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West nile virus infection Risk Factors

Introduction

Overview

Overview

Certain factors may increase the risk of infection with WNV by a mosquito bite, such as warm temperatures, extensive outdoor exposure, homelessness, and absence of window screens. Occupational risk factors include in-field occupations, such as agriculture. Severe clinical disease is often associated with advanced age, immunosuppression, malignancy, diabetes mellitus, hypertension, and renal disease. An increased risk of death is observed among immunosuppressed patients and those presenting with altered level of consciousness. Certain conditions such as encephalitis, advanced cardiovascular disease, and hepatitis C virus may also carry an increased risk of death among patients infected with WNV.

Risk Factors

Risk Factors

Risk factors for infection with West Nile virus include:

Risk of infection Description
Outdoor exposure Persons who work outdoors or have outdoor activities have higher risk of being infected.[1][2]
Homeless status Prolonged outdoor exposure and low or no income to acquire mosquito repellents.[1][2]
Lack of adequate window screens Absence of adequate windows may increase exposure to mosquito bites.[1][2]
Warmer temperatures Associated with higher periods of incidence of disease due to shorter incubation periods of the virus in mosquitoes, and increased efficiency of viral transmission to birds.[3][4][5]
Regional factors

Agricultural lands[6]; irrigated terrains[7]; heavy rain periods[8]; weak rain periods[8]

Risk of severe disease Description
Age > 50 years While persons of any age can be infected with WNV, US surveillance data indicate that persons over age 50 are at higher risk for severe disease and death due to WNV infection.[1]
Organ recipients

Higher risk of developing neuroinvasive disease after:[9]

Risk of neuroinvasive disease in certain conditions[10][11][12][13][14]
Risk of death Description
Risk of death in certain conditions[15][14][12]
References

References

  1. ↑ 1.0 1.1 1.2 1.3 “Epidemic/epizootic West Nile virus in the United StatesΒ : guidelines for surveillance, prevention, and control. 3rd revision”.
  2. ↑ 2.0 2.1 2.2 Campbell, Grant L; Marfin, Anthony A; Lanciotti, Robert S; Gubler, Duane J (2002). “West Nile virus”. The Lancet Infectious Diseases. 2 (9): 519–529. doi:10.1016/S1473-3099(02)00368-7. ISSNΒ 1473-3099.
  3. ↑ Soverow JE, Wellenius GA, Fisman DN, Mittleman MA (2009). “Infectious disease in a warming world: how weather influenced West Nile virus in the United States (2001-2005)”. Environ Health Perspect. 117 (7): 1049–52. doi:10.1289/ehp.0800487. PMCΒ 2717128. PMIDΒ 19654911.
  4. ↑ Kilpatrick AM, Meola MA, Moudy RM, Kramer LD (2008). “Temperature, viral genetics, and the transmission of West Nile virus by Culex pipiens mosquitoes”. PLoS Pathog. 4 (6): e1000092. doi:10.1371/journal.ppat.1000092. PMCΒ 2430533. PMIDΒ 18584026.
  5. ↑ Reisen WK, Fang Y, Martinez VM (2006). “Effects of temperature on the transmission of west nile virus by Culex tarsalis (Diptera: Culicidae)”. J Med Entomol. 43 (2): 309–17. PMIDΒ 16619616.
  6. ↑ Bowden SE, Magori K, Drake JM (2011). “Regional differences in the association between land cover and West Nile virus disease incidence in humans in the United States”. Am J Trop Med Hyg. 84 (2): 234–8. doi:10.4269/ajtmh.2011.10-0134. PMCΒ 3029173. PMIDΒ 21292890.
  7. ↑ DeGroote JP, Sugumaran R (2012). “National and regional associations between human West Nile virus incidence and demographic, landscape, and land use conditions in the coterminous United States”. Vector Borne Zoonotic Dis. 12 (8): 657–65. doi:10.1089/vbz.2011.0786. PMIDΒ 22607071.
  8. ↑ 8.0 8.1 Landesman WJ, Allan BF, Langerhans RB, Knight TM, Chase JM (2007). “Inter-annual associations between precipitation and human incidence of West Nile virus in the United States”. Vector Borne Zoonotic Dis. 7 (3): 337–43. doi:10.1089/vbz.2006.0590. PMIDΒ 17867908.
  9. ↑ DeSalvo D, Roy-Chaudhury P, Peddi R, Merchen T, Konijetti K, Gupta M; et al. (2004). “West Nile virus encephalitis in organ transplant recipients: another high-risk group for meningoencephalitis and death”. Transplantation. 77 (3): 466–9. doi:10.1097/01.TP.0000101434.98873.CB. PMIDΒ 14966429.
  10. ↑ Cho H, Diamond MS (2012). “Immune responses to West Nile virus infection in the central nervous system”. Viruses. 4 (12): 3812–30. doi:10.3390/v4123812. PMCΒ 3528292. PMIDΒ 23247502.
  11. ↑ Lindsey NP, Staples JE, Lehman JA, Fischer M (2012). “Medical risk factors for severe West Nile Virus disease, United States, 2008-2010”. Am J Trop Med Hyg. 87 (1): 179–84. doi:10.4269/ajtmh.2012.12-0113. PMCΒ 3391046. PMIDΒ 22764311.
  12. ↑ 12.0 12.1 Murray K, Baraniuk S, Resnick M, Arafat R, Kilborn C, Cain K; et al. (2006). “Risk factors for encephalitis and death from West Nile virus infection”. Epidemiol Infect. 134 (6): 1325–32. doi:10.1017/S0950268806006339. PMCΒ 2870518. PMIDΒ 16672108.
  13. ↑ Bode AV, Sejvar JJ, Pape WJ, Campbell GL, Marfin AA (2006). “West Nile virus disease: a descriptive study of 228 patients hospitalized in a 4-county region of Colorado in 2003”. Clin Infect Dis. 42 (9): 1234–40. doi:10.1086/503038. PMIDΒ 16586381.
  14. ↑ 14.0 14.1 “Surveillance for Human West Nile Virus Disease – United States, 1999-2008”.
  15. ↑ Nash D, Mostashari F, Fine A, Miller J, O’Leary D, Murray K; et al. (2001). “The outbreak of West Nile virus infection in the New York City area in 1999”. N Engl J Med. 344 (24): 1807–14. doi:10.1056/NEJM200106143442401. PMIDΒ 11407341.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: JoΓ£o AndrΓ© Alves Silva, M.D. [2]