See West Nile virus infection. Read more. Weekly updates: West Nile virus transmission season Map. Twitter Facebook Linked In Mail. Situation update The last weekly epidemiological update of the WNV transmission season was published on 12 November Interactive dashboard.
View in full screen Download the data Short description of the data, including file formats and link to some kind of data dictionary. Although cases of milder febrile illness concomitant with the outbreak of CNS infection were not observed, it was noted that surveillance was rather insensitive and may have been unable to detect such cases Following the outbreak in Romania, several subsequent epidemics associated with relatively high rates of CNS infection were observed throughout the Middle East and Europe, including Morocco in , Tunisia in , and large outbreaks in Italy and Israel in Thus, it appeared that outbreaks of WNV were occurring more frequently; in addition, these outbreaks were associated with higher rates of severe CNS disease and higher fatality rates, predominantly among older individuals.
The Tunisian outbreak of involved patients hospitalized with meningitis or meningoencephalitis, and 8 deaths; more than half of all these patients were over 50 years of age A large outbreak of WNV occurring in the Volgograd region of Russia during the early Summer of involved serologically confirmed cases, with 84 cases of acute meningoencephalitis and 40 fatalities.
By the time the virus was first detected in North America in , it had already had a recent history of more frequent outbreaks and more severe illness. In late August of , a cluster of severe cases of encephalitis was noted in an area around Queens in New York City An epidemiologic investigation by the New York City Department of Health identified eight such cases, and revealed that all of the patients had been previously healthy, had resided within the same 16 square mile area, and had recently engaged in outdoor activities.
All but one had developed severe acute flaccid paralysis in the setting of encephalitis. As the initial suspicion was that of an arthropod-borne virus arbovirus encephalitis, early testing was directed at common eastern North American arboviruses.
Early serologic testing displayed IgM antibodies against St. Louis encephalitis virus by enzyme-linked immunosorbent assay. Both before and during the human encephalitis investigation, an epizootic among birds associated with a high fatality rate had been noted in and around New York City These were initially felt to be unrelated to the human epidemic.
Pathologic assessment of the dead birds displayed involvement of multiple organs, including evidence of encephalitis; however, common avian pathogens were not detected Genomic analyses using polymerase chain reaction and genome sequencing with specimens from New York City birds, infected mosquitoes collected in Connecticut, and human brain tissue from a fatal case of encephalitis, as well as expanded serological testing of specimens from suspected human cases identified WNV as the etiologic agent of this outbreak 4 weeks after the outbreak in humans was first reported to New York City public health officials 21— By the end of the Summer of , 62 patients with serologic evidence of acute WNV infection, including 59 hospitalized patients, had been identified.
Similar to more recent outbreaks of the virus, the epidemic seemed to be associated with a high rate of CNS involvement and a preponderance of cases in patients older than 60 years Although the mechanism of the introduction of the virus into North America remains unknown, it seems clear that the source of the WNV strain detected in New York City originated in the Middle East.
A similar avian epizootic among domestic geese in Israel during and had been attributed to WNV 21 , Human cases of WNV occurred simultaneously in Israel and New York in August of , and when the genomic sequences of WNV isolates or infected human brain tissue from the New York City outbreak were compared to various non-US strains, the greatest homology was found with a WNV strain isolated from a goose from the Israeli epizootic and subsequently with a strain detected in the brain tissue of an Israeli patient who died of West Nile encephalitis in In addition, both the pattern of high avian mortality previously not associated with WNV outbreaks and the severity of human CNS disease seen in New York City and in Israel were similar during the outbreaks.
During the Summer of , 21 cases of human WNV illness occurred among 10 counties in northeastern states The following year, 66 cases were detected among a much more widespread geographic area, involving 38 counties in 10 states. The spread of human cases seemed to follow avian deaths; thus, avian death surveillance and, to a lesser extent, mosquito pool surveillance became important parts of public health efforts to track the virus and predict potential human cases In addition to avian and human illness, a substantial number of equine cases were documented throughout the US, a pattern also being observed in other parts of the world.
Large epizootics, particularly among equines, were noted in Italy in and 28 and in France in However, these outbreaks did not seem to be associated with significant human disease. Human cases appeared to be relegated to Israel, Russia, and the US.
This was the largest outbreak of West Nile meningoencephalitis ever recorded anywhere, and also the largest outbreak of arboviral meningoencephalitis ever documented in the western hemisphere. WNV expanded its geographic range from the Mississippi River area at the conclusion of the season to the Pacific Coast by the end of As of January , the provisional human case count from the season was , including cases of meningoencephalitis and deaths 2.
Particular regions of the US including parts of Louisiana, Mississippi, and the Chicago area, saw particularly high numbers of cases. Severe CNS disease continued to be predominantly seen in older individuals, but more cases of milder febrile illness in younger patients were detected, possibly as a result of enhanced surveillance efforts.
The factors contributing to the magnitude of the epidemic remain unclear, but it is interesting to note that in several areas of the country, climatic and geographic factors during the Spring and Summer of were very similar to those in , when a large epidemic of the related flavivirus, St.
Louis encephalitis virus, occurred in the US The particular factors and an understanding of how they may have contributed to or facilitated these large arboviral outbreaks require further elucidation.
The reason for the increase in frequency and severity of outbreaks of WNV since remains unclear. The movement of the virus into areas with large immunologically naive populations, with an age structure including many elderly and immunocompromised individuals, may account in part for this observation 1 ; however, a more virulent strain of the virus has been suggested as well The future epidemiology of WNV in North America is uncertain, and the historic pattern of the virus provides little guidance as to its potential course in the US.
Whether continued infection among the population will lead to a decline in susceptible avian and human hosts, with a subsequent decline in the number of cases, remains to be seen. Following the large outbreak in , Romania continued to experience cases during following years, although at greatly diminished rates, and seroprevalence rates among avians appeared to remain high Comparison with the epidemiologic patterns of other related flaviviruses may be illustrative: St.
Louis encephalitis tends to occur sporadically in various regions of the US, with the appearance of occasional larger clusters and, rarely, large geographically dispersed epidemics On the other hand, Japanese encephalitis tends to be a hyperendemic disease in areas of Southeast Asia, where symptomatic illness predominates in serologically naive children The fact that WNV illness in the US seems to predominate in adults and the elderly, with children less frequently developing symptomatic illness, may suggest that a substantial immune population will develop over time; however, the future pattern cannot be predicted.
During the period of WNV transmission in North America, arbovirus surveillance capacity has been increased substantially; however, the complex epidemiology of the illness and the difficulties associated with serologic testing for the virus continue to present challenges for surveillance and prevention measures. Efforts to control and reduce vector populations, reinforcement of public health messages of personal protection from mosquitoes, and vigilant surveillance and public awareness campaigns are likely to remain the cornerstones of the public health response to WNV.
Through continued surveillance and further study, it is hoped that the remaining questions regarding the epidemiologic and clinical features of WNV may be answered. Image of the Day Land. EO Explorer. Maps of West Nile Virus Risk. At the time of publication, it represented the best available science. Image of the Day for October 9,
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