In today’s presentation we will cover information regarding the organism that causes West Nile fever and its epidemiology. We will also talk about the history of the disease, how it is transmitted, species that it affects (including humans, if applicable), and clinical and necropsy signs observed. Finally, we will address prevention and control measures for West Nile virus.
West Nile virus (WNV) is a single-stranded RNA virus of the family Flaviviridae, genus Flavivirus . WNV is a member of the Japanese encephalitis virus antigenic complex of arthropod-borne flaviviruses. This complex also includes Saint Louis encephalitis virus (SLE), Japanese encephalitis virus (JE) Kunjin virus, and Murray Valley encephalitis virus. Photo: Electron micrograph of West Nile virus isolated from brain tissue from a crow found in New York. From CDC website.
WNV was first recognized when isolated from a feverish woman in the West Nile District of Uganda in 1937. Since then, WNV has been found in humans, birds, and other vertebrates in Africa, Eastern Europe, West Asia, and the Middle East. Over the last 50 years, there have been several significant outbreaks of WNV. Based on extensive studies done in Egypt in the 1950s, the ecology of the disease was found to vary greatly depending on the prevalence of the disease. At one epidemiological extreme are areas where WNV circulates in most years and uncomplicated WN fever is a mild and common childhood disease that is easily overlooked among many other febrile conditions. Therefore, high prevalence of background immunity is present and increases with age, and WN fever epidemics and WN meningoencephalitis cases are rare. At the other extreme are the industrialized urban areas, where little or no previous WNV activity has occurred. Aging and immunologically naive populations encounter this virus for the first time, and a preponderance of neuroinvasive cases have been observed. Israel also experienced several outbreaks in the 1950s. In 1957, nursing homes in Israel reported severe neurologic disease and death associated with West Nile fever.
There have been many West Nile outbreaks throughout the world. The outbreak in Romania seemed to spark the beginning of several outbreaks worldwide in large industrialized urban areas. WNV was first documented in the western hemisphere in 1999.
West Nile was first discovered in the United States in 1999. There were seven deaths and sixty-two cases (12% case fatality rate) in New York City and surrounding counties. Exotic zoo birds, crows, and horses were also found to be infected. Initially, Saint Louis Encephalitis virus was thought to be the cause of the human infections until WNV was isolated in both zoo animal and human samples. This marked the first of appearance of WNV in the western hemisphere. The U.S. virus is a lineage 1 virus which is antigenically similar to a strain that circulated in Israel from 1997 to 2000.
This map shows the distribution of cases in New York City in 1999. The green dots indicate where WNV positive mosquitoes were found. The red dots indicate cases of WNV in humans, and the large circles show areas where WNV positive birds were found.
This chart depicts the cases of infection by week occurring in New York City in 1999. Most of the cases occurred during the month of August. Mosquito control began the first week of September, and while cases were decreasing in number by that time, the control measures were likely to have helped stop transmission. This chart was taken from MMWR October 22, 1999;48(41):944-946, 955.
There are many speculations concerning the introduction of WNV into the United States. It is not known where the U.S. virus originated, but it is most closely related genetically to strains found in the Middle East. It was made public in 2002 that the CDC sent Iraq samples of WNV in 1980s-90s.
This map depicts the spread of West Nile Virus since its appearance in the United States in 1999. This illustrates WNV activity in birds, horses, mosquitoes, other animals, and humans. Image taken from: www.cdc.gov/ncidod/dvbid/westnile/surv&control.htm#map1
This is the monthly onset distribution of West Nile meningoencephalitis and West Nile fever cases, from 1999-2001. Most cases were reported in the months of July through September. Chart from: Campbell G, Marlin A, Lanciotti R, Gubler D. West Nile Virus. THE LANCET Infectious Diseases 2002;2:519-529.
This chart shows the age distribution of West Nile meningoencephalitis cases, from 1999-2001. The age category with the highest number of cases was ages 70-79, followed by the 60-69 age group. Chart from: Campbell G, Marlin A, Lanciotti R, Gubler D. West Nile Virus. THE LANCET Infectious Diseases 2002;2:519-529.
