Systemic and Ophthalmic Manifestations of West Nile Virus Infection

Yos Priestley; Marcia Thiel; Steven B. Koevary


Expert Rev Ophthalmol. 2008;3(3):279-292. 

In This Article


West Nile virus is a vector-borne disease that is transmitted through the bite of infected Culex mosquitoes. The mosquitoes act as a maintenance vector by infecting birds that act as amplifying hosts. Birds that are most susceptible to WNV disease are crows and blue jays of the family Corvidae. Infection in birds results in a high level of viremia, which facilitates the enzootic cycle of mosquito transmission.[6,29] At any point during this cycle, an infected mosquito can act as a 'bridge vector' by spreading the virus to humans through a bite.[6] Viral amplification occurs during the summer months in the enzootic cycle and culminates in the early fall when the mosquitoes begin to bite humans. Thus, upwards of 85% of human infections occur during the months of August and September.[8] Vectoral transmission of WNV by mosquitoes from human to human is not thought to occur because of the low reported levels of viremia in infected individuals.[29] However, WNV has been reported to have been passed on to others by blood transfusion, organ transplantation and vertically from mother to child.

The first cases of WNV that were acquired through blood transfusion and organ transplantation were reported in August of 2002 during a major outbreak in the USA. Of note was the reported case of transmission to four recipients of organs transplanted from a common donor.[30] The organ donor had received blood products from 63 donors before her death, one of whom had asymptomatic WNV. Following her last transfusion, her serum and plasma tested positive for the presence of WNV isolates. Three of the four organ recipients developed West Nile encephalitis (WNE) while the fourth developed symptoms of WN fever (WNF; see later). More recently, additional cases of viral transmission through tainted blood transfusions and organ transplants have been reported.[31,32,33]

Shortly after reports surfaced that WNV could be transmitted by infected blood and transplanted organs, came reports of transmission of the virus to the fetus and neonate through the placenta and breast milk, respectively. In 2003, it was reported that a woman of 20 years of age contracted WNV 2 months before delivering a live infant at 38 weeks of gestation. The infant had normal physical features, but was found to have bilateral chorioretinitis, severe bilateral loss of white matter in both temporal and occipital lobes of the brain, and cystic cerebral tissue destruction in one temporal lobe.[34] The infant's serum and CSF tested positive for WNV-specific IgM.[34] While additional complications have been reported following WNV infection in utero, it remains unclear whether the virus played a role in their development. Data suggest that congenital WNV infection can not be ruled out, based on a negative serological finding of cord blood.[35,94] Though confirmed transmission of WNV through breast milk has only been reported in one case, it is perhaps prudent to counsel against this practice in mothers who have been diagnosed with WNV infection.[93]


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