Westward Ho? — The Spread of West Nile Virus
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《新英格兰医药杂志》
West Nile virus, a mosquito-borne flavivirus, was first isolated from a febrile patient in the West Nile region of Uganda in 1937. For the next 60 years, it remained a little-understood cause of febrile illness and sporadic encephalitis in parts of Africa, Europe, and Asia, garnering scant medical attention. After its surprising detection in New York City in 1999, West Nile virus became a major clinical and public health concern in North America. The next year, the Centers for Disease Control and Prevention collaborated with state and local health departments to establish ArboNet, an electronic surveillance system for tracking West Nile virus infections in humans, mosquitoes, birds, and other animals in the United States. Data from ArboNet have documented the dramatic westward spread of West Nile virus across North America (see maps).
Spread of West Nile Virus in Birds, Horses, Mosquitoes, Other Animals, and Humans in the United States, 1999–2004.
The incidence of human neuroinvasive disease (meningitis, encephalitis, and acute flaccid paralysis) is indicated according to county. Data for 2004 are reported cases as of October 15.
As of October 15, 2004, ArboNet had received reports of West Nile virus infection in 58 mosquito species and 284 bird species and had recorded 6690 cases of neuroinvasive West Nile virus disease (meningitis, encephalitis, or acute flaccid paralysis) among persons in the United States. Results from serologic surveys indicate that symptoms develop in approximately 20 percent of persons with West Nile virus and that neuroinvasive disease occurs in 1 in 140. Given these proportions, it would seem that approximately 940,000 persons have been infected with West Nile virus in the United States, and 190,000 of them have become ill. The risk of neuroinvasive disease increases with age and appears to be substantially higher among organ-transplant recipients than in the general population. ArboNet has also recorded 629 deaths due to West Nile virus, and clinical-outcome studies suggest that many survivors of neuroinvasive disease have long-term disability.
Nearly all infections result from mosquito bites; however, transmission through transplanted organs and transfused blood, transplacental transmission, and occupational transmission by means of percutaneous exposure have occurred, and there has probably been transmission through breast milk. Prospective evaluations to determine the risk of congenital West Nile virus infection are under way. Screening of the U.S. blood supply was initiated in 2003, and it has substantially reduced the risk of transmission through transfusion. To date, 1006 viremic donors have been identified through such screening and reported to ArboNet (818 in 2003 and 188 in 2004). However, blood donors with very low levels of viremia may still escape detection, and vigilance for West Nile virus infections due to transfusion and organ transplantation must continue.
In 2004, only 741 cases of neuroinvasive disease due to West Nile virus infection had been reported through October 15, as compared with 2866 in all of 2003 and 2946 in 2002. Although one third of the cases of neuroinvasive disease reported in 2004 occurred in Arizona and California, the risk of West Nile virus disease remains sporadically distributed throughout the country. The annual recurrence of West Nile virus activity suggests that transmission will continue during the coming years.
Future patterns of transmission are hard to predict. The epidemiology of St. Louis encephalitis virus, a closely related arbovirus, might lend some insight. Each year since 1932, between 0 and 1967 cases of St. Louis encephalitis (median, 26), occurring either sporadically or in focal or regional epidemics, have been reported in the United States. However, West Nile virus produces higher levels of viremia in birds than St. Louis encephalitis virus, infects more mosquito species, and is more likely to cause symptoms, making a higher incidence of disease likely. Herd immunity in humans will have a minimal effect on the incidence of disease, because even in areas of the United States that have had epidemics of West Nile virus, studies have shown that less than 5 percent of the population has been exposed to the virus and developed protective antibody. For reasons that are unclear, the spread of West Nile virus into Latin America and the Caribbean has resulted in surprisingly scarce reports of human disease, despite conditions that should favor the transmission of mosquito-borne arboviruses.
The risk of neuroinvasive disease due to West Nile virus is relatively low, and the foci of highest incidence are likely to shift with ecologic variations. This variability complicates prospective clinical studies and could encumber vaccine efficacy trials. Research efforts to identify new treatment strategies for West Nile virus may need to seek enrollment of patients in smaller community-based hospitals and ambulatory care centers and should be flexible enough to adapt to emerging outbreaks. Over the coming years, mosquito-control and other prevention programs should be designed and funded to prevent sporadic outbreaks, with the understanding that the risk of West Nile virus disease is likely to vary considerably over time and place.