Since the first detected case in 1999, the number of cases and deaths in humans has increased dramatically almost every year. These are the final numbers for 2003. Source CDC:http://www.cdc.gov/ncidod/dvbid/westnile/surv&controlCaseCount03_detailed.htm.
The states in red are those with human WNV cases; states in yellow (Maine) indicate avian, animal or mosquito infections. These are the final numbers for 2003. Data from CDC website.
This map shows the number of cases by state for human, avian, animal or mosquito infections as of July 6, 2004. Data from CDC website: http://www.cdc.gov/ncidod/dvbid/westnile/surv&control04Maps.htm.
Horses are affected by WNV much more often than any other domestic animals. In 2003, 4,554 horses were diagnosed with WNV. The number of reported cases in canids grew from two in 2002 to 30 in 2003. Seventeen squirrels, one cat and 32 other unidentified animal species were reported WNV positive in 2003. Cases reported as of November 25, 2003.
Distribution of equine cases in 2003. Figure from USDA-APHIS http://www.aphis.usda.gov/vs/nahps/equine/wnv/maps.html.
Distribution of equine cases in 2004 as of June 16, 2004. Figure from USDA-APHIS (http://www.aphis.usda.gov/vs/nahps/equine/wnv/map2004.html)
World distribution of West Nile virus as of early, 2002. As shown by the map, West Nile Virus is present in North America, Africa, parts of Asia, Europe, the Middle East, and Australia. West Nile Virus has since spread across the contiguous United States. Figure from: Campbell G, Marlin A, Lanciotti R, Gubler D. West Nile Virus. THE LANCET Infectious Diseases 2002;2:519-529.
This schematic gives a general representation of the transmission of West Nile Virus. Birds (especially Corvids: ravens, jays, and crows) serve as a reservoir for WNV. Certain female mosquitoes only feed on birds (ornithophilic) and keep the virus transmission in the avian host. Other female mosquitoes act as bridge vectors picking up the virus when they feed on birds and then transmit the virus when they bite other species of animals. At this time it is not believed the level of viremia in humans, horses or other animals is high enough for them to serve as reservoirs making them incidental hosts.
Although it is unknown which species are most responsible for transmission to humans in the U.S., the Culex species are the most important vectors in maintaining the West Nile virus cycle. However, 43 different species of mosquitoes have been found harboring WNV in the US. Many different types of mosquitoes throughout the world have also been found to transmit WNV. WNV has been isolated from ticks in Asia and Russia, but their role in virus transmission is still unclear at this time. Upper photo: Mosquito larvae in water. Lower photo: Female Culex mosquito laying eggs on water in an egg raft formation. Image from CDC website.
This map shows the distribution of Culex pipiens across the United States. Satellites can "track" mosquitoes by focusing on geographical regions of the species’ most favorable conditions. Conventional techniques in mosquito tracking have already produced maps showing these favorable regions. Side by side, recent satellite data matches the published mosquito habitats almost identically. Habitats determined by satellite data are shown in red. Mosquito distribution maps determined by means other than satellite surveillance are outlined in yellow. The four species represented in the next four slides have tested positive for West Nile Virus in each of the past four years. They are: Culex salinarius, Culex pipiens, Culex restuans, and Aedes vexans . Source: NASA at http://www.gsfc.nasa.gov/topstory/20020828phap.html
This map shows the distribution of Culex restuans across the United States. Source: NASA at http://www.gsfc.nasa.gov/topstory/20020828phap.html
This map shows the distribution of Culex salinarius across the United States. Source: NASA at http://www.gsfc.nasa.gov/topstory/20020828phap.html
This map shows the distribution of Aedes vexans across the United States. Source: NASA at http://www.gsfc.nasa.gov/topstory/20020828phap.html
The exact mechanism of the persistence of West Nile Virus in the environment is not exactly known. However, recent studies have demonstrated several possible mechanism which may work in concert to provide the distribution picture seen. The presence of overwintering Culex mosquitoes was found in New York City following the initial discovery of WNV in 1999. A study in India confirmed that transovarial transmission does occur in Culex vishnui mosquitoes in low rates in laboratory settings. Studies completed in birds also indicate that contact transmission between birds may occur and migratory birds may have a large role in transporting West Nile and its vectors to unaffected regions. Photo: Culex quinquefasciatus, mosquito blood-feeding on a human finger, has also been proven to be a vector associated with transmission of the WNV. Image is from the CDC. .
