of the effort to control WNV–infected mosquitoes. Since the bite of a WNV–infected mosquito is the most important risk factor for developing WNV encephalitis, measures that individuals can take on their own to prevent mosquito bites are of particular importance. These measures include minimizing outdoor exposure where potential mosquito vectors occur, keeping windows closed or well screened, wearing long-sleeved shirts and long pants outdoors, covering exposed skin and clothing with repellants such as those containing diethyltoluamide, and removing all containers capable of holding water from personal surroundings to eliminate mosquito breeding sites.26 Use of insecticide under appropriate conditions has been demonstrated to reduce adult Culex mosquito populations.27-32 Reducing the numbers of adult mosquitoes in the community requires the application of pesticides when the local health department finds through surveillance programs that human-biting mosquitoes are infected and present in sufficient numbers. Widespread application of insecticides is subject to a number of regulatory and environmental factors. Spraying near water is often forbidden by statutes designed to protect wildlife in those habitats. Wind and temperature are important factors; too much wind makes it difficult to control where the spray goes. Temperatures that are too low keep mosquitoes from seeking blood meals. These and a number of other factors must be considered when mass applications of insecticide are contemplated. When applications of insecticide are delayed or halted as a result of external factors, reliance on personal protective measures assumes even greater importance. Conclusion The WNV appears to have become enzootic in the United States and has the potential to spread over much of remaining North America. The medical community should maintain vigilance for human cases and report those cases to local public health authorities. The public health community is working to strengthen infrastructure to deal with WNV and other vector-borne viral diseases. The enlightened clinician will remain a crucial partner. References 1. Centers for Disease Control and Prevention. Outbreak of West Nile-like viral encephalitis—New York, 1999. MMWR Morb Mortal Wkly Rep.1999;48:845-849.Google Scholar 2. Centers for Disease Control and Prevention. Update: West Nile-like viral encephalitis—New York, 1999. MMWR Morb Mortal Wkly Rep.1999;48:890-892.Google Scholar 3. Centers for Disease Control and Prevention. Update: West Nile virus encephalitis—New York, 1999. MMWR Morb Mortal Wkly Rep.1999;48:944-946.Google Scholar 4. Lanciotti RS, Roehrig JT, Deubel V. et al. Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States. Science.1999;286:2333-2337.Google Scholar 5. Hayes CG. West Nile fever. In: Monath TP, ed. The Arboviruses: Epidemiology and Ecology, Vol V. Boca Raton, Fla: CRC Press; 1988:59-88. 6. Craven RB. Yellow fever. In: Belshe R, ed. Textbook of Human Virology. 2nd ed. St Louis, Mo: Mosby–Year Book Inc; 1991:645-649. 7. Craven RB. Dengue. In: Belshe R, ed. Textbook of Human Virology. 2nd ed. St Louis, Mo: Mosby–Year Book Inc; 1991:649-656. 8. Centers for Disease Control and Prevention. Update: surveillance for West Nile virus in overwintering mosquitoes—New York, 2000. MMWR Morb Mortal Wkly Rep.2000;49:178-179.Google Scholar 9. Centers for Disease Control and Prevention. Serosurveys for West Nile virus infection—New York and Connecticut counties, 2000. MMWR Morb Mortal Wkly Rep.2000;50:37-39.Google Scholar 10. Centers for Disease Control and Prevention. Update: West Nile virus activity—Northeastern United States, 2000. MMWR Morb Mortal Wkly Rep.2000;49:820-822.Google Scholar 11. Peyton EL, Campbell SR, Candeletti TM. et al. AEDES (FINLAYA) Japonicus Japonicus (Theobald), a new introduction into the United States. J Am Mosq Control Assoc.1999;15:238-241.Google Scholar 12. Tsai TF, Popovici F, Cernescu C. et al. West Nile encephalitis epidemic in southeastern Romania. Lancet.1998;352:767-771.Google Scholar 13. Marburg K, Goldblum H, Sterk VV. et al. The natural history of West Nile fever: clinical observations during an epidemic in Israel. Am J Hyg.1956;64:259-263.Google Scholar 14. Monath TP. West Nile fever. In: Strickland GT, ed. Tropical Medicine. Philadelphia, Pa: WB Saunders Co; 1991:206-207. 