Source Information
From the Centers for Disease Control and Prevention, Fort Collins, Colo.(Lyle R. Petersen, M.D., M)
Spread of West Nile Virus in Birds, Horses, Mosquitoes, Other Animals, and Humans in the United States, 1999–2004.
The incidence of human neuroinvasive disease (meningitis, encephalitis, and acute flaccid paralysis) is indicated according to county. Data for 2004 are reported cases as of October 15.
As of October 15, 2004, ArboNet had received reports of West Nile virus infection in 58 mosquito species and 284 bird species and had recorded 6690 cases of neuroinvasive West Nile virus disease (meningitis, encephalitis, or acute flaccid paralysis) among persons in the United States. Results from serologic surveys indicate that symptoms develop in approximately 20 percent of persons with West Nile virus and that neuroinvasive disease occurs in 1 in 140. Given these proportions, it would seem that approximately 940,000 persons have been infected with West Nile virus in the United States, and 190,000 of them have become ill. The risk of neuroinvasive disease increases with age and appears to be substantially higher among organ-transplant recipients than in the general population. ArboNet has also recorded 629 deaths due to West Nile virus, and clinical-outcome studies suggest that many survivors of neuroinvasive disease have long-term disability.
Nearly all infections result from mosquito bites; however, transmission through transplanted organs and transfused blood, transplacental transmission, and occupational transmission by means of percutaneous exposure have occurred, and there has probably been transmission through breast milk. Prospective evaluations to determine the risk of congenital West Nile virus infection are under way. Screening of the U.S. blood supply was initiated in 2003, and it has substantially reduced the risk of transmission through transfusion. To date, 1006 viremic donors have been identified through such screening and reported to ArboNet (818 in 2003 and 188 in 2004). However, blood donors with very low levels of viremia may still escape detection, and vigilance for West Nile virus infections due to transfusion and organ transplantation must continue.
In 2004, only 741 cases of neuroinvasive disease due to West Nile virus infection had been reported through October 15, as compared with 2866 in all of 2003 and 2946 in 2002. Although one third of the cases of neuroinvasive disease reported in 2004 occurred in Arizona and California, the risk of West Nile virus disease remains sporadically distributed throughout the country. The annual recurrence of West Nile virus activity suggests that transmission will continue during the coming years.
Future patterns of transmission are hard to predict. The epidemiology of St. Louis encephalitis virus, a closely related arbovirus, might lend some insight. Each year since 1932, between 0 and 1967 cases of St. Louis encephalitis (median, 26), occurring either sporadically or in focal or regional epidemics, have been reported in the United States. However, West Nile virus produces higher levels of viremia in birds than St. Louis encephalitis virus, infects more mosquito species, and is more likely to cause symptoms, making a higher incidence of disease likely. Herd immunity in humans will have a minimal effect on the incidence of disease, because even in areas of the United States that have had epidemics of West Nile virus, studies have shown that less than 5 percent of the population has been exposed to the virus and developed protective antibody. For reasons that are unclear, the spread of West Nile virus into Latin America and the Caribbean has resulted in surprisingly scarce reports of human disease, despite conditions that should favor the transmission of mosquito-borne arboviruses.
The risk of neuroinvasive disease due to West Nile virus is relatively low, and the foci of highest incidence are likely to shift with ecologic variations. This variability complicates prospective clinical studies and could encumber vaccine efficacy trials. Research efforts to identify new treatment strategies for West Nile virus may need to seek enrollment of patients in smaller community-based hospitals and ambulatory care centers and should be flexible enough to adapt to emerging outbreaks. Over the coming years, mosquito-control and other prevention programs should be designed and funded to prevent sporadic outbreaks, with the understanding that the risk of West Nile virus disease is likely to vary considerably over time and place.
Source Information
From the Centers for Disease Control and Prevention, Fort Collins, Colo.(Lyle R. Petersen, M.D., M)