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      Increase in West Nile Neuroinvasive Disease after Hurricane Katrina

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          Abstract

          After Hurricane Katrina, the number of reported cases of West Nile neuroinvasive disease (WNND) sharply increased in the hurricane-affected regions of Louisiana and Mississippi. In 2006, a >2-fold increase in WNND incidence was observed in the hurricane-affected areas than in previous years.

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          Epidemiology and Transmission Dynamics of West Nile Virus Disease

          West Nile virus (WNV) was first detected in the Western Hemisphere in 1999 during an outbreak of encephalitis in New York City. Over the next 5 years, the virus spread across the continental United States as well as north into Canada, and southward into the Caribbean Islands and Latin America (1). This article highlights new information about the epidemiology and transmission dynamics of human WNV disease obtained over the past 5 years of intensified research. Epidemiology WNV is transmitted primarily by the bite of infected mosquitoes that acquire the virus by feeding on infected birds. The intensity of transmission to humans is dependent on abundance and feeding patterns of infected mosquitoes and on local ecology and behavior that influence human exposure to mosquitoes. Although up to 55% of affected populations became infected during epidemics in Africa, more recent outbreaks in Europe and North America have yielded much lower attack rates (1,2). In the area of most intense WNV transmission in Queens, New York, in 1999, ≈2.6% of residents were infected (most of these were asymptomatic infections), and similarly low prevalence of infection has been seen in other areas of the United States (3,4). WNV outbreaks in Europe and the Middle East since 1995 appear to have caused infection in 1,000 potentially WNV-viremic blood donations were identified, and the corresponding blood components were sequestered. Nevertheless, 6 WNV cases due to transfusion were documented in 2003, and at least 1 was documented in 2004, indicating that infectious blood components with low concentrations of WNV may escape current screening tests (19). One instance of possible WNV transmission through dialysis has been reported (20). WNV transmission through organ transplantation was also first described during the 2002 epidemic (15). Chronically immunosuppressed organ transplant patients appear to have an increased risk for severe WNV disease, even after mosquito-acquired infection (16). During 2002, the estimated risk of neuroinvasive WNV disease in solid organ transplant patients in Toronto, Canada, was approximately 40 times greater than in the general population (16). Whether other immunosuppressed or immunocompromised patients are at increased risk for severe WNV disease is uncertain, but severe WNV disease has been described among immunocompromised patients. WNV infection has been occupationally acquired by laboratory workers through percutaneous inoculation and possibly through aerosol exposure (21,22). An outbreak of WNV disease among turkey handlers at a turkey farm raised the possibility of aerosol exposure (17). Dynamics of Transmission: Vectors WNV is transmitted primarily by Culex mosquitoes, but other genera may also be vectors (23). In Europe and Africa, the principal vectors are Cx. pipiens, Cx. univittatus, and Cx. antennatus, and in India, species of the Cx. vishnui complex (6,24). In Australia, Kunjin virus is transmitted primarily by Cx. annulirostris (11). In North America, WNV has been found in 59 different mosquito species with diverse ecology and behavior; however, 40%. Field studies during and after WNV outbreaks in several areas of the United States have confirmed that house sparrows were abundant and frequently infected with WNV, characteristics that would allow them to serve as important amplifying hosts (23,25,37). The importance of birds in dispersing WNV remains speculative. Local movements of resident, nonmigratory birds and long-range travel of migratory birds may both contribute to the spread of WNV (38,39). Although WNV was isolated from rodents in Nigeria and a bat in India, most mammals do not appear to generate viremia levels of sufficient titer to contribute to transmission (24,40–42). Three reptilian and 1 amphibian species (red-ear slider, garter snake, green iguana, and North American bullfrog) were found to be incompetent as amplifying hosts of a