15. Nash D, Moshtashari F, Fine A. et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med.2001;344:1807-1814.Google Scholar 16. Roehrig JT. Arboviruses. In: Specter S, Young SA, eds. Clinical Virology Manual. 3rd ed. Washington, DC: American Society for Microbiology; 2000:356-373. 17. Martin DA, Karabatsos N, Roehrig JT. Standardization of immunoglobulin M capture enzyme-linked immunosorbent assays (MAC-ELISA) for routine diagnosis of arboviral infections. J Clin Microbiol.2000;38:1823-1826.Google Scholar 18. Johnson AJ, Martin DM, Karabatsos N. et al. Detection of anti-arboviral IgG by using a monoclonal antibody-based capture ELISA. J Clin Microbiol.2000;38:1827-1831.Google Scholar 19. Beaty BJ, Calisher CH, Shope RE. Arboviruses. In: Schmidt NJ, Emmons RW, eds. Diagnostic Procedures for Viral, Rickettsial and Chlamydial Infections. 6th ed. Washington, DC: American Public Health Association; 1989:797-855. 20. Tardei G, Ruta S, Chitu V. et al. Evaluation of immunoglobulin M (IgM) and IgG enzyme immunoassays in serologic diagnosis of West Nile virus infection. J Clin Microbiol.2000;38:2232-2239.Google Scholar 21. Lanciotti RS, Kerst AJ, Nasci RS. et al. Rapid detection of West Nile virus from human clinical, field-collected mosquitoes, and avian samples by a TaqMan reverse transcriptase-PCR assay. J Clin Microbiol.2000;38:4066-4071.Google Scholar 22. Shieh W-J, Guarner J, Layton M. et al. The role of pathology in an investigation of an outbreak of West Nile encephalitis in New York, 1999. Emerg Infect Dis.2000;6:370-372.Google Scholar 23. Jordan I, Briese T, Fischer N. et al. Ribavirin inhibits West Nile virus replication and cytopathic effect in neural cells. J Infect Dis.2000;182:1214-1217.Google Scholar 24. Centers for Disease Control and Prevention. Guidelines for Arbovirus Surveillance in the United States. Fort Collins, Colo: US Dept of Health and Human Services, Centers for Disease Control and Prevention; 1993. 25. Anderson JF, Andreadis TG, Vossbrinck CR. et al. Isolation of West Nile virus from mosquitoes, crows, and a Cooper's Hawk in Connecticut. Science.1999;286:2331-2333.Google Scholar 26. Cecchine G, Golomb BA, Hilborne LH. et al. Pesticides. Washington, DC: National Defense Research Institute; 1996. A Review of the Scientific Literature as it Pertains to Gulf War Illnesses; vol 8. 27. Andis MD, Sackett SR, Carroll MK, Bordes ES. Strategies for the emergency control of arboviral epidemics in New Orleans. J Am Mosq Control Assoc.1987;3:125-130.Google Scholar 28. Leiser LB, Beier JC, Craig GB. The efficacy of malathion ULV spraying for urban Culex control in South Bend, Indiana. Mosquito News.1982;42:617-618.Google Scholar 29. Mitchell CJ, Hayes RO, Holden P. et al. Effects of ultra-low volume applications of malathion in Hale County, Texas. J Med Entomol.1969;6:155-162.Google Scholar 30. Mitchell CJ, Kilpatrick JW, Hayes RO, Curry HW. Effects of ultra-low volume applications of malathion in Hale County, Texas. J Med Entomol.1970;7:85-91.Google Scholar 31. Mount GA, Biery TL, Haile DG. A review of ultralow-volume aerial sprays of insecticide for mosquito control. J Am Mosq Control Assoc.1996;12:601-618.Google Scholar 32. Reisen WK, Milby MM, Reeves WC. et al. Aerial adulticiding for the suppression of Culex tarsals in Kern County, California, using low volume propoxur. J Am Mosq Control Assoc.1985;1:154-163.Google Scholar http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA American Medical Association

West Nile Virus

JAMA , Volume 286 (6) – Aug 8, 2001

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References (29)

Publisher
American Medical Association
Copyright
Copyright © 2001 American Medical Association. All Rights Reserved.