In 2002, the CDC documented WNV in a lab worker as a result of a wound sustained from a scalpel while removing the brain from a blue jay. A second laboratory acquired case was also reported in 2002 by CDC. This case was the result of a needle stick to the finger in a worker harvesting WNV-infected mouse brains. West Nile virus was also found to be present in the blood supply in 2002. Twenty three cases of WNV infection were reported to have been acquired after receiving blood components from 16 WNV-viremic blood donors. This prompted blood collection agencies to begin screening blood donations with WNV nucleic acid-amplification tests. During 2003, 737 donors were found to be presumptive West Nile viremic donors and their donations were subsequently quarantined and discarded. Two cases of confirmed blood transfusion associated WNV were documented in 2003.
In August 2002, 4 patients receiving organ transplants from one organ donor were diagnosed with WNV infection. One transplant recipient subsequently died from the infection. The organ donor had received blood products from 63 blood donors to help combat injuries sustained in an accident. The last blood transfusion received had been from a WNV-viremic blood donor. In October 2002, a women who had suffered from WNV-induced menigioencephalitis during her 27 th week of pregnancy gave birth to an infant suffering from bilateral chorioretinits and severe cerebral abnormalities. The infant was positive for WNV-specific IgM and neutralizing antibodies at the time of birth. However, it is important to note that this case simply demonstrates the possibility of transplacental transmission and not a causal relationship between WNV and congenital abnormalities. In September 2002, a women gave birth to a healthy infant, but required two units of blood following delivery. One of the units was from a WNV-viremic blood donor. She subsequently developed WNV fever twelve days later and was hospitalized. The mother had been breastfeeding her child until the second day of hospitalization. The infant remained healthy, however was WNV-specific IgM positive at 25 days of age. The breast milk was tested for WNV and WNV genetic material was found.
The incubation period for WNV is approximately 3-14 days. Approximately 80% are persons infected with WNV have no signs or symptoms. Approximately 20% of those infected develop a mild illness, termed “West Nile Fever.” Uncomplicated WN fever typically begins with sudden onset of fever (usually >39 o C), headache, and myalgia, often accompanied by gastrointestinal symptoms. The acute illness usually lasts 3-6 days, but prolonged fatigue is common. In earlier epidemics in which WN fever cases predominated—up to half of the patients had a generalized roseolar or maculopapular rash that lasted up to a week and resolved without desquamation. Generalized lymphadenopathy was also common. Rash is typically seen more commonly in children. By contrast, in more recent epidemics in which WN meningoencephalitis cases predominated, no more than 22% of patients had skin rash and less than 5% had lymphadenopathy. The reasons for these apparent differences are unknown.
Approximately 1 in 150 WNV infections will result in severe neurological disease. The more severe disease due is called “West Nile encephalitis,” “West Nile meningitis” or “West Nile meningoencephalitis.” Encephalitis refers to an inflammation of the brain, meningitis is an inflammation of the membrane around the brain and the spinal cord, and meningoencephalitis refers to inflammation of the brain and the membrane surrounding it. The symptoms of these severe infections include headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. Severe neurological disease due to WNV infection has occurred in patients of all ages. Year-round transmission is possible in some areas, therefore WNV should be considered in all persons with unexplained encephalitis and meningitis.
Among those with severe illness due to West Nile virus, case-fatality rates range from 3% to 15% and are highest among the elderly. Overall deaths occur in approximately 1 in 1,000 infections.
In order to diagnose WNV in humans, antibodies must be detected in the serum or cerebral spinal fluid (CSF). The most efficient diagnostic method is using the IgM antibody capture enzyme-linked immunosorbent assay (MAC-ELISA) on serum or cerebral spinal fluid (CSF) collected within 8 days of illness onset Another test is to monitor a rise in antibody titer with the acute-phase sera collected on the first day of illness and convalescent-phase specimens more than 3 weeks later, looking for a four-fold increase. The development of WN virus-specific antibodies between the acute and convalescent phases of illness is strong evidence of infection, and is most often associated with long-term immunity. Since IgM antibody does not cross the blood-brain barrier, IgM antibody in CSF strongly suggests central nervous system infection. Patients who have been recently vaccinated against or recently infected with related flaviviruses (yellow fever, Japanese encephalitis, dengue) may have positive WNV MAC-ELISA results and must be ruled out as possible causes of illness.