North American WNV strain, and no signs of illness developed in these animals (43). Viremia levels of sufficient titer to infect mosquitoes were found after experimental infection of young alligators (Alligator mississippiensis) (44). In Russia, the lake frog (Rana ridibunda) appears to be a competent reservoir (45). Nonmosquitoborne WNV transmission has been observed or strongly suspected among farmed alligators, domestic turkeys in Wisconsin, and domestic geese in Canada (17,46,47). Transmission through close contact has been confirmed in both birds and alligators in laboratory conditions but has yet to be documented in wild vertebrate populations (23,36,44). Control of WNV Transmission Avoiding human exposure to WNV-infected mosquitoes remains the cornerstone for preventing WNV disease. Source reduction, application of larvicides, and targeted spraying of pesticides to kill adult mosquitoes can reduce the abundance of mosquitoes, but demonstrating their impact on the incidence of human WNV disease is challenging because of the difficulty in accounting for all determinants of mosquito abundance and human exposure. One study indicated that clustering of human WNV disease in Chicago varied between mosquito abatement districts, suggesting that mosquito control may have some impact on transmission to humans (14). Persons in WNV-endemic areas should wear insect repellent on skin and clothes when exposed to mosquitoes and avoid being outdoors during dusk to dawn when mosquito vectors of WNV are abundant. Of insect repellents recommended for use on skin, those containing N,N-diethyl-m-toluamide (DEET), picaridin (KBR-3023), or oil of lemon eucalyptus (p-menthane-3,8 diol) provide long-lasting protection (48). Both DEET and permethrin provide effective protection against mosquitoes when applied to clothing. Persons' willingness to use DEET as a repellent appears to be influenced primarily by their level of concern about being bitten by mosquitoes and by their concern that DEET may be harmful to health, despite its good safety record (49). To prevent transmission of WNV through blood transfusion, blood donations in WNV-endemic areas should be screened by using nucleic acid amplification tests. Screening of organ donors for WNV infection has not been universally implemented because of concern about rejecting essential organs after false-positive screening results (50). Pregnant women should avoid exposure to mosquito bites to reduce the risk for intrauterine WNV transmission. Future Directions WNV disease will likely continue to be a public health concern for the foreseeable future; the virus has become established in a broad range of ecologic settings and is transmitted by a relatively large number of mosquito species. WNV will also likely continue to spread into Central and South America, but the public health implications of this spread remain uncertain. Observations thus far in North America indicate that circulation of other flaviviruses, such as dengue, viral mutation, and differing ecologic conditions may yield different clinical manifestations and transmission dynamics. Over the next few years, research efforts might well be focused in several areas. Research into new methods to reduce human exposure to mosquitoes is crucial and can help prevent other mosquitoborne illnesses. This should include development of new methods to reduce mosquito abundance, development of new repellents, and behavioral research to enhance the use of existing effective repellents and other personal protective measures against mosquito bites. A better understanding of the dynamics of nonmosquitoborne transmission is essential to prevent disease among infants of infected mothers and recipients of blood transfusions and transplanted organs. Currently available prevention strategies such as the dissemination of knowledge and products for personal protection from mosquito exposure and the application of existing techniques for reducing mosquito abundance in communities at risk of WNV transmission need to be vigorously implemented. National and international surveillance for WNV transmission will be important to monitor spread of the virus and the effect of control strategies. Finally, further research into the ecologic determinants of WNV transmission, including climatic factors and dynamics of reservoir and vector populations, could help in determining geographic areas of higher risk for WNV disease.
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            Effect of Hurricane Katrina on Arboviral Disease Transmission

            To the Editor: Rarely has the aftermath of a natural disaster in the continental United States resulted in increased transmission of mosquitoborne viruses (1). However, on August 29, 2005, Hurricane Katrina struck Louisiana and Mississippi, where mosquito-borne West Nile (WNV) and St. Louis encephalitis viruses are endemic. Using data from the ArboNET system of the Centers for Disease Control and Prevention, we evaluated the short-term effects of Hurricane Katrina on the reported incidence of human West Nile neuroinvasive disease (WNND) and Saint Louis encephalitis (SLE) in Louisiana and Mississippi using the reported week of onset and the year (2003–2005). We also evaluated incidence by onset date and county (or parish) over 3 time intervals (January 1–August 31, September 1–September 30, and October 1–October 30) in 2005. Reporting lag was evaluated by onset dates and corresponding dates of reports. Because the completeness of reporting of West Nile fever and other arboviral fever cases is highly variable, only reports of human WNND and SLE were considered. In Louisiana, the highest reported incidence of WNND occurred in the second week of August 2005, before Hurricane Katrina made landfall. Although the number of cases reported in 2005 (117) was higher than in 2003 (85) or 2004 (101), the number of cases peaked during roughly the same weeks in each year. In Mississippi, the total number of cases reported in 2005 (39) was only slightly higher than in previous years (31 in 2004 and 34 in 2003). The number of cases peaked in mid-September 2005, later than the peak in 2004, but similar to when a second peak occurred in 2003. Thus, the increase in WNND incidence for either state does not appear to be hurricane-related. In Louisiana, 82 WNND cases in 20 parishes had onset between January 1, 2005 and August 31, 2005. In comparison, 25 WNND cases had onset between September 1, 2005 and September 30, 2005; a total of 14 of these cases in 7 parishes had not reported WNND cases previously in 2005; a total of 5 of these parishes had detected WNV activity in animals before the hurricane. From October 1, 2005 to October 31, 2005, a total of 10 additional WNND cases were reported in Louisiana, including 1 case from a parish that had not previously reported cases. Only 5 cases with illness onset after the hurricane resided in coastal parishes. In Mississippi, 17 WNND cases in 10 counties had onset between January 1, 2005 and August 31, 2005. Twenty cases had onset between September 1, 2005 and September 30, 2005, including 9 cases in 4 counties that had not reported WNND cases previously in 2005; a total of 2 of these counties had detected WNV activity in animals before the hurricane. From October 1, 2005 to October 31, 2005 2 more WNND cases were reported in Mississippi, including 1 from a county that had not reported cases previously. All cases with illness onset after the hurricane resided in inland counties. Thus, in both states the coastal counties and parishes that were hardest hit by the hurricane had the fewest number of posthurricane WNND cases. In 2005, Louisiana reported 2 SLE cases and Mississippi reported 5. Both Louisiana cases and 4 of the Mississippi cases had onset of illness after September 1. In 2004, no SLE cases had been reported by either of these states. In 2003, a total of 9 cases were reported in Louisiana (3 with onset in September) and 2 in Mississippi (with onsets in May and June). Thus, Hurricane Katrina did not appear to increase SLE incidence in Louisiana, and if it did increase incidence in Mississippi, the increase was minimal. In both 2003 and 2004, Louisiana’s median reporting time to ArboNET was ≈30 days. In 2005, the median reporting time prehurricane was 36 days and posthurricane was 69 days. Louisiana state officials believed that this reporting lag was largely due to impaired transport and collection of biologic samples and relocation of diagnostic facilities immediately following the hurricane. In contrast, in 2003 and 2004, Mississippi’s median reporting time to ArboNET was 21 days and 36 days, respectively. In 2005, the median reporting time prehurricane was 23 days and posthurricane was 14 days. Mississippi state officials believed that the improved reporting time was due to the additional help and longer hours worked by health department officials following the hurricane. Although Hurricane Katrina disrupted WNV surveillance in Louisiana, it did not appear to increase the incidence of WNND and SLE in either Louisiana or Mississippi. In coastal areas, the hurricane destroyed housing and impeded vector control, thus possibly increasing the risk of mosquito-borne infections ( 1 , 2 ). However, hurricane-force winds and heavy flooding might have actually decreased the risk of WNV and SLE transmission by dispersing or killing birds and mosquitoes, and destroying their habitat. Many people were promptly evacuated to less affected areas, where, on the basis of previous years’ data showing seasonality of WNV transmission, the risk of infection was probably decreasing. Natural disasters do not usually cause an immediate increase in arboviral diseases ( 1 , 2 ). However, if hurricanes strike early in transmission season, there could be a late increase in risk after vector and host populations are re-established. In addition, risk could increase when people are relocated to areas where transmission is intense.
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              Author and article information

              Journal
              Emerg Infect Dis
              EID
              Emerging Infectious Diseases
              Centers for Disease Control and Prevention
              1080-6040
              1080-6059
              May 2008
              : 14
              : 5
              : 804-807
              Affiliations
              [* ]Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, USA
              Author notes
              Address for correspondence: Kevin A. Caillouët, Department of Tropical Medicine, Tulane University School of Public Health and Tropical Medicine, 1430 Tulane Ave, SL-17, New Orleans, LA 70112, USA; email: kcaillou@ 123456tulane.edu
              Article
              07-1066
              10.3201/eid1405.071066
              2600257
              18439367
              ae5de3c3-97e7-47f4-801c-209cfb2a65bd
              History
              Categories
              Dispatch

              Infectious disease & Microbiology
              natural disasters,dispatch,hurricane katrina,arbovirus,west nile virus,encephalitis,neuroinvasive disease

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