ISSN
0098-7484
eISSN
1538-3598
DOI
10.1001/jama.286.6.651
Publisher site
See Article on Publisher Site

Abstract

West Nile virus (WNV) first appeared in North America in the summer of 1999 in New York City causing 62 cases of human neurologic disease, 7 deaths, and leaving thousands of crows, other birds, and horses dead in its wake.1-3 At this time, there is no specific therapy available for WNV, which reappeared in 2000 and is expected to cause disease this year as well. Vaccines for WNV have been developed but still must undergo lengthy safety and efficacy testing. In this article, we will consider the epidemiology, clinical manifestations, diagnosis, and treatment of WNV infections and review currently available strategies for surveillance, prevention, and control of WNV. Epidemiology The WNV, an arbovirus (arthropod-borne virus) in the Flaviviridae family, was first isolated on the African continent and has since been found in the Middle East and Europe along major bird migration flyways (aerial routes that migratory birds usually follow on their annual north/south migrations) that connect Europe, Africa, and the Middle East. The strain of WNV currently active in the United States is most closely related to a strain that was recently circulating in Israel.4 The WNV is transmitted between the natural bird reservoir hosts primarily by mosquitoes.5 The primary mosquito vectors for WNV are in the Culex family.5 These mosquitoes prefer to feed on birds, but some will bite people as well. Humans are thought to be incidental or dead-end hosts, since they can become infected and may become ill as a result, but they do not develop a viremia that is sufficient for the continuation of a transmission cycle if bitten by another mosquito. The WNV produces a viremia that usually disappears with the onset of clinical symptoms, in contrast to the flaviviruses that cause yellow fever and dengue. In these illnesses, viremias persist into the early, acute stages of onset of symptoms.6,7 The WNV occasionally produces symptomatic infections in horses and other mammals that, like humans, act as dead-end hosts.5 In temperate climates, WNV is only active during the warmer months when mosquitoes can become infected from biting infected birds and transmit the virus. It is not known how the virus overwinters (is able to survive the cold temperatures that would ordinarily kill the mosquitoes harboring it), but this does appear to be possible. Evidence supporting both the presence of and a possible mechanism for local overwintering was obtained when New York City Department of Health and Centers for Disease Control and Prevention (CDC) investigators found, in February 2000, infected Culex pipiens mosquitoes that were overwintering in protected underground sites in New York.8 The WNV may also be reintroduced by migrating birds in subsequent years. Whether by overwintering or reintroduction, WNV did reappear again in 2000. The virus was discovered in a hawk in February in Connecticut and in another hawk in April in Suffolk County, New York. Later, there were cases of overt human encephalitis on Staten Island in Richmond County, New York and in New Jersey.9 Other foci of intense enzootic transmission occurred in other counties in New York and in several areas of Connecticut, Massachusetts, and Pennsylvania, although there were no reports of human cases of WNV encephalitis in these areas despite heightened publicity and active surveillance. Human serosurveys conducted in 3 of these areas in October and November 2000 showed very low overall infection rates compared with surveys in 1999, suggesting that conditions favoring epizootic transmission do not always place humans at risk. An additional explanation for the observed disparity between rates of infection in animals and humans may be the high ratio of inapparent infections to apparent cases of encephalitis produced by WNV. It has been estimated that there are as many as 120 to 160 inapparent infections for every overt infection.9,10 As the 2000 transmission season progressed, infection with WNV was found in 12 mosquito species. New control problems were posed by the recovery of the virus from the newly introduced species Ochlerotatus (Aedes) japonicus, which bites humans during the daylight hours and breeds in water containers that may be in the proximity of human households.11 In 2001, WNV–infected crows have been reported in Connecticut, Maryland, New Jersey, New York, Rhode Island, and Florida. As of early July 2001, no human cases have been documented (CDC, unpublished surveillance data, 2001). Clinical Considerations The vast majority of WNV infections are clinically silent. There is a low statistical likelihood of overt clinical disease, which does not always present as clinical encephalitis.9,10 Less than 1% of all infections (overt and clinically silent) will have a neurologic component.12 Milder infections are characterized by fever, malaise, lymphadenopathy, periocular pain, gastrointestinal symptoms, muscle pains, and possibly a headache. A fine maculopapular rash may be present; this occurs more frequently in children than in adults.13 Identification of these less severe cases may be difficult due to their resemblance to a mild viral syndrome. Elderly and young persons are at highest risk of developing severe clinical encephalitis.13,14 Fulminant encephalitis and death may occur. Among the cases seen in 1999, some patients had evidence of a transverse myelitis or Guillain-Barré syndrome; these patients exhibited symptoms ranging from pronounced proximal muscle weakness to flaccid paralysis of their extremities. While not universal, this presentation may be a useful additional clinical sign pointing toward a WNV etiology. The other hallmarks of encephalitis—fever, confusion, disorientation, and/or coma—may also be present.13,14 Of 62 case-patients identified in the 1999 New York outbreak, there were 7 deaths for a case fatality rate of 12%.15 Diagnosis and Treatment Diagnostic tests for WNV are available in state health department laboratories in the northeastern United States and most other states. Testing is also available from the CDC, although the CDC recommends that specimens be submitted through state health departments so that these departments are aware of potential human cases of WNV infection. Serologic diagnosis of WNV infection may be misleading because of cross-reactivity among flaviviruses; the diagnosis may remain unclear until the arboviral agent is actually isolated and identified.16-19 False-positive results for WNV may be obtained when the infecting virus is St Louis encephalitis, dengue, and several others, or when the patient has been immunized with yellow fever or Japanese encephalitis vaccines. When WNV appeared in North America in 1999, human cases of encephalitis were initially diagnosed as St Louis encephalitis due to cross-reactivity between these related members of the Flavivirus genus. The serologic screening test of choice is the WNV enzyme-linked immunosorbent assay (ELISA).17,18 If positive, the ELISA results should be verified by the much more specific plaque reduction neutralization test, which takes 7 to 10 days to complete.19 Separate ELISA tests are performed for IgM and IgG antibodies.20 In some cases, IgM antibodies will persist for up to a year, occasionally causing confusion as to whether the antibodies reflect a current or previous infection. For patients with encephalitis, cerebrospinal fluid (CSF) should be tested by ELISA for IgM antibodies and analyzed by polymerase chain reaction (PCR) for the detection of viral nucleic acid.21 Detection of IgM antibodies against WNV in CSF from a patient with encephalitis is considered to be strong evidence of a WNV etiology. Postmortem specimens of brain tissue are useful for detection of viral nucleic acid by PCR or for detection of viral antigens by immunohistochemical (IHC) staining techniques using polyclonal or monoclonal antibodies.22 Detection of WNV by either technique is considered to be definitive evidence of WNV infection, although negative PCR results on CSF or tissue or negative IHC results on tissue do not rule out WNV infection. In a recent study, PCR testing of CSF specimens from patients with clinically evident and serologically confirmed WNV infection was positive only 50% to 60% of the time.21 Clinical outcome was not associated with PCR results. Negative PCR results on CSF may be due to the WNV having been cleared by the time diagnostic lumbar puncture was performed or could reflect a sensitivity threshold for PCR. There is no specific therapy for WNV encephalitis. Ribavirin has been shown to inhibit the virus in neural cell cultures23 and has also been administered to a small number of patients. Well-controlled clinical trials of ribavirin therapy are needed. Supportive care is the currently accepted mode of therapy. Surveillance in Nature Surveillance of WNV has been established to monitor prevalence of infection in birds, horses, and adult mosquitoes.24 Since WNV is new in North America, its normal avian hosts will be susceptible to it as an infecting virus and some will also be susceptible to disease and death when infected. Crows and blue jays are particularly susceptible to WNV and large numbers of them become ill and die when infected.2 Examination of fresh bird carcasses by traditional virus isolation techniques or by the newer, less labor intensive TaqMan PCR technology (PE Applied Biosystems, Foster City, Calif) can detect the presence of WNV and thus the general geographic location of WNV–infected mosquitoes.21,25 Because WNV has been shown to cause disease in a wide variety of wild and domestic animals, vigilance by the veterinary community is important. Another surveillance method involves using domestic chickens as sentinel animals. Maintained in outdoor cages where they can be fed upon by local mosquitoes, chickens can be periodically tested for WNV antibody seroconversion. Such seroconversion should alert officials to virus activity. This technique has apparently been less successful for WNV surveillance in the northeastern United States than it has been for surveillance of other arboviruses.24 Surveillance for infected mosquitoes is also a useful technique.24 Placement of traps near sewage treatment plants or irrigated fields will capture Culex mosquitoes that are common vectors for WNV. Clinically apparent encephalitis cases in horses have been used as sentinel events to monitor arboviruses in nature.24 The occurrence of equine cases has been thought to represent an increased risk for the surrounding human population. However, many equine cases in the 2000 epidemic season occurred after the incidence of WNV infection in humans peaked, suggesting that equine encephalitis cases due to WNV are not always useful for predicting human risk, although they are good indicators of the geographic location of virus activity. Personal and Community Protective Measures Mosquito surveillance, public education programs, and application of pesticides are the main components of the effort to control WNV–infected mosquitoes. Since the bite of a WNV–infected mosquito is the most important risk factor for developing WNV encephalitis, measures that individuals can take on their own to prevent mosquito bites are of particular importance. These measures include minimizing outdoor exposure where potential mosquito vectors occur, keeping windows closed or well screened, wearing long-sleeved shirts and long pants outdoors, covering exposed skin and clothing with repellants such as those containing diethyltoluamide, and removing all containers capable of holding water from personal surroundings to eliminate mosquito breeding sites.26 Use of insecticide under appropriate conditions has been demonstrated to reduce adult Culex mosquito populations.27-32 Reducing the numbers of adult mosquitoes in the community requires the application of pesticides when the local health department finds through surveillance programs that human-biting mosquitoes are infected and present in sufficient numbers. Widespread application of insecticides is subject to a number of regulatory and environmental factors. Spraying near water is often forbidden by statutes designed to protect wildlife in those habitats. Wind and temperature are important factors; too much wind makes it difficult to control where the spray goes. Temperatures that are too low keep mosquitoes from seeking blood meals. These and a number of other factors must be considered when mass applications of insecticide are contemplated. When applications of insecticide are delayed or halted as a result of external factors, reliance on personal protective measures assumes even greater importance. Conclusion The WNV appears to have become enzootic in the United States and has the potential to spread over much of remaining North America. The medical community should maintain vigilance for human cases and report those cases to local public health authorities. The public health community is working to strengthen infrastructure to deal with WNV and other vector-borne viral diseases. The enlightened clinician will remain a crucial partner. References 1. Centers for Disease Control and Prevention. Outbreak of West Nile-like viral encephalitis—New York, 1999. MMWR Morb Mortal Wkly Rep.1999;48:845-849.Google Scholar 2. Centers for Disease Control and Prevention. Update: West Nile-like viral encephalitis—New York, 1999. MMWR Morb Mortal Wkly Rep.1999;48:890-892.Google Scholar 3. Centers for Disease Control and Prevention. Update: West Nile virus encephalitis—New York, 1999. MMWR Morb Mortal Wkly Rep.1999;48:944-946.Google Scholar 4. Lanciotti RS, Roehrig JT, Deubel V. et al. Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States. Science.1999;286:2333-2337.Google Scholar 5. Hayes CG. West Nile fever. In: Monath TP, ed. The Arboviruses: Epidemiology and Ecology, Vol V. Boca Raton, Fla: CRC Press; 1988:59-88. 6. Craven RB. Yellow fever. In: Belshe R, ed. Textbook of Human Virology. 2nd ed. St Louis, Mo: Mosby–Year Book Inc; 1991:645-649. 7. Craven RB. Dengue. In: Belshe R, ed. Textbook of Human Virology. 2nd ed. St Louis, Mo: Mosby–Year Book Inc; 1991:649-656. 8. Centers for Disease Control and Prevention. Update: surveillance for West Nile virus in overwintering mosquitoes—New York, 2000. MMWR Morb Mortal Wkly Rep.2000;49:178-179.Google Scholar 9. Centers for Disease Control and Prevention. Serosurveys for West Nile virus infection—New York and Connecticut counties, 2000. MMWR Morb Mortal Wkly Rep.2000;50:37-39.Google Scholar 10. Centers for Disease Control and Prevention. Update: West Nile virus activity—Northeastern United States, 2000. MMWR Morb Mortal Wkly Rep.2000;49:820-822.Google Scholar 11. Peyton EL, Campbell SR, Candeletti TM. et al. AEDES (FINLAYA) Japonicus Japonicus (Theobald), a new introduction into the United States. J Am Mosq Control Assoc.1999;15:238-241.Google Scholar 12. Tsai TF, Popovici F, Cernescu C. et al. West Nile encephalitis epidemic in southeastern Romania. Lancet.1998;352:767-771.Google Scholar 13. Marburg K, Goldblum H, Sterk VV. et al. The natural history of West Nile fever: clinical observations during an epidemic in Israel. Am J Hyg.1956;64:259-263.Google Scholar 14. Monath TP. West Nile fever. In: Strickland GT, ed. Tropical Medicine. Philadelphia, Pa: WB Saunders Co; 1991:206-207. 15. Nash D, Moshtashari F, Fine A. et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med.2001;344:1807-1814.Google Scholar 16. Roehrig JT. Arboviruses. In: Specter S, Young SA, eds. Clinical Virology Manual. 3rd ed. Washington, DC: American Society for Microbiology; 2000:356-373. 17. Martin DA, Karabatsos N, Roehrig JT. Standardization of immunoglobulin M capture enzyme-linked immunosorbent assays (MAC-ELISA) for routine diagnosis of arboviral infections. J Clin Microbiol.2000;38:1823-1826.Google Scholar 18. Johnson AJ, Martin DM, Karabatsos N. et al. Detection of anti-arboviral IgG by using a monoclonal antibody-based capture ELISA. J Clin Microbiol.2000;38:1827-1831.Google Scholar 19. 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