The CDC can also perform a plaque reduction neutralization test (PRNT) to differentiate cross-reacting flaviviruses, such as St. Louis encephalitis virus, in order to confirm exposure to WNV. This test is also used when a state finds its initial case of human WNV illness. This test requires growth of the virus and may take a week or longer to conduct. The results from the PRNT are often needed before CDC considers a human WNV infection confirmed. Other laboratory tests exist to confirm WNV infection but are less commonly used. Negative IgM tests of specimens collected less than 14 days after illness should be reconfirmed by tests of a later specimen. IgM antibody may persist for 6 months or longer in blood, and up to 16 months in CSF.
Since WNV is a viral disease, there is no specific treatment other than supportive care. Antivirals have been used in vitro, but none are currently on the market. For example, ribavirin in high doses and interferon alpha-2b were found to have some activity against WNV in vitro, but no controlled studies have been completed on the use of these or other medications, including steroids, anti-seizure drugs, or osmotic agents, in the management of WNV encephalitis. The vaccine manufacture, Acambis, has began Phase 1 of a vaccine clinical trial in 60 healthy human volunteers for a WNV vaccine.
A broad range of mammalian species are susceptible to natural or experimental infection with WN virus. The role, if any, that mammals play in the WN virus transmission cycle is unknown. The (*) indicates animal species that have been reported to show signs of WNV infection. Current as of Nov. 2002. The image is a gray squirrel.
West Nile virus has been detected in dead birds of at least 138 species. Although birds, particularly crows and blue jays, infected with WN virus can die or become ill, most infected birds do survive. The nations first documented cases of domestic canine and squirrel deaths due to WNV occurred in August 2002 in Illinois. The Illinois Department of Natural Resources saw a decrease in the state’s squirrel population and sent animals for testing. It is thought that the number of squirrels in the area may drop temporarily, but that the population should not be decimated. They do not believe that the squirrels develop a viremia so the risk should be relatively low for spread of the virus with the information they had at the time.
A report from Nebraska, in 2002, stated that two bovine sera tested positive for WNV. The first animal was down for 3 weeks, but was still alive at the time of report. The animal was described as thin, experiencing rear limb ataxia, but was still alert and eating. The second animal exhibited ataxia in the hind limbs progressing to paresis. The owners elected euthanasia after 3 weeks of illness, and no further testing was performed. In September of 2002, samples sent to the Lincoln Veterinary Diagnostic Laboratory of the University of Nebraska from a mountain goat and sheep were positive for WNV by Reverse Transcriptase Polymerase Chain Reaction (RT-PCR). The sheep was a 6-year-old Suffolk ewe and was febrile (104 to 106 degrees Fahrenheit) with hind-limb paralysis that progressed to convulsions that died 2 days after the onset of clinical signs. A flock of 12 Rocky Mountain goats that ranged in age from 16 to 24 months had 7 animals show neurological signs and die over a two week period. Clinical signs included horizontal nystagmus, ataxia, head tilt and lateral recumbency. The remaining 5 goats were not affected clinically. Samples from a Suri Alpaca tested positive for WNV by Reverse Transcriptase Polymerase Chain Reaction (RT-PCR). The PCR results were confirmed at the National Veterinary Services Laboratory. The animal exhibited clinical signs for 3.5 days prior to death. Upon necropsy, the alpaca had mild to moderate, diffuse, non-suppurative meningoencephalitis.
Small animals rarely exhibit clinical illness. Case reports of dogs and cats positive with WNV report fever, depression, muscle weakness, spasms, seizures and paralysis. Myocarditis can also be found. A serologic survey conducted in the initial epidemic area of New York showed a low infection rate of dogs and cats. WNV was confirmed by the Illinois Department of Public Health laboratory in Chicago to have caused the deaths of a dog, a wolf and three gray squirrels. The wolf was 3 months old and in a small zoological collection southwest of Chicago. It displayed CNS signs but apparently did not show signs of any other diseases. Again, officials stress that people have a very low risk of contacting the infection from affected animals as mosquitoes are the only proven vector. WNV should be suspected in animals that exhibit neurological and cardiac symptoms.
