Since its introduction to the United States in 1999, West Nile virus has become the major vector-borne disease in the U.S., with 770 reported deaths, 20,000 reported illnesses, and perhaps around a million people infected. The virus is transmitted by Culex mosquitoes (the "vector") and cycles between birds that the mosquitoes feed on. Humans can also be infected with the virus when bitten by these mosquitoes.
Scientists have struggled to explain these large outbreaks in the U.S., which stand in stark contrast to the sporadic European infections. In a new study published in the open access journal PLoS Biology, Drs. Marm Kilpatrick, Peter Daszak, and colleagues now present evidence that the major vector of West Nile virus in the USA, Culex pipiens mosquitoes, change their feeding behavior in the fall from their preferred host, American robins, to humans, resulting in large scale outbreaks of disease.
These feeding shifts appear to be a "continent-wide phenomenon," the researchers conclude, and may explain why West Nile virus outbreaks are so intense in the U.S. compared to Europe and Africa, where the virus originates.
From May through September 2005,Dr. Kilpatrick, senior research scientist with the Consortium for Conservation Medicine, and his team collected mosquitoes and caught birds at six sites in Maryland and Washington, D.C. They determined the changes in mosquito populations throughout the West Nile virus transmission season, the abundance and diversity of bird species at these sites, and tested samples for West Nile virus.
Dr. Kilpatrick says, "To find out which species mosquitoes favored as hosts, we collected thousands of Culex pipiens mosquitoes and selected those that had just fed and still had bloodmeals in them. We sequenced the DNA in the bloodmeal to identify the species of host they had fed on."
Their findings showed that from May to June, the American robin, which represented just 4.5% bird population at their sites, accounted for more than half of Culex pipiens' meals. As the summer wore on and robins left their breeding grounds, the probability that humans were fed on increased sevenfold. Because the overall number of birds increased during this time, Kilpatrick and his team concluded that mosquitoes changed to humans as a result of robin dispersal, rather than a lack of avian hosts. "This feeding shift happened, even though the total number of birds at our site increased as other species' offspring joined the population," said Kilpatrick.
With the data collected from the Washington, D.C., area, the researchers presented a model of the risks of infection of the West Nile virus in humans. The model predicted that the risk of human infection peaked in late July to mid-August, declined toward the end of August, and then rose slightly at the end of September. The actual human cases in the area that year, the authors point out, "showed a strikingly similar pattern." This same pattern was seen in California and Colorado, with numbers of infected Culex tarsalis mosquitoes (the main vectors in the western USA) peaking in June and July, followed by a late-summer spike in human infections, suggesting a continent-wide phenomenon.
Dr. Peter Daszak, Executive Director of the Consortium for Conservation Medicine, comments: "This is a case study in how to understand emerging diseases. Our collaborative team includes ecologists, virologists, and entomologists, and uses state-of-the-art techniques, including DNA sequencing of mosquito blood meals, to piece together what drives a virus to cause outbreaks in people. At the CCM we study the ecology of diseases and develop predictive models that can help us prevent future outbreaks. We are now using this approach to help understand the emergence and spread of other viruses such as SARS, Nipah virus and avian influenza."
The study is funded by the National Institute of Allergy and Infectious Disease.
Citation: Kilpatrick AM, Kramer LD, Jones MJ, Marra PP, Daszak P (2006) West Nile virus epidemics in North America are driven by shifts in mosquito feeding behavior. PLoS Biol 4(4): e82.
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