In a recent study, dogs and cats were experimentally infected with West Nile Virus. Four dogs and four cats were infected by mosquito bite: all four of the dogs showed a viremia of low magnitude and short duration, and did not show clinical symptoms of disease; all four of the cats became viremic, and all but one showed mild, non-neurological signs of disease. During the period of viremia, WNV was not isolated from the saliva of either the infected dogs or cats. In addition, four different cats were exposed to West Nile Virus by consuming an infected mouse: viremia developed in these cats also, but none showed clinical signs of disease. The study showed that dogs and cats can readily be infected with WNV, and that prey animals may serve as an important source of infection. However, neither dogs nor cats would likely serve as amplifying hosts of the disease. Source: Emerging Infectious Diseases, www.cdc.gov/eid Vol. 10, No.1, Jan 2004.
Listed are clinical signs that have been observed in horses with West Nile Virus. It should be suspected in horses exhibiting neurological signs of any sort, especially if they have not been vaccinated. Many horses infected with WNV do not develop any illness, but of horses that become ill, about 40% result in death.
Horses infected by WN virus develop a brief low-level viremia that is rarely, if ever, infectious to mosquitoes. There is no reason to euthanize a horse infected with WNV because the data suggests that most horses recover from the infection. Diagnosis is primarily made by serology, especially if the animal is showing clinical signs. Immunity may last months or longer. Necropsies should be performed using proper biohazard precautions. Treatment would consist of supportive care for clinical signs.
A killed West Nile virus vaccine for horses has been available since August 2001 and became fully licensed in November of 2002. It requires two doses of the vaccine given 3 to 6 weeks apart followed by an annual booster. This product is restricted in use to licensed veterinarians. Clients should be cautioned that effectiveness of the vaccine occurs AFTER the second dose and it is best to set a vaccination schedule to get the second dose into them at least 2 weeks before the mosquito season begins.
All of these methods play important roles in successful mosquito management. Surveillance, source reduction, and personal protection are techniques used by individuals in order to monitor mosquito populations, reduce their numbers, and limit human exposure. Biological control, larvicide, and adulticide control methods are techniques most commonly employed on a large, community-wide basis.
Corvids are especially susceptible to WNV, so many states test dead birds. Sentinel caged chicken flocks are maintained and periodically tested for WNV, as they are good indicators of increased virus activity. Mosquitoes can be tested for WNV and other pathogens, alerting us to emerging diseases. Mosquito species counting programs are also useful surveillance methods. When established mosquito larval and adult threshold populations are exceeded, control activities are initiated. Seasonal records are kept in addition to weather data in order to predict mosquito larval occurrence and adult flights. Public health officials must make the distinction between nuisance complaints or situations that pose a real public health threat with mosquitoes and potential pathogens that they may carry. Image: working with a sentinel chicken flock in Iowa.
Source reduction consists of elimination of larval habitats or rendering of such habitats unsuitable for larval development. Empty standing water in old tires, cemetery urns, buckets, plastic covers, toys, or any other container. The water that stands in old tire piles is the ideal site for mosquito breeding. No matter how a tire sits on the ground it is always capable of collecting rain water. Empty and change the water in bird baths, fountains, wading pools, rain barrels, and potted plant trays at least once a week. Drain or fill temporary pools with dirt. Keep swimming pools treated and circulating, and keep rain gutters unclogged.
Many mosquitoes that carry West Nile Virus need to lay their eggs in a raft on standing water. By emptying containers such as the one pictured, you are doing your part in making the habitat unsuitable for egg laying and thus larval development. Public education is an important component of source reduction. Other forms of source reduction include open marsh water management, in which mosquito-producing areas on the marsh are connected by shallow ditches to deep water habitats to allow drainage or fish access; and rotational impoundment management, in which the marsh is minimally flooded during summer but is flap-gated to reintegrate impoundments to the estuary for the rest of the year.
West Nile Virus infection can be prevented by reducing contact with mosquitoes. Personal protection measures include reducing time outdoors, particularly in early evening hours, wearing long pants and long sleeved shirts, and applying mosquito repellent containing DEET to exposed skin areas. Do not use DEET products on your pets. The concentration of DEET in mosquito products is to high to be safe for cats and dogs. Exposed pets may develop severe neurological problems. Use dog and cat approved mosquito repellant products on pets, but note that not all products labeled for use on dogs can be used on cats (American Veterinary Medical Association website). Make sure window and door screens are intact (bug tight). Replace your outdoor lights with yellow (bug) lights.
Biological control involves using different predators that eat mosquito larvae and pupae. The mosquito fish, Gambusia affinis and G. holbrooki are the most commonly used supplemental control because they are easily reared. They are indiscriminate feeders and may eat other things, such as tadpoles, zooplankton, aquatic insects, and other fish eggs. Some naturally occurring fish such as Fundulus spp., Rivulus spp., and killifish play an important role in controlling mosquitoes in open marsh water and rotational impoundment management. There are other agents such as fungus, protozoa, and nematodes that have been tried but are not readily available. A predacious copepod, Mesocyclops longisetus, preys on mosquito larvae and is a candidate for local rearing with Paramecium spp. for food.
Larvicides are used when immature mosquito populations become larger than source reduction can manage or biological control can handle. They are often more effective and target-specific than adulticides, making them less controversial. They can be applied to smaller geographic areas than adulticides because larvae are often concentrated in specific locations, such as standing water.
This chart depicts the various types of larvicides used in the United States with their chemical or biological name as well as the commercial product name. There may be others on the market that this chart does not cover.
Despite the efforts listed in previous slides, there are times when the environment prevails or humans are unable to prevent large swarms of mosquitoes. Adulticide use then becomes necessary. It is often the least efficient control program but ultra low volume spray either on the ground or aerially can reduce the population when the proper type and time of application is followed. Effective adult mosquito control with adulticides requires small droplets that drift through mosquito areas and come in contact with adults to kill them. Large droplets settle on the ground or vegetation and do not contact mosquitoes and may cause undesirable effects on nontargeted organisms. Insecticides are applied in a concentrated form at very low volumes such as 1 oz (29.6 mL) per acre. Excessive wind and updrafts reduce control, but light wind is necessary for drifting spray droplets.
This chart displays the various types of chemicals used as adulticides, namely the organophosphates, malathion and naled. Natural pyrethrins, fenthion, and synthetic pyrethroids such as permethrin, resmethrin and sumithrin and their product names are also listed.
This is a list of recommendations from Office of Laboratory Security, Canada Health Department for field investigations and handling dead animals and their tissues that may be infected with WNV. Website: www.hc-sc.gc.ca/pphb-dgspsp/ols-bsl/wnvbio_e
Transcript of "West nile"
West Nile Virus
Center for Food Security anOverview• Organism• History• Epidemiology• Transmission• Disease in Humans• Disease in Animals• Prevention and Control
Center for Food Security anHistory• 1937: West Nile District, Uganda• 1950− Egypt Ecology studied Disease varies− Israel 1951-54 1957 Meningoencephalitis in elderly
Center for Food Security anHistory• 1962, 2000: France• 1973-74: South Africa• 1996: Romania− First outbreak inindustrialized urban area• 1998: Italy• 1999− Russia− United States, New York First occurrence in the western hemisphere
Center for Food Security anUnited States - 1999• New York City− 62 cases− 7 deaths− Zoo birds, crows,horses• St. Louis Encephalitisvirus first suspected• Similar to virus strainfound in Israel
Center for Food Security an1999 NYC area - WNV activityMosquitoesMosquitoesBirdsBirdsHumansHumans
Center for Food Security an1999 – NYC WNV Cases
Center for Food Security anPossible Modes of Introductionof West Nile Virus into the U.S.• Infected human host• Human-transported vertebrate host− Legal− Illegal• Human-transported vector(s)• Storm-transported vertebrate host (bird)• Intentional introduction
Center for Food Security anSpread of WNV in the U.S.:1999-2002
Center for Food Security anWNV Monthly Onset: 1999-2001
Center for Food Security anAge distribution of WNV cases:1999-2001
Center for Food Security anWNV in the U.S., HumansYear Cases Deaths1999 62 72000 21 22001 66 92002 4156 2842003 9862 264
Center for Food Security anWNV in the U.S.: 2003
Center for Food Security anWNV in U.S.:as of July 6, 2004
Center for Food Security anWNV Positive Animals, 2003• U.S. Cases− 4,554 equine− 30 dogs− 17 squirrels− 1 cat− 32 unidentifiedanimal species
Center for Food Security anWNV Equine Cases: 2003
Center for Food Security anWNV Equine Cases: 2004
Center for Food Security an2002 WNV World Distribution
Center for Food Security anEcology & Transmission• Infectedmosquitoesoverwinter• Transovarialtransmission• Birds− Contacttransmission− Migratory transport
Center for Food Security anHuman Transmission• Laboratory acquired− Laceration during necropsy on blue jay− Needle stick• Blood transfusions− 23 cases in 2002− Implemented screening in 2003 737 presumptive West Nile viremic donors 2 transfusion associated cases
Center for Food Security anHuman Transmission• Organ transplantation− 4 documented cases from 1 organ donor− Organ donor received blood fromviremic blood donor• Transplacental transmission− WNV 27th week gestation• Breast feeding− Mother received contaminated blood− Infant WNV positive
Center for Food Security anHuman Disease• Incubation: 3-14 days− 80% asymptomatic or mild flu-like illness− 20% develop sudden fever, weakness,headache, myalgia, nausea, vomiting• Symptoms last 3-6 days• Fine maculopapular rash More frequent in children• Recent epidemics: menigoencephalitis
Center for Food Security anHuman Disease• Less than 1% (1:150) infected− Develop severe illness With neurological component− Encephalitis (meningoencephalitis) Fever, confusion, disorientation, seizures,ataxia, tremors, neck stiffness, ± coma− Muscle weakness to flaccid paralysis ofextremities
Center for Food Security anHuman Disease• Severe illness− Case-fatality rate: 3-15%− Highest among elderly Those over 50 yrs at greatest risk• Overall death rate: 0.1%− 1:1,000 infections
Center for Food Security anDiagnosis in Humans• Antibody detection− Serum or CSF− IgM capture ELISA (MAC-ELISA) Within 8 days− Fourfold or greater rise in titer Acute/convalescent – 3 weeks apart Strong evidence of infection− IgM in CSF strongly suggestsCNS infection− Cross reaction to other viruses
Center for Food Security anDiagnosis in Humans• Plaque reduction neutralization test− To differentiate cross-reaction− CDC test for state’s initial case− Negative tests Collected within 14 days of illness Reconfirm• Duration of immunity− Unknown− IgM may last 6 months or more in blood− Up to 16 months in CSF
Center for Food Security anTreatment in Humans• No specific therapy• Supportive care• Ribavirin?• Interferon alpha-2b?• Vaccine in Phase 1 of clinical trial
Center for Food Security anWNV in AnimalsHorses (*) Black Bear BatsGoats (*) Wolf (*) Llama (*)Sheep (*) Alpaca (*) Cattle (*)Dog (*) Mountain Goat Seal (*)Rabbit Alligator (*) Cat (*)Chipmunk Gray Squirrels (*) DeerSkunkCrocodile (*)
Center for Food Security anClinical Signs in Wildlife• Birds− Commonly found dead (Corvids esp.)• Bats, chipmunks, skunks, anddomestic rabbits− Majority do not develop clinical signs• Gray Squirrels− Lethargy, biting paws,vocalization, ataxia, circling,encephalitis, myocarditis
Center for Food Security anClinical Signs in Large Animals• Bovine− Ataxia progressing to paresis• Alpaca, Sheep, Goats− Fever, horizontal nystagmus,torticollis, ataxia, recumbency− Vocalization− The alpaca had mild to moderate,diffuse, non-suppurativemeningoencephalitis
Center for Food Security anClinical Signs in Small Animals• Dogs and Cats• Rarely exhibit clinical illness• Fever, depression• Muscle weakness, spasms• Seizures, paralysis, myocarditis• Wolf- 1 case− 3 months old, zoo animal, CNS signs• Suspect WNV in animals exhibitingneurological and cardiac symptoms
Center for Food Security anClinical Signs in Small Animals• Dogs and cats experimentally infected− Mosquito bite: dogs All dogs showed viremia, no clinical signs− Mosquito bite: cats All cats showed viremia All but one showed mild clinical signs− Infected prey: cats All cats developed viremia None showed clinical signs• Conclusion: readily infected, but notamplifying hosts
Center for Food Security anClinical Signs in Horses• Paralysis of lips,facial muscles, ortongue• Head tilt, difficultyswallowing• Altered mentation• Sound sensitive• Blindness• Troubling righting• Drowsiness• Flu-like, anorexia,depression• Muscle and skintwitching• Hyperesthesia• Propulsive walking• Weakness, ataxia,recumbency• Seizures
Center for Food Security anDiagnosis and Treatmentin Horses• Diagnosis− Serology Seropositive & unvaccinated= WNV infection• Immunity− Many months or longer• Perform necropsies with properprecautions• Supportive treatment
Center for Food Security anWNV Vaccine for Horses• Fully licensed vaccine−November 2002−Killed product−2 doses 3-6 weeks apart−Annual booster−Restricted useto veterinarians only
Center for Food Security anMosquito Management• Surveillance• Source reduction• Personal protection• Biological control• Larvicide• Adulticide
Center for Food Security anSurveillance• Dead bird testing• Sentinel chicken flocks• Mosquito collection− Test for pathogens− Account for species• Larval and adult mosquitoes− Map habitats− Record keeping• Determining nuisance vs. vectors
Center for Food Security anSource Reduction• Eliminating larval habitats− Tires, bird baths, containers, raingutters, unused swimming pools
Center for Food Security anSource Reduction• Making habitatsunsuitable for larvaldevelopment• Public education• Marsh watermanagement− Drain, fish access,gated
Center for Food Security anPersonal Protection• Reduce time outdoors− Especially evening hours• Wear long pants and sleeves• Use mosquito repellent− 35% DEET• Do not use DEET onyour animals• Make sure all window screens are intact• Use yellow “bug” light bulbs in outdoorlight fixtures
Center for Food Security anBiological Control• Utilizes predators, both natural andintroduced, to eat larvae and pupae− Mosquito fish Gambusia affinis, G. holbrooki most common Fundulus spp., Rivulus spp., killifish• Other agents have been used but arenot readily available− Fungus, protozoa, nematodes• Copepods
Center for Food Security anLarvicides• Use when source reduction andbiological control not feasible• More effective and target-specific• Less controversial than adulticides• Applied to smaller geographic areas− Larvae concentrate in specific locations
Center for Food Security anLarvicidesProductNameProduct(Larvae, Pupae, Adult)Temephos Abate (L)Methoprene Altosid (L)Oils BVA, Golden Bear (L, P)Monomolecular film Agnique (L, P)Bacillusthuringiensisisraelensis (BTI)Aquabac, Bactimos,LarvX, Teknar, Dunks (L)Bacillus sphaericus VectoLex (L)Pyrethrins Pyrenone, Pyronyl (A, L)
Center for Food Security anAdulticides• When other controlmeasures unsuccessful• Least efficient• Proper type and time ofapplication helps efficacy− Ultra Low Volume foggers 1 ounce per acre− Small droplets contact andkill adults
Center for Food Security anAdulticidesChemicalNameProductMalathion Fyfanon, Atrapa,PrentoxNaled Dibrom, TrumpetFenthion BatexPermethrin Permanone,AquaResilin, Biomist,Mosquito BeaterResmethrin ScourgeSumithrin Anvil
Center for Food Security anBiosafety• Mosquito avoidance precautions− Bug spray, long sleeves, etc• Wear gloves or double plastic bags tocollect dead birds• Wash hands after handling• Manipulate carcasses in biosafetycabinet when possible for necropsy
Center for Food Security anAcknowledgmentsDevelopment of thispresentation was fundedby a grant from theCenters for Disease Controland Prevention to theCenter for Food Securityand Public Health at IowaState University.
Center for Food Security anAcknowledgmentsAuthor:Co-authors:Reviewer:Radford Davis, DVM, MPHAnn Peters, DVM, MPHStacy Holzbauer, DVMJean Gladon